Hepatitis B Acute & Chronic Infections

DIFFERENTIATION OF ACUTE & CHRONIC HBV:

HBs Ag Anti HBs Ag HBe Ag Anti HBe Ag Anti HBc Ag
Acute HBV
(high infectivity)
+ + IgM
Acute HBV
(low infectivity)
+ + IgM
Chronic HBV
(high infectivity)
+ - + IgG
Chronic HBV
(low infectivity)
+ - + IgG
Recovery + - + IgG
Immunized - +
CLINICAL FINDINGS:
  • Acute infection :
  1. Loss of appetite, nausea, vomiting, body aches, mild fever, dark urine, and then progresses to development of jaundice.
  2. Itchy skin has been an indication as a possible symptom of all hepatitis virus types.
  3. Fulminant hepatic failure may arise.
  4. The infection may be entirely asymptomatic and may go unrecognized.
  5. DNA polymerase,Anti HBc (+), HBsAg (+) is a marker of acute hepatitis B infection
  • Chronic infection with hepatitis B virus
  1. It may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis)
  2. 90 % chance for chronic infection if infected at birth
  3. Mild chronic hepatitis B has 5 year survival 97 %
  4. Adult infection is usually symptomatic
COMPLICATIONS OF ACUTE HBV:
  • Fulminant hepatitis
  • Cirrhosis
  • Hepatocellular carcinoma
  • Chronic hepatitis
  • Papular acrodermatitis of child hood (Gianotti - crosti syndrome)
  • Glomerulonephritis
  • Essential mixed cryoglobulinemia (more common with HCV)
  • Polyarteritis nodosa (PAN) may be associated with HBV infection.
  • Hepatocellular carcinoma is the only vaccine preventable cancer.
CHRONIC HBV:
  1. Chronic HBV infection has two stages :
  2. Replicative stage (early)
  • HBV DNA is found both in serum and hepatocyte nuclei, where it is present in free or episomal form.
  • HBe Ag (+)ve - Patient has high infectivity
  • Serum analysis yields elevated ALT, HBsAg, Anti-HBc, HBeAg, and bilirubin.
  • Antiviral therapy with interferon is indicated in patients with active viral replication (is HBV DNA) and elevated ALT levels
  • Non-replicative stage
  • HBV DNA (marker of level of liver injury) present only in hepatocyte nuclei, integrated into the host genome.
  1. Anti HBe (+)ve
  2. Patient has low infectivity
EXTRAHEPATIC MANIFESTATION OF HBV:
  • Nephrotic syndrome
  1. Membranous nephropathy,
  2. Minimal change nephropathy,
  3. Mesangial proliferative glomerulonephritis,
  4. Membranoproliferative glomerulonephritis
  5. IgA nephropathy
  • PAN
  • Essential mixed cryoglobulinemia
  • Lichen planus
  • Sjogren syndrome

