HEPATITIS
Types of hepatitis
1) Viral hepatitis
2) Alcoholic hepatitis
3) Drug induced hepatitis
4) Other toxins that induced hepatitis
5) Metabolic disorder
6) Cholestatic
7) Autoimmune
8) Alpha-1 antitrypsin deficiency
9) Nonalcoholic steatohepatitis
I Acute viral hepatitis
Symptoms and signs: ( prodromal phase icteric phase recovery phase )
malaise, nausea, vomiting, diarrhea, and low-grade fever followed by dark urine, jaundice, and
tender hepatomegaly. Hepatitis like illness may be caused not only by hepatotropic viruses
(A,B,C,D,E) but also by other viruses (EB virus, CMV, coxsackie virus, etc.)
Laboratory data:
Complete LFT, prothrombin time, glucose, hepatitis profile (Anti-HAV IgM, HBsAg, Anti-HBc
IgM, Anti-HCV )
Therapy:
1) Diet: high calorie, high protein diet, fatty food need not be restricted unless they produce
nausea, vomiting, or diarrhea
2) Bed rest and physical isolation
3) Supportive care
a) IV volume expansion
b) Metoclopramide for protracted nausea and vomiting
c) Multivitamin supplement
d) Cholestyramine up to 4g po qid for severe pruritus
4) Avoid narcotics, analgesics, and tranquilizers
5) Alcohol abstinence
6) Treatment of acute HCV with IFN-alpha for 6 months ↑ sustained HCV-RNA clearance
Indication for hospitalization:
1)
2)
3)
4)
Evidence of significant impaired coagulation function, ( prothrombin time > 16 seconds)
Encephalopathy
Ascites
Dehydration resulting from nausea and vomiting
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5) Severe jaundice ( total bilirubin > 10 mg/dl )
6) Elderly patient and those with significant medical problems
Complication and sequelae
1)
2)
3)
4)
5)
relapsing hepatitis
cholestatic hepatitis
fulminant hepatitis ( massive hepatic necrosis )
chronic viral hepatitis
enhanced risk of hepatocellular carcinoma
6) serum sickness-like syndrome
II
Chronic viral hepatitis
1. Presence of liver inflammation persisting for at least 6 months
2. Subdivided into
1) Carrier state
2) Chronic persistent hepatitis
3) Chronic active hepatitis
4) Cirrhosis
3. Treatment
1) Chronic HBV: IFN-alfa-2b (5 million units SC qd or 10 million units SC 3
times/week) for 16 weeks, restricted to patients with active viral replication
with no evidence of decompensated liver disease. Lamivudine ( 100 mg PO
qd ) or Adefovir dipivoxil ( 10mg PO qd )
2) Chronic HCV: PEG-IFN and ribavirin ( 10.6-13.0 mg/kg/day, PO bid ) for
6-12 months. PEG-IFN alpha-2a (180μg SC/week) and PEG-IFN alpha-2b
(1.5μg/kg, SC/week) are similar in efficacy.
III Alcoholic hepatitis
Significant liver damage develops in only 10-20% of chronic alcoholics.
 Additional factors ( genetic, nutritional, environmental ) may be important in the pathogenesis
of alcoholic liver disease.
Symptoms and signs
1) Fatty liver: most commonly observed abnormality, usually asymptomatic, hepatomegaly, mild
liver enzyme abnormality
2) Alcoholic hepatitis: clinically silent or severe to hepatic failure and death, fever, upper
abdominal pain, anorexia, nausea, vomiting, weight loss,↑AST higher than ↑ALT, ↑AP,
Hyperbilirubinemia and prolongation of PT, leukocytosis, renal failure, A discriminatory factor
(DF)= 4.6 X ( PTpatient—PTcontrol) + serum bilirubin can be determined to assess in-hospital
mortality (DF>3250% mortality)
3) Alcoholic cirrhosis: a common cause of cirrhosis and HCC
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Treatment
1) abstinence from alcohol and nutritional support ( high protein diet, 1.5g/kg )
2) Corticosteroids is controversial.
3) DF > 32 with hepatic encephalopathy may benefit from steroid therapy.
( Oral prednisone 40-60 mg/day and subsequently tapered as clinically indicated )
4) Pentoxifylline (400 mg PO, tid) is a nonselective phosphodiesterase inhibitor with anti-inflammatory
properties and an excellent safety profile that has shown improved survival in severe (DF>32)
alcoholic hepatitis.
IV Toxic and drug-induced hepatitis
1. Pathogenesis
1) Direct hepatotoxins
CCl4, phosphorus tetracycline, methotrexate, 6-mercaptopurine, acetaminophen,
mushroom toxin, alkylated anabolic steroids )
2) Idiosyncratic hepatotoxins
Sulfonamides, nitrofurantoin, paraaminosalicylic acid, phenytoin, halothane
Isoniazid, methyldopa
2. Clinical characterization
1) Direct hepatotoxin
a) high incidence of toxicity in exposed persons
b) dose-dependent injury
c) brief period between exposure and onset of illness
d) reproducibility in experimental animals
2) Idiosyncratic hepatotoxin
a) hepatic injury in only small proportion of exposed persons
b) lack of relationship between dose and extent of injury
c) relatively long latent period
d) failure of experimental reproducibility
3. Morphologic pattern
1) Hepatitis: marked increase of GPT/GOT
2) Cholestatic: marked increase of alkaline phosphatase
3) Mixed: mixture of 1) and 2)
4) Fatty liver
5) Granulomas
4. Therapy
1) Cessation of the causative agent
2) An attempt to remove the agent from the GI tract using lavage or cathartics
3) Supportive care is crucial
4) Specific therapy for acetaminophen ( antidote: N-Acetylcysteine )
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5) Large doses of glucocorticoids: hepatic failure accompanied by hallmark of hypersensitivity
6) Hemodialysis
Acute hepatic failure
Massive hepatic necrosis with impaired consciousness occurring within 8 weeks of the onset of
illness
Clinical manifestations
Neuropsychiatric changes-- delirium, personality change, stupor, coma; cerebral
edema—suggested by profuse sweating, hemodynamic instability, tachyarrhythmias, tachypnea,
fever, papilledemia, decerebrate rigidity ( though all may be absent ); deep jaundice, coagulopathy,
bleeding, renal failure, acid-base disturbance, hypoglycemia, acute pancreatitis, cardiorespiratory
failure, infections ( bacterial, fungal ).
Adverse prognostic indicators
1)Age < 10 or > 40,
2)Certain causes ( eg., halothane, hepatitis C )
3)Duration of jaundice > 7 days before onset of encephalopathy
4)Serum bilirubin > 18 mg/dl
5)Coma ( survival <20% )
6)Rapid reduction in liver size
7)Respiratory failure
8)Marked prolongation of PT, factor V level <20% ( In FHF, the level of factor V predicts
outcome. )
Treatment
1).Endotracheal intubation often required
2).Monitor serum glucose with IV supplement
3).Prevent GI bleeding with H2-blocker and antacids
4).Intracranial pressure is monitored—more sensitive than CT
5).Value of dexamethasone for cerebral edema unclear, IV mannitol may be
beneficial.
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