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CHRONIC HEPATITIS B SEROLOGY

CHRONIC HEPATITIS B SEROLOGY. Antigens. HBsAg Found on the surface of the intact virus and in serum as unattached particles Earliest detectable marker in serum indicates current Hepatitis B infection. HBcAg Found within the core of the intact virus Not detectable in serum.

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CHRONIC HEPATITIS B SEROLOGY

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  1. CHRONIC HEPATITIS B SEROLOGY

  2. Antigens HBsAg • Found on the surface of the intact virus and in serum as unattached particles • Earliest detectable marker in serum • indicates current Hepatitis B infection HBcAg • Found within the core of the intact virus • Not detectable in serum Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1933-1934

  3. Antigens HBeAg • Readily detectable serologic marker of HBV infection • Appears shortly after HBsAg • Coincides w/high levels of virus replication • Indicates highly infective stage of HBV Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1935

  4. Antibodies Anti-HBs • Antibody to HBsAg • Becomes detectable in serum after HBsAg disappears • indicates immunity to Hepatitis B infection • “protective antibody” Anti-HBc • Total antibody to HBcAg • Only serologic evidence of recent HBV infection during the “window period” • May indicate acute or chronic infection Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1933-1934

  5. Antibodies Anti-HBc IgM • IGM antibody to HBcAg • Seen in the 1st 6 months after acute infection • indicates recent acute Hepatitis B infection Anti-Hbc IgG -IgG antibody to HBcAg -predominates beyond 6 months - Seen in chronic HBV infection Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1934-1935

  6. Antibodies Anti-HBe - Antibody to HBeAg - Signifies low infectivity Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1935

  7. Chronic Hepatitis B Serologic Patterns Reference: 17th Ed. Harrison’s Principles of Internal Medicine p.1943

  8. CHRONIC HEPATITIS B CLINICAL and laboratory FEATURES

  9. Progression of acute hepatitis to chronic hepatitis: Clinical and Laboratory features: • lack of complete resolution of clinical symptoms of anorexia, weight loss, and fatigue and the persistence of hepatomegaly; 2. the presence of bridging or multilobular hepatic necrosis on liver biopsy during protracted, severe acute viral hepatitis; • failure of the serum aminotransferase, bilirubin, and globulin levels to return to normal within 6 to 12 months after the acute illness; and 4. the persistence of HBeAg beyond 3 months or HBsAg beyond 6 months after acute hepatitis. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17th Ed., pp.1945

  10. CHRONIC HEPATITIS B CLINICAL FEATURES • Onset: insiduous • Incubation period: 30-180 days (mean, 8-12 weeks) • Fatigue is a common symptom • Low grade fever between 38° and 39°C (100° - 102°F) when heralded with serum-sickness syndrome Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17th Ed., pp.1941-1942

  11. CHRONIC HEPATITIS B • Persistent or Intermittent jaundiceis a common feature in severe or advanced cases. • It may lead to progressive liver injury and in cases with superimposed cirrhosis --- hepatic decompensation. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17th Ed., p. 1957

  12. CHRONIC HEPATITIS B LABORATORY FEATURES • Aminotransferase elevations tend to be modest but may fluctuate in the range of 100-1000 units. • Alanineaminotransferase (ALT) tends to be more elevated than aspartateaminotransferase (AST) • When cirrhosis is established, AST tends to exceed ALT. • Levels of alkaline phosphatase activity tend to be normal or only marginally elevated. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17th Ed., p. 1957

  13. CHRONIC HEPATITIS B • In severe cases, moderate elevations in serum bilirubin [51.3 to 171 µmol/L (3 to 10 mg/dL)] occur. • Hypoalbuminemia and prolongation of the prothrombin time occur in severe or end-stage cases. • Hyperglobulinemia and detectable circulating autoantibodies are distinctly absent in chronic hepatitis B (in contrast to autoimmune hepatitis). Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17th Ed., p. 1957

  14. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 16th Ed., p. 1844

  15. TREATMENT

  16. Candidates for therapy • Chronically infected individuals with: • persistently elevated alanineaminotransferase • a marker of liver damage • HBV DNA levels Lai, CL; Yuen (2007). "The natural history and treatment of chronic hepatitis B: a critical evaluation of standard treatment criteria and end points". Annals of internal medicine147 (1): 58–61

  17. Candidates for therapy HBeAg-positive patients (w/ evidence of chronic HBV): • HBV DNA level is ≥20,000 IU/mL (105 copies/mL) • Serum ALT is elevated for 3-6 months. HBeAg-negative patients(w/ evidence of chronic HBV): • HBV DNA is ≥ 2000 IU/mL (104 copies/mL) • Serum ALT is elevated (ALT levels >20 U/L for females and 30 U/L for males) for 3-6 months. Pyrsopoulos, Nikolaos. Chronic Hepatitis B: treatment and medication. Emedicine.com. June 19,2009

  18. Goals of Treatment • to suppress HBV replication • to induce remission of liver disease before development of cirrhosis and hepatocellular carcinoma

  19. Approved Drugs for Chronic Hepatitis B treatment • Interferon (INF) α • Pegylated interferon • Lamivudine • Adefovirdipivoxil • Entecavir

  20. Interferon (INF) α • Protein product manufactured by recombinant DNA technology • Modulates host immune responses • Direct antiviral activity • HBeAg negative patients: 1 and ½ yr txresults in sustained remissions, with suppressed HBV DNA and aminotransferase activity, in 20%

  21. Complications of Interferon (INF) α • systemic "flu-like" symptoms • marrow suppression • Irritability,depression/anxiety • autoimmune reactions • miscellaneous side effects • alopecia, rashes, diarrhea, and numbness and tingling of the extremities. *With the possible exception of autoimmune thyroiditis, all these side effects are reversible upon dose lowering or cessation of therapy.

  22. Lamivudine • inhibits reverse transcriptase activity of both HIV and HBV • HBeAg-reactive patients: daily doses of 100 mg for 48–52 weeks • HBeAg- negative patients: 1 year of lamivudine therapy

  23. Adefovirdipivoxil • prodrug that is converted to the diphosphate salt • active drug : antiviral nucleotide reverse transcriptase inhibitor • oral daily dose of 10 mg reduces HBV DNA

  24. Pegylated interferon • once-a-week PEG IFN was more effective than the more frequently administered, standard IFN • After 6 months of therapy: • HBeAg loss (30%) • HBeAgseroconversion (22%–27%) • undetectable HBV DNA (<400 copies/mL by PCR) in 10–25% • normal ALT in 34–39% • a mean reduction in HBV DNA of 2 log10 copies/mL (PEG IFN-2b) to 4.5 log10 copies/mL (PEG IFN-2a)

  25. Entecavir • Guanosine nucleoside analogue with activity against HBV polymerase • Competes with natural substrate deoxyguanosinetriphosphate (dGTP) to inhibit HBV polymerase activity • Less effective for lamivudine-refractory HBV infection • available as a tablet and as oral solution (0.05 mg/mL; 0.5 mg = 10 mL).

  26. Harrison’s Principles of Internal Medicine, 17 edition

  27. Harrison’s Principles of Internal Medicine, 17 edition

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