This lecture was conducted during the
Nephrology Unit Grand Ground by Medical
Student rotated under Nephrology Division
under the supervision and administration of
Prof. Jamal Al Wakeel, Head of Nephrology
Unit, Department of Medicine and Dr.
Abdulkareem Al Suwaida, Chairman of the
Department of Medicine. Nephrology
Division is not responsible for the content
of the presentation for it is intended for
learning and/or education purpose only.
Acute Viral Hepatitis
Presented By:
Dr. Mahdi Al Namankani
Medical Student
May, 2008
Definition:
Diffuse liver inflammation lasting less than
6 months
Causes:
Hepatitis A
HAV
Infective
hepatitis
Hepatitis B
HBV
serum
hepatitis
Hepatitis
D
HDV
Hepatitis C
HCV
Post
transfusion
hepatitis
Hepatitis E
HEV
Epidemic/
Entral
virus
27 nm RNA
42 nm DNA
Hepa virus
35 nm
Incomplete
RNA+HBsAg
30 – 60 nm
RNA flavi firus
32 nm RNA
transmission
Feco-oral
Incubation p.
2 – 6 weeks
2 – 6 months
2 – 6 months
2 – 6 months
2 – 6 weeks
Chronicity
&liver cancer
no
Yes
Yes
Yes
No
Immunization
-passive
Non specific
Ig
Specific Ig
IgM
-active
HAV vaccine
danger
Heptavax
HBV vaccine
Heptavax
HBV vaccine
Paraentral and post transfusion
Sexual
low risk 1-5 %
Intrauterine
low risk <5%
Feco-oral
Non specific
Ig
Pathogenesis
Initial viremia, with inflammation of GIT mucosa.
Intrahepatic localization
lead to
A- diffuse centrilobular necrosis, with cellular infiltration around portal
tracts
B- intrahepatic cholestasis due to cellualar edema & inspissation of bile
Other organ: splenomegaly –
lymphoadenopathy
Hypoplasia of BM
Clinical picture
1. Preicetric stage or prodromal stage:3 – 9 days
Sudden onset of influenza like picture: fever - headache –
malaise – muscular pain
Anorexia is marked with nausea – vomiting – distension
Pain in Rt hypochondrium & epigastrium
Dark urine – pale stool
Transient itching
Examination: fever with relative bradycardia + enlarged
tender liver
Clinical picture
Icteric stage: 2-4 w
Jaundice with fever & improvement of general
condition
Anorexia nausea & vomiting diminish or disappear
Urine is dark brown & frothy
Stool are clay in color – bulky – offensive – greasy
Examination:
Soft tender enlarged liver Spleen is enlarged in 20 %
L N 10% geralized lymphoadenopathy with LN of
post. Triangle of neck
Clinical picture
Convalescence stage:
Signs & symptoms gradually disappear
Jaundice may persist for some times due to affinity of
bile pigment to elastic tissue
Complete recovery of liver may take up to 6 months
Investigation:
LFT:
1. serum bilirubin : total, direct and indirect
2. ALT – AST : from 500 – 2000 IU/L
ALT > AST
3. Alkaline phosphatase – 5’nucleotidase – GGT:
Blood :
Leucopenia with relative lymphocytosis, ESR
Urine :
Early bilirubin appearance
Bile salt : granular casts – frothy urine - +ve hay sulfur
test
Stool:
Pale – clay with staetorrhea
Diminished stercobilinogen
Serology
Acute stage
Chronic stage
others
Hepatitis A
Anti HAV IgM
Anti HAV IgG
Fecal
HAV
Hepatitis D
Anti HDV IgM
Anti HDV IgG
Hepatitis E
Anti HEV IgM
Anti HEV IgG
Hepatitis B marker:
antigen
Significance
Corresponding
Ab
significance
Appear after 6 week
Acute infection, remain
for 3 ms
Chronic infection if >6
ms
Anti HBs
Appear after 3 m
Reflecting recovery &
immunity
HBcAg
(core)
Detected on Liver
Biopsy only (not serum)
Anti HBc
Appear after 2 m
Reflecting sever
acute & chronic form
HBeAg
(envolop)
Reflect ongoing viral
replication (chronicity)
Anti HBe
