H339 Acute Viral Hepatitis

Introduction

Virology and etiology

Hepatitis A

Hepatitis B

Viral proteins and particles

Serologic and virologic markers

HBV has no direct cytotoxic effect, but the presence of viral HBsAg/cAg on the cell surface stimulate the host?s cytotoxic CD8+ T lymphocytes to destroy infected hepatocytes.

HBsAg ???? ?? ??? – mutation?? ?? ??? ??? ???? ? HBV DNA
HBs? Ag, Ab? ?? ??? – ?? ?? ???? or HBV? ?? or ???? Ab? x

Molecular variants

Extrahepatic sites

Hepatitis D

Hepatitis C

Hepatitis E

Pathogenesis

Hepatitis B

Hepatitis C

Extrahepatic manifestations

by immune complex-mediated tissue damage

Serum sickness syndrome

related to the deposition in tissue blood vessel walls of HBsAg–anti-HBs circulating immune complexes, leading to activation of the complement system and depressed serum complement levels.

Glomerulonephritis

Essential mixed cryoglobulinemia (EMC)

The association with HBV is limited.
A substantial proportion has chronic HCV infection.

H363 The Vasculitis Syndromes

Treatment

  • Mild disease
    • e.g., only nonulcerating skin lesions ± mild neuropathy
    • Direct-acting antiviral (DAA) therapy
  • Severe disease
    • e.g., renal failure requiring hemodialysis (d/t RPGN)

Pathology

Epidemiology and global features

Hepatitis A

Hepatitis B

Hepatitis D

Hepatitis C

Hepatitis E

Clinical and laboratory features

Symptoms and signs

  • Serum sickness-like syndrome
    • Fever
    • Pruritic urticarial rash
    • Arthralgia
    • Lymphadenopathy
  • Polyarteritis nodosa
    • Beads on a string appearance
    • Membranous, MPGN

Laboratory features

HBsAgANTI- HBsANTI- HBcHBeAgANTI- HBeINTERPRETATION
+IgM+Acute hepatitis B, high infectivity
+IgG+Chronic hepatitis B, high infectivity
+IgG+1. Late acute or chronic hepatitis B, low infectivity
2. HBeAg-negative (?precore-mutant?) hepatitis B (chronic or, rarely, acute)
++++/-+/-1. HBsAg of one subtype and heterotypic anti-HBs (common)
2. Process of seroconversion from HBsAg to anti-HBs (rare)
IgM+/-+/-1. Acute hepatitis Ba
2. Anti-HBc ?window?
IgG+/-1. Low-level hepatitis B carrier
2. Hepatitis B in remote past
+IgG+/-Recovery from hepatitis B
+1. Immunization with HBsAg (axer vaccination)
2. Hepatitis B in the remote past (?)
3. False-positive

Prognosis

HBV

  • 95%: acute hepatitis? ?? completely resolve
  • 4-5%: develop chronic hepatitis
    • 50-80% remain stable 

Complications and sequelae

Fulminant hepatitis

Etiology

HBV? m/c cause, ??? HDV? ?? ?
? ? drug toxicity, HAV, autoimmune hepatitis, ischemia, Wilson disease, and malignant infiltration of the liver.

Pathophysiology & Diagnosis

  • Severe acute liver injury without cirrhosis or underlying liver disease.
  • The diagnosis requires:
    • Elevated aminotransferases (often >1,000 U/L)
    • Signs of hepatic encephalopathy (HE)
    • Impaired hepatic synthetic function (defined as INR ?1.5)

?? ??? ?? 8? ?? ??? ??, ????? ???? ?. -> ?? ????? ??? ??, ???.

Prognosis

Prognostic factors
???? ?? ??
Bilirubin  ??? ?
PT ??
??
??? ?? 
AST, ALT, albumin, virus titer

Management

????? glucocorticoid, prostaglandin, ???? ?. ???? ??? ?? ??.

Differential diagnosis

Treatment

Prophylaxis

Hepatitis A

Hepatitis B

???? 3? ? ???? ???? ??? protective effect? ??? ?????/???? booster ?? ?? ??.

?? ? ??

  • Perinatal exposure
    • HBIG 0.5mL 1? IM + 12hr ?? vaccine (3?)
  • Direct percutaneous/transmucosal exposure
    • HBIG 0.06mL/kg IM + 1? ?? vaccine
    • Booster: ?????? ?? ??
  • Direct sexual contact
    • HBIG 0.06mL/kg IM + 2? ?? vaccine

Hepatitis D

Hepatitis C

Hepatitis E