Mallory-Denk bodiesCharacteristically seen in: Alcoholic liver disease Ballooning degeneration Piecemeal
1° biliary cirrhosis
Wilson disease
Hepatocellular tumors
Non-alcoholic fatty liver disease
Focal nodular hyperplasia
Indian childhood cirrhosis
Chronic cholestatic syndromes
Bileduct obstruction
Acute viral hepatitis
Alcoholic hepatitis
Drug induced
α-1antitrypsin ↓
1o biliary cirrhosis
Chronic hepatitis
on Meyenburg complexes - bite duct micro-hamartomas
  • Caroli disease - biliary cysts + ascending cholangitis
  • Nut meg liver - CVC liver
  • Infarct of Zahn - acute thrombosis of intrahepatic portal vein radical
  • Vanishing bile duct syndrome - Chronic rejection of transplanted liver
  • Fatty change is not seen in Indian childhood cirrhosis
  • Jaundice is not seen in Reye's syndrome and hepatocellular carcinoma
HISTOPATHOLOGY:
  • Chronic hepatitis B
  1. Ground glass cytoplasmic inclusions are seen within hepatocytes in case of chronic hepatitis B.
  2. These inclusions represent hepatitis B virus surface antigen.
  • Acute hepatitis B
  1. Signs of hepatocellular injury, mononuclear inflammatory infiltrate, kupffer cell hyperplasia, cholestasis and regeneration
  2. The characteristic histopathological changes includes ballooning degeneration, Councilman body or acidophil body, dropout necrosis, and bridging necrosis.
  3. Ballooning degeneration: In this hepatocytes appear swollen with granular cytoplasm which tends to condense around the nucleus.
  4. Councilman body: Cells show acidophilic degeneration with intensely eosinophilic cytoplasm and a small pyknotic nucleus which gets eventually extruded leaving behind necrotic acidophilic mass called Councilman bodies.
PROPHYLAXIS:
  • Passive prophylaxis is by hepatitis B immune globulin (HBIG).
  • Active immunization is by recombinant hepatitis B vaccine.
  • These are two recombinant vaccines :Vaccine is given intramuscular into the deltoidor in infants into the anterolateral aspect of thigh. Gluteal injection is not recommended as it may result in poor immune response.
  1. Recombivax - HB
  2. Engerix - B
  • Three doses are given at 0, 1 and 6 months.
  • For pre exposure prophylaxis only hepatitis B vaccine is given. For post exposure prophylaxis combination of HBIG and hepatitis B vaccine is recommended.
  • For perinatal exposure single dose of HBIG at birth along with complete course of vaccination is recommended.
  • First dose of vaccine should be given within 12 hours after birth.
Exam Question
  •  Serum analysis yields elevated ALT, HBsAg, Anti-HBc, HBeAg, and bilirubin in active chronic hepatitis B
  • DNA polymerase,Ig M anti-HBc antibody, HBsAg (+) is a marker of acute hepatitis B infection
  • Liver biopsy in acute hepatitis due to hepatitis B virus is likely to show ballooning degeneration, Councilman body or acidophil body, dropout necrosis, and bridging necrosis The incidence of chronic carrier state in liver disease is due to hepatitis B infection.
  • The patterns of glomerular injury in HBV related chronic liver disease shows Membranous nephropathy, Minimal change nephropathy, Mesangial proliferative glomerulonephritis, Membranoproliferative glomerulonephritisIgA nephropathy
  • Most widely accepted mechanism associated with nephropathy in chronic HBV patients is Deposition of immune complex particles attributed to viral antigens and host antibodies Adult infection is usually symptomatic in chronic hepatitis B
  • 90 % chance for chronic infection if HBV infection occur at birth
  • Mild chronic hepatitis B has 5 year survival 97 %
  • Complications of acute HBV include Fulminant hepatitis, Cirrhosis,Hepatocellular carcinoma, Chronic hepatitis, Gianotti - crosti syndrome, Glomerulonephritis, Essential mixed cryoglobulinemia, Polyarteritis nodosa (PAN), Hepatocellular carcinoma
  • Best means of giving hepatitis B vaccine is Intramuscular deltoid
  • Ground glass hepatocytes are seen in HBV chronic infection
  • Increased SGPT & SGOT with HBs Ag antigen positive HBe Ag antigen negative and anti-HBe antibody positive shows chronic active hepatitis is diagnosed as HBV precore mutant Marker of level of liver injury in cases of hepatitis B is HBV DNA
  • Hepatitis B associated with Polyarteritis nodosa
  • Hepatitis B vaccine should be given as per which schedule 0,1,6 months
  • Antiviral therapy with interferon is indicated in patients with active viral replication (is HBV DNA) and elevated ALT levels
  • Extrahepatic Manifestations of Hepatitis B include Aplastic Anemia ,Cryoglobulinaemia, Diabetes mellitus, Dermatomyositis-like syndrome ,Gianotti- Crosti syndrome, Glomerulonephritis, Guillain- Barre syndrome, Myasthenia gravis, Pericarditis and myocarditis, Pancreatitis, Peripheral Neuropathy, Polyarteritis Nodosa ,Polyarthritis, Polymyalgia rheumatica, Polymyositis, Porphyria cutanea tarda ,Psychosis, Raynaud's syndrome, Serum sickness like illness, Splenomegaly and lymph node enlargement, Skin alterations, Thrombopenic. purpura ,Thyroiditis ,Urticaria
  • Positive HBs Ag with Other serological tests for hepatitis negative & normal liver enzymes are suggestive of inactive HBV carrier
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