Appear after 2.5 m
Non replicating virus
HBsAg
(surface)
HBV DNA
Most sensitive indication for viral replication & chronicity (Dan
particle)
It is detected by PCR
•Serological gap:
It is a window last several weeks between
disappearing of HBs Ag & appearance of Anti
Hbs. Anti HBc Ab may represent serological
evidence of recent HBV infection
Blood free from Hbs Ag & Anti Hbs (but
containing anti – HBC) is the major cause of
trasfusion HBV infection
Hepatitis C markers:
Marker
technique
time
significance
HCV Ab
2nd & 3rd generation ELISA or RIBA
test
After 3 – 6 ms of
infection
Exposure to infection
not immunity
HCV
RNA
PCR – quantitative PCR is more
accurate & assess interferon ttt
After 1 – 2 weeks
Indicate active virus
Course & Complication:
Complete recovary:
Occur in most cases of virus A – E
Less common in virus B – D & in small case of virus C
Relapse:
Characteristic of virus C – less common in B – D
Present by reappearance of CL.p. or
biochemical
Abnormalities ( biliruben & enzymes )
Fulminant hepatitis: ( Acute liver failure )
Acute hepatic necrosis – acute yellow atrophy
After typical onset
deep jaundice , vomiting ,
encephalopathy & coma
Patient usually dies in 10 days
• Prolonged cholestasis
• Cholestatic jaundice Watson’s syndrom
• After 3 W of jaundice, condition improves but jaundice
deepens & patients starts to itch
• This is due to intra hepatic Biliary obstruction by
inflammation
• Jaundice persist to 6 m then recovery
post hepatitis syndrome:
Common intelligent
Features : anxiety , fatigue , anorexia, Rt upper
abdominal discomfort
Palpable liver raised copula of diaphragm in X Ray
LFT & biopsy are normal
Chronic sequelae:
In C, B, D not in A & E
Chronic active hepatits
Chronic persistent hepatitis
Post hepatic cirrhosis
Hepatocellular carcinoma
Extrahepatic manifestation of hepatitis
Clinical condition
Associated
virus
comments
Polyarteitis nodosea
HBV
60 % have HBV
Glomeronephritis
HCV & HBV
Mainly mesengioproliferative –result in CRF
Porphyria cutnea tarda
HCV
Blistering lesion on back of hands
Cryoglobulinemia
HCV
Type 2 (mixed – essential)
Sjogren syndrom
HCV
Virus isolated from salivary tissue
Lichen planus
HCV
60 % have HCV
Others associated with HCV
Erythema nodusm – erythema multiforme
Polymyosistis – hachimoto’s thyroiditis
Diabetes mellitus – bahcet’s syndrome
Down syndrome – Aplastic anemia
Studies involve small number of patients
Impotance need evaluation
Treatment:
Rest:
Bed rest till LFT normal
Diet:
Protein: gives freely except with Liver failure
CHO: gives freely
Fats: better avoided
Alcohol & hepatotoxic: contraindicated
Drugs:
Vitamins especially K parental
Cholestyramine: for itching
Corticosteroids are indicated in : fulminant cases –
cholestatic jaundice
Interferon: reduce risk of chronic hepatitis in acute
hepatitis C
Prophylaxis:
Screening: of blood for hepatitis Ag , disposable
syringes, avoid sharing razors or tooth brush
passive prophylaxis:
Hepatitis A : gamma globulin in contact or preicteric phase
patient
Hepatitis B: (HBIG) rich with anti HBs
Active prophylaxis:
Hepatitis A:
Inactivated HAV 0.5 – 1 ml IM to be repeated after 6 -12m
Hepatitis B:
Recombinant HBV vaccine (Heptavax) IM in 3doses at
0-1-6m
High risk people:
Medical doctors & nurses
Hemophiliacs & hemolytic anemia
Prenatal drug abusers
Babies porn to HBsAg +ve mother
Now for all infant & children
N.P: HBV is prophylactic against hepatitis D viral infection