Siddha cure for Jaundice
Jaundice
Definition And Explanation
Jaundice (also known as icterus; from the Greek word icteric) is a yellowish
pigmentation of the skin, the conjunctival membranes over the sclerae (whites of
the eyes), and other mucous membranes caused by hyperbilirubinemia (increased
levels of bilirubin in the blood).
The term jaundice also have an origin from the French word jaune, meaning
yellow.
People with jaundice have a problem with their liver, which stops it from removing
dead red blood cells properly.
These blood cells contain a chemical called bilirubin. The yellow colour of the skin
and mucous membranes happens because of an increase in the bile pigment,
bilirubin, in the blood.
This hyperbilirubinemia subsequently causes increased levels of bilirubin in the
extracellular fluid.
Concentration of bilirubin in blood plasma does not normally exceed 1 mg/dL
(>17µmol/L).
A concentration higher than 1.8 mg/dL (>30µmol/L) leads to jaundice.
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Jaundice is often seen in liver disease such as hepatitis or liver cancer.
It may also indicate leptospirosis or obstruction of the biliary tract, for example by
gallstones or pancreatic cancer, or less commonly be congenital in origin.
Yellow discoloration of the skin, especially on the palms and the soles, but not of
the sclera and mucous membranes (i.e. oral cavity) is due to carotenemia—a
harmless condition important to differentiate from jaundice.
Jaundice can also be caused by other diseases, like malaria, hepatitis, or gallstones.
Jaundice is the most common of all liver problems.
The bile, made by the liver, is a vital digestive fluid needed for proper nutrition. It
also stops decaying changes in food.
If the bile is stopped from entering the intestines there is an increase in gases and
other products.
Types of Jaundice
There are three types of jaundice:
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Haemolytic jaundice {Pre-hepatic} - caused by destruction of red blood
cells. This causes increased bilirubin formation and anaemia
Obstructive jaundice{Post-hepatic} - caused by a blockage in the pathway
where bilirubin is made in the liver cells and where bile goes into the
duodenum
Hepatocellular jaundice{Hepatic} - caused by damage to liver cells. The
damage could be from a viral infection or toxic drugs.
Pathology of the different types of jaundice
When a pathological process interferes with the normal functioning of the
metabolism and excretion of bilirubin just described, jaundice may be the result.
Jaundice is classified into three categories, depending on which part of the
physiological mechanism the pathology affects.
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The three categories are:
Category
Definition
Pre-hepatic/ hemolytic The pathology is occurring prior to the liver.
Hepatic/
hepatocellular
The pathology is located within the liver.
Post-Hepatic/
cholestatic
The pathology is located after the conjugation of bilirubin
in the liver.
Pre-hepatic
Pre-hepatic jaundice is caused by anything which causes an increased rate of
hemolysis (breakdown of red blood cells).
In tropical countries, malaria can cause jaundice in this manner.
Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia and
glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis
and therefore hemolytic jaundice.
Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also
lead to coloration.
Defects in bilirubin metabolism also present as jaundice, as in Gilbert's syndrome
(a genetic disorder of bilirubin metabolism which can result in mild jaundice,
which is found in about 5% of the population) and Crigler-Najjar syndrome.
In jaundice secondary to hemolysis, the increased production of bilirubin, leads to
the increased production of urine-urobilinogen.
Bilirubin is not usually found in the urine because unconjugated bilirubin is not
water-soluble, so, the combination of increased urine-urobilinogen with no
bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.
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Laboratory findings include:
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Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia
causes increased heme metabolism; exception: infants where gut flora has
not developed).
Serum: increased unconjugated bilirubin.
Kernicterus is associated with increased unconjugated bilirubin, neonates
are especially vulnerable to this.
Hepatocellular
Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis,
hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease.
Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading
to a buildup of unconjugated bilirubin in the blood.
Other causes include primary biliary cirrhosis leading to an increase in plasma
conjugated bilirubin because there is impairment of excretion of conjugated
bilirubin into the bile.
The blood contains abnormally raised amount of conjugated bilirubin and bile salts
which are excreted in the urine.
Jaundice seen in the newborn, known as neonatal jaundice, is common in
newborns as hepatic machinery for the conjugation and excretion of bilirubin does
not fully mature until approximately two weeks of age.
Rat fever (leptospirosis) can also cause hepatic jaundice.
In hepatic jaundice, there is invariably cholestasis.
Laboratory findings depend on the cause of jaundice.
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Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable
(except in children). Kernicterus is a condition not associated with increased
conjugated bilirubin.
Plasma protein show characteristic changes.
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
Plasma albumin level is low but plasma globulins are raised due to an
increased formation of antibodies.
Bilirubin transport across the hepatocyte may be impaired at any point between the
uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin
into biliary canaliculi.
In addition, swelling of cells and oedema due to inflammation cause mechanical
obstruction of intrahepatic biliary tree.
Hence in hepatocellular jaundice, concentration of both unconjugated and
conjugated bilirubin rises in the blood.
In hepatocellular disease, there is usually interference in all major steps of
bilirubin metabolism—uptake, conjugation and excretion.
However, excretion is the rate-limiting step, and usually impaired to the greatest
extent.
As a result, conjugated hyperbilirubinaemia predominates.
The unconjugated bilirubin still enters the liver cells and becomes conjugated in
the usual way.
This conjugated bilirubin is then returned to the blood, probably by rupture of the
congested bile canaliculi and direct emptying of the bile into the lymph leaving the
liver.
Thus, most of the bilirubin in the plasma becomes the conjugated type rather than
the unconjugated type.
Post-hepatic
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption
to the drainage of bile in the biliary system.
The most common causes are gallstones in the common bile duct, and pancreatic
cancer in the head of the pancreas.
Also, a group of parasites known as "liver flukes" can live in the common bile
duct, causing obstructive jaundice. Other causes include strictures of the common
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bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic
pseudocysts.
A rare cause of obstructive jaundice is Mirizzi's syndrome.
In complete obstruction of the bile duct, no urobilinogen is found in the urine,
since bilirubin has no access to the intestine and it is in the intestine that bilirubin
gets converted to urobilinogen to be later released into the general circulation.
In this case, presence of bilirubin (conjugated) in the urine without urineurobilinogen suggests obstructive jaundice, either intra-hepatic or post-hepatic.
The presence of pale stools and dark urine suggests an obstructive or post-hepatic
cause as normal feces get their color from bile pigments.
However, although pale stools and dark urine are a feature of biliary obstruction,
they can occur in many intra-hepatic illnesses and are therefore not a reliable
clinical feature to distinguish obstruction from hepatic causes of jaundice.
Patients also can present with elevated serum cholesterol, and often complain of
severe itching or "pruritus" because of the deposition of bile salts.
No single test can differentiate between various classifications of jaundice.
A combination of liver function tests is essential to arrive at a diagnosis.
Table of diagnostic tests
Function test
Total bilirubin
Conjugated bilirubin
Unconjugated bilirubin
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Pre-hepatic
Jaundice
Hepatic Jaundice
Post-hepatic
Jaundice
Normal /
Increased
Increased
Normal
Increased
Increased
Normal /
Increased
Increased
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Normal /
Increased
Increased
Urine Color
Normal
Dark
Dark (urobilinogen +
(conjugated
conjugated bilirubin)
bilirubin)
Stool Color
Normal
Normal/Pale
Urobilinogen
Alkaline phosphatase
levels
Decreased /
Negative
Pale
Increased
Alanine transferase and Normal
Aspartate transferase
levels
Increased
Conjugated Bilirubin in
Not Present
Urine
Present
Neonatal jaundice
Neonatal jaundice is usually harmless: this condition is often seen in infants
around the second day after birth, lasting until day 8 in normal births, or to around
day 14 in premature births.
Causes of neonatal jaundice
Typical causes for neonatal jaundice include
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normal physiologic jaundice,
jaundice due to breast feeding, and
hemolytic disorders that include hereditary spherocytosis,
glucose-6-phosphate dehydrogenase deficiency,
pyruvate kinase deficiency,
ABO/Rh blood type autoantibodies, or infantile pyknocytosis.
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Pathology of neonatal jaundice
Serum bilirubin normally drops to a low level without any intervention required:
the jaundice is presumably a consequence of metabolic and physiological
adjustments after birth.
Complications
In cases where bilirubin rises higher, a brain-damaging condition known as
kernicterus can occur, leading to significant lifelong disability; there are concerns
that this condition has been rising in recent years due to inadequate detection and
treatment of neonatal hyperbilirubinemia.
Treatment of neonatal jaundice
A Bili light is often the tool used for early treatment, which often consists of
exposing the baby to intensive phototherapy.
However, in third world countries where procuring such treatment is prohibitably
expensive, parents often subject their children to regular daily treatments of baking
in the sunlight and sunbathing.
Bilirubin count is lowered through bowel movements and urination so regular and
proper feedings are especially important.
Pathophysiology of Common Hepatitis
In order to understand how jaundice results, the pathological processes that cause
jaundice to take their effect must be understood.
Jaundice itself is not a disease, but rather a sign of one of many possible
underlying pathological processes that occur at some point along the normal
physiological pathway of the metabolism of bilirubin.
When red blood cells have completed their life span of approximately 120 days, or
when they are damaged, their membranes become fragile and prone to rupture.
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As each red blood cell traverses through the reticuloendothelial system, its cell
membrane ruptures when its membrane is fragile enough to allow this.
Cellular contents, including hemoglobin, are subsequently released into the blood.
The hemoglobin is phagocytosed by macrophages, and split into its heme and
globin portions.
The globin portion, a protein, is degraded into amino acids and plays no role in
jaundice.
Two reactions then take place with the heme molecule.
The first oxidation reaction is catalyzed by the microsomal enzyme heme
oxygenase and results in biliverdin (green color pigment), iron and carbon
monoxide.
The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment
called bilirubin by cytosolic enzyme biliverdin reductase.
This bilirubin is "unconjugated," "free" or "indirect" bilirubin.
Approximately 4 mg of bilirubin per kg of blood is produced each day.
The majority of this bilirubin comes from the breakdown of heme from expired red
blood cells in the process just described.
However approximately 20 percent comes from other heme sources, including
ineffective erythropoiesis, and the breakdown of other heme-containing proteins,
such as muscle myoglobin and cytochromes.
Hepatic events
The unconjugated bilirubin then travels to the liver through the bloodstream.
Because this bilirubin is not soluble, however, it is transported through the blood
bound to serum albumin.
Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin
diglucuronide, or just "conjugated bilirubin") to become more water soluble.
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The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts
as part of bile.
Intestinal bacteria convert the bilirubin into urobilinogen.
From here the urobilinogen can take two pathways.
It can either be further converted into stercobilinogen, which is then oxidized to
stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal
cells, transported in the blood to the kidneys, and passed out in the urine as the
oxidised product urobilin.
Stercobilin and urobilin are the products responsible for the coloration of feces and
urine, respectively.
Causes
Jaundice is basically a summer disease which is caused due to high concentration
of Bilirubin.
Bilirubin is yellow substance which is found in bile and helps liver break down the
worn out red blood cells, which ideally should be transformed into waste and new
red blood cells should be formed.
Jaundice is a sign that the liver is not working.
It may be caused by a blockage of the bile ducts which release bile salts and
pigment into the intestines.
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The bile then gets mixed with blood and this gives a yellow colour to the skin.
Jaundice is caused when the number of damaged red blood cells multiply, the
amount of bilirubin in the blood increases fast.
The causes of jaundice are:
1. Enlarged Liver:
Inflammation (swelling or enlargement) of the liver, called hepatitis.
One of the basic causes of jaundice is liver enlargement, which happens due
to liver infections.
This is caused by a virus.
The virus can spread and may lead to epidemics caused by:
o
o
o
o
overcrowding
dirty surroundings
insanitary conditions
contamination of food and water.
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Liver cirrhosis
Hepatitis E
- these are all caused by those viruses
When the liver is enlarged, it finds it difficult to convert bilirubin into waste
and thus, it results in mixing of bilirubin with blood.
This is when the skin and urine get the dark yellow colour.
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2. Bile Disorder
The blockage of the bile ducts could be caused by Gallstones.
Bile is a substance which substance which promotes the digestive process
and produces by the liver.
If this bile shrinks due to stone, tumour or birth defect, then it gets released
in the blood.
The skin and urine becomes yellow but the stool is white or brown in colour.
The patient is unable to digest fat and may also suffer blood clotting.
3. Loss Of Blood
The decreased number of red blood cells is the next cause.This condition is
called as Pernicious anaemia.
Due to certain illness like malaria, typhoid etc, the production of the red
blood cells may fall or cells may even damage.
This lack of red blood cells and the problem of the liver to process bilirubin
leads to this disease.
4. Other causes of jaundice are
 Pancreatic cancer
 Alcoholic liver disease
 Diseases affecting the liver such as:
i. typhoid,
ii. malaria,
iii. yellow fever and
iv. tuberculosis.
v. Certain medication
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vi.
vii.
Pregnancy
liver cancer
Symptoms
Yellow eyes caused by jaundice from hepatitis
The conjunctiva of the eye are one of the first tissues to change color as bilirubin
levels rise in jaundice. This is sometimes referred to as scleral icterus.
However, the sclera themselves are not "icteric" (stained with bile pigment) but
rather the conjunctival membranes that overlie them.
The yellowing of the "white of the eye" is thus more properly termed conjunctival
icterus.
The term "icterus" itself is sometimes incorrectly used to refer to jaundice that is
noted in the sclera of the eyes, however its more common and more correct
meaning is entirely synonymous with jaundice.
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The symptoms of jaundice are:
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Extreme weakness
Headache
Fever
Loss of appetite
Tiredness
Severe constipation
Nausea
Yellow coloration of the eyes, tongue, skin and urine.
Dull pain in the liver region.
Obstructive jaundice may also cause intense itching.
Jaundice in case of pregnancy leads to is vaginal bleeding, frequent fainting and
feeling of thrist.
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Diagnosis
Biliary tract dilation due to obstruction as seen on
CAT scan
Biliary tract dilation due to obstruction
Most patients presenting with jaundice will have various predictable patterns of
liver panel abnormalities, though significant variation does exist.
The typical liver panel will include :
Blood levels of enzymes found primarily from the liver, such as
 the aminotransferases (ALT, AST),
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 alkaline phosphatase (ALP);
 bilirubin (which causes the jaundice); and
 protein levels, specifically, total protein and albumin.
Other primary lab tests for liver function include GGT and prothrombin time (PT).
Some bone and heart disorders can lead to an increase in ALP and the
aminotransferases, so the first step in differentiating these from liver problems is to
compare the levels of GGT, which will only be elevated in liver-specific
conditions.
The second step is distinguishing from biliary (cholestatic) or liver (hepatic) causes
of jaundice and altered lab results.
The former typically indicates a surgical response, while the latter typically leans
toward a medical response.
ALP and GGT levels will typically rise with one pattern while AST and ALT rise
in a separate pattern.
If the ALP (10–45 IU/L) and GGT (18–85) levels rise proportionately about as
high as the AST (12–38 IU/L) and ALT (10–45 IU/L) levels, this indicates a
cholestatic problem.
On the other hand, if the AST and ALT rise is significantly higher than the ALP
and GGT rise, this indicates an hepatic problem.
Finally, distinguishing between hepatic causes of jaundice, comparing levels of
AST and ALT can prove useful.
AST levels will typically be higher than ALT.
This remains the case in most hepatic disorders except for hepatitis (viral or
hepatotoxic).
Alcoholic liver damage may see fairly normal ALT levels, with AST 10x higher
than ALT.
On the other hand, if ALT is higher than AST, this is indicative of hepatitis. Levels
of ALT and AST are not well correlated to the extent of liver damage, although
rapid drops in these levels from very high levels can indicate severe necrosis.
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Low levels of albumin tend to indicate a chronic condition, while it is normal in
hepatitis and cholestasis.
Lab results for liver panels are frequently compared by the magnitude of their
differences, not the pure number, as well as by their ratios.
The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic
liver damage (10), some other form of liver damage (above 1), or hepatitis (less
than 1).
Bilirubin levels greater than 10x normal could indicate neoplastic or intrahepatic
cholestasis.
Levels lower than this tend to indicate hepatocellular causes.
AST levels greater than 15x tends to indicate acute hepatocellular damage.
Less than this tend to indicate obstructive causes.
ALP levels greater than 5x normal tend to indicate obstruction, while levels greater
than 10x normal can indicate drug (toxic) induced cholestatic hepatitis or
Cytomegalovirus.
Both of these conditions can also have ALT and AST greater than 20× normal.
GGT levels greater than 10x normal typically indicate cholestasis.
Levels 5–10× tend to indicate viral hepatitis.
Levels less than 5× normal tend to indicate drug toxicity.
Acute hepatitis will typically have ALT and AST levels rising 20–30× normal
(above 1000), and may remain significantly elevated for several weeks.
Acetaminophen toxicity can result in ALT and AST levels greater than 50x
normal.
Complications
Complications of jaundice include : sepsis
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
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cholangitis,
biliary cirrhosis,
pancreatitis,
coagulopathy,
renal and
liver failure.
Other complications are related to the underlying disease and the procedures
employed in the diagnosis and management of individual diseases.
Cholangitis especially the suppurative type (Charcot’s triad or Raynaud’s pentad)
is usually secondary to choledocholithiasis.
It may also complicate procedures like ERCP.
Management
Treatment should include correction of coagulopathy, fluid/electrolyte anomaly,
antibiotics and biliary drainage with ERCP where available or trans-hepatic
drainage or surgery.
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Other Varities Of Hepatitis
Hepatitis A
Definition and Explanation
Hepatitis A (formerly known as infectious hepatitis and epidemical virus) is an
acute infectious disease of the liver caused by the hepatitis A virus (Hep A), an
RNA virus, usually spread by the fecal-oral route; transmitted person-to-person by
ingestion of contaminated food or water or through direct contact with an
infectious person.
Tens of millions of individuals worldwide are estimated to become infected with
Hep A each year.
Incubation period
The time between infection and the appearance of the symptoms (the incubation
period) is between two and six weeks and the average incubation period is 28 days.
About Hepatitis A
In developing countries, and in regions with poor hygiene standards, the incidence
of infection with this virus is high and the illness is usually contracted in early
childhood.
As incomes rise and access to clean water increases, the incidence of HAV
decreases.
Hepatitis A infection causes no clinical signs and symptoms in over 90% of
infected children and since the infection confers lifelong immunity, the disease is
of no special significance to those infected early in life.
In Europe, the United States and other industrialized countries, on the other hand,
the infection is contracted primarily by susceptible young adults, most of whom are
infected with the virus during trips to countries with a high incidence of the disease
or through contact with infectious persons.
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HAV infection produces a self-limited disease that does not result in chronic
infection or chronic liver disease.
However, 10–15% of patients might experience a relapse of symptoms during the 6
months after acute illness.
Acute liver failure from Hepatitis A is rare (overall case-fatality rate: 0.5%).
The risk for symptomatic infection is directly related to age, with >80% of adults
having symptoms compatible with acute viral hepatitis and the majority of children
having either asymptomatic or unrecognized infection.
Antibody produced in response to HAV infection persists for life and confers
protection against reinfection.
The disease can be prevented by vaccination, and hepatitis A vaccine has been
proven effective in controlling outbreaks worldwide.
Signs and symptoms
Early symptoms of hepatitis A infection can be mistaken for influenza, but some
sufferers, especially children, exhibit no symptoms at all. Symptoms typically
appear 2 to 6 weeks, (the incubation period), after the initial infection.
Symptoms usually last less than 2 months, although some people can be ill for as
long as 6 months.
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Fatigue
Fever
Abdominal pain
Nausea
Appetite loss
Jaundice, a yellowing of the skin or whites of the eyes
Bile is removed from blood stream and excreted in urine, giving it a dark
amber colour
Clay-coloured feces
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Virology
Hepatitis A
Electron micrograph of
hepatitis A virions.
Virus classification
Group:
Group IV
((+)ssRNA)
Family: Picornaviridae
Genus: Hepatovirus
Species:
Hepatitis A
virus
Pathology of Hepatitis A
Following ingestion, HAV enters the bloodstream through the epithelium of the
oropharynx or intestine.
The blood carries the virus to its target, the liver, where it multiplies within
hepatocytes and Kupffer cells (liver macrophages).
Virions are secreted into the bile and released in stool.
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HAV is excreted in large quantities approximately
11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the
blood.
The incubation period is 15–50 days and mortality is less than 0.5%.
Within the liver hepatocytes the RNA genome is released from the protein coat and
is translated by the cell's own ribosomes.
Unlike other members of the Picornaviruses this virus requires an intact eukaryote
initiating factor 4G (eIF4G) for the initiation of translation.
The requirement for this factor results in an inability to shut down host protein
synthesis unlike other picornaviruses.
The virus must then inefficiently compete for the cellular translational machinery
which may explain its poor growth in cell culture.
Presumably for this reason the virus has strategically adopted a naturally highly
deoptimized codon usage with respect to that of its cellular host.
Precisely how this strategy works is not quite clear yet.
There is no apparent virus-mediated cytotoxicity presumably because of the virus'
own requirement for an intact eIF4G and liver pathology is likely immunemediated.
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Structure of HAV
The Hepatitis virus (HAV) is a Picornavirus; it is non-enveloped and contains a
single-stranded RNA packaged in a protein shell.
There is only one serotype of the virus, but multiple genotypes exist.
Codon use within the genome is biased and unusually distinct from its host.
It also has a poor internal ribosome entry site
In the region that codes for the HAV capsid there are highly conserved clusters of
rare codons that restrict antigenic variability.
Genotypes
Only one serotype and seven different genetic groups (four humans and three
simian) have been described.
The human genotypes are numbered I-III. Six subtypes have been described (IA,
IB, IIA, IIB, IIIA, IIIB).
The simian genotypes have been numbered IV-VI. A single isolate of genotype VII
isolated from a human has also been described.
Genotype III has been isolated from both humans and owl monkeys.
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Most human isolates are of genotype I. Of the type I isolates subtype IA accounts
for the majority.
The mutation rate in the genome has been estimated to be 1.73 - 9.76 x 10−4
nucleotide substitution per site per year.
The human strains appear to have diverged from the simian ~3600 years ago.]
The mean age of genotypes III and IIIA strains has been estimated to be 592 and
202 years respectively.
Transmission
The virus spreads by the fecal-oral route and infections often occur in conditions of
poor sanitation and overcrowding.
Hepatitis A can be transmitted by the parenteral route but very rarely by blood and
blood products.
Food-borne outbreaks are not uncommon, and ingestion of shellfish cultivated in
polluted water is associated with a high risk of infection.
Approximately 40% of all acute viral hepatitis is caused by HAV. Infected
individuals are infectious prior to onset of symptoms, roughly 10 days following
infection.
The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform),
drying, and temperatures up to 60 °C.
It can survive for months in fresh and salt water.
Common-source (e.g., water, restaurant) outbreaks are typical.
Infection is common in children in developing countries, reaching 100% incidence,
but following infection there is lifelong immunity.
HAV can be inactivated by:
 chlorine treatment (drinking water),
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
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formalin (0.35%, 37 °C, 72 hours),
peracetic acid (2%, 4 hours),
beta-propiolactone (0.25%, 1 hour), and
UV radiation (2 μW/cm2/min).
Diagnosis
Serum IgG, IgM and ALT following Hepatitis A virus infection
Although HAV is excreted in the feces towards the end of the incubation period,
specific diagnosis is made by the detection of HAV-specific IgM antibodies in the
blood.
IgM antibody is only present in the blood following an acute hepatitis A infection.
It is detectable from one to two weeks after the initial infection and persists for up
to 14 weeks.
The presence of IgG antibody in the blood means that the acute stage of the illness
is past and the person is immune to further infection.
IgG antibody to HAV is also found in the blood following vaccination and tests for
immunity to the virus are based on the detection of this antibody.
During the acute stage of the infection, the liver enzyme alanine transferase (ALT)
is present in the blood at levels much higher than is normal.
The enzyme comes from the liver cells that have been damaged by the virus.
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Hepatitis A virus is present in the blood, (viremia), and feces of infected people up
to two weeks before clinical illness develops.
Prevention
Hepatitis A can be prevented by vaccination, good hygiene and sanitation.[1][19]
The vaccine protects against HAV in more than 95% of cases for longer than 20
years.
It contains inactivated hepatitis A virus providing active immunity against a future
infection.
In the USA the vaccine was first phased in 1996 for children in high-risk areas, and
in 1999 it was spread to areas with elevating levels of infection.
The vaccine is given by injection.
An initial dose provides protection starting two to four weeks after vaccination; the
second booster dose, given six to twelve months later, provides protection for over
twenty years.
Treatment in allopathy
There is no specific treatment for hepatitis A.
Sufferers are advised to rest, avoid fatty foods and alcohol (these may be poorly
tolerated for some additional months during the recovery phase and cause minor
relapses), eat a well-balanced diet, and stay hydrated.
Prognosis
The United States Centers for Disease Control and Prevention (CDC) in 1991
reported a low mortality rate for hepatitis A of 4 deaths per 1000 cases for the
general population but a higher rate of 17.5 per 1000 in those aged 50 and over.
The risk of death from acute liver failure following HAV infection increases with
age and when the person has underlying chronic liver disease.
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Young children who are infected with hepatitis A typically have a milder form of
the disease, usually lasting from 1–3 weeks, whereas adults tend to experience a
much more severe form of the disease.
Epidemiology
Hepatitis A Distribution 2005
Antibodies to HAV (anti-HAV) in the blood are a marker of past or current
infection.
High-income regions (Western Europe, Australia, New Zealand, Canada, the
United States, Japan, the Republic of Korea, and Singapore) have very low HAV
endemicity levels .
A high proportion of susceptible adults, low-income regions (sub-Saharan Africa
and parts of South Asia) have high endemicity levels and almost no susceptible
adolescents and adults.
Most middle-income regions have a mix of intermediate and low endemicity
levels.
Anti-HAV prevalence suggest that middle-income regions in Asia, Latin America,
Eastern Europe, and the Middle East currently have an intermediate or low level of
endemicity.
The countries in these regions may have an increasing burden of disease from
hepatitis A.
There were 30,000 cases of Hepatitis A reported to the CDC in the U.S. in 1997.
The agency estimates that there were as many as 270,000 cases each year from
1980 through 2000.
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Hepatitis B
Definition
Hepatitis B is an infectious inflammatory illness of the liver caused by the
hepatitis B virus (HBV) that affects hominoidea, including humans. Originally
known as "serum hepatitis".
The disease has caused epidemics in parts of Asia and Africa, and it is endemic in
China. About a third of the world population has been infected at one point in their
lives, including 350 million who are chronic carriers.
About HBV
Hepatitis B virus is an hepadnavirus—hepa from hepatotropic (attracted to the
liver) and dna because it is a DNA virus—and it has a circular genome of partially
double-stranded DNA.
The viruses replicate through an RNA intermediate form by reverse transcription,
which in practice relates them to retroviruses.
Although replication takes place in the liver, the virus spreads to the blood where
viral proteins and antibodies against them are found in infected people.
History
World Hepatitis Day, observed July 28, aims to raise global awareness of hepatitis
B and hepatitis C and encourage prevention, diagnosis and treatment.
It has been led by the World Hepatitis Alliance since 2007 and in May 2010, it got
global endorsement from the World Health Organization.[91]
The earliest record of an epidemic caused by hepatitis B virus was made by
Lurman in 1885.
An outbreak of smallpox occurred in Bremen in 1883 and 1,289 shipyard
employees were vaccinated with lymph from other people.
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After several weeks, and up to eight months later, 191 of the vaccinated workers
became ill with jaundice and were diagnosed as suffering from serum hepatitis.
Other employees who had been inoculated with different batches of lymph
remained healthy.
Lurman's paper, now regarded as a classical example of an epidemiological study,
proved that contaminated lymph was the source of the outbreak.
Later, numerous similar outbreaks were reported following the introduction, in
1909, of hypodermic needles that were used, and, more importantly, reused, for
administering Salvarsan for the treatment of syphilis.
The virus was not discovered until 1965 when Baruch Blumberg, then working at
the National Institutes of Health (NIH), discovered the Australia antigen (later
known to be hepatitis B surface antigen, or HBsAg) in the blood of Australian
aboriginal people.
Although a virus had been suspected since the research published by MacCallum
in 1947, D.S. Dane and others discovered the virus particle in 1970 by electron
microscopy.
By the early 1980s the genome of the virus had been sequenced, and the first
vaccines were being tested.
Causes, incidence, and risk factors
Hepatitis B infection can be spread through having contact with the
 blood,
 semen,
 vaginal fluids, and
 other body fluids of someone who already has a hepatitis B infection.
Infection can be spread through:





Blood transfusions (not common in the United States)
Direct contact with blood in health care settings
Sexual contact with an infected person
Tattoo or acupuncture with unclean needles or instruments
Shared needles during drug use
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
Shared personal items (such as toothbrushes, razors, and nail clippers) with
an infected person
The hepatitis B virus can be passed to an infant during childbirth if the mother is
infected.
However, Hepatitis B viruses cannot be spread by holding hands, sharing eating
utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding.
Risk factors for hepatitis B infection include:





Being born, or having parents who were born in regions with high infection
rates (including Asia, Africa, and the Caribbean)
Being infected with HIV
Being on hemodialysis
Having multiple sex partners
Men having sex with men
How does hepatitis B virus cause liver injury?
Most of the damage from the hepatitis B virus occurs because of the way the body
responds to the infection.
The hepatitis B virus reproduces in liver cells, but the virus itself is not the direct
cause of damage to the liver.
Rather, the presence of the virus triggers an immune response from the body as the
body tries to eliminate the virus and recover from the infection.
When the body's immune system detects the infection, it sends out special cells to
fight it off.
However, these disease-fighting cells can lead to liver inflammation.
Therefore, there is a balance between the protective and destructive effects of the
immune response to the hepatitis B virus.
This infection has two possible phases;
1) Acute and
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2) Chronic.
1. Acute hepatitis B refers to newly acquired infections. Affected individuals
notice symptoms approximately 1 to 4 months after exposure to the virus. In
most people with acute hepatitis, symptoms resolve over weeks to months
and they are cured of the infection. However, a small number of people
develop a very severe, life-threatening form of acute hepatitis called
fulminant hepatitis.
2. Chronic hepatitis B is an infection with HBV that lasts longer than 6
months. Once the infection becomes chronic, it may never go away
completely.
Signs and symptoms
Acute infection with hepatitis B virus is associated with acute viral hepatitis – an
illness that begins with









general ill-health,
loss of appetite,
nausea,
vomiting,
body aches,
mild fever, and
dark urine, and
then progresses to development of jaundice.
It has been noted that itchy skin has been an indication as a possible
symptom of all hepatitis virus types.
 The illness lasts for a few weeks and then gradually improves in most
affected people.
 A few people may have more severe liver disease (fulminant hepatic
failure), and may die as a result.
 The infection may be entirely asymptomatic and may go
unrecognized.
Chronic infection with hepatitis B virus
 either may be asymptomatic or
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 may be associated with a chronic inflammation of the liver (chronic
hepatitis), leading to cirrhosis over a period of several years.
 This type of infection dramatically increases the incidence of hepatocellular
carcinoma (liver cancer).
 Chronic carriers are encouraged to avoid consuming alcohol as it increases
their risk for cirrhosis and liver cancer.
 Hepatitis B virus has been linked to the development of Membranous
glomerulonephritis (MGN).
Symptoms outside of the liver are present in 1–10% of HBV-infected people and
include











serum-sickness–like syndrome,
acute necrotizing vasculitis (polyarteritis nodosa),
membranous glomerulonephritis, and
papular acrodermatitis of childhood (Gianotti-Crosti syndrome).
The serum-sickness–like syndrome occurs in the setting of acute hepatitis B,
often preceding the onset of jaundice.
The clinical features are fever, skin rash, and polyarteritis.
The symptoms often subside shortly after the onset of jaundice, but can
persist throughout the duration of acute hepatitis B.
About 30–50% of people with acute necrotizing vasculitis (polyarteritis
nodosa) are HBV carriers.
HBV-associated nephropathy has been described in adults but is more
common in children.
Membranous glomerulonephritis is the most common form.
Other immune-mediated hematological disorders, such as essential mixed
cryoglobulinemia and aplastic anemia
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Virology
Structure
The genome organisation of HBV. The genes overlap.
Hepatitis B virus (HBV) is a member of the Hepadnavirus family.
The virus particle, (virion) consists of an outer lipid envelope and an icosahedral
nucleocapsid core composed of protein.
These virions are 42 nM in diameter and are sometimes referred to as "Dane
particles".
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The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse
transcriptase activity.
The outer envelope contains embedded proteins that are involved in viral binding
of, and entry into, susceptible cells.
The virus is one of the smallest enveloped animal viruses, but pleomorphic forms
exist, including filamentous and spherical bodies lacking a core.
These particles are not infectious and are composed of the lipid and protein that
forms part of the surface of the virion, which is called the surface antigen
(HBsAg), and is produced in excess during the life cycle of the virus.
Hepatitis B virus replication.
The life cycle of hepatitis B virus is complex.
Hepatitis B is one of a few known pararetroviruses: non-retroviruses that still do
use reverse transcription in their replication process.
The virus gains entry into the cell by binding to an unknown receptor on the
surface and being endocytosed in.
Because the virus multiplies via RNA made by a host enzyme, the viral genomic
DNA has to be transferred to the cell nucleus by host proteins called chaperones.
The partially double stranded viral DNA is then made fully double stranded and
transformed into covalently closed circular DNA (cccDNA) that serves as a
template for transcription of four viral mRNAs.
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The largest mRNA, (which is longer than the viral genome), is used to make the
new copies of the genome and to make the capsid core protein and the viral DNA
polymerase.
These four viral transcripts undergo additional processing and go on to form
progeny virions that are released from the cell or returned to the nucleus and recycled to produce even more copies.
The long mRNA is then transported back to the cytoplasm where the virion P
protein synthesizes DNA via its reverse transcriptase activity.
Serotypes and genotypes
The virus is divided into four major serotypes (adr, adw, ayr, ayw) based on
antigenic epitopes presented on its envelope proteins, and into eight genotypes (AH) according to overall nucleotide sequence variation of the genome.
The genotypes have a distinct geographical distribution and are used in tracing the
evolution and transmission of the virus.
Differences between genotypes affect the disease severity, course and likelihood of
complications, and response to treatment and possibly vaccination.
Genotypes differ by at least 8% of their sequence and were first reported in 1988
when six were initially described (A-F).
Two further types have since been described (G and H).
Most genotypes are now divided into subgenotypes with distinct properties.
Genotype A is most commonly found in the Americas, Africa, India and Western
Europe. Genotype B is most commonly found in Asia and the United States.
Genotype B1 dominates in Japan, B2 in China and Vietnam while B3 confined to
Indonesia.
B4 is confined to Vietnam.
All these strains specify the serotype ayw1.
B5 is most common in the Philippines.
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Genotype C is most common in Asia and the United States.
Subgenotype C1 is common in Japan, Korea and China.
C2 is common in China, South-East Asia and Bangladesh and C3 in Oceania.
All these strains specify the serotype adrq.
C4 specifying ayw3 is found in Aborigines from Australia.
Genotype D is most commonly found in Southern Europe, India and the United
States and has been divided into 8 subtypes (D1–D8).
In Turkey genotype D is also the most common type.
A pattern of defined geographical distribution is less evident with D1–D4 where
these subgenotypes are widely spread within Europe, Africa and Asia.
This may be due to their divergence having occurred before than of genotypes B
and C.
D4 appears to be the oldest split and is still the dominating subgenotype of D in
Oceania.
Type E is most commonly found in West and Southern Africa.
Type F is most commonly found in Central and South America and has been
divided into two subgroups (F1 and F2).
Genotype G has an insertion of 36 nucleotides in the core gene and is found in
France and the United States.
Type H is most commonly found in Central and South America and California in
United States.
Africa has five genotypes (A-E). Of these the predominant genotypes are A in
Kenya, B and D in Egypt, D in Tunisia, A-D in South Africa and E in Nigeria.
Genotype H is probably split off from genotype F within the New World.
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Pathogenesis
Hepatitis B virus primarily interferes with the functions of the liver by replicating
in liver cells, known as hepatocytes.
The receptor is not yet known, though there is evidence that the receptor in the
closely related duck hepatitis B virus is carboxypeptidase D.
The virions bind to the host cell via the preS domain of the viral surface antigen
and are subsequently internalized by endocytosis.
PreS and IgA receptors are accused of this interaction.
HBV-preS-specific receptors are expressed primarily on hepatocytes; however,
viral DNA and proteins have also been detected in extrahepatic sites, suggesting
that cellular receptors for HBV may also exist on extrahepatic cells.
During HBV infection, the host immune response causes both hepatocellular
damage and viral clearance.
Although the innate immune response does not play a significant role in these
processes, the adaptive immune response, in particular virus-specific cytotoxic T
lymphocytes(CTLs), contributes to most of the liver injury associated with HBV
infection.
CTLs eliminate HBV infection by killing infected cells and producing antiviral
cytokines, which are then used to purge HBV from viable hepatocytes.
Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific
inflammatory cells can worsen CTL-induced immunopathology, and platelets
activated at the site of infection may facilitate the accumulation of CTLs in the
liver.
Transmission
Transmission of hepatitis B virus results from exposure to infectious blood or body
fluids containing blood.
Possible forms of transmission include
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




sexual contact,
blood transfusions
transfusion with other human blood products,
re-use of contaminated needles and syringes, and
vertical transmission from mother to child (MTCT) during childbirth.
Without intervention, a mother who is positive for HBsAg confers a 20% risk of
passing the infection to her offspring at the time of birth.
This risk is as high as 90% if the mother is also positive for HBeAg.
HBV can be transmitted between family members within households, possibly by
contact of nonintact skin or mucous membrane with secretions or saliva containing
HBV.
However, at least 30% of reported hepatitis B among adults cannot be associated
with an identifiable risk factor.
And Shi et al. showed that breastfeeding after proper immunoprophylaxis did not
contribute to MTCT of HBV.
Diagnosis
Signs and tests
The following tests are done to identify and monitor liver damage from hepatitis B:



Albumin level
Liver function tests
Prothrombin time
The following tests are done to help diagnose and monitor people with hepatitis B:



Antibody to HBsAg (Anti-HBs) -- a positive result means you have either
had hepatitis B in the past, or have received a hepatitis B vaccine
Antibody to hepatitis B core antigen (Anti-HBc) -- a positive result means
you had a recent infection or an infection in the past
Hepatitis B surface antigen (HBsAg) -- a positive result means you have an
active infection
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
Hepatitis E surface antigen (HBeAg) -- a positive result means you have a
hepatitis B infection and are more likely to spread the infection to others
through sexual contact or sharing needles
Patients with chronic hepatitis will need ongoing blood tests to monitor their status.
Hepatitis B viral antigens and antibodies detectable in the blood following acute
infection.
Hepatitis B viral antigens and antibodies detectable in the blood of a chronically
infected person.
The tests, called assays, for detection of hepatitis B virus infection involve serum
or blood tests that detect either viral antigens (proteins produced by the virus) or
antibodies produced by the host. Interpretation of these assays is complex.
The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the
presence of this infection.
It is the first detectable viral antigen to appear during infection.
However, early in an infection, this antigen may not be present and it may be
undetectable later in the infection as it is being cleared by the host.
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The infectious virion contains an inner "core particle" enclosing viral genome.
The icosahedral core particle is made of 180 or 240 copies of core protein,
alternatively known as hepatitis B core antigen, or HBcAg.
During this 'window' in which the host remains infected but is successfully clearing
the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the
only serological evidence of disease.
Therefore most hepatitis B diagnostic panels contain HBsAg and total antiHBc(both IgM and IgG).
Shortly after the appearance of the HBsAg, another antigen called hepatitis B e
antigen (HBeAg) will appear.
Traditionally, the presence of HBeAg in a host's serum is associated with much
higher rates of viral replication and enhanced infectivity; however, variants of the
hepatitis B virus do not produce the 'e' antigen, so this rule does not always hold
true.
During the natural course of an infection, the HBeAg may be cleared, and
antibodies to the 'e' antigen (anti-HBe) will arise immediately afterwards.
This conversion is usually associated with a dramatic decline in viral replication.
Ground glass hepatocytes as seen in a chronic
hepatitis B. Liverbiopsy. H&E stain.
If the host is able to clear the infection, eventually the HBsAg will become
undetectable and will be followed by IgG antibodies to the hepatitis B surface
antigen and core antigen, (anti-HBs and anti HBc IgG).
The time between the removal of the HBsAg and the appearance of anti-HBs is
called the window period.
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A person negative for HBsAg but positive for anti-HBs either has cleared an
infection or has been vaccinated previously.
Individuals who remain HBsAg positive for at least six months are considered to
be hepatitis B carriers.
Carriers of the virus may have chronic hepatitis B, which would be reflected by
elevated serum alanine aminotransferase (ALT) levels and inflammation of the
liver, as revealed by biopsy.
Carriers who have seroconverted to HBeAg negative status, in particular those who
acquired the infection as adults, have very little viral multiplication and hence may
be at little risk of long-term complications or of transmitting infection to others.
PCR tests have been developed to detect and measure the amount of HBV DNA,
called the viral load, in clinical specimens.
These tests are used to assess a person's infection status and to monitor treatment.
Individuals with high viral loads, characteristically have ground glass hepatocytes
on biopsy.
Prevention
Several vaccines have been developed for the prevention of hepatitis B virus
infection.
These rely on the use of one of the viral envelope proteins (hepatitis B surface
antigen or HBsAg).
The vaccine was originally prepared from plasma obtained from people who had
long-standing hepatitis B virus infection.
However, it is made using a synthetic recombinant DNA technology that does not
contain blood products.
One cannot be infected with hepatitis B from this vaccine.
The risk of transmission from mother to newborn can be reduced from 20–90% to
5–10% by administering to the newborn hepatitis B vaccine (HBV 1) and hepatitis
B immune globulin (HBIG) within 12 hours of birth, followed by a second dose of
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hepatitis B vaccine (HBV 2) at 1–2 months and a third dose at and no earlier than
6 months (24 weeks).
Since 2% of infants vaccinated will not develop immunity after the first three dose
series, infants born to hepatitis B-positive mothers are tested at 9 months for
hepatitis B surface antigen (HBsAg) and the antibody to the hepatitis B surface
antigen (anti-HBs).
If post-vaccination test results indicate that the child is still susceptible, a second
three dose series at (0, 1 and 6 months) is administered.
If the child is still susceptible after the second series, a third series is not
recommended.
Following vaccination, hepatitis B surface antigen may be detected in serum for
several days; this is known as vaccine antigenaemia.
The vaccine is administered in either two-, three-, or four-dose schedules into
infants and adults, which provides protection for 85–90% of individuals.
Protection has been observed to last 12 years in individuals who show adequate
initial response to the primary course of vaccinations, and that immunity is
predicted to last at least 25 years.
Unlike hepatitis A, hepatitis B does not generally spread through water and food.
Instead, it is transmitted through body fluids; thus, prevention is the avoidance of
such transmission: unprotected sexual contact, blood transfusions, re-use of
contaminated needles and syringes, and vertical transmission during child birth.
Infants may be vaccinated at birth.
Lifestyle measures for preventing transmission of hepatitis B:





Avoid sexual contact with a person who has acute or chronic hepatitis B.
Use a condom and practice safe sex.
Avoid sharing personal items, such as razors or toothbrushes.
Do not share drug needles or other drug equipment (such as straws for
snorting drugs).
Clean blood spills with a solution containing 1 part household bleach to 10
parts water.
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Prognosis
Hepatitis B virus infection may be either acute (self-limiting) or chronic (longstanding).
Persons with self-limiting infection clear the infection spontaneously within weeks
to months.
Children are less likely than adults to clear the infection.
More than 95% of people who become infected as adults or older children will
stage a full recovery and develop protective immunity to the virus.
However, this drops to 30% for younger children, and only 5% of newborns that
acquire the infection from their mother at birth will clear the infection.
This population has a 40% lifetime risk of death from cirrhosis or hepatocellular
carcinoma.
Of those infected between the age of one to six, 70% will clear the infection.
Hepatitis D (HDV) can occur only with a concomitant hepatitis B infection,
because HDV uses the HBV surface antigen to form a capsid.
Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer.
Polyarteritis nodosa is more common in people with hepatitis B infection.
Reactivation
Hepatitis B virus DNA persists in the body after infection, and in some people the
disease recurs.
Although rare, reactivation is seen most often following alcohol or drug use, or in
people with impaired immunity.
HBV goes through cycles of replication and non-replication.
Approximately 50% of overt carriers experience acute reactivation.
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Males with baseline ALT of 200 UL/L are three times more likely to develop a
reactivation than people with lower levels.
Although reactivation can occur spontaneously, people who undergo chemotherapy
have a higher risk.
Immunosuppressive drugs favor increased HBV replication while inhibiting
cytotoxic T cell function in the liver.
The risk of reactivation varies depending on the serological profile; those with
detectable HBsAg in their blood are at the greatest risk, but those with only
antibodies to the core antigen are also at risk.
The presence of antibodies to the surface antigen, which are considered to be a
marker of immunity, does not preclude reactivation.
Treatment with prophylactic antiviral drugs can prevent the serious morbidity
associated with HBV disease reactivation.
Epidemiology
Estimate of disability-adjusted life year for hepatitis B per 100,000 inhabitants as
of 2004.
no data
100-125
<10
125-150
10-20
150-200
20-40
200-250
40-60
250-500
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60-80
>500
80-100
Prevalence of hepatitis B virus as of 2005.
In 2004, an estimated 350 million individuals were infected worldwide.
National and regional prevalence ranges from over 10% in Asia to under 0.5% in
the United States and northern Europe.
Routes of infection include vertical transmission (such as through childbirth), early
life horizontal transmission (bites, lesions, and sanitary habits), and adult
horizontal transmission (sexual contact, intravenous drug use).
The primary method of transmission reflects the prevalence of chronic HBV
infection in a given area.
In low prevalence areas such as the continental United States and Western Europe,
injection drug abuse and unprotected sex are the primary methods, although other
factors may also be important.
In moderate prevalence areas, which include Eastern Europe, Russia, and Japan,
where 2–7% of the population is chronically infected, the disease is predominantly
spread among children.
In high-prevalence areas such as China and South East Asia, transmission during
childbirth is most common, although in other areas of high endemicity such as
Africa, transmission during childhood is a significant factor.
The prevalence of chronic HBV infection in areas of high endemicity is at least
8%. As of 2010, China has 120 million infected people, followed by India and
Indonesia with 40 million and 12 million, respectively.
According to World Health Organization (WHO), an estimated 600,000 people die
every year related to the infection.
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Complications
There is a much higher rate of hepatocellular carcinoma in people who have
chronic hepatitis B than in the general population.
Other complications may include:



Chronic persistent hepatitis
Cirrhosis
Fulminant hepatitis, which can lead to liver failure and possibly death
What is the scope of the problem?
Hepatitis B is estimated that 350 million individuals worldwide are infected with
the virus, which causes 620,000 deaths worldwide each year.
According to the Centers for Disease Control (CDC), approximately 46,000 new
cases of hepatitis B occurred in the United States in 2006.
In the United States, rates of new infection were highest among people aged 25 to
44 years (3.1 cases per 100,000 population) and lowest among those younger than
15 years of age (0.02 per 100,000).
This reflects the major modes of transmission of hepatitis B (sexual transmission,
illicit drug use, exposure to infected blood) and the effect of universal vaccination
of infants.
In the United States, there has been a 75% decrease in newly diagnosed cases of
hepatitis B during the past decade.
This decrease is attributed to increased vaccination and to heightened public
awareness of HIV/AIDS and the resulting safer sexual practices.
When a person first gets hepatitis B, they are said to have an 'acute' infection.
Most people are able to eliminate the virus and are cured of the infection.
Some are not able to clear the virus and have 'chronic' infection with hepatitis B
that is usually life-long .
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In the United States an estimated 800,000 to 1.4 million people are chronically
infected with hepatitis B and the disease causes about 3000 deaths each year.
Hepatitis B is found throughout the world. Some countries have much higher rates
of infection than the United States; for example, in Southeast Asia and SubSaharan Africa, as many as 15% to 20% of adults are chronically infected with
hepatitis B.
The good news is that infection with HBV is usually preventable because there is
an effective vaccine. Use of the vaccine has resulted in an 82% decrease in the
number of new infections reported in the United States each year.
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Hepatitis C
Definition
Hepatitis C is an infectious disease affecting primarily the liver, caused by the
hepatitis C virus (HCV).
Explanation
The infection is often asymptomatic, but chronic infection can lead to scarring of
the liver and ultimately to cirrhosis, which is generally apparent after many years.
In some cases, those with cirrhosis will go on to develop liver failure, liver cancer
or life-threatening esophageal and gastric varices.
HCV is spread primarily by blood-to-blood contact associated with intravenous
drug use, poorly sterilized medical equipment and transfusions.
An estimated 130–170 million people worldwide are infected with hepatitis C.
The existence of hepatitis C (originally "non-A non-B hepatitis") was postulated in
the 1970s and proven in 1989.
Hepatitis C only infects humans and chimpanzees.
The virus persists in the liver in about 85% of those infected.
This persistent infection can be treated with medication: the standard therapy is a
combination of peginterferon and ribavirin, with either boceprevir or telaprevir
added in some cases.
Overall, 50–80% of people treated are cured.
Those who develop cirrhosis or liver cancer may require a liver transplant.
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Hepatitis C is the leading cause of liver transplantation, though the virus usually
recurs after transplantation.
No vaccine against hepatitis C is available.
History
In the mid-1970s, Harvey J. Alter, Chief of the Infectious Disease Section in the
Department of Transfusion Medicine at the National Institutes of Health, and his
research team demonstrated how most post-transfusion hepatitis cases were not
due to hepatitis A or B viruses.
Despite this discovery, international research efforts to identify the virus, initially
called non-A, non-B hepatitis (NANBH), failed for the next decade.
In 1987, Michael Houghton, Qui-Lim Choo, and George Kuo at Chiron
Corporation, collaborating with Dr. D.W. Bradley at the Centers for Disease
Control and Prevention, used a novel molecular cloning approach to identify the
unknown organism and develop a diagnostic test.
In 1988, the virus was confirmed by Alter by verifying its presence in a panel of
NANBH specimens.
In April 1989, the discovery of HCV was published in two articles in the journal
Science.
The discovery led to significant improvements in diagnosis and improved antiviral
treatment.
In 2000, Drs. Alter and Houghton were honored with the Lasker Award for
Clinical Medical Research for "pioneering work leading to the discovery of the
virus that causes hepatitis C and the development of screening methods that
reduced the risk of blood transfusion-associated hepatitis in the U.S. from 30% in
1970 to virtually zero in 2000."
Chiron filed for several patents on the virus and its diagnosis.
A competing patent application by the CDC was dropped in 1990 after Chiron paid
$1.9 million to the CDC and $337,500 to Bradley.
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In 1994, Bradley sued Chiron, seeking to invalidate the patent, have himself
included as a coinventor, and receive damages and royalty income.
He dropped the suit in 1998 after losing before an appeals court.
Pathophysiology
The cause of hepatitis C, HCV, is a spherical, enveloped, single-stranded RNA
virus belonging to the Flaviviridae family and Flavivirus genus.
The natural targets of HCV are hepatocytes and, possibly, B lymphocytes.
Viral clearance is associated with the development and persistence of strong virusspecific responses by cytotoxic T lymphocytes and helper T cells.
In most infected people, viremia persists and is accompanied by variable degrees
of hepatic inflammation and fibrosis.
Findings from studies suggest at least 50% of hepatocytes may be infected with
HCV in patients with chronic hepatitis C.
RNA-dependent RNA polymerase, an enzyme critical in HCV replication, lacks
proofreading capabilities and generates a large number of mutant viruses known as
quasispecies.
These represent minor molecular variations with only 1-2% nucleotide
heterogeneity.
HCV quasispecies pose a major challenge to immune-mediated control of HCV
and may explain the variable clinical course and the difficulties in vaccine
development
Signs and symptoms
About 75% of people have no symptoms when they first acquire hepatitis C viral
infection.
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The remaining 25% may complain of fatigue, loss of appetite, muscle aches or
fever.
Yellowing of the skin or eyes (jaundice) is rare at this early stage of infection.
Over time, the liver in people with chronic infection may begin to experience the
effects of the persistent inflammation caused by the immune reaction to the virus.
Blood tests may show elevated levels of liver enzymes, a sign of liver damage,
which is often the first suggestion that the infection may be present.
Patients may become easily fatigued or complain of nonspecific symptoms.
As cirrhosis develops, symptoms increase and may include :







weakness,
loss of appetite,
weight loss,
breast enlargement in men,
a rash on the palms,
difficulty with the clotting of blood, and
spider-like blood vessels on the skin.
Acute infection
Hepatitis C infection causes acute symptoms in 15% of cases.
Symptoms are generally mild and vague, including a decreased appetite, fatigue,
nausea, muscle or joint pains, and weight loss.
Most cases of acute infection are not associated with jaundice.
The infection resolves spontaneously in 10-50% of cases, which occurs more
frequently in individuals who are young and female.
Chronic infection
About 80% of those exposed to the virus develop a chronic infection.
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Most experience minimal or no symptoms during the initial few decades of the
infection, although chronic hepatitis C can be associated with fatigue.
Hepatitis C after many years becomes the primary cause of cirrhosis and liver
cancer.
About 10–30% of people develop cirrhosis over 30 years.
Cirrhosis is more common in those co-infected with hepatitis B or HIV, alcoholics,
and those of male gender.
Those who develop cirrhosis have a 20-fold greater risk of hepatocellular
carcinoma, a rate of 1–3% per year, and if this is complicated by excess alcohol the
risk becomes 100 fold greater.
Hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular
carcinoma worldwide.
Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in
the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the
stomach and esophagus), jaundice, and a syndrome of cognitive impairment known
as hepatic encephalopathy.
It is a common cause for requiring a liver transplant.
Extrahepatic
Hepatitis C is also rarely associated with Sjögren's syndrome (an autoimmune
disorder), thrombocytopenia, lichen planus, diabetes mellitus, and B-cell
lymphoproliferative disorders.
Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic
hepatitis C.
Putative associations with Hyde's prurigo nodularis and membranoproliferative
glomerulonephritis have been reported.
Hepatitis C infection is also associated with a condition called mixed
cryoglobulinemia, which is inflammation of small and medium sized blood vessels
(or vasculitis) caused by deposition of immune complexes involving cryoglobulins.
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Virology
.
The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense
RNA virus.
It is a member of the hepacivirus genus in the family Flaviviridae.
There are seven major genotypes of HCV, which are indicated numerically from
one to seven.
In the United States, about 70% of cases are caused by genotype 1, 20% by
genotype 2, and about 1% by each of the other genotypes.
Genotype 1 is also the most common in South America and Europe.
The HCV genome consists of a single, open reading frame and 2 untranslated,
highly conserved regions, 5'-UTR and 3'-UTR, at both ends of the genome.
The genome has approximately 9500 base pairs and encodes a single polyprotein
of 3011 amino acids that are processed into 10 structural and regulatory proteins
(see the image below).
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Hepatitis C viral genome. Courtesy of Hepatitis
Resource Network.
Structural components include the core and 2 envelope proteins, E1 and E2.
Two regions of the E2 protein, designated hypervariable regions 1 and 2, have an
extremely high rate of mutation, thought to result from selective pressure by virusspecific antibodies.
The envelope protein E2 also contains the binding site for CD-81, a tetraspanin
receptor expressed on hepatocytes and B lymphocytes that acts as a receptor or
coreceptor for HCV.
The nonstructural components include NS2, NS3, NS4A, NS4B, NS5A, NS5B,
and p7, whose proteins function as helicase-, protease-, and RNA-dependent RNA
polymerase, although the exact function of p7 is unknown.
One region within NS5A is linked to an interferon (IFN) response and is called the
IFN sensitivity–determining region.
These enzymes are critical in viral replication and are attractive targets for future
antiviral therapy.
HCV genomic analysis by means of arduous gene sequencing of many viruses has
led to the division of HCV into 6 genotypes based on homology.
Numerous subtypes have also been identified.
Arabic numerals denote the genotype, and lower-case letters denote the subtypes
for lesser homology within each genotype.
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Genotypes
Molecular differences between genotypes are relatively large, and they have a
difference of at least 30% at the nucleotide level.
The major HCV genotype worldwide is genotype 1, which accounts for 40-80% of
all isolates.
Genotype 1 also may be associated with more severe liver disease and a higher risk
of HCC.
Genotypes 1a and 1b are prevalent in the United States, whereas in other countries,
genotype 1a is less frequent.
HCV genotype 1, particularly 1b, does not respond to therapy as well as genotypes
2 and 3. Genotype details are as follows:








Genotype 1a occurs in 50-60% of patients in the United States; this type is
difficult to eradicate using current medications
Genotype 1b occurs in 15-20% of patients in the United States; subtype 1b is
also difficult to eradicate using current medications; this type is most
prevalent in Europe, Turkey, and Japan
Genotype 1c occurs in less than 1% of patients in the United States
Genotypes 2a, 2b, and 2c occur in 10-15% of patients in the United States;
these subtypes are widely distributed and are most responsive to medication
Genotypes 3a and 3b occur in 4-6% of patients in the United States; these
subtypes are most prevalent in India, Pakistan, Thailand, Australia, and
Scotland
Genotype 4 occurs in less than 5% of patients in the United States; it is most
prevalent in the Middle East and Africa
Genotype 5 occurs in less than 5% of patients in the United States; it is most
prevalent in South Africa
Genotype 6 occurs in less than 5% of patients in the United States; it is most
prevalent in Southeast Asia, particularly Hong Kong and Macao
Within a region, a specific genotype may also be associated with a specific mode
of transmission, such as genotype 3 among persons in Scotland who abuse
intravenous drugs.
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Transmission
The primary route of transmission in the developed world is intravenous drug use
(IDU), while in the developing world the main methods are blood transfusions and
unsafe medical procedures.
The cause of transmission remains unknown in 20% of cases; however, many of
these are believed to be accounted for by IDU.
Intravenous drug use
IDU is a major risk factor for hepatitis C in many parts of the world.
Of 77 countries reviewed 25 (including the United States) were found to have
prevalences of hepatitis C in the intravenous drug user population of between 60%
and 80%.
While twelve countries had rates greater than 80%. Occurrence of hepatitis C
among prison inmates in the United States are ten to 20 times that of the
occurrence observed in the general population; this has been attributed to high-risk
behavior in prisons such as IDU and tattooing with nonsterile equipment.
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Healthcare exposure
Blood transfusion, transfusion of blood products, or organ transplantation without
HCV screening carry significant risks of infection.
The United States instituted universal screening in 1992 and Canada instituted
universal screening in 1990.
This decreased the risk from one in 200 units of blood to one in 10,000 to one in
10,000,000 per unit of blood.
This low risk remains as there is a period of about 11–70 days between the
potential blood donor acquiring hepatitis C and their blood testing positive
depending on the method.
Those who have experienced a needle stick injury from someone who was HCV
positive have about a 1.8% chance of subsequently contracting the disease
themselves.
The risk is greater if the needle in question is hollow and the puncture wound is
deep.
There is a risk from mucosal exposures to blood; but this risk is low, and there is
no risk if blood exposure occurs on intact skin.
Hospital equipment has also been documented as a method of transmission of
hepatitis C including: reuse of needles and syringes, multiple-use medication vials,
infusion bags, and improperly sterilized surgical equipment, among others.
Limitations in the implementation and enforcement of stringent standard
precautions in public and private medical and dental facilities are known to be the
primary cause of the spread of HCV in Egypt, the country with highest rate of
infection in the world.
Sexual intercourse
Whether hepatitis C can be transmitted through sexual activity is controversial.
While there is an association between high-risk sexual activity and hepatitis C, it is
not known whether transmission of the disease is due to drug use that has not been
admitted to or sex as a risk factor.
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The majority of evidence supports there being no risk for monogamous
heterosexual couples.
Sexual practices that involve higher levels of trauma to the anogenital mucosa,
such as anal penetrative sex, or that occur when there is a concurrent sexually
transmitted infection, including HIV or genital ulceration, do present a risk.
The United States government only recommends condom use to prevent hepatitis
C transmission in those with multiple partners.
Body piercings
Tattooing is associated with two to threefold increased risk of hepatitis C.
This can be due to either improperly sterilized equipment or contamination of the
dyes being used. Tattoos or piercings performed either before the mid-1980s,
"underground," or nonprofessionally are of particular concern, since sterile
techniques in such settings may be lacking.
The risk also appears to be greater for larger tattoos.
It is estimated that nearly half of prison inmates share unsterilized tattooing
equipment.
It is rare for tattoos in a licensed facility to be directly associated with HCV
infection.
Shared personal items
Personal-care items such as razors, toothbrushes, and manicuring or pedicuring
equipment can be contaminated with blood.
Sharing such items can potentially lead to exposure to HCV. Appropriate caution
should be taken regarding any medical condition that results in bleeding, such as
cuts and sores.
HCV is not spread through casual contact, such as hugging, kissing, or sharing
eating or cooking utensils.
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Vertical transmission
Vertical transmission of hepatitis C from an infected mother to her child occurs in
less than 10% of pregnancies.
There are no measures that alter this risk.
It is not clear when during pregnancy transmission occurs, but it may occur both
during gestation and at delivery.
A long labor is associated with a greater risk of transmission.
There is no evidence that breast-feeding spreads HCV; however, to be cautious, an
infected mother is advised to avoid breastfeeding if her nipples are cracked and
bleeding, or her viral loads are high.
Diagnosis
There are a number of diagnostic tests for hepatitis C including:




HCV antibody enzyme immunoassay or ELISA,
recombinant immunoblot assay, and
quantitative HCV RNA polymerase chain reaction (PCR).
HCV RNA can be detected by PCR typically one to two weeks after
infection, while antibodies can take substantially longer to form and thus be
detected.
Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for
more than six months based on the presence of its RNA.
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Chronic infections are typically asymptomatic during the first few decades, and
thus are most commonly discovered following the investigation of elevated liver
enzyme levels or during a routine screening of high risk individuals.
Testing is not able to distinguish between acute and chronic infections.
Serology
Hepatitis C testing typically begins with blood testing to detect the presence of
antibodies to the HCV using an enzyme immunoassay.
If this test is positive, a confirmatory test is then performed to verify the
immunoassay and to determine the viral load.
A recombinant immunoblot assay is used to verify the immunoassay and the viral
load is determined by a HCV RNA polymerase chain reaction.
If there are no RNA and the immunoblot is positive it means that the person had a
previous infection but cleared it either with treatment or spontaneously; if the
immunoblot is negative, it means that the immunoassay was wrong.
It takes about 6–8 weeks following infection before the immunoassay will test
positive.
Liver enzymes are variable during the initial part of the infection and on average
begin to rise at seven weeks after infection.
Liver enzymes are poorly related with disease severity.
Biopsy
Liver biopsies are used to determine the degree of liver damage present; however,
there are risks from the procedure.
The typical changes seen are lymphocytes within the parenchyma, lymphoid
follicles in portal triad, and changes to the bile ducts.
There are a number of blood tests available that try to determine the degree of
hepatic fibrosis and alleviate the need for biopsy.
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Screening
It is believed only 5–50% of those infected in the United States and Canada
become aware of their status.
Testing is recommended in those at high risk, which includes those with tattoos.
Screening is also recommended in those with elevated liver enzymes as this is
frequently the only sign of chronic hepatitis.
Routine screening is not currently recommended in the United States.
However, in 2012, the U.S. Centers for Disease Control and Prevention (CDC)
recommended a single screening test for those born between 1945 and 1965.
Prevention
As of 2011, no vaccine protects against contracting hepatitis C.
However, a number are under development and some have shown encouraging
results.
A combination of harm reduction strategies, such as the provision of new needles
and syringes and treatment of substance use, decrease the risk of hepatitis C in
intravenous drug users by about 75%.
The screening of blood donors is important at a national level, as is adhering to
universal precautions within healthcare facilities.
In countries where there is an insufficient supply of sterile syringes, medications
should be given orally rather than via injection.
Treatment
HCV induces chronic infection in 50–80% of infected persons.
Approximately 40-80% of these clear with treatment.
In rare cases, infection can clear without treatment.
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Those with chronic hepatitis C are advised to avoid alcohol and medications toxic
to the liver, and to be vaccinated for hepatitis A and hepatitis B.
Ultrasound surveillance for hepatocellular carcinoma is recommended in those
with accompanying cirrhosis.
Prognosis
Responses to treatment vary by genotype. Sustained response is about 40-50% in
people with HCV genotype 1 given 48 weeks of treatment.
Sustained response is seen in 70-80% of people with HCV genotypes 2 and 3 with
24 weeks of treatment.
Sustained response is about 65% in those with genotype 4 given 48 weeks of
treatment.
The evidence for treatment in genotype 6 disease is sparse, and the evidence that
exists is for 48 weeks of treatment at the same doses as are used for genotype 1
disease.
Epidemiology
Prevalence of hepatitis C worldwide in 1999
Disability-adjusted life year for hepatitis C in 2004 per 100,000 inhabitants
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no data
35-40
<10
40-45
10-15
45-50
15-20
50-75
20-25
75–100
25-30
>100
30-35
It is estimated that 130–170 million people, or ~3% of the world's population, are
living with chronic hepatitis C.
About 3–4 million people are infected per year, and more than 350,000 people die
yearly from hepatitis C-related diseases.
Rates have increased substantially in the 20th century due to a combination of IDU
and intravenous medication or poorly sterilized medical equipment.
Among those chronically infected, the risk of cirrhosis after 20 years varies
between studies but has been estimated at ~10%-15% for men and ~1-5% for
women.
The reason for this difference is not known.
Once cirrhosis is established, the rate of developing hepatocellular carcinoma is
~1%-4% per year.
Prevalence is higher in some countries in Africa and Asia.
Countries with particularly high rates of infection include Egypt (22%), Pakistan
(4.8%) and China (3.2%).
It is believed that the high prevalence in Egypt is linked to a now-discontinued
mass-treatment campaign for schistosomiasis, using improperly sterilized glass
syringes.
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Hepatitis C. Causes of chronic liver disease
Hepatitis D
Definition
Hepatitis D, also referred to as hepatitis D virus (HDV) and classified as
Hepatitis delta virus, is a disease caused by a small circular enveloped RNA virus.
Explanation
It is one of five known hepatitis viruses: A, B, C, D, and E. HDV is considered to
be a subviral satellite because it can propagate only in the presence of the hepatitis
B virus (HBV).
Transmission of HDV can occur either via simultaneous infection with HBV
(coinfection) or superimposed on chronic hepatitis B or hepatitis B carrier state
(superinfection).
Both superinfection and coinfection with HDV results in more severe
complications compared to infection with HBV alone.
These complications include a greater likelihood of experiencing liver failure in
acute infections and a rapid progression to liver cirrhosis, with an increased chance
of developing liver cancer in chronic infections.
In combination with hepatitis B virus, hepatitis D has the highest mortality rate of
all the hepatitis infections of 20%.
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History
Hepatitis D virus was first reported in the mid-1977, by an Italian researcher,
Mario Rizzetto, as a nuclear antigen in patients infected with HBV who had severe
liver disease .
This nuclear antigen was then thought to be a hepatitis B antigen and was called
the delta antigen.
Subsequent experiments in chimpanzees showed that the hepatitis delta antigen
(HDAg) was a structural part of a pathogen that required HBV infection to
replicate.
The entire virus was cloned and sequenced in 1986, and obtained its own genus
deltavirus
Virology
Structure and Genome
Hepatitis delta virus delta antigen
The HDV is a small, spherical virus with a 36 nm diameter.
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It has an outer coat containing three HBV envelope proteins (called large, medium,
and small hepatitis B surface antigens, and host lipids surrounding an inner
nucleocapsid.
The nucleocapsid contains single-stranded, circular RNA of 1679 nucleotides and
about 200 molecules of hepatitis D antigen (HDAg) for each genome.
The central region of HDAg has been shown to bind RNA.
Several interactions are also mediated by a coiled-coil region at the N terminus of
HDAg.
The hepatitis D circular genome is unique to animal viruses because of its high GC
nucleotide content.
The HDV genome exists as an enveloped negative sense, single-stranded, closed
circular RNA nucleotide sequence is 70% self-complementary, allowing the
genome to form a partially double stranded RNA structure that is described as rodlike.
With a genome of approximately 1700 nucleotides, HDV is the smallest "virus"
known to infect animals.
It has been proposed that HDV may have originated from a class of plant viruses
called viroids.
Life Cycle
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The receptor that HDV recognizes on human hepatocytes has not been identified;
however it is thought to be the same as the HBV receptor because both viruses
have the same outer coat.
HDV recognizes its receptor via the N-terminal domain of the large hepatitis B
surface antigen, HBsAg.
Mapping by mutagenesis of this domain has shown that aminoacid residues 9-15
make up the receptor binding site.
After entering the hepatocyte, the virus is uncoated and the nucleocapsid
translocated to the nucleus due to a signal in HDAg Since the nucleocapsid does
not contain an RNA polymerase to replicate the virus’ genome, the virus makes
use of the cellular RNA polymerases
Initially just RNA pol II, now RNA polymerases I and III have also been shown to
be involved in HDV replication.
Normally RNA polymerase II utilizes DNA as a template and produces mRNA.
Consequently, if HDV indeed utilizes RNA polymerase II during replication, it
would be the only known pathogen capable of using a DNA-dependent polymerase
as an RNA-dependent polymerase.
The RNA polymerases treat the RNA genome as double stranded DNA due to the
folded rod-like structure it is in.
Three forms of RNA are made; circular genomic RNA, circular complementary
antigenomic RNA, and a linear polyadenylated antigenomic RNA, which is the
mRNA containing the open reading frame for the HDAg.
Synthesis of antigenomic RNA occurs in the nucleous, mediated by RNA Pol I,
whereas synthesis of genomic RNA takes place in the nucleoplasm, mediated by
RNA Pol II.
HDV RNA is synthesized first as linear RNA that contains many copies of the
genome.
The genomic and antigenomic RNA contain a sequence of 85 nucleotides that acts
as a ribozyme, which self-cleaves the linear RNA into monomers.
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This monomers are then ligated to form circular RNA.
There are eight reported genotypes of HDV with unexplained variations in their
geographical distribution and pathogenicity.
Delta antigens
A significant difference between viroids and HDV is that, while viroids produce no
proteins, HDV is known to produce one protein, namely HDAg.
It comes in two forms; a 27kDa large-HDAg, and a small-HDAg of 24kDa.
The N-terminals of the two forms are identical, they differ by 19 more amino acids
in the C-terminal of the large HDAg.
Both isoforms are produced from the same reading frame which contains an UAG
stop codon at codon 196, which normally produces only the small-HDAg.
However, editing by cellular enzyme adenosine deaminase-1 changes the stop
codon to UCG, allowing the large-HDAg to be produced .
Despite having 90% identical sequences, these two proteins play diverging roles
during the course of an infection.
HDAg-S is produced in the early stages of an infection and enters the nucleus and
supports viral replication.
HDAg-L, in contrast, is produced during the later stages of an infection, acts as an
inhibitor of viral replication, and is required for assembly of viral particles.
Thus RNA editing by the cellular enzymes is critical to the virus’ life cycle
because it regulates the balance between viral replication and virion assembly.
Evolution
Three genotypes (I-III) were originally described.
Genotype I has been isolated in Europe, North America, Africa and some Asia.
Genotype II has been found in Japan, Taiwan, and Yakutia (Russia).
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Genotype III has been found exclusively in South America (Peru, Colombia, and
Venezuela).
Some genomes from Taiwan and the Okinawa islands have been difficult to type
but have been placed in genotype 2.
However it is not known that there are at least 8 genotypes of this virus (HDV-1 to
HDV-8).
Phylogenetic studies suggest an African origin for this pathogen.
Hepatitis D Symptoms
When a person becomes infected with the hepatitis D virus (HDV), the virus
begins to multiply within the liver.
Fourteen days to 180 days later, a person may develop hepatitis D symptoms.
However, not everyone infected with the hepatitis D virus will actually have
symptoms.
Also, some of the people who do develop symptoms will have only very mild
symptoms.
You can look and feel perfectly healthy, yet still be infected with the disease and
infect others.
Specific Hepatitis D Symptoms
For a person with hepatitis D, symptoms (especially early symptoms) may include
one or several of the following:

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

Fatigue
Excessive tiredness
Not feeling very hungry
Nausea or vomiting
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
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


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Diarrhea
A low-grade fever
Muscle pain
Joint pain
Sore throat
Mild abdominal pain (or stomach pain)
Dark urine
Light-colored stool.
Oftentimes, these early symptoms may be confused with those commonly seen
with the stomach flu .
Jaundice (yellowing of the skin or the whites of the eyes) usually occurs several
days after early symptoms of hepatitis D first appear.
However, it may occur up to two weeks after symptoms begin.
At this point, early symptoms tend to improve; but other new symptoms, such as
abdominal pain (or stomach pain) on the right side, may appear.
Clinical features
An HDV infection absolutely requires an associated HBV infection.
The outcome of disease largely depends on whether the two viruses infect
simultaneously (coinfection), or whether the newly HDV-infected person is a
chronically infected HBV carrier (superinfection).
Coinfection of HBV and HDV (simultaneous infection with the two viruses)
results in both acute type B and acute type D hepatitis.
The incubation period depends on the HBV titre of the infecting inoculum.
Depending on the relative titres of HBV and HDV, a single bout or two bouts of
hepatitis may be seen.
Coinfections of HBV and HDV are usually acute, self-limited infections.
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The chronic form of hepatitis D is seen in less than 5% of HBV - HDV coinfected
patient.
Acute hepatitis D occurs after an incubation period of 3 - 7 weeks, and a preicteric
phase begins with symptoms of




fatigue,
lethargy,
anorexia and
nausea, lasting usually 3 to 7 days.
During this phase, ALT and AST activities become abnormal.
The appearance of jaundice is typical at the onset of the icteric phase.
Fatigue and nausea persist, clay-colored stools and dark urine appear, and serum
bilirubin levels become abnormal.
In patients with acute, self-limiting infection, convalescence begins with the
disappearance of clinical symptoms.
Fatigue may persist for longer periods of time.
Superinfection of HBV and HDV (HDV infection of a chronically infected HBV
carrier) causes a generally severe acute hepatitis with short incubation time that
leads to chronic type D hepatitis in up to 80% of cases.
Superinfection is associated with fulminant acute hepatitis and severe chronic
active hepatitis, often progressive to cirrhosis.
During the acute phase of HDV infection, synthesis of both HBsAg and HBV
DNA are inhibited until the HDV infection is cleared.
Chronic viral hepatitis D is usually initiated by a clinically apparent acute
infection.
Symptoms are less severe than in acute hepatitis, and while serum ALT and AST
levels are elevated, bilirubin and albumin levels and prothrombin time may be
normal.
In chronic hepatitis D, the HBV markers are usually suppressed.
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Progression to cirrhosis usually takes 5 - 10 yrs, but it can appear 2 years after
onset of infection.
About 60 to 70% of patients with chronic hepatitis D develop cirrhosis. A high
proportion of these patients die of hepatic failure.
Hepatocellular carcinoma (HCC) occurs in chronically infected HDV patients with
advanced liver disease with the same frequency as in patients with ordinary
hepatitis B.
HCC may actually be more a secondary effect of the associated cirrhosis than a
direct carcinogenic effect of the virus.
Taken together, three phases of chronic hepatitis D have been proposed:
a) an early active phase with active HDV replication and suppression of HBV,
b) a second moderately active one with decreasing HDV and reactivating HBV,
c) a third late one with development of cirrhosis and hepatocellular carcinoma
caused by replication of either virus or with remission resulting from marked
reduction of both viruses.
Complications
One serious complication that can occur during this acute hepatitis D infection is
fulminant hepatitis -- a serious condition that results in liver failure.
Up to 5 percent of people who get infected with the hepatitis B virus at the same
time as the hepatitis D virus will develop fulminant hepatitis.
Up to 20 percent of people with chronic hepatitis B will develop fulminant
hepatitis with an acute hepatitis D infection.
Fulminant viral hepatitis is rare, but still about 10 times more common in hepatitis
D than in other types of viral hepatitis.
It is characterized by hepatic encephalopathy showing changes in
 personality,
 disturbances in sleep,
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
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confusion
difficulty concentrating,
abnormal behavior,
somnolence and
coma.
The mortality rate of fulminant hepatitis D reaches 80%.
Liver transplantation is indicated.
Some factors that can increase the risk of developing fulminant hepatitis include:



Being older
Having severe liver disease (cirrhosis)
Having had a liver transplant.
Transmission
The routes of transmission of hepatitis D are similar to those for hepatitis B.
Infection is largely restricted to persons at high risk of hepatitis B infection,
particularly injecting drug users and persons receiving clotting factor concentrates.
Worldwide more than 15 million people are co-infected.
HDV is rare in most developed countries, and is mostly associated with
intravenous drug use.
However, HDV is much more common in the immediate Mediterranean region,
sub-Saharan Africa, the Middle East, and the northern part of South America.
In all, about 20 million people may be infected with HDV.
Treatment and Prevention
There is no vaccine for Hepatitis D virus, but there is a vaccine for Hepatitis B.
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Hepatitis D needs the presence of the Hepatitus B virus in order become infectous.
Hepatitis E
Definition
Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a
virus called hepatitis E virus (HEV).
HEV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase
genome.
HEV has a fecal-oral transmission route.
It is one of five known hepatitis viruses: A, B, C, D, and E.
Infection with this virus was first documented in 1955 during an outbreak in New
Delhi, India.
Explanation
Every year there are 20 million hepatitis E infections, over three million acute
cases of hepatitis E, and 70 000 hepatitis E-related deaths.
Hepatitis E is usually self-limiting but may develop into fulminant hepatitis (acute
liver failure).
The hepatitis E virus is transmitted via the faecal-oral route, principally via
contaminated water.
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Hepatitis E is found worldwide, but the prevalence is highest in East and South
Asia.
China has produced and licensed the first vaccine to prevent hepatitis E virus
infection, although it is not yet available globally.
Globally, there are approximately 20 million incident hepatitis E infections every
year.
Virology
.
Although it was originally classified in the Caliciviridae family, the virus has since
been classified into the genus Hepevirus, but was not assigned to a viral family.
The virus itself is a small non-enveloped particle.
The genome is approximately 7200 bases in length, is a polyadenylated singlestrand RNA molecule that contains three discontinuous and partially overlapping
open reading frames (ORFs) along with 5' and 3' cis-acting elements, which have
important roles in HEV replication and transcription.
ORF1 encode a methyltransferase, protease, helicase and replicase; ORF2 encode
the capsid protein and ORF3 encodes a protein of undefined function.
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A three-dimensional, atomic-resolution structure of the capsid protein in the
context of a virus-like particle has been described.
An in vitro culture system is not yet available.
As of 2009 there are approximately 1,600 sequences of both human and animal
isolates of HEV available in open-access sequence databases.
Species of this genus infect humans, pigs, boars, deer, rats, rabbits and birds.
Epidemology
There is only one serotype of the virus and classification is based on the nucleotide
sequences of the genome.
Genotype 1 has been classified into five subtypes.
The number of genotype 2 can be classified into two subtypes.
Genotypes 3 and 4 have been into ten and seven subtypes respectively.
Hepatitis E is found worldwide and different genotypes of the hepatitis E virus
determine differences in epidemiology.
For example, genotype 1 is usually seen in developing countries and causes
community level outbreaks while genotype 3 is usually seen in the developed
countries and does not cause outbreaks.
Globally, 70 000 deaths and 3.4 million cases of acute hepatitis E are attributable
to infection with hepatitis E virus genotypes 1 and 2.
The highest seroprevalence rates (number of persons in a population who test
positive for the disease) are observed in regions where low standards of sanitation
increase the risk for transmission of the virus.
Over 60% of all hepatitis E infections and 65% of all hepatitis E deaths occur in
East and South Asia, where seroprevalence rates of 25% are common in some age
groups.
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In Egypt, half the population aged above five years is serologically positive for the
hepatitis E virus.
Recent outbreaks
In 2004, there were two major outbreaks, both of them in sub-Saharan Africa.
There was an outbreak in Chad in which, as of September 27, there were 1,442
reported cases and 46 deaths.
The second was in Sudan with, as of September 28, 6,861 cases and 87 deaths.
Increasingly, hepatitis E is being seen in developed nations, with reports of cases in
the UK, US and Japan.
The disease is thought to be a zoonosis in that animals are thought to be the source.
Both deer and swine have been implicated.
In 2011, a minor outbreak was reported in Tangail, a neighborhood of Dhaka,
Bangladesh.
In June 2012, an outbreak was reported in city of Ichalkaranji, Maharashtra, India.
As of June 14, 2012, 3232 cases were reported and 18 died. and 3 died in Shirol
taluka of Kolhapur Maharashtra ,India in june 2012
In July 2012, an outbreak was reported in South Sudanese refugee camps in Maban
County near the Sudan border.
South Sudan's Ministry of Health reported over 400 cases and 16 fatalities.
Animals as a reservoir
Domestic animals have been reported as a reservoir for the hepatitis E virus, with
some surveys showing infection rates exceeding 95% among domestic pigs.
Transmission after consumption of wild boar meat and uncooked deer meat has
been reported as well.
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The rate of transmission to humans by this route and the public health importance
of this are, however, still unclear.
A number of other small mammals have been identified as potential reservoirs:
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the lesser bandicoot rat (Bandicota bengalensis),
the black rat (Rattus rattus brunneusculus) and
the Asian house shrew (Suncus murinus).
A new virus designated rat hepatitis E virus has been isolated.
An avian virus has been described that is associated with hepatitis-splenomegaly
syndrome in chickens.
This virus is genetically and antigenically related to mammalian HEV, and
probably represents a new genus in the family.
Replicative virus has been found in the small intestine, lymph nodes, colon and
liver of experimentally infected pigs.
Transmission
The hepatitis E virus is transmitted mainly through the faecal-oral route due to
faecal contamination of drinking water. Other transmission routes have been
identified, which include:

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foodborne transmission from ingestion of products derived from infected
animals;
zoonotic transmission from animals to humans;
transfusion of infected blood products;
vertical transmission from a pregnant woman to her fetus.
Although humans are considered the natural host for the hepatitis E virus,
antibodies to the hepatitis E virus or closely related viruses have been detected in
primates and several other animal species.
Hepatitis E is a waterborne disease, and contaminated water or food supplies have
been implicated in major outbreaks.
The ingestion of raw or uncooked shellfish has also been identified as the source of
sporadic cases in endemic areas.
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The risk factors for hepatitis E are related to poor sanitation in large areas of the
world and shedding of the hepatitis E virus in faeces.
Symptoms
The incubation period following exposure to the hepatitis E virus ranges from three
to eight weeks, with a mean of 40 days.
The period of communicability is unknown.
The hepatitis E virus causes acute sporadic and epidemic viral hepatitis.
Symptomatic infection is most common in young adults aged 15–40 years.
Although infection is frequent in children, the disease is mostly asymptomatic or
causes a very mild illness without jaundice (anicteric) that goes undiagnosed.
Typical signs and symptoms of hepatitis include:
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jaundice (yellow discoloration of the skin and sclera of the eyes, dark urine
and pale stools);
anorexia (loss of appetite);
an enlarged, tender liver (hepatomegaly);
abdominal pain and tenderness;
nausea and vomiting;
fever.
These symptoms are largely indistinguishable from those experienced during any
acute phase of hepatic illness and typically last for one to two weeks.
In rare cases, acute hepatitis E can result in fulminant hepatitis (acute liver failure)
and death.
Overall population mortality rates from hepatitis E range from 0.5% to 4.0%.
Fulminant hepatitis occurs more frequently during pregnancy.
Pregnant women are at greater risk of obstetrical complications and mortality from
hepatitis E, which can induce a mortality rate of 20% among pregnant women in
their third trimester.
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Cases of chronic hepatitis E infection have been reported in immunosuppressed
people.
Reactivation of hepatitis E infection has also been reported in
immunocompromised people.
Diagnosis
Cases of hepatitis E are not clinically distinguishable from other types of acute
viral hepatitis.
Diagnosis of hepatitis E infection is therefore usually based on the detection of
specific antibodies to the virus in the blood.
Two additional diagnostic tests require specialized laboratory facilities and are
used only in research studies.
These are:


reverse transcriptase polymerase chain reaction (RT-PCR) to detect the
hepatitis E virus RNA;
immune electron microscopy to detect the hepatitis E virus.
Hepatitis E should be suspected in outbreaks of waterborne hepatitis occurring in
developing countries, especially if the disease is more severe in pregnant women,
or if hepatitis A has been excluded.
Treatment
There is no available treatment capable of altering the course of acute hepatitis.
Prevention is the most effective approach against the disease.
As hepatitis E is usually self-limiting, hospitalization is generally not required.
However, hospitalization is required for people with fulminant hepatitis and should
also be considered for infected pregnant women.
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Prevention
The risk of infection and transmission can be reduced by:


maintaining quality standards for public water supplies ;
establishing proper disposal systems to eliminate sanitary waste.
On an individual level, infection risk can be reduced by:

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
maintaining hygienic practices such as hand washing with safe water,
particularly before handling food;
avoiding drinking water and/or ice of unknown purity;
avoiding eating uncooked shellfish, and uncooked fruits or vegetables that
are not peeled or that are prepared by people living in or travelling in highly
endemic countries.
A vaccine based on recombinant viral proteins has been developed and
recently tested in a high-risk population (military personnel of a developing
country).
The vaccine appeared to be effective and safe, but further studies are needed
to assess the long-term protection and the cost-effectiveness of hepatitis E
vaccination.
In 2011, the first vaccine to prevent hepatitis E infection was registered in
China.
A different vaccine (HEV 239, sold as Hecolin by its developer Xiamen
Innovax Biotech) was approved for the disease in 2012 by the Chinese
Ministry of Science and Technology, following a phase 3 trial on two groups
of 50,000 people each from Jiangsu Province where none of the vaccinated
became infected during a 12 month period, compared to 15 in the group
given placebo treatment.
Although it is not available globally, it could potentially become available in a
number of other countries.
Guidelines for epidemic measures
In epidemics, WHO recommends:


determining the mode of transmission;
identifying the population specifically exposed to increased risk of infection;
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eliminating a common source of infection;
improving sanitary and hygienic practices to eliminate faecal contamination
of food and water.
WHO response
WHO is working in the following areas to prevent and control viral hepatitis:

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
raising awareness, promoting partnerships and mobilizing resources;
evidence-based policy and data for action;
prevention of transmission; and
screening, care and treatment.
WHO also organizes World Hepatitis Day on 28 July every year to increase
awareness and understanding of viral hepatitis
Hepatitis F
Definition
Hepatitis F is a hypothetical virus linked to hepatitis.
Several hepatitis F candidates emerged in the 1990s; none of these reports have
been substantiated.
Virology
Hepatitis F is a new virus in the Hepatitis family, that is affecting may people
worldwide.
A disease that became more evident in the 1990s, this virus has often been
referred to as the ‘non-existent virus’ or even a ‘hypothetical virus’.
The virus is also called as VLP or Virus like Particles because of their small size.
Soon, the virus affects the liver like all other cases of Hepatitis and around 20% of
cases result in fatality.
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In 1994, Deka et al. reported that novel viral particles had been discovered in the
stool of post-transfusion, non-hepatitis A, non-hepatitis B, non-hepatitis C, nonhepatitis E patients.
Injection of these particles into the bloodstream of Indian rhesus monkeys caused
hepatitis, and the virus was named hepatitis F or Toga virus.
Further investigations failed to confirm the existence of the virus, and it was
delisted as a cause for infectious hepatitis.
A subsequently-discovered virus thought to cause hepatitis was named Hepatitis G
virus, though its role in hepatitis has not been confirmed and it is now considered
synonymous with GB virus C and is an "orphan virus" with no causal links to any
human disease.
Hepatitis F’s discovery
After scientists discovered Hepatitis A, B, C, D and E, they noticed another strand
of Hepatitis virus that couldn’t exactly be classified within the reaches of these 5
types.
Sometimes between 1991 and 1992, Japanese doctors noticed that this was a
completely new class of virus and named it Hepatitis F.
It was in 1993 that Hepatitis F was termed as a mutant virus from HBV in Japan
and this was verified by the help of a PCR study.
Further studies were done until 1994, when this virus was understood better by
means of experimentations and lab examinations and doctors were better able to
understand the symptoms of Hepatitis F and its treatment.
symptoms
Like other forms of Hepatitis, Hepatitis F also has symptoms that include:

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Abdominal pain
Vomiting
Fatigue and fever
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Appetite loss
Jaundice or dark yellow urine
Nausea & Diarrhea
Anorexia
It is also accompanied by joint pain and a rash, though this symptom is seen only at
the last stages of the disease.
Diagnosis
To diagnose Hepatitis F is very important in order for the patient to get the right
medical treatment.
Since the disease can be fatal, timely treatment is based on accurate diagnostics.
The doctor will study a variety of things

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Patient’s medical history
Sexual activity
Surgeries done in the past
Based on these, the doctor will recommend a liver panel test along with blood tests
to diagnose the disease.
Some doctors will also suggest a RIBA II and ELISA II tests.
In certain cases, diagnosis becomes very difficult which will create the need for a
liver biopsy.
Since the right treatment is very important, the patient will need to undergo a small
treatment where a small tissue sample of the liver will be studied under the
microscope to give more accurate results.
Fact is; since the Hepatitis F virus is a fairly new virus, the tests and diagnostics to
accurately pin point the disease is not yet very advanced.
Treatment
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Currently, there is no cure for Hepatitis F. since the virus is fairly new and a
mutant of the HBV virus, many scientists and doctors around the globe are
working round the clock to come up with a cure.
Until medicines and vaccination for curing Hepatitis F are discovered, the doctor
can do nothing more than trying to treat the immediate symptoms of the disease to
bring comfort to the patient.
This is why diagnosing Hepatitis F timely is so important.
If the doctors can detect the Hepatitis F virus early on, the case for survival
improves in patients.
Hepatitis G
Definition
Hepatitis G is a liver disease or rather inflammation of liver that is caused by the
hepatitis G virus or the HGV.
Virology
The HGV is the newly discovered far off relative of the hepatitis C virus.
The other term for HGV is GB.
The virus is benign is nature.
It was mentioned for the first time in the early 1996.
Not much is known about the nature of sickness HGV causes or the infection
frequency or the prevention procedure and so on.
Transmission
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Reports reveal that most cases of hepatitis were due to transfusion of blood
containing the HGV virus.
Thus patients with conditions like hemophilia or any other condition that demands
the supply of blood were highly susceptible to getting hepatitis G.
Also
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health care workers,
hemodialysis patients,
injected drug users,
acupuncturists,
those who use tattoos or
other body piercing arts etc
can contact hepatitis G infection.
Furthermore infected mothers can transfer the virus to her newborn.
So can the virus be sexually transmitted as well.
Causes & Symptoms
Whether hepatitis G actually makes one sick is not very clear.
Some believe it does whereas some believe it does not.
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Some researchers hold the opinion that the sickness is mild whereas others think it
is chronic enough to lead to a liver failure even.
Some researchers believe that a single HGV acts on the liver whereas others
believe that the virus acts in a group to produce a cumulative result.
In some cases Hepatitis G co-exists with HIV or Hepatitis C virus and often go
undiagnosed since it shows up no symptom and remains in latent form for as long
as nine years at a stretch.
Diagnosis & treatment
Diagnosis plays a key role in the treatment of any disease.
It is in fact the first step towards treatment.
Without proper diagnosis you cannot at all treat a disease.
The means of detecting or diagnosing hepatitis G is the DNA test.
It is the only diagnosis means and quite an expensive one.
The DNA diagnosis procedure is a complicated procedure and is not very much
available.
Efforts are being made however to generate an assay for the HGV antibody which
develops as a result of the virus invasion
Hepatitis G: Do’s & Don’ts
A patient with Hepatitis G has to observe the following ‘do’s’ and ‘don’ts’:

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He should not consume fatty or spice-rich food and also should limit the
intake of protein.
He should get adequate rest and sleep.
He should stay away from alcohol.
He should not smoke.
He should dink at least 8-10 glasses of water per day to flush out the toxins.
He should curb the intake of caffeinated beverages.
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He should live a stress-free life. He should practice yoga and meditation to
get rid of his stress
He should practice light free-hand exercises
He should use contraceptive measures while indulging in sexual activities
He should take his medicines timely and go for timely check-ups
Autoimmune Hepatitis
Definition
Autoimmune Hepatitis is a disease of the liver that occurs when the body's
immune system attacks cells of the liver.
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface
of hepatocytes, possibly due to genetic predisposition or acute liver infection,
causes a cell-mediated immune response against the body's own liver, resulting in
autoimmune hepatitis.
This abnormal immune response results in inflammation of the liver, which can
lead to further complications, including cirrhosis.
Immune serum markers frequently are present, autoantibodies against liver-specific
and non–liver-specific antigens and increased immunoglobulin G (IgG) levels.
The disease often is associated with other autoimmune diseases.
Autoimmune hepatitis cannot be explained on the basis of chronic viral infection,
alcohol consumption, or exposure to hepatotoxic medications or chemicals.
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Explanation
Autoimmune hepatitis has an incidence of 1-2 per 100,000 per year, and a
prevalence of 10-20/100,000.
As with most other autoimmune diseases, it affects women much more often than
men (70%).
Liver enzymes are elevated, as may be bilirubin.
Historical background
In 1950, Waldenstrom first described a form of chronic hepatitis in young women.
This condition was characterized by cirrhosis, plasma cell infiltration of the liver,
and marked hypergammaglobulinemia.
Kunkel, in 1950, and Bearn, in 1956, described other features of the disease,
including hepatosplenomegaly, jaundice, acne, hirsutism, cushingoid facies,
pigmented abdominal striae, obesity, arthritis, and amenorrhea.
In 1955, Joske first reported the association of the lupus erythematosus (LE) cell
phenomenon in active chronic viral hepatitis.
This association led to the introduction of the term lupoid hepatitis by Mackay and
associates in 1956.
Researchers currently know that no direct link exists between systemic lupus
erythematosus (SLE) syndrome and autoimmune hepatitis; thus, lupoid hepatitis is
not associated with SLE.
The development of viral serologic tests represented another important step
forward.
These permitted hepatologists to differentiate chronic viral hepatitis from other
types of chronic liver disease, including autoimmune hepatitis.
Autoimmune hepatitis now is recognized as a multisystem disorder that can occur
in males and females of all ages.
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This condition can coexist with other liver diseases (eg, chronic viral hepatitis) and
also may be triggered by certain viral infections (eg, hepatitis A) and chemicals
(eg, minocycline).
The histopathologic description of autoimmune hepatitis has undergone several
revisions over the years.
In 1992, an international panel codified the diagnostic criteria.
The term autoimmune hepatitis was selected to replace terms such as autoimmune
liver disease and autoimmune chronic active hepatitis.
The panel waived the requirement of 6 months of disease activity to establish
chronicity, expanded the histologic spectrum to include lobular hepatitis, and
reaffirmed the nonviral nature of the disease.
The panel also designated incompatible histologic features, such as cholestatic
histology, the presence of bile duct injury, and ductopenia.
Etiology
The etiology of autoimmune hepatitis is unknown.
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Several factors (eg, viral infection, drugs, environmental agents) may trigger an
autoimmune response and autoimmune disease.
In a few patients with autoimmune hepatitis, illness onset follows acute hepatitis
A, hepatitis B, or Epstein-Barr virus infections.
Autoantibodies are common in patients with chronic hepatitis C virus (HCV)
infection.
Some patients with chronic HCV infection exhibit liver-kidney microsomal type 1
(LKM-1) antibody.
Some cases of drug-induced liver disease have an immune-mediated basis.
A number of drugs (eg, methyldopa, nitrofurantoin, minocycline, adalimumab,
infliximab,) can produce an illness with the clinical features of autoimmune
hepatitis.
Although most cases improve when the drug is stopped, chronic cases of
autoimmune hepatitis may be seen, even after drug withdrawal.
Casswall et al found Helicobacter species DNA in 50% of liver biopsies from
patients with autoimmune hepatitis and ulcerative colitis.
Classification
Four subtypes are recognised, but the clinical utility of distinguishing subtypes is
limited.
1. positive ANA and SMA, elevated immunoglobulin G (classic form,
responds well to low dose steroids);
2. positive LKM-1 (typically female children and teenagers; disease can be
severe), LKM-2 or LKM-3;
3. positive antibodies against soluble liver antigen (this group behaves like
group 1) (anti-SLA, anti-LP)
4. no autoantibodies detected (~20%)
Clinical features
Clinical features of autoimmune hepatitis widely vary.
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Most cases have an insidious onset.
Patients may be asymptomatic or have nonspecific symptoms (eg, fatigue,
anorexia, weight loss, behavioral changes, amenorrhea).
Systemic or cutaneous abnormalities occur in 25% of patients.
Epistaxis, bleeding gums, and bruises with minimal trauma are frequent
complaints.
Autoimmune hepatitis may present as acute hepatitis, chronic hepatitis, or wellestablished cirrhosis.
Autoimmune hepatitis rarely presents as fulminant hepatic failure.
Approximately one third of patients present with symptoms of acute hepatitis
marked by fever, hepatic tenderness, and jaundice.
In some patients, the acute illness may appear to resolve spontaneously; however,
patients invariably develop signs and symptoms of chronic liver disease.
Other patients experience rapid progression of the disease to acute liver failure, as
marked by coagulopathy and jaundice.
Ascites and hepatic encephalopathy also may ensue.
The chronic hepatitis associated with autoimmune hepatitis may range in severity
from a subclinical illness without symptoms and with abnormal results on liver
chemistries to a disabling chronic liver disease.
Symptoms and physical examination findings may stem from the various
extrahepatic diseases associated with autoimmune hepatitis.
Common symptoms include the following:
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Fatigue
Upper abdominal discomfort
Mild pruritus
Anorexia
Myalgia
Diarrhea
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Cushingoid features
Arthralgias
Skin rashes (including acne)
Edema
Hirsutism
Amenorrhea
Chest pain from pleuritis
Weight loss and intense pruritus (unusual)
Many patients have histologic evidence of cirrhosis at the onset of symptoms.
This is true both for patients with an initial presentation of acute hepatitis and for
patients with chronic hepatitis.
Thus, subclinical disease often precedes the onset of symptoms.
As many as 20% of patients present initially with signs of decompensated
cirrhosis.
In other patients, chronic hepatitis progresses to cirrhosis after years of
unsuccessful immunosuppressant therapy marked by multiple disease relapses.
This is said to occur in 20-40% of patients.
Patients with cirrhosis may experience classic symptoms of portal hypertension,
namely variceal bleeding, ascites, and hepatic encephalopathy.
Patients with complications of cirrhosis should be referred for consideration of
liver transplantation.
Associated disease
Autoimmune hepatitis, especially type 2, is associated with a wide variety of other
disorders.
Involvement of other systems may present at disease onset or may develop during
the course of active liver disease.
Most of these conditions are immunologic in origin.
Patients may present with manifestations of the following hematologic disorders:
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Hypersplenism
Autoimmune hemolytic anemia
Coombs-positive hemolytic anemia
Pernicious anemia
Idiopathic thrombocytopenic purpura
Eosinophilia
Gastrointestinal disease associated with autoimmune hepatitis includes
inflammatory bowel disease, which is seen in 6% of cases.
The presence of ulcerative colitis in patients with autoimmune hepatitis should
prompt performance of cholangiography to exclude primary sclerosing cholangitis
(PSC).
A study of 140 pediatric patients with autoimmune hepatitis, autoimmune
cholangitis, and overlap syndrome identified 23 patients with celiac disease.
Associated endocrinologic conditions include Graves disease (6%) and
autoimmune thyroiditis (12%).
Associated rheumatologic complications include the following:

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Rheumatoid arthritis and Felty syndrome
Sjögren syndrome
Systemic sclerosis
Mixed connective-tissue disease
Erythema nodosum
Leukocytoclastic vasculitis (patients may present with leg ulcers)
Other associated conditions are as follows:
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Proliferative glomerulonephritis
Fibrosing alveolitis
Pericarditis and myocarditis
Febrile panniculitis
Lichen planus
Uveitis
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Pediatric presentation
In 1997, Gregorio et al published a series of 52 cases of autoimmune hepatitis in
children (32 children with autoimmune hepatitis type 1 [AIH-1] and 20 children
with autoimmune hepatitis type 2 [AIH-2]).
The following summary of clinical features of AIH was based on 20 years of
treating these children at King's College Hospital.
Median patient ages were 10 years for AIH-1 and 7.4 years for AIH-2.
Other autoimmune disorders occurred in 20% of patients and 40% of their
relatives; these included autoimmune thyroiditis, celiac disease, inflammatory
bowel disease, diabetes mellitus, and other disorders.
AIH-2 can be part of autoimmune polyendocrinopathy-candidiasis-ectodermal
dystrophy (APECED), an autosomal recessive genetic disorder in which liver
disease is reportedly present in about 20% of cases.
In 50% of the children, acute presentation mimicked acute viral hepatitis (ie,
abdominal discomfort, vomiting, nausea, jaundice).
Fulminant hepatic failure occurred in 11% of the children and was more common
in patients with AIH-2.
Insidious presentation was characterized by intermittent jaundice or nonspecific
symptoms.
Routine blood analysis revealed incidental findings of abnormal liver enzymes.
Patients with autoimmune hepatitis developed cirrhosis and portal hypertension.
In 2005, Oettinger et al published a series of 142 children with autoimmune
hepatitis.
Clinical findings included the following:


Jaundice (58%)
Nonspecific weakness (57%)
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Anorexia (47%)
Abdominal pain (38%)
Paleness (26%)
AIH-1 was found in 73% of the children, AIH-2 was found in 25% of the children,
and 4 children could not be classified.
Liver biopsy showed active hepatitis (52%), cirrhosis (38%), and mild
inflammatory activity (10%).
Additional autoimmune disorders often occur in children with autoimmune
hepatitis.
In children with AIH-1, associated autoimmune disorders include the following:






Ulcerative colitis
Sclerosing cholangitis
Arthritis
Vasculitis
Glomerulonephritis
Diabetes mellitus
In children with AIH-2, associated autoimmune disorders include the following:




Polyendocrinopathy
Alopecia areata
Diabetes mellitus
Thyroiditis
Acute liver failure occurs primarily between the ages of 13 months and 4 years in
children with AIH-2. It typically occurs after puberty in patients with AIH-1.
Symptoms in females
If the patient is classically a young female ,they may present with signs of chronic
liver disease (cirrhosis, low albumin, spider nivae etc) or acute hepatitis (25%
present with fever, jaundice, painful hepatomegaly etc).
Commonly, the patient will have amenorrhoea - this may be the presenting
complaint.
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The proposed pathogenesis of autoimmune hepatitis involves the combination of
genetic predisposition and environmental triggers.
The genetic predisposition may relate to several defects in immunologic control of
autoreactivity.
An environmental agent triggers the autoimmune response against liver antigens,
causing necroinflammatory liver damage, fibrosis, and, eventually, cirrhosis, if left
untreated.
Genetic predisposition
Genetic susceptibility to developing autoimmune hepatitis has been associated with
the HLA haplotypes B8, B14, DR3, DR4, and Dw3.
C4A gene deletions are associated with the development of autoimmune hepatitis
in younger patients.
HLA-DR3–positive patients are more likely than other patients to have aggressive
disease, which is less responsive to medical therapy and more often results in liver
transplantation; in addition, these patients are younger than other patients at the
time of their initial presentation.
HLA-DR4–positive patients are more likely to develop extrahepatic manifestations
of their disease.
Patients with autoimmune hepatitis have low levels of T lymphocytes that express
the CD8 marker and a specific defect in a subpopulation of T cells that controls the
immune response to specific liver cell membrane antigens.
Autoimmune hepatitis has also been associated with the complement allele
C4AQO, resulting in a partial deficiency of complement component C4.
C4 has a well-known role in virus neutralization; failure to eliminate viruses may
lead to immune reaction against antigen on infected cells.
Environmental triggers
Among the several viruses implicated as triggering agents are rubella, EpsteinBarr, and hepatitis A, B, and C.
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Some authors have shown a high amino acid sequence homology between hepatitis
C virus (HCV) polyprotein and CYP2D6, the molecular target of liver-kidney
microsomal type 1 (LKM-1) antibody, which suggests that molecular mimicry may
trigger production of LKM-1 antibody in HCV infection.
Drugs may also trigger autoimmune hepatitis; however, no specific drug has been
identified as an etiologic agent for autoimmune hepatitis.
Drug-metabolizing enzymes of phase 1 and phase 2 (ie, cytochrome P-450, uridine
diphosphate glucuronosyltransferase proteins) are targets of virus-induced and
drug-induced autoimmunity, as well as autoimmune hepatitis.
Pathogenesis
Current evidence suggests that liver injury in a patient with autoimmune hepatitis
is the result of a cell-mediated immunologic attack.
Aberrant display of human leukocyte antigen (HLA) class II on the surface of
hepatocytes facilitates the exposure of normal liver cell membrane constituents to
antigen-presenting cells (APCs).
APCs present hepatic antigens to uncommitted helper T lymphocytes (TH 0). APCs
and helper T lymphocytes interact at the ligand-ligand level, which, in turn,
activates TH 0.
This activation is followed by functional differentiation into helper T cell 1 (TH 1)
or helper T cell 2 (TH 2), according to the cytokines prevailing in the tissue and the
nature of the antigen.
TH 1 primarily secretes interleukin 2 (IL-2) and interferon gamma, which activate
macrophages and enhance expression of HLA classes I and II, thus perpetuating
the immune recognition cycle.
TH 2 cells primarily produce interleukins 4, 5, and 10, which stimulate
autoantibody production by B lymphocytes.
The reasons for the aberrant HLA display are unclear.
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It may be initiated or triggered by genetic factors, viral infections (eg, acute
hepatitis A or B, Epstein-Barr virus infection), and chemical agents (eg, interferon,
melatonin, alpha methyldopa, oxyphenisatin, nitrofurantoin, tienilic acid).
The asialoglycoprotein receptor and the cytochrome mono-oxygenase P-450 IID6
are proposed as the triggering autoantigens.
Physiologically, TH 1 and TH 2 cells antagonize each other.
Regulatory mechanisms strictly control the autoantigen recognition process; their
failure perpetuates an autoimmune attack.
Liver cell injury can be caused by the action of cytotoxic lymphocytes that are
stimulated by IL-2, complement activation, engagement of natural killer
lymphocytes by the autoantibody bound to the hepatocyte surface, or reaction of
autoantibodies with liver-specific antigens expressed on hepatocyte surfaces.
Autoantibody-coated hepatocytes from patients with autoimmune hepatitis are
killed when incubated with autologous allogenic lymphocytes.
The effector cell was shown to be an Fc receptor-positive mononuclear cell.
Wen and others have shown that T-cell clones from liver biopsy specimens in
children with autoimmune hepatitis who express the γ/δ T-cell receptor are
preferentially cytotoxic to liver-derived cells.
Evidence for an autoimmune pathogenesis includes the following:

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


Hepatic histopathologic lesions composed predominantly of cytotoxic T
cells and plasma cells
Circulating autoantibodies (ie, nuclear, smooth muscle, thyroid, liver-kidney
microsomal, soluble liver antigen, hepatic lectin)
Association with hypergammaglobulinemia and the presence of a
rheumatoid factor
Association with other autoimmune diseases
Response to steroid and/or immunosuppressive therapy
The autoantibodies described in these patients include the following:


Antinuclear antibody (ANA), primarily in a homogeneous pattern
Anti–smooth muscle antibody (ASMA) directed at actin
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
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
Anti–liver-kidney microsomal antibody (anti–LKM-1)
Antibodies against soluble liver antigen (anti-SLA) directed at cytokeratins
types 8 and 18
Antibodies to liver-specific asialoglycoprotein receptor or hepatic lectin
Antimitochondrial antibody (AMA) - AMA is the sine qua non of primary
biliary cirrhosis (PBC) but may be observed in the so-called overlap
syndrome with autoimmune hepatitis.
Antiphospholipid antibodies.
Epidemiology
International statistics
The prevalence of autoimmune hepatitis is estimated to be 0.1-1.2 cases per
100,000 individuals in Western Europe.
The reported prevalence of autoimmune hepatitis in Europe ranges from 11.6-16.9
cases per 100,000 persons.
The reported prevelance is higher than the estimated prevalance.
This is approximately the same prevalence as primary biliary cirrhosis and twice as
high as the prevalence of primary sclerosing cholangitis.
Autoimmune hepatitis accounts for about 3% of liver transplantations in Europe.
The reported prevalence in Japan is only 0.08-0.015 cases per 100,000 persons in
Japan.
The ratio of incidence of AIH-1 to AIH-2 is
 1.5-2:1 in Europe and Canada and
 6-7:1 in North America, South America, and Japan.
AIH-2 is more commonly described in southern Europe than in northern Europe,
the United States, or Japan.
In an analysis of data from 33,379 patients with liver cirrhosis, Michitaka et al
concluded that autoimmune hepatitis is the etiologic agent in 1.9% of such cases in
Japan.
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Racial, sexual, and age-related differences in incidence
The disease is most common in whites of northern European ancestry with a high
frequency of HLA-DR3 and HLA-DR4 markers.
The Japanese population has a low frequency of HLA-DR3 markers. In Japan,
autoimmune hepatitis is associated with HLA-DR4.
Women are affected more often than men (70-80% of patients are women).
Autoimmune hepatitis has a bimodal age distribution, with a first peak of incidence
at age 10-20 years and a second at age 45-70 years.
Approximately one half of affected individuals are younger than 20 years;
incidence peaks in premenstrual girls.
Patients with AIH-2 tend to be younger; 80% of patients with AIH-2 are children.
However, autoimmune hepatitis may occur in people of any age, including infants
and older adults.
The diagnosis should not be overlooked in individuals older than 70 years.
Men may be affected more commonly than women in older age groups.
Physical Examination
Common findings on physical examination are as follows:






Hepatomegaly (83%)
Jaundice (69%)
Splenomegaly (32%)
Spider angiomata (58%)
Ascites (20%)
Encephalopathy (14%)
All of these findings may be observed in patients with disease that has progressed
to the point of cirrhosis with ensuing portal hypertension.
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However, hepatomegaly, jaundice, splenomegaly, and spider angiomata also may
be observed in patients who do not have cirrhosis.
Complications
Complications may include the following:




Cirrhosis and complications of cirrhosis (eg, ascites, coagulopathy, hepatic
coma)
Portal hypertension
Esophageal varices
Malnutrition (with poor growth in children)
GI tract bleeding as a complication of portal hypertension is usually rare.
Diagnosis
The diagnosis of autoimmune hepatitis is best achieved with a combination of
clinical, laboratory and histological findings.
Clinicians must consider the diagnosis of autoimmune hepatitis in any patient who
has acute hepatitis or acute liver failure (defined by the new onset of
coagulopathy).
The workup of such patients should include testing for :
 serum autoantibodies,
 serum protein electrophoresis, and
 quantitative immunoglobulins.
Urgent liver biopsy, transjugular if appropriate, may help to confirm the clinical
suspicion of acute autoimmune hepatitis.
A number of specific antibodies found in the blood
 antinuclear antibody (ANA),
 anti-Smooth Muscle Antibody (SMA),
 liver/kidney microsomal antibody (LKM-1, LKM-2, LKM-3)
 anti soluble liver antigen (SLA/LP) and
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 anti-mitochondrial antibody (AMA)) are of use, as is finding an increased
Immunoglobulin G level.
However, the diagnosis of autoimmune hepatitis always requires a liver biopsy.
Expert oppinion has been summarized by the International Autoimmune Hepatitis
Group, which has published criteria which utilize clinical and laboratory data that
can be used to help determine if a patient has autoimmune hepatitis.
Overlapping presentation with primary biliary cirrhosis and primary sclerosing
cholangitis has been observed.
Laboratory findings in autoimmune hepatitis include the following:



Elevated serum aminotransferase levels (1.5-50 times reference values)
Elevated serum immunoglobulin levels, primarily immunoglobulin G (IgG)
Seropositive results for ANAs, SMAs, or LKM-1 or anti–liver cytosol 1
(anti-LC1) antibodies
In 50% of patients, abnormal results on liver function tests include decreased
albumin levels and prolonged prothrombin time.
Alcoholic hepatitis
Definition
Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake
of alcohol.
Explanation
It is usually found in association with hepatosteatosis, an early stage of alcoholic
liver disease, and may contribute to the progression of fibrosis, leading to cirrhosis
Symptoms are jaundice, ascites (fluid accumulation in the abdominal cavity),
fatigue and hepatic encephalopathy (brain dysfunction due to liver failure).
Mild cases are self-limiting, but severe cases have a high risk of death.
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Symptoms and signs
Alcoholic hepatitis is characterized by a variable constellation of symptoms, which
may include feeling unwell, enlargement of the liver, development of fluid in the
abdomen (ascites), and modest elevation of liver enzyme levels (as determined by
liver function tests).
Alcoholic hepatitis can vary from mild with only liver enzyme elevation to severe
liver inflammation with development of jaundice, prolonged prothrombin time, and
even liver failure.
Severe cases are characterized by either obtundation (dulled consciousness) or the
combination of elevated bilirubin levels and prolonged prothrombin time; the
mortality rate in both severe categories is 50% within 30 days of onset.
Alcoholic hepatitis is distinct from cirrhosis caused by long-term alcohol
consumption.
Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and
alcoholic cirrhosis.
Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more
common in patients with long term alcohol consumption.
Some alcoholics develop acute hepatitis as an inflammatory reaction to the cells
affected by fatty change.
This is not directly related to the dose of alcohol.
Some people seem more prone to this reaction than others.
This is called alcoholic steatonecrosis and the inflammation probably predisposes
to liver fibrosis.
Etiology and Pathophysiology
Some signs and pathological changes in liver histology include:
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

Mallory's hyaline - a condition where pre-keratin filaments accumulate in
hepatocytes. This sign is not limited to alcoholic liver disease, but is often
characteristic.
Ballooning degeneration - hepatocytes in the setting of alcoholic change
often swell up with excess fat, water and protein; normally these proteins are
exported into the bloodstream. Accompanied with ballooning, there is
necrotic damage. The swelling is capable of blocking nearby biliary ducts,
leading to diffuse cholestasis.
Inflammation - neutrophilic invasion is triggered by the necrotic changes
and presence of cellular debris within the lobules. Ordinarily the amount of
debris is removed by Kupffer cells, although in the setting of inflammation
they become overloaded, allowing other white cells to spill into the
parenchyma. These cells to hepatocytes with Mallory bodies.
If chronic liver disease is also present:


Fibrosis
Cirrhosis - a progressive and permanent type of fibrotic degeneration of liver
tissue.
Although the association of alcohol and liver disease has been known since
antiquity, the precise mechanism of alcoholic liver disease remains in dispute.
Genetic, environmental, nutritional, metabolic, and immunologic factors, as well as
cytokines and viral disease have been invoked.
Ethanol metabolism
Most tissues of the body, including the skeletal muscles, contain the necessary
enzymes for the oxidative or nonoxidative metabolism of ethanol.
However, the major site of ethanol metabolism is the liver.
Within the liver, 3 enzyme systems—
 the cytosolic alcohol dehydrogenase (ADH) system,
 microsomal ethanol-oxidizing system (MEOS), and
 peroxisomal catalase system—can oxidize ethanol.
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Cytosolic ADH uses nicotinamide adenine dinucleotide (NAD) as an oxidizing
agent.
ADH exists in numerous isoenzyme forms in the human liver and is encoded by 3
separate genes, designated as ADH1, ADH2, and ADH3. Variations in ADH
isoforms may account for significant differences in ethanol elimination rates.
The microsomal ethanol-oxidizing system (MEOS) uses nicotinamide adenine
dinucleotide phosphate (NADPH) and molecular oxygen.
The central enzyme of MEOS is cytochrome P-450 2E1 (CYP2E1).
This enzyme, in addition to catalyzing ethanol oxidation, is also responsible for the
biotransformation of other drugs, such as acetaminophen, haloalkanes, and
nitrosamines.
Ethanol upregulates CYP2E1, and the proportion of alcohol metabolized via this
pathway increases with the severity and duration of alcohol use.
Peroxisomal catalase uses hydrogen peroxide as an oxidizing agent.
The product of all 3 reactions is acetaldehyde, which is then further metabolized to
acetate by acetaldehyde dehydrogenase (ALDH).
Acetaldehyde is a reactive metabolite that can produce injury in a variety of ways.
Genetic factors
Although the evidence to prove a genetic predilection to alcoholism is adequate,
the role of genetic factors in determining susceptibility to alcoholic liver injury is
much less clear.
Most people who are alcoholics do not develop severe or progressive liver injury.
Attempts to link persons who are susceptible with specific human leukocyte
antigen (HLA) groups have yielded inconsistent results, as have studies of genetic
polymorphisms of collagen, ADH, ALDH, and CYP2E1.
Similar conclusions were reached in a meta-analysis of 50 studies pertaining to the
association of alcoholic liver disease and genetic polymorphism.
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Nonetheless, the fact remains that only a small fraction of even heavy alcoholics
develop severe liver disease (ie, cirrhosis).
Thus, future case-control studies investigating the genetic basis of alcohol-induced
liver disease are urgently needed.
The genetic factor that most clearly affects susceptibility is sex.
For a given level of ethanol intake, women are more susceptible than men to
developing alcoholic liver disease
Malnutrition
Most patients with alcoholic hepatitis exhibit evidence of protein-energy
malnutrition (PEM).
In the past, nutritional deficiencies were assumed to play a major role in the
development of liver injury.
This assumption was supported by several animal models in which susceptibility to
alcohol-induced cirrhosis could be produced by diets deficient in choline and
methionine.
This view changed in the early 1970s after key studies by Lieber and DeCarli
performed in baboons demonstrated that alcohol ingestion could lead to
steatohepatitis and cirrhosis in the presence of a nutritionally complete diet.
However, subsequent studies have suggested that enteral or parenteral nutritional
supplementation in patients with alcoholic hepatitis may improve survival.
Toxic effects on cell membranes
Ethanol and its metabolite, acetaldehyde, have been shown to damage liver cell
membranes.
Ethanol can alter the fluidity of cell membranes, thereby altering the activity of
membrane-bound enzymes and transport proteins.
Ethanol damage to mitochondrial membranes may be responsible for the giant
mitochondria (megamitochondria) observed in patients with alcoholic hepatitis.
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Acetaldehyde-modified proteins and lipids on the cell surface may behave as
neoantigens and trigger immunologic injury.
Hypermetabolic state of the hepatocyte
Hepatic injury in alcoholic hepatitis is most prominent in the perivenular area
(zone 3) of the hepatic lobule.
This zone is known to be sensitive to hypoxic damage.
Ethanol induces a hypermetabolic state in the hepatocytes, partially because
ethanol metabolism via MEOS does not result in energy capture via formation of
ATP.
Rather, this pathway leads to loss of energy in the form of heat.
In some studies, antithyroid drugs, such as propylthiouracil (PTU), that reduce the
basal metabolic rate of the liver have shown to be beneficial in the treatment of
alcoholic hepatitis.
Generation of free radicals and oxidative injury
Free radicals, superoxides and hydroperoxides, are generated as byproducts of
ethanol metabolism via the microsomal and peroxisomal pathways.
In addition, acetaldehyde reacts with glutathione and depletes this key element of
the hepatocytic defense against free radicals.
Other antioxidant defenses, including selenium, zinc, and vitamin E, are often
reduced in individuals with alcoholism.
Peroxidation of membrane lipids accompanies alcoholic liver injury and may be
involved in cell death and inflammation.
Steatosis
Oxidation of ethanol requires conversion of NAD to the reduced form NADH.
Because NAD is required for the oxidation of fat, its depletion inhibits fatty acid
oxidation, thus causing accumulation of fat within the hepatocytes (steatosis).
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Some of the excess NADH may be reoxidized in the conversion of pyruvate to
lactate.
Accumulation of fat in hepatocytes may occur within days of alcohol ingestion;
with abstinence from alcohol, the normal redox state is restored, the lipid is
mobilized, and steatosis resolves.
Although steatosis has generally been considered a benign and reversible
condition, rupture of lipid-laden hepatocytes may lead to focal inflammation,
granuloma formation, and fibrosis, and it may contribute to progressive liver
injury.
Nonoxidative metabolism of ethanol may lead to the formation of fatty acid ethyl
esters, which may also be implicated in the pathogenesis of alcohol-induced liver
damage.
Formation of acetaldehyde adducts
Acetaldehyde may be the principal mediator of alcoholic liver injury.
The deleterious effects of acetaldehyde include impairment of the mitochondrial
beta-oxidation of fatty acids, formation of oxygen-derived free radicals, and
depletion of mitochondrial glutathione.
In addition, acetaldehyde may bind covalently with several hepatic
macromolecules, such as amines and thiols, in cell membranes, enzymes, and
microtubules to form acetaldehyde adducts.
This binding may trigger an immune response through formation of neoantigens,
impair function of intracellular transport through precipitation of intermediate
filaments and other cytoskeletal elements, and stimulate hepatic stellate cells to
produce collagen.
Levels of acetaldehyde in the liver represent a balance between its rate of
formation (determined by the alcohol load and activities of the 3 alcoholdehydrogenating enzymes) and its rate of degradation by ALDH.
ALDH is downregulated by long-term ethanol abuse, with resultant acetaldehyde
accumulation.
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Role of the immune system
Active alcoholic hepatitis often persists for months after cessation of drinking.
In fact, its severity may worsen during the first few weeks of abstinence.
This observation suggests that an immunologic mechanism may be responsible for
perpetuation of the injury.
Levels of serum immunoglobulins, especially the immunoglobulin A (IgA) class,
are increased in persons with alcoholic hepatitis.
Antibodies directed against acetaldehyde-modified cytoskeletal proteins can be
demonstrated in some individuals.
Autoantibodies, including antinuclear and anti–single-stranded or anti–doublestranded DNA antibodies, have also been detected in some patients with alcoholic
liver disease.
B and T lymphocytes are noted in the portal and periportal areas, and natural killer
lymphocytes are noted around hyalin-containing hepatocytes.
Patients have decreased peripheral lymphocyte counts with an associated increase
in the ratio of helper cells to suppressor cells, signifying that lymphocytes are
involved in a cell-mediated inflammatory process.
Lymphocyte activation upon exposure to liver extracts has been demonstrated in
patients with alcoholic hepatitis.
Immunosuppressive therapy with glucocorticoids appears to improve survival and
accelerate recovery in patients with severe alcoholic hepatitis.
Cytokines
Tumor necrosis factor-alpha (TNF-alpha) can induce programmed cellular death
(apoptosis) in liver cells.
Several studies have demonstrated extremely high levels of TNF and several TNFinducible cytokines, such as interleukin (IL)–1, IL-6, and IL-8, in the sera of
patients with alcoholic hepatitis.
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Inflammatory cytokines (TNF, IL-1, IL-8) and hepatic acute-phase cytokines (IL6) have been postulated to play a significant role in modulating certain metabolic
complications in alcoholic hepatitis, and they are probably instrumental in the liver
injury of alcoholic hepatitis and cirrhosis, as shown in the images below.
Ethanol (ETOH) and cytokine production. CYP =
cytochrome P; IL = interleukin; NF-κB = nuclear factor-kappa B; ROS = reactive
oxygen species; TNF = tumor necrosis factor.
Mechanisms of cytokine injury. IL = interleukin ; NO =
nitric oxide; O2- = superoxide anion; OH- = hydroxyl radical; PMN =
polymorphonuclear lymphocyte; TNF = tumor necrosis factor.
Role of concomitant viral disease
Alcohol consumption may exacerbate injury caused by other pathogenic factors,
including hepatitis viruses.
Extensive epidemiologic studies suggest that the risk of cirrhosis in patients with
chronic hepatitis C infection is greatly exacerbated by heavy alcohol ingestion.
Possible mechanisms include the impairment of immune-mediated viral killing or
enhanced virus gene expression due to the interaction of alcohol and hepatitis C
virus.
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Acetaminophen-alcohol interactions
Long-term alcohol abuse has been established as potentiating acetaminophen
toxicity via induction of CYP2E1 and depletion of glutathione.
Alcoholic patients may develop severe, even fatal, toxic liver injury after ingestion
of standard therapeutic doses of acetaminophen.
Diagnosis
The diagnosis is made in a patient with history of significant alcohol intake who
develops worsening liver function tests, including elevated bilirubin and
aminotransferases.
The ratio of aspartate aminotransferase to alanine aminotransferase is usually 2 or
more.In most cases, the liver enzymes do not exceed 500.
The changes on liver biopsy are important in confirming a clinical diagnosis.
Physical examination
Patients with alcoholic hepatitis are commonly febrile with tachycardia. Mild
tachypnea with primary respiratory alkalosis may be observed.
The liver is usually enlarged, often with mild hepatic tenderness.
Hepatomegaly results from both steatosis and swelling of injured hepatocytes.
Manifestations of hepatic failure or portal hypertension may include :





scleral icterus with darkening of the urine,
splenomegaly,
asterixis (a flapping tremor characteristic of metabolic encephalopathies),
peripheral edema, and
bulging flanks with shifting abdominal dullness (indicating the presence of
ascites).
 Spider angiomata,
 proximal muscle wasting,
 altered hair distribution, and
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 gynecomastia may be observed, although these findings most commonly
reflect coexistent cirrhosis.
Epidemiology
Alcohol abuse is the most common cause of serious liver disease in Western
societies.
In the United States alone, alcoholic liver disease affects more than 2 million
people (ie, approximately 1% of the population).
The true prevalence of alcoholic hepatitis, especially of its milder forms, is
unknown, because patients may be asymptomatic and never seek medical attention.
Globally, the prevalence of alcoholic hepatitis appears to differ widely among
different countries.
In the Western hemisphere, when liver biopsies were performed in people who
drank moderate to heavy amounts of alcohol and were asymptomatic, the
prevalence of alcoholic hepatitis was found to be approximately 25-30%.
Racial and age differences in incidence
Although no genetic predilection is noted for any particular race, alcoholism and
alcoholic liver disease are more common in minority groups, particularly among
Native Americans.
Likewise, since the 1960s, death rates of alcoholic hepatitis and cirrhosis have
consistently been far greater for the nonwhite population than the white population.
The nonwhite male rate of alcoholic hepatitis is 1.7 times the white male rate, 1.9
times the nonwhite female rate, and almost 4 times the white female rate.
Alcoholic hepatitis can develop at any age.
However, its prevalence parallels the prevalence of ethanol abuse in the
population, with a peak incidence in individuals aged 20-60 years.
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Sexual differences in incidence
Women are more susceptible than men to the adverse effects of alcohol.
Women develop alcoholic hepatitis after a shorter period and smaller amounts of
alcohol abuse than men, and alcoholic hepatitis progresses more rapidly in women
than in men.
The estimated minimum daily ethanol intake required for the development of
cirrhosis is 40 g for men and 20 g for women older than 15-20 years.
Furthermore, for patients who continue to drink after a diagnosis of alcoholic liver
disease, the 5-year survival rate is approximately 30% for women compared with
70% for men.
To date, no single factor can account for this increased female susceptibility to
alcoholic liver damage.
Lower gastric mucosal alcohol dehydrogenase (ADH) content in women has been
suggested to possibly lead to less first-pass clearance of alcohol in the stomach.
A higher prevalence of autoantibodies has been found in the sera of alcoholic
females compared with alcoholic males, but their clinical significance is
questionable.
Perhaps hormonal influences on the metabolism of alcohol or the higher
prevalence of immunologic abnormalities is responsible for the differences
described in the prevalence of alcoholic liver damage between men and women.
Prognosis
The long-term prognosis of individuals with alcoholic hepatitis depends heavily on
whether patients have established cirrhosis and whether they continue to drink.
With abstinence, patients with this disease exhibit progressive improvement in
liver function over months to years, and histologic features of active alcoholic
hepatitis resolve.
If alcohol abuse continues, alcoholic hepatitis invariably persists and progresses to
cirrhosis over months to years.
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Mild alcoholic hepatitis is a benign disorder with negligible short-term mortality.
However, when alcoholic hepatitis is of sufficient severity to cause hepatic
encephalopathy, jaundice, or coagulopathy, mortality can be substantial.
The overall 30-day mortality rate in patients hospitalized with alcoholic hepatitis is
approximately 15%; however, in patients with severe liver disease, the rate
approaches or exceeds 50%.
In those lacking encephalopathy, jaundice, or coagulopathy, the 30-day mortality
rate is less than 5%.
Overall, the 1-year mortality rate after hospitalization for alcoholic hepatitis is
approximately 40%.
In one study, the overall mortality among patients with severe alcoholic hepatitis
was 66%. Age, white blood cell (WBC) count, prothrombin time (PT), and female
sex were all independent risk factors for the dismal outcome.
Jaundice In Siddha(Manjal kamalai)
According to siddhars jaundice is named as “ Manjal Kamalai” or
“Manjal Noi”.
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Yellowish colouration of urine,eyes,tongue,body as a whole is defined as kamalai.
Kamalai means “Kamam + Illai”,it means “not interested in any thing or action” .
It is also named as pithu noi means “pithu in the body travels against the normal
physiological route and get mixed with the blood and shows it externally by
changing the normal body’s colour in to the colour of pitham that is yellow in
colour.
It is also named as “Manjal Noi” because the body changes in to yellow colour
during the disease period.
Noi varum valli: Taking food which induces the rise of pitham and kabam.
 Taking excess food than the need which causes indigestion,this condition
along with the increased pithakabam destroys the work of all vayues and
seneer(blood) there by attacks the valapateeral (Liver) and causes its
thapitham(inflammation),makes the bile to mix with blood and this blood
flow in to muscles,skin,nailbeds,tongue,uvula and stay there and causes this
disease.
 Another reason is when there occurs rain during the peak of summer there
occurs increase of kapam in the prevalence of increased pitha kutram and
causes kamalai .
Signs and symptoms :











Hand,face,palm,eyes,body becomes white.
Geneeral body tiredness.
Shivering of body.
Frequent breathlessness.
Constipation.
Excessive sleep.
Heaviness of head.
Yellowishness of body.
General anasarca.
Dumpness of ear.
Hyper salivation.
Nausea.
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





Bitterness of tongue.
Dyspepsia.
Indigestion.
Dryness of skin.
Shrinking of skin like toads skin.
Yellowishness of urine.
These are the signs and symptoms of manjal kamalai as per yukimuni’s thought.
Types of kamalai:There are 13 types of kamalai according to yuki muni.
They are:












Udhu kamalai
Varal kamalai
Vatha kamalai
Pitha kamalai
Kaba kamalai
Vathakaba kamalai
Pithakaba kamalai
Mukutra kamalai
Perum kamalai
Alagu kamalai
Senkamala kamalai
Kumba kamalai
Kunma kamalai
Types that can be treated and cured are:




Pitha kamalai
Perumkamalai
Kaba kamalai
Udhu kamalai
Varal kamalai
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 Vathakaba kamalai
 Pithakaba kamalai.
Types which cannot be easily treated and cured are:





Kumba kamalai
Kunma kamalai
Mukkutra kamalai
Vatha kamalai
Senkamala kamalai
Alagu kamalai
Mukutra verupadu:- Due to excessive intake of
food which increases
Pitha kutram and also due to sleeplessness,roaming excessively in sun the pitha
kutram increases than it’s normal level,at this time if some extrinsic or intrinsic
factors induces the increase of kaba kutram it joins pitham and destroys the work
of paravukal(viyanan) and blood and causes the diseases kamalai. Then other
vayues function also gets affected.
Nadi nadai:- Pithakabam and Pithavatham are the nadi for kamalai.
Siddha management:-More than half of all liver disease could be
prevented if we acted on the knowledge we already have.
Avoiding or limiting the use of alcoholic beverages. Man-made chemicals also
pose an extreme threat to the liver
Once cirrhosis has been diagnosed, sodium and fluids should be restricted, and all
alcohol consumption must cease.
Antiemetics, diuretics, and supplemental vitamins are prescribed.
Patients should avoid exposure to infections and eat small but frequent meals of
nutritious foods.
The liver is the only organ that can generate healthy, new tissue.
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It is therefore possible to regenerate a cirrhosis-damaged liver if extraordinary
therapies are followed and the underlying cause of the cirrhosis is eliminated.
Herbs in siddhaMedicine for Treating Liver
Disease:Hepatitis A virus can be taken care of very easily with herbs.
Many of the herbs have shown remarkable results in clinical trials and studies.
Some of these are :-



Eclipta Alba (Bhringaraj),
Boerhavia diffusa (Punarnava) , and
Picrorhiza kurroa (Katuki).
We can supply Concentrated Extracts in Tablet form of all these Herbs
It is recommend that people take these herbs on a prophylactic basis when
travelling to parts of the world where hepatitis infection is a risk.
Siddha Treatment for Hepatitis B / Hepatitis C :HBV and HCV are more serious infections.
We must be careful how we use herbs for prevention of HBV and HCV.
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The herbs mentioned earlier have shown a protective action in HBV, and using
them on a regular basis may be a good way to prevent HBV.
Siddha medicines play a significant role in protecting the liver from cirrhosis and
from liver cancer.
Animal and clinical studies done with Phyllanthus Amarus, Phyllanthus Niruri, and
Eclipta Alba have proven their ability to reverse HBV infections in approximately
60% to 70% of patients.
More significantly, with these herbs we are able to stop the process, which leads to
cirrhosis and cancer of the liver.
This means that even if we are not able to make some patients negative for HBV
and HCV, we can still protect them from cirrhosis of the liver, in which the liver
stops functioning, and liver cancer.
Take very good care of your health. To protect your liver, avoid alcohol and
caffeine. Drink green tea, exercise, reduce stress, and use the herbs mentioned
above. Give this hard-working and essential part of your body a rest and a tune-up,
and you will be rewarded with better health, more energy and higher disease
resistance.
Research work on Hepatoprotective Plants Andrographis paniculata (kalmegh)
Andrographolide, the active constituent isolated from the plant Andrographis
paniculata, showed a significant dose dependent (0.75 - 12 mg/kg p.o. x7)
protective activity against paracetamol-induced toxicity on ex vivo preparation of
isolated rat hepatocytes.
It significantly increased the percent viability of the hepatocytes as tested by trypan
blue exclusion and oxygen uptake tests.
It completely antagonized the toxic effects of paracetamol on certain enzymes
(GOT, GPT and alkaline phosphatase) in serum as well as in isolated hepatic cells.
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Andrographolide was found to be more potent than silymarin, a standard
hepatoprotective agent.
For centuries Andrographis has been an important herb in the Asian healing
systems of Ayurveda, Unani and Traditional Chinese Medicine.
Traditionally this herb has been used to potentiate immune system response to
inflammation and infections, and as an anti-inflammatory, antipyretic (lowers
fevers) and a hepatoprotective (liver protector).
Boerhavia diffusa (Punarnava)
An alcoholic extract of whole plant Boerhavia diffusa given orally exhibited
hepatoprotective activity against experimentally induced carbon tetrachloride
hepatotoxicity in rats and mice.
The extract also produced an increase in normal bile flow in rats suggesting a
strong choleretic activity.
The extract does not show any signs of toxicity up to an oral dose of 2g/kg in mice.
Eclipta alba (Bhringaraj)
The hepatoprotective effect of the ethanol/water (1:1) extract of Eclipta alba was
studied at subcellular levels in rats against (CCl4) -induced hepatotoxicity.
The loss of hepatic lysomal acid phosphatase and alkaline phosphatase by (CCl4)
was significantly restored by Ea.
The study shows that hepatoprotective activity of Ea is by regulating the levels of
hepatic microsomal drug metabolising enzymes.[6]
Swertia Chirata(Chirayata)
Simultaneous treatments with S. Chirata (in different doses, viz, 20, 50, and 100
mg/kg body wt daily) and (CCl4) caused improvement at both biochemical and
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histopathological parameters compared to that of (CCl4) treatment alone but it was
most effective when S. chirata was administered in a moderate dose (50 mg/kg
body wt).
Terminalia belerica(Baheda)
Compound I isolated from fraction TB5 of Terminalia belerica and finally
identified as 3,4,5-trihydroxy benzoic acid (gallic acid) was evaluated for its
hepatoprotective activity against carbon tetrachloride (CCl4) - induced
physiological and biochemical alterations in the liver.
Administration of compound I led to significant reversal of majority of the altered
parameters.
Our results confirm the presence of hepatoprotective activity in altered parameters.
Our results confirm the presence of hepatoprotective activity in Compound I.
Tinospora cordifolia(Guduchi)
Outstanding results in people suffering from jaundice have been obtained using a
herb called Tinospora Cordifolia.
The herb is used in malignant obstructive jaundice: half of the group received
conventional treatment - drugs and drainage - the other half were treated with
drainage plus T. Cordifolia.
After conclusion of treatment, 50% of the drug-treated group were found to have
blood poisoning while none of the herb treated group developed this problem.
After surgery, only 40% of the drug-treated group survived, whereas an amazing
92.4% 0f those treated with the herb lived.
The hepatoprotective effect of T. Cordifolia has been studied in carbon
tetrachloride induced liver damage in rats.
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While acute damage was enhanced by prior exposure to the drug, it proved
effective in the prevention of fibrosis, and in stimulating regeneration of hepatic
tissue.
Picrorhiza kuroa (Katuki)
Picrorrhiza Kurroa is one of the herbs they recommend to support the liver not
only in everyday situations, but in cases where severe viral infections attack found
protection against viral hepatitis, and other studies have demonstrated its
helpfulness in protecting against alcohol.
The hepatoprotective activity of picroliv, the irridoid glycoside mixture from
Picrorhiza kuroa, was determined in adult male albino rats.
Pretreatment with picroliv prevented the hepatotoxic effects of paracetamol and
galactosamine as evidenced by various biochemical and histopathological
observations.
Maximum hepatoprotective effect was observed with daily oral doses of 6 and 12
mg/kg for 7 or 8 days.
The antihepatotoxic action of picroliv seems likely due to an alteration in the
biotransformation of the toxic substances resulting in decreased formation of
reactive metabolites.
Siddha Medicine for Jaundice
The best Siddha medicine for jaundice is Keelanelli herb.
It grows abundantly in almost all areas of Tamil nadu.
In ancient days people are not aware of jaundice vaccine and they know the power
of this plant to in jaundice treatment.
Keelanelli medicine is still used in nattu vaitiyam to get fast and complete cure
against this disease.
This is the best Siddha medicine for jaundice.
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It is used to treat :
 urine problems,
 intestinal problems,
 throat infection,
 stomach infections,
 eye problems,
 heat,
 menstrual problems,
 anemia, and wound healing and not feeling hungry.
It is having tiny leaves with small bud like below the stem area. The whole part of
the plant is used to treat jaundice disease.
Aravindh Herbals Treatment
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For
Jaundice
Jaundice which is named as kamalai by sidhars is having best known remedy n
siddha medicine. One of the best treatment is from aravindh herbal labs
formulation “Aeroliv Capsule”
Aeroliv capsule contains the following ingredients:
 Indigofera tinctoria
 Phyllanthus amarus or Phyllanthus niruri
 Andrographis paniculata
 Glycyrrhiza glabra
 Annabedi chendorum
 Mandora chenduram
 Velli parpam
The explanation of the above combination of the drug is explained below with
evidences for their action against jaundice.
Indigofera tinctoria
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Kingdom: Plantae
Phylum:
Angiosperms
Class:
Eudicots
Sub class: Rosids
Order:
Fabales
Family:
Fabaceae
Genus:
Indigofera
Species:
tinctoria
Binomial name
Indigofera tinctoria
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Common vernacular names
English : Indian indigo
Hindi : Nil
Malayalam : Nilamari Amri.
Sanskrit:Neelini
Explanation
Indigofera tinctoria bears the common name True indigo. The plant was one of
the original sources of indigo dye.
Today most dye is synthetic, but natural dye from I. tinctoria is still available,
marketed as natural coloring.
The plant is also widely grown as a soil-improving groundcover.
Dye is obtained from the processing of the plant's leaves.
They are soaked in water and fermented in order to convert the glycoside indican
naturally present in the plant to the blue dye indigotin.
The precipitate from the fermented leaf solution is mixed with a strong base such
as lye, pressed into cakes, dried, and powdered.
The powder is then mixed with various other substances to produce different
shades of blue and purple.
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Distribution
It has been naturalized to tropical and temperate Asia, as well as parts of Africa,
but its native habitat is unknown since it has been in cultivation worldwide for
many centuries.
Morphological Description
True indigo is a densely branching shrub one to two meters high.
It may be an annual, biennial, or perennial, depending on the climate in which it is
grown.
It has light green pinnate compound leaves with 6-14 leaflets. Leaves are green
with bluish tint.
Pink or violet flowers many, small and nearly sessile in spicate receme
inflorescence are seen.
Tender branches are also bluish green colored.
Fruits are cylindric pods, 2-3 cm long, greenish grey when young and dark brown
on ripening.
Seeds are 10-15 per pods.
The plant is a legume, so it is rotated into fields to improve the soil in the same
way that other legume crops such as alfalfa and beans are.
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Chemical constitutions
The rotenoids deguelin, dehydrodeguelin, rotenol, rotenone, tephrosin and
sumatrol can be found in I. tinctoria.
Whole plant contains flavonoids, apigenin, kaempferol, luteolin and quercetin.
It contains alkaloid indican.
Actions :









Hepato-protective,
Anti-periodic,
Stimulant,
Antidote,
Alterative,
Deobstruent,
Purgative,
Antiseptic,
Astringent dye.
Siddha Medicinal Uses :
1. The leaves are dried in shade, powdered and given in dose of 1 to 5 grams
for three times a day for any type of toxicity (herbal,metal or poison of any
living creature), fever due to derranged vatham, kamalai (jaundice),
mantham (indigestion) etc.
2. The root is crushed and prepared into decoction, and given for gunmam
(abdominal disorders), vellai(leucorrhoea), all types of toxicities etc.
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3. The leaves are crushed, prepared into decoction and given for
toxicities,fever,arthritis etc.
4. The leaf juice is given in the dose of 10-20ml along with honey twice daily
for jaundice, inflammation of liver etc.
5. For poisonous bites the samoolam or the whole plant is ground and applied
as a paste over the bitten area. Also the leaf juice is given internally to the
patient.
6. Its Stem chewed to cure cough and decoction of Leaves used to cure chest
pains .
7. The twine paste cures dislocation.
8. It is used in asities, snake poison, diseases due to metallic toxemia and in
dog bite and extract in rabid dog bite, epilepsy and other nervous disorders.
9. Ointment used in sores, old ulcers and piles.
10.Decoction of leaves used in menorrhagia.
11.Roots used in urinary complaints and hepatitis.
Pharmacological studies
Anti hyperglycemic activity
Anti-diabetic and nephroprotective activity of Indigofera tinctoria leaves, using
STZinduced diabetic rats as model for clinical type-1and type-2 diabetes is
investigated.
At a regular interval of an experimental protocol blood glucose, urinary creatinine,
total proteins and organs to body weight ratio were studied.
The histo-pathological study was carried out by STZ-induced diabetic and
antidiabetic rat’s pancreas.
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Statistical analysis of the results shown that in STZ-induced diabetic rats
chloroform and alcohol extracts of I.tinctoria leaves at 40, 80, 160 and 200 mg/kg
doses.
Significant effect of alcoholic extract from 4th day to 16th day of the study.
I.tinctoria leaves extract improved renal creatinine clearance and reduce
renal total protein loss demonstrating nephro protective properties.
The organ to body weight ratio studies carried out on last day, shown
pancreas and liver specific effects of I.tinctorialeaves.
These results were also supported by histopathological studies. The present study
conclude that alcoholic extract of I.tinctoria leaves with long-term treatment may
be beneficial in the management of type-1 and type-2 diabetes13.
Anti bacterial,Anti oxidant and Cyto toxicity Effect
Antibacterial, anti oxidant and cytotoxic activity of the leaf extract of indigofera
tinctoria isdetermined
Antibacterial activity was carried out on in vitro lung cancer cell line. The extract
screened for phytochemical analysis was found to contain bioactive compounds
like falvonoid, saponins, tannins,steroidal terpens, phenols and anthroquinone were
identified by GC -MS analysis.
The leaf extract I.tinctoria having the ability to inhibit the growth of gram positive
bacteria namely Staphylococcus aureus, Bacillus pumilus and Streptococcus
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pyrogens and zone of inhibition was observed 16 and 17 mm, respectively but not
shown growth of inhibition on gram negative bacteria Escherichia and
pseudomonas aeruginosa.
Strong antioxidant activity was observed both qualitatily and quantitatively.
The strong antioxidant was observed at 250ugml-1 with an IC 50 value of 51.66
which is higher than that of standarad ascorbic acid.
The cytotoxic effect of I.tinctoria leaf extract on lung cancer cell line NCI-H69
was studied.
The percentage cell viability of cells was found to decrease at increasing
concentration.
GC-MS analysis of the leaf extract shows 6 compounds.
This study suggests that ethanol extract of Indigofera tinctoria have profound
antibacterial,antioxidant and cytotoxic effect14.
Anti-Inflamatory effect
The anti-inflammatory activity of Ethanolic extract of I.tinctoria leaves is
elucidated (500 & 1000mg/kg).
When compare to control as well as positive control Ibuprofen (Standard drug)
group values are expressed as mean and SD.
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Statistical significance was determinded using the student’s t-test.
Values with p<0.01 were considered significance.
The present study indicated thar oral administration of ethanol extract of I.tinctoria
linn dose dependently improve the potent anti inflammatory activity.
The extract lowers the carrageen an induced rat paw oedema.
Anti hepatoprotective activity
The antihepatotoxic efficacy of aqueous extract of I.tinctoria (250, 500 mg/kg) is
investigated and silymarin (25mg/kg) against paracetamol induced liver damage
in rats.
Paracetamol at the dose of 3 g/kg body weight orally one day only produced liver
damage in rats as manifested by the significant rise in serum levels of aspartate
aminotransferas (AST),alanine-aminotransferase (ALT), alkaline phosphatase
(ALP), glutamyltranspeptidase (GGT),lactate dehydrogenase (LDH), bilirubin,
cholesterol and decrease the protein level compared to control.
Treatment of rats with I.tinctoria and silymarin once daily for twenty eight days to
paracetamol treated will increased in protein level.
Furthermore,liver tissues were processed for histopathologialobservation.
The extract alone treated rats did not adversely affect the serum biochemical and
histopathologial observation.
The antihepatotoxic efficacies of the Indigofera tinctoria extracts were reported to
be significant.
Anti-Epilective property
The anti-Epilective property of I.tinctoriais investigated in malealbino Wistar rats
by injection of lithium chloride(3 mEq/kg, i.p.) follow after 24 h administration of
pilocarpine (30 mg/kg, i.p.).
After 1h injection of pilocarpine different doses of the ethanol extract of
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I.tinctoria were administered orally.
The severity of status epilepticus was observed and recorded using Racine scoring
system for every 15 min for 90 min and thereafter every 30 min for another 90
min.
In terms of the thiobarbiturate-reactive substances (TBARS) in-vivo lipid
peroxidation of rat brain tissue was measured.
Determined both invitro free radical nitric oxide (NO) and 2-diphenyl-2-picryl
hydrazyl (DPPH) scavenging activities of the extract.
The status epilepticus was significantly reduced following oral administration of
the extract at a dose of 500 and 1000 mg/kg.
No test animal group exhibited stage 4 seizure.
The extract also exhibited antioxidant activities in both in-vivo and in-vitro studies.
The ethanol extract of I.tinctoria was found to be useful in controllinglithium /
pilocarpine induced status epilepticus in albino rats.
Neurotransmitters concentrations
The effect of methanolic extract of Indigofera tinctoria (MEIT) on
neurotransmitters concentrations in rat brain after induction of seizures by MES
and PTZ is evaluated.
The leaves of Indigofera tinctoria Linn. (Family:Fabaceae) is traditionally used in
the epilepsy and other nervous disorders, bronchitis and liver
ailments.
The relationship between seizure activities and altered the neurotransmitters such
as noradrenaline, dopamine and serotonin in forebrain of rats in MES and PTZ
seizure models is estimated.
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In MES model, MEIT(200 & 400mg/kg) showed significantly restored the
decreased levels of brain monoamines such as noradrenaline,dopamine and
serotonin.
Similarly in PTZ model,MEIT showed significantly increased the
neurotransmitters in forebrain of rats.
Thus, this study conclude that methanol extract of Indigofera tinctoria increased
the neurotransmitters on rat brain, which may be decreased the susceptibility to
MES and PTZ induced seizure in rats.
CONCLUSION
The vast study done on the plant proved that the plant has many important
phytochemical compounds like galactomannan, composed of galactose and
mannose in molar ratio of 1:1.52,Glycoside (Indian), Coloring matter (Indigotin),
Flavonoids, terpinoids, alkaloids and glycosides,Indigotine, Indiruben, rotenoids
and other related compounds .
These compounds were found to be responsible for many pharmacological
activities such as Cyto toxicity Effect, Anti hyperglycemic activity, Anti oxidant,
Anti -inflammatory activity,Anti bacterial, Anti hepatoprotective activity, Anti
diabetic activity,Anticonvulsive agent.
Plant has therapuetic uses as medicinal properties as it is used in constipation,liver
disease , heart palpitation and gout , bitter, thermogenic, laxative,trichogenous,
expectorant, anthelminthic, tonic and diuretic and are useful for promoting growth
of hair and in naturopathy, splenomegaly,echolalia, cardiopathy, chronic
bronchitis, asthama,ulcers, and skin diseases.
Hence ,this plant provides a significant role in the prevention and treatment
of a various disease and in the protection of the system from damage.
The therapeutic potential of I.tinctoria is effective .
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Phyllanthus amarus(P.niruri)
Kingdom: Plantae
Division: Angiosperms
Class:Eudicots
Sub class:Rosids
Order: Malpighiales
Family: Phyllanthaceae
Genus: Phyllanthus
Species: P. niruri
Binomial name: Phyllanthus niruri
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Explanation
The annual herb Phyllanthus niruri is best known by the common names
English:Stonebreaker or Seed-Under-Leaf
Sanskrit:Bhumyamalaki
Tamil:Keela Nelli.
Kannada:Nela Nelli
Telugu:Nela Usiri
Distribution
It is a widespread tropical plant commonly found in coastal areas.
It grows widely in the tropical parts of all countries except Australia.
It is found mainly as a weed in waste lands, agricultural lands and riverbanks.
In waste lands it grows abundabtly during the rainy season.
Morphology
It is an annual, glabrous herb.
It grows 50 to 70 centimeters tall and bears ascending herbaceous branches.
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Has an errect stem, naked below and slender and spreading leaf branches above.
The bark is smooth and light green.
Leaves are numerous, subsessile, pale green, often distichously imbricating,
glaucous below, elliptic to oblong, obtuse, and stipules subulate.
It bears numerous pale green flowers which are often flushed with red.
Flowers arise in leaf axis, very numerous, males 1-3 and females solitary.
Sepels of male orbicular and obovate to oblong in females.
Stamens 3, anthers sessile and in a short column.
Disc of male minute glands and of females annular and lobed.
Capsules depressed globose, smooth and hardly 3 lobed.
Seeds are trigonous, rounded and with longitudinal regular parallel ribes on the
back.
The fruits are tiny, smooth capsules containing seeds.
Parts Used
Leaves or aerial parts are used.
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Chemical constituents
Phyllanthin (bitter constituent) and hypophyllanthin (non-bitter compound) are
isolated from the leaves.
From the aerial parts phyllanthine (4-methoxy-securinine) and 4- methoxynorsecurinine are identified1.
From the roots glycoflavones were isolated2.
Lintetralin was also isolated from the plant3.
Amariin, a novel hydrolysable tannin together with geraniin, corilagin, 1,6digalloyl-glucopyranoside as well as a rutin and quercetin- 3-O-lucopyranoside
have been isolated .
An unusual hydrolysable tannin, phyllanthusiin D has also been isolated.
Also a number of






alkaloids
flavonoids
geraniin, a tannin which is an in vitro anti-viral agent
lignans
hypophyllanthin
phyllanthin
are isolated from Phyllanthus amarus.
(Abbrevation
Rt – Rt culture
Pl – Plant
Lf – Leaf
Sd – Seed
Ol – Oil
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Aer – Aerial plant
EO – Essential oils)
Following are chemical constituents from parts of phyllanthus niruri
1. Kaempferol-4-o-alpha-L-rhamnoside, Aer 0.9%, Rt
2. (-) Limonine, Lf EO 4.5%
3. Ascorbic acid, Lf 0.41%
4. Cymene, Lf EO 11%
5. Hypophyllanthin, Pl 0.05-0.17%
6. Geranin, Pl .23%
7. Linoleic acid, Sd Ol 21%
8. Linolenic acid, Sd Ol 51.4%
9.Ricinoleic acid, Sd Ol 1.2%
10.Phyltetralin, Pl, Lf 0.14%
11.&Phyllanthin, Lf, Aer
Following are from the parts of the whole plant
1. (-)-Nor-secrurinine, Pl
2. 4-Hydroxy-sesamin, Pl
3. Corilagin, Pl
4. Ellagic acid, Pl
5. Estradiol, Pl
6. Fisetin-41-O-beta-D-dlucoside, Pl
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7. Hinokinin, Pl
8. Iso-lintetralin, Pl
9. Nirurin, Pl
10.Nirurinetin, Pl
11.Phyllanthus, Pl
12.Trans-phytol, Pl
13.Repandusinic acid A, Pl
Following are from the parts of the roots:
1. (+)-Catechin, Rt cult
2. (+)-Gallocatechin, Rt Cult
3. (-)-Epi-catechin, Rt Cult
4. (-)-Epi-catechin-3-gallate, Rt Cult
5. (-) Epi-gallocatechin, Rt Cult
6. Gallic acid, Rt cult
7. (-)-Epi-gallocatechin-3-O-gallate, Rt
8. Eriodictyol-7-o-alpha-L-rhamnoside, Rt
9. Fisetin-41-O-alpha-L-rhamoniside, Rt
10.Lupeol acetate, Rt
11.Lupeol, Rt
12.Nor-securinine, Rt
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Following are from the parts of the Leaves:
1. 4-Hydroxy-lintetralin, Lf
2. 2,3-dimethoxy-iso-lintertralin, Lf
3. Astragalin, Lf
4. Beta sitosterol, Lf
5. Demethylenedioxy niranthin, Lf
6. Hydroxy niranthin, Lf
7. Hypophyllanthin, Lf Aer
8. Iso-quercitin, Lf
9. Linnanthin, Lf
10.Lintetralin, Lf
11.Niranthin, Lf
12.Quercitrin, Lf
13.Salicylic acid methyl ester, Lf EO
14.Seco-4-hydroxy-lintetralin, Lf
Following are from the parts of the aerial plant:
1.24- Isopropyl Cholestrol, Aer
2.Dotriacontanoic acid, Aer
3.Nirphyllin, Aer
4.Nirurine, Aer
5.Phyllanthenol, Aer
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6.Phyllantheol, Aer
7.Phyllester, Aer
8.Phyllinurin, Aer
9.Phylltetrin, Aer
10.Triacontan-1-al, Aer
11.Triancontan-1-ol, Aer
Following are present in all leaf, stem, aerial plant, roots
1.Nirtetralin, Pl, Lf
2.4-Methoxy-nor-securinine, Aer, Rt, St
3.Rutin, Pl, Lf
4. Phyllanthine, Rt, Lf, St
5. Phyllochrysine, Lf, St
6. Quercetin, Lf, Pl
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Chemical Structures
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Action
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anti-viral [an agent that destroys viruses]
hepatoprotective [liver protector]
hypoglycemic [lowers blood sugar]
deobstruent,
diuretic,
astringent
cooling,
bitter,
stomachic,
febrifuge ,
antiseptic.
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Medicinal uses
P. niruri is an important plant of Indian siddha system of medicine which is used
for problems of the stomach, genitourinary system, liver, kidney and spleen.
The plant has also been used in Brazil and Peru as a supposed herbal remedy for
kidney stones.
Phyllanthus Amarus is also used for:
Liver Conditions
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Hepatitis B
jaundice
may have a support role in Diabetes
Viral Conditions
Viral liver diseases including:
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acute hepatitis
chronic persistent hepatitis
part of the treatment for chronic active hepatitis
The plant was also used in skin diseases like scabby affections, offensive sores and
bruises.
In western parts of India it was used as a diuretic in gonorrhoea and acidity of the
urine.
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The root with rice water was a remedy for menorrhagia.
In chronic dysentery, the plant along with fenugreek was given.
Whole plant is used in dropsy, gonorrhoea, menorrhagia and other genital
affections.
It is useful in dropsy, jaundice, diarrhoea, dysentery, intermittent fevers, scabies,
ulcers and wounds.
Young shoots and leaves are given in dysentery and ulcers.
Fresh root is an excellent remedy for jaundice.
The decoction of the plant is a remedy for intermittent fevers and intermittents with
infracts of the spleen and liver.
It is also a good tonic and diuretic.
Phyllanthus niruri is very effective in treating viral infection of the liver,
specifically hepatitis B.
It also has diuretic effect.
It has demonstrated hypoglycemic effects in animals and humans.
It is recommended for kidney stones and gallstones (active stones and as a
preventative).
It is used to tone, balance, strengthen, detoxify and protect the liver (and to balance
liver enzymes).
It helps to tone, balance, strengthen, detoxify and protect the kidneys and to reduce
uric acid and increase urination.
In ayurvedic medicine, it is used to treat diabetes.
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Pharmacological studies
A clincial study with Phyllanthus niruri, indicated that it has no significant effect
on either stone voiding or pain levels, but it may reduce the levels of urinary
calcium.
The alcoholic extract of the whole plant has anti-cancer activity against Freund
virus Leukaemia (solid) in the mouse and antispasmodic activity on isolated guinea
pig ileum.
Aqueous extract of whole plant has hypoglycaemic action in normal and alloxandiabetic rabbits and leaves to be higher than that of tolbutamide.
It is effective in treatment of infective hepatitis without any adverse effect.
It shown to be effective with other Siddha drugs in the treatment of jaundice due to
infective hepatitis.
Hepatoprotective Effect
Hepatitis B is one of the major diseases inflicting human population. Conventional
treatment with interferon – alpha is very expensive and has many serious side
effects.
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Alternative herbal medicine using extracts of Phyllanthus niruri and Phyllanthus
urinaria have been reported to be effective against Hepatitis B and other viral
infections.
A study reports quantitative determination of the anti viral effect of these herbs in
well-defined in vitro systems.
Phyllanthus niruri has been reported to exhibit marked antihepatitis B virus
surface antigen activity in in-vivo and in-vitro studies.
Infectious hepatitis is due to the inability of the bodies’ immune system to
eliminate the virus from the liver cells: hence the “carrier state”.
An infection with the virus is documented by detectable levels of various viral
antigens in the blood, including HbaAg (the surface antigen of the virus) as well as
antibodies to the core of virus (HBc antibodies).
In one study, 37 patients with chronic viral hepatitis B were treated with a daily
dose of 600mg of Phyllanthus niruri for 30 days.
59% of the patients lost the HBsAg two weeks after the end of the treatment.
Furthermore, none of the cases followed for up to 9 months had any symptoms of
HBsAg.
The authors postulated that Phyllanthus niruri might inhibit proliferation of the
virus by inhibiting replication of the genetic material of the virus. 4
Research in Japan and India in the 1980's has demonstrated the liver -healing
properties of Phyllanthus niruri.
The primary compounds responsible are phyllanthin, hypophyllanthin and
triacontanal.
Glycosides found in Phyllanthus niruri demonstrated Aldose reductase (AR)
inhibitory activity in studies conducted by a Japanese research group in 1988 and
1989.
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HIV Replication Inhibition
Aqueous extract of Phyllanthus niruri is reported to have inhibitory effect on
human immunodeficiency virus.
The investigation examines the anti-HIV effects of the alkaloidal extract of
Phyllanthus niruri in human cell lines.
The inhibitory effect on HIV replication was monitored in terms of inhibition of
virus induced cytopathogenecity in MT-4 cells.
The alkaloidal extract of Phyllanthus niruri showed suppressing activity on strains
of HIV-1 cells cultured on MT-4 cell lines.
The CC50 for the extract was found to be 279.85μgmL-1 whereas the EC50 was
found to be 20.98μgmL.
Interestingly the Selectivity Index (SI) was found to be 13.34, which showed a
clear selective toxicity of the extract for the viral cells.
The alkaloidal extract of Phyllanthus niruri was thus found to exhibit sensitive
inhibitory response on cytopathic effects induced by both the strains of human
immunodeficiency virus on human MT-4 cells in the tested concentrations.
Lipid Lowering Activity
Lipid lowering activity of Phyllanthus niruri alcoholic extracts in triton induced
hyperlipidaemia was examined in rats.
It was observed that administration of triton in rat caused increase in serum
cholesterol by 3.5 fold, phospholipid 2 fold and triglyceride 1.2 fold.
Administration of Phyllanthus niruri at the dose of 200mg/kg simultaneously with
triton lowered the level of total cholesterol, phospholipid and triglyceride by 27, 25
and 24 percent respectively.
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In an experiment with cholesterol fed rats, Phyllanthus niruri at a dose of 100
mg/kg lowered the elevated level of low-density lipoprotein lipids in
hyperlipidemic and drug fed animals.
Anti – Diabetic Activity
An alcoholic extract of Phyllanthus niruri was found to reduce significantly the
blood sugar in normal rats and in alloxan diabetes rats.
In normal rats, administration of Phyllanthus niruri 200mg/kg body weight
reduced the blood sugar by 34.5 percent and to 47.4 percent at the concentration of
1000mg/kg by weight at 1 hour.
However at 6th hour, values are almost similar to normal value.
Continuous administration of the drug produced significant reduction in normal
blood sugar in rats, which on 15th day was also found to reduce the blood sugar in
alloxan diabetic rats.
In short term experiment, drug was found to reduce the blood sugar at 4th hour by
6.07 percent at dose level of 200mg/kg by weight and 18.7 percent at concentration
of 1000mg/kg by weight.
Continuous administration of drug produced significant reduction in blood sugar in
alloxan diabetic rats.
On 15th day values were almost similar to normal in the group taking 1000mg/kg
by weight.
Plant extract did not produce any toxicity as seen from liver and kidney function
test and in hematological parameters.
The results indicate potential antidiabetic action of Phyllanthus niruri.
Anti Malarial Activity
The ethanolic, dichloromethane and lyophilized aqueous extracts of
Cassia occidentalis root bark, Morinda morindoides leaves and whole plants of
Phyllanthus niruri were evaluated for their antimalarial activity in vivo, in 4-day,
suppressive assays against Plasmodium berghei ANKA in mice.
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No toxic effect or mortality was observed in mice treated, orally, with any of the
extracts as a single dose, of 500 mg/kg body weight, or as the same dose given
twice weekly for 4 weeks (to give a total dose of 4 g/kg).
No significant lesions were observed, by eye or during histopathological
examinations, in the hearts, lungs, spleens, kidneys, livers, large intestines or
brains of any mouse.
At doses of 200 mg/kg, all the ethanolic and dichloromethane extracts produced
significant chemosuppressions of parasitaemia (of > 60% for C.occidentalis root
bark and Phyllanthus niruri whole plant, and of 30% for M.morindoides leaves)
when administered orally.
The most active ethanolic extract, that of Phyllanthus niruri, reduced parasitaemia
by 73%.
The dichloromethane extracts of M.morindoides and Phyllanthus niruri produced
similar reductions (74% and 72% chemosuppression, respectively), whereas that of
C.occidentalis was slightly less active (60% chemosuppression).
Each lyophilized aqueous extract was less active than the corresponding ethanolic
extract.
Anti- spasmodic activity
Research done in Brazil at the Federal University of Santa Catarina in 1984 on
Phyllanthus niruri revealed an alkaloid (phyllanthoside) in the leaves and stem
with strong antispasmodic activity.
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It served as a relaxing agent for smooth muscles and they concluded that its
spasmolytic action probably accounted for the efficacy of Phyllanthus niruri in
expelling stones.
Analgesic activity
Methanol extract of dried callus tissue at a concentration of 10mg/kg,
administered intraperitonially to mice was active vs. acetic acid induced writhin
and vs. formalin – induced pedal edema.
The extract, at 50mg/kg was inactive vs tail flick response to radiant heat.
Ethanol/ water (1:1) extract of dried entire plant at a dose of 50mg/kg,
administered intragastric to male mice was active.
The extract also administered intraperitonially to male mice at a dose of 0.3mg/kg
was active.
Chromosome Aberration Inhibition –
Water extract of dried fruit and leaves, at a dose of 685.0 mg/kg, administered to
mice by gastric incubation was active vs. chromosome damage induced by lead
nitrate and aluminium sulphate in bone marrow chromosomes. Dosing was for 7
days.
Comparative pharmacognostic studies of 3 Phyllanthus
species
The detailed pharmacognostic evaluation of the 3 species of Phyllanthus namely
Phyllanthus amarus Schum & Thonn or Phyllanthus maderaspatensis Linn or
mixture of Phyllanthus amarus, Phyllanthus fraternus Webster and Phyllanthus
maderaspatensis has been carried out with the aim to establish the identification
markers of this important hepatoprotective agents (effective in Hepatitis B too).
The study concluded that the 3 species can be differentiated on the micro and
macroscopic characters, physicochemical values, HPTLC fingerprint profile and
the detection of phyllanthin and hypophyllanthin as marker components.
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Besides, an interesting conclusion can be drawn that phyllanthin and
hypophyllanthin said to protect the hepatocytes against CCl 4 and galactose amine
induced toxicity may not be exclusively responsible for hepatoprotective activity
as these are present in Phyllanthus amarus while Phyllanthus fraternus and
Phyllanthus maderaspatensis also possess significant hepatoprotective activity.
Andrographis Paniculata
Andrographis paniculata has white flowers and green leaves.
Kingdom: Plantae
Division: Angiosperms
Class:Magno
Sub class: Asterids
Order: Lamiales
Family: Acanthaceae
Genus: Andrographis
Species: A. paniculata
Binomial name :Andrographis paniculata
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English Name: Creat , Green Chirayta, King of bitters.
Common (Indian) Name:
Hindi: Kalmegh, Kiryat, Mahatit,
Gujrati: Kiriyata, Olikiriyat
Marathi: Olen Kirayat,
Canarese: Nelabevu gida
Sanskrit: Bhuinimb, Kirata, Mahateet
Malyalam: Nilaveppu, Kiriyatta,
Telugu: Nela Vemu
Tamil: Nilavempui
Explanation
Andrographis paniculata is a herbaceous plant native to Southeast Asia.
The plant is known to have medicinal properties and can be used to treat the
common cold and to boost the immune system. The herb is also commonly used as
a folk medicinal remedy for fever,jaundice and pain reduction.
Distribution
Kalmegh is an annual herb found through India, specially in dense forests.
It is under cultivation in many states of India.
Andrographis paniculata plant grows to a height of between 1 and 4 feet.
It grows in moist shady places and it has glabrous leaves and with flowers with
rose-purple spots on the petals.
It also has a dark green stem.
Andrographis paniculata grows abundantly in Southeast Asia, including India, Sri
Lanka, Pakistan, Java, Malaysia and Indonesia.
It is cultivated extensively in India, China and Thailand.
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Morphology
It is an erect branched annual, 0.3-0.9 meters high, branches sharply quadrangular
winged in the upper part;
Leaves - lanceolate, acute, undulate, pale beneath;
Flowers small, solitary distant, in axillary or terminal racemes or panicles, bracts
lanceolate;
Corolla - 2 lipped, upper lip 2-toothed, lower 2 lobed, rose coloured;
Flowers - Capsule, linear - oblong, acute at both ends;
Seeds many, rugosely pitted, yellowish brown.
Flowering time in India is November - December.
Useful parts:
Whole plant.
Chemical Constituents
Andrographis paniculata contains bitter principles andrographolide, a bicyclic
diterpenoid lactone and Kalmeghin (upto 2.5%).
The leaves contain the maximum active principle content while in the stem it is in
lesser amount.
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Andrographolide, a diterpene lactone compound, is believed to be the principal
active agent.
Other possibly active constituents include :
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neoandrographolide,
andrographiside,
14-deoxy-11,12-didehydroandrographolide,
deoxyandrographolide, and arabinoglycan proteins.
5-Hydroxy-7,
8-dimethoxy (2R)-flavanone-5-O-beta-D-glucopyranoside,
5-hydroxy-7,8,2',
5'-tetramethoxy-flavone-5-O-beta-D-glucopyranoside,
andrographic acid, and andrographidine A have also been isolated from
Andrographis paniculata.
Action
The plant has the following actions:
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bitter,
acrid,
cooling,
laxative,
vulnerary,
antipyretic,
antiperiodic,
anti-inflammatory,
expectorant,
depurative,
soporific,
anthelmintic,
digestive
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Medicinal uses
It is useful in treating
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hyperdispsia,
buring sensation,
wounds,
ulcers,
chronic fever,
malarial and intermittent fevers,
inflammations,
cough,
bronchitis,
skin diseases,
leprosy,
colic,
flatulence,
diarrhoea,
dysentery,
haemorrhoids etc.
In Bengal (India), household medicine known as "Alui" is prepared from fresh
leaves and is given to children suffering from stomach complaints.
Pharmacological actions
Recent experimental finding indicated that Kalmegh is having antityphoid and
antibiotic properties.
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It has been proved to be hepatopratective drug.
Andrographis paniculata can reduce cold symptoms.
Andrographis can also be used to supplement the performance of the immune
system.
Andrographis contains andrographolides, which are responsible for this immune
system stimulation.
The use of Andrographis paniculata as a folk medicine is recorded in the Journal of
Health Science, which argues it is used in this capacity to treat fever and reduce
pain.
Independent medical research cited in the Journal of Health Science supports the
effectiveness of the herb as a treatment to reduce fever.
Side Effects
Possible side effects reported from the use of Andrographis paniculata include a
reaction from the user's digestive system.
This can manifest itself as intestinal upset or indigestion.
A report by the University of Michigan Health System shows nausea, vomiting and
diarrhea are other possible side effects related to the digestive system.
Irritation of the liver is another possible side effect, and this discovery led to the
University of Michigan recommending a lower dosage of Andrographis paniculata
to reduce the risk of liver problems.
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Prooved pharmacological actions
Anti-HIV effects (proposed)
14-dehydroandroandrographolide succinic acid monoester (DASM) may inhibit
proteolytic cleavage of the HIV envelope glycoprotein, thus acting as a protease
inhibitor for HIV (in vitro).
In a Phase I dosing trial in HIV positive patients, investigators reported a
significant rise in CD4 counts at a dose of 10mg/kg/day; however, this dose was
not well-tolerated by most patients with adverse reactions that included multiple
cases of allergic reactions, fatigue, headache, painful lymphadenopathy, nausea,
and diarrhea.
Anti-inflammatory
Andrographolide inhibits NK-kappaB binding to DNA in vitro, reducing
expression of a variety of inflammatory proteins, including COX-2.
In rat neutrophils, it also appears to exert anti-inflammatory action via a decrease
in gene expression required for neutrophil adhesion and transmigration.
In mice with experimental autoimmune encephalomyelitis, an inflammatory
demyelinating disease that serves as an animal model for multiple sclerosis,
andrographolide significantly inhibited T-cell and antibody responses to myelin
antigens.
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Andrographolide also reduced immune-stimulated nitric oxide production in vitro,
either through accelerated degradation of the iNOS nitric-oxide producing protein
or by suppressing expression of this protein.
Neoandrographolide has also been shown in vitro and ex vivo to suppress nitric
oxide synthesis in mice.
Other in vitro studies suggest that the anti-inflammatory/anti-apoptotic action may
be mediated by a decrease in free radical production through inhibition of release
of cytochrome C by mitochondria.
Andrographolide may also have mast-cell stabilizing activity in rats.
Antineoplastic effects
Several in vitro studies have indicated that andographolide has anticancer effects.
Specifically, andrographolide and isoandrographolide have ED50 values of 6.5 and
5.1mcg/mL, respectively, when added to KB cells.
Based on their experience with andographolide and human cancer cells, Zhou et al.
postulate that andrographolide may induce apoptosis in human cancer cells via
activation of caspase 8 in the extrinsic death receptor pathway and subsequently
with the participation of mitochondria.
Cardiovascular effects
Studies in dogs have shown a decrease in myocardial reperfusion injury following
ischemic events, possibly mediated by a decrease in the level of free radicals
generated by ischemia.
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Studies in rabbits report that andrographolide may help reduce restenosis after
angioplasty by reducing the secretion of endothelial growth factors that contribute
to restenosis.
Rat studies show a possible hypotensive effect as well.
Genitourinary effects
Animal studies show possible decreased spermatogenesis by preventing
cytokinesis of dividing spermatogenic cell lines.
Hematologic effects
In vitro studies have demonstrated an antithrombotic effect via inhibition of PAFinduced platelet aggregation.
Hepatoprotective effects
In mouse models of chemically-induced hepatotoxicity, andrographolide,
neoandrographolide, and andrographiside all reduced levels of lipid
peroxidation, glutathione depletion, and enzymatic leakage, possibly through
antioxidant effects.
A choleretic effect was seen in rats and guinea pigs with paracetamol-induced
liver damage.
Hypoglycemic effect
Studies in rabbits suggest that a water extract of andrographis can prevent
hyperglycemia induced by oral glucose administration, probably through an effect
on glucose absorption from the gut; there is no effect on fasting blood sugar levels
with chronic administration of the extract.
A rat study showed increased digestion and absorption of carbohydrates in rats
after the administration of andrographolide.
This is believed to be mediated by activation of intestinal disaccharidases.
Recent animal studies report that there may also be an increased glucose
metabolism in rats treated with andrographolide.
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Immunomodulatory properties
Andrographolide alone and the standardized andrographis combination product
Kan Jang were found to increase the formation of TNF-alpha and Beta2MG in
vitro; the fixed combination was more effective than the andrographolide alone.
In vitro andrographolide also increased TNF-alpha production and cytotoxic
activity of lymphocytes against certain cancer cell lines, as well as demonstrating
potential direct anticancer activity by induction of cell-cycle inhibitory protein p27
and decreased expression of cyclin-dependent kinase.
Pharmacodynamics/Kinetics:
Time to peak:
In humans, maximum plasma levels of andrographolide after a typical therapeutic
dose of 20mg (four tablets of Kan Jan preparation) are reached after 1.5-2 hours.
Metabolism:
Andrographolide appears to be intensively metabolized in a dose-dependent
fashion.
Renal excretion does not play a significant role in its elimination. The half-life of
andrographolide is approximately 6.6 hours.
EC50 and IC50:
In an in vitro study using mouse cells, bisandrographolide A extracted from
Andrographis paniculata potently activated transient receptor potential 4 (TRPV4)
channels with an EC50 of 790-950nm.
The ethanol extract of Andrographis paniculata significantly inhibited growth of
human acute myeloid leukemic HL-60 cells with an IC50 value of 14.01mcg/mL
after 24 hours of treatment.
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Glycyrrhiza glabra
Kingdom:
Plantae
Division:
Angiosperms
Class:
Eudicots
Sub class:
Rosids
Order:
Fabales
Family:
Fabaceae
Subfamily:
Faboideae
Tribe:
Galegeae
Genus:
Glycyrrhiza
Species:
glabra
Binomial name
Glycyrrhiza glabra
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Explanation
Glycyrrhizaglabra,also known as licorice and sweet wood,is native to
the Mediterranean and certain areas of Asia.
In modern medicine, licorice extracts are often used as a flavoring
agent to mask bitter taste in preparations, and as an expectorant in
cough and cold preparations.
Licorice extracts have been used for more than 60 years in Japan to
treat chronic hepatitis, and also have therapeutic benefit against other
viruses, including human immunodeficiency virus (HIV),
cytomegalovirus (CMV), and Herpes simplex.
Deglycyrrhizinated licorice (DGL) preparations are useful in treating
various types of ulcers, while topical licorice preparations have been
used to sooth and heal skin eruptions, such as psoriasis and herpetic
lesions.
Distribution
The Liquorice plants are shrubs, natives of South-east Europe and
South-west Asia, as far as Persia, the G. glabra ranging more
especially to the westward, the G. glandulifera more to the eastward
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and being the source of the Eastern Liquorice root of commerce.
Morphology
The licorice shrub is a member of the pea family and grows in
Sub-tropical climate in rich soil to a height of four or five feet.
It has oval leaflets, white to purplish flower clusters, and flat pods.
Below ground, the licorice plant has an extensive root system with a
main taproot and numerous runners.
The main taproot, which is harvested for medicinal use, is soft, fibrous, and has a bright
yellow interior.
Glycyrrhiza is derived from the ancient Greek term glykos, meaning
sweet, and rhiza meaning root.
Chemical constitutions
A number of components have been isolated from licorice, including a
water-soluble, biologically active complex that accounts for 40-50
percent of total dry material weight.
This complex is composed of :
 triterpene
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saponins,
flavonoids,
polysaccharides,
pectins,
simple sugars,
amino acids,
mineral salts, and various other substances.
Glycyrrhizin, a triterpenoid compound, accounts for the sweet taste of
licorice root.
This compound represents a mixture of potassium-calcium-magnesium
salts of glycyrrhizic acid that varies within a 2-25 percent range.
Among the natural saponins, glycyrrhizic acid is a molecule composed
of a hydrophilic part, two molecules of glucuronic acid, and a
hydrophobic fragment, glycyrrhetic acid.
The yellow color of licorice is due to the flavonoid content of
the plant, which includes liquiritin, isoliquiritin (a chalcone), and other
compounds.
The isoflavones glabridin and hispaglabridins A and B have significant
antioxidant activity and both glabridin and glabrene possess estrogenlike activity.
It contains 3-dehydro-18 beta-glycyrrhetinic acid, 2-15% triterpenoid saponins,
largely glycyrrhizin that is ammonium and calcium salts of glycyrrhizinic acid and
24-hydroxyglycyrrhizin.
Glycyrrhizinic acid hydrolyzes to diglucuronic acid and the aglycone
glycyrrhetinic acid.
There are other triterpenoid saponins, including sitosterol and stigmasterol,
flavonoids and isoflavonoids, coumestans, coumarins, resins, gums, tannin, starch
and a bitter principle.
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Part used
Root.
Taste/smell
Sweet, nutritious.
Action
(a) Demulcent,
(b) Adrenalmodulator,
(c) Antibacterial,
(d) Antiviral,
(e) Antimutagen,
(f) Anti-allergenic,
(g) Expectorant with secretolytic and secretomotor activity,
(h) Anti-inflammatory,
(i) Nutritive,
(j) Spasmolytic,
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(k) Antioxidant,
(l) Estrogenic,
(m) Immunomodulator,
(n) Mild laxative,
(o) Hepatoprotective.
Medicinal uses
Licorice is most known for its soothing effect on inflamed mucous membranes of
the throat, lungs, stomach and intestines.
The root is used for coughs, all throat and bronchial irritations, urinary tract
irritation, adrenal fatigue, immune deficient states, allergies, gastric and duodenal
ulcers, liver disorders, exhaustion due to adrenal stress, and dermatological
detoxification.
It is effective for chronic hepatitis, useful in HIV and is specific for conditions like
mononucleosis, where the patient has abnormally high liver enzymes, a sore throat
and needs immune system support.
It is also a wonderful herb for Chronic Fatigue Syndrome.
Due to its sweet taste, licorice makes a nice addition to formulas that are
unpalatable.
Respiratory Benefits
Siddha, the traditional medicinal system of India, considers Glycyrrhiza glabra to
be a tonic, expectorant and a demulcent.
A demulcent has soothing, coating properties, while an expectorant eliminates
phlegm and mucous from the respiratory tract.
These properties account for the traditional use of licorice as a cough reliever and
an asthma treatment.
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Ulcer Treatment
It may be beneficial for treating stomach ulcers.
A small number of studies indicate that glycyrrhiza glabra combined with antacids
had results comparable to prescription drugs.
One study found a high rate of success with licorice root fluid extract for treating
stomach ulcers.
Animal research suggests glycyrrhiza glabra may protect against ulcers caused by
aspirin use.
Acid Reflux Treatment
Licorice may help relieve heartburn or symptoms of gastroesophageal reflux
disease.
Taking orally significantly decreases the severity of acid reflux and other
symptoms, including :
 heartburn pain,
 cramping,
 nausea and vomiting.
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Topical and Oral Benefits
Licorice may have topical and oral uses. Applying licorice content reduced skin
itching, swelling and redness, and gargling with it and warm water reduced the
pain of canker sores.
Weight and Fat Reduction
Although research is limited, Glycyrrhiza glabra may be beneficial for people who
want to lose weight or decrease body fat.
The University of Maryland Medical Center cites a study in which participants
consumed 900 mg of licorice flavonoid oil per day for eight weeks and
experienced significant reductions in body fat and weight, along with lowered
cholesterol levels.
In another study cited by the Medical Center, applying a topical preparation of the
licorice component glycyrrhetinic acid decreased the thickness of fat on the thigh.
Hepato protective and Anti-hepatic
Glycyrrhiza glabra has anti viral action which protects liver cells from the viral
infection due to which jaundice is caused. By its demulcent action it reduces the
body heat which is the main cause of jaundice according to siddha system of
medicine
Prooved pharmacological actions
Experiments with both methanol extract of licorice and the constituent glycyrrhizin
appear to activate glucuronidation and suggest the possibility that it may influence
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detoxification of xenobiotics in the liver.Thus its hepato protective action is
proved.
Subdural injection of licorice root has inhibited RC mammary carcinoma and
lympho sarcoma 150 in mice. A number of constituents in licorice have shown
anti-tumor activity in animal research.
The saponin known as glycyrrhizin, also known as glycyrrhizic acid or
glycyrrhizinic acid, is the main ingredient in licorice root. It and its aglycone,
glycyrrhetinic acid, exert most of the medicinal effects and are essential active
components.
Glycyrrhetinic acid is formed from glycyrrhizin via hydrolysis that is assisted by
intestinal flora enzymes.
It decreases inflammation by enhancing movement of leucocytes towards
inflammed areas.
Glycyrrhizin also increases interferon production and inhibits the activity of
phospholipase A and the formation of prostaglandin E2 in activated peritoneal
macrophages.
Additionally it inhibits the effect of several tumor promoters.
The isoflavone in licorice called formononetin, has very weak estrogenic activity
compared with natural estrone or synthetic DES.
Phytoestrogens can behave like anti-estrogens by competing with estradiol for
cytoplasmic receptors in estrogen-sensitive tissues, possibly acting as protection
against stronger estrogenic action from estradiol and protecting against cancers that
are estrogen receptor positive.
Since licorice inhibits 5-beta-reductase that regulates cortisol and aldosterone
metabolism, it may retard the metabolic excretion of corticosteroids and extend the
biological half-life of cortisol and aldosterone.
Licorice potentiates the activity of anthraquinone drugs or herbs containing
anthraquinones, like cascara and buckthorn, by increasing the wettability of the
bowel contents because of the high surfactant activity of glycyrrhizin.
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It also potentiates the toxicity of cardiac glycosides like digitalis due to potassium
loss in the urine. There may also be an additive effect with thiazide diuretics.
When used with corticoid treatment, glycyrrhizin interferes with 5 beta-reductase
breakdown of corticosteroids, thus prolonging its biological half-life.
The compound glycyrrhizic acid, found in liquorice, is now routinely used
throughout Japan for the treatment and control of chronic viral hepatitis, and there
is a possible transaminase-lowering effect.
Hepatoprotective mechanisms have been demonstrated in mice.
Recent studies indicate that glycyrrhizic acid disrupts latent Kaposi's sarcoma (as
also demonstrated with other herpesvirus infections in the active stage), exhibiting
a strong anti-viral effect.
The Chinese use liquorice to treat Tuberculosis.
Liquorice affects the body's endocrine system as it contains isoflavones
(phytoestrogens).
It might lower the amount of serum testosterone slightly, but whether it affects the
amount of free testosterone is unclear.
Consuming liquorice may prevent the development of hyperkalemia in persons on
hemodialysis.
Large doses of glycyrrhizinic acid and glycyrrhetinic acid in liquorice extract can
lead to hypokalemia and serious increases in blood pressure, a syndrome known as
apparent mineralocorticoid excess.
These side effects stem from the inhibition of the enzyme 11β-hydroxysteroid
dehydrogenase (type 2) and subsequent increase in activity of cortisol on the
kidney.
11β-hydroxysteroid dehydrogenase normally inactivates cortisol in the kidney;
thus, liquorice's inhibition of this enzyme makes the concentration of cortisol
appear to increase.
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Cortisol acts at the same receptor as the hormone aldosterone in the kidney and the
effects mimic aldosterone excess, although aldosterone remains low or normal
during liquorice overdose.
To decrease the chances of these serious side effects, deglycyrrhizinated
liquorice preparations are available.
The disabling of similar enzymes in the gut by glycyrrhizinic acid and
glycyrrhetinic acid also causes increased mucus and decreased acid secretion.
As it inhibits Helicobacter pylori, is used as an aid for healing stomach and
duodenal ulcers, and in moderate amounts may soothe an upset stomach.
Liquorice can be used to treat ileitis, leaky gut syndrome, irritable bowel
syndrome and Crohn's disease as it is antispasmodic in the bowels.
Studies of the use of liquorice extract (usually at 7%) in the treatment of melasma
have shown that glabridin inhibits tyrosinase activity of melanocytes.
The compounded carbenoxolone is derived from liquorice.
Some studies indicate that it inhibits 11β-Hydroxysteroid dehydrogenase type 1, an
enzyme that is highly expressed in liver and fat tissues, where it plays a role in
metabolism, and in the brain, where the same enzyme is involved in stress response
that has been associated with age-related mental decline.
In siddha it is used in the Hoxsey anti-cancer formula, and is a considered
adaptogen which helps reregulate the hypothalamic-pituitary-adrenal axis.
It can also be used for auto-immune conditions including lupus, scleroderma,
rheumatoid arthritis and animal dander allergies.
Glycyrrhizin from Glycyrrhiza root has been shown to modulate airway
constriction, lung inflammation and infiltration of eosinophils in bronchial areas by
stimulating CD4 and CD8 immune cell function.
Liquorice may be useful in conventional and naturopathic medicine for both mouth
ulcers and peptic ulcers.
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
Sliver of liquorice root

Various liquorice root slivers

Liquorice root with bark
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Annabedi chendooram
Chemical name: Ferri sulphas, Greenvitriol
Taste: Astringent
Nature: Heat
Action:








Tonic,
Astringent,
Emmenogogue,
Deodarent,
Anthelmintic,
Antimicrobial,
Antiperiodic.
Liver tonic.
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Mandoora Chendooram
Chemical name: Ferroso ferric sulphide
Taste: Astringent,sour,bitter
Nature: Heat
Action:





Tonic,
Appetiser,
Haematemic,
Carminative,
Diuretic.
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Velli parpam
Chemical name: Argenium
Taste: Sour,Astringent,Sweet
Nature: Cold
Action:









Antispasmodic,
Tonic,
Stimulent,
Tonic,
Anti-Emetic,
Aprodisiac,
Laxative,
Carminative,
Demulcent.
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Over all view of capsule’s action:
Indigofera tinctoria&Annabedi chendooram:
Both by their anti microbial action acts against the HAV virus and thus helps to
lower the infection .
Andrographis paniculata & Phyllanthus niruri &Annabedi
chendooram :
All these by their anti periodic action reduces the fever and the body heat,all these
by their hepatic tonic action heals the liver’s damage and strengthens the liver.
Glycyrrhiza glabra,mandoora chendooram,velli parpam :
By their demulcent,diuretic action reduces the body heat,increases the excreation
of excess bile through urine and there by decreases the bilirubin level in the blood.
Annabedi chendooram, mandoora chendooram
All these by their haemetinic action increases the RBC production and by their
astringent taste avoids the destruction of RBC and thus lowers the bilirubin level in
the blood.
Conclusion
All the ingredients of the capsule is having proved hepato protective action and
by their nature of being hepatic tonic strengthens the liver and by their stimulant
and carminative action improves the appetite and by their nature of being good
tonic nature improves the immunity of the body and avoids the occurance of the
same jaundice repeatedly.
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