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Dr kgm hep b

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  • 1. Hepatitis B virus Dr. K. G. Maharjan Liver unit, Bir hospital
  • 2. Introduction• Hepatitis is an inflammation of the liver.• It is usually caused by viral & non viral infections also due to toxins (alcohol) & drugs (mostly ATT)• In our setup it maybe due to bacterial infection but may be an autoimmune response as well.• It is characterized by anorexia , jaundice, abdominal pain, liver enlargement and sometimes fever.• Others , usually bacterial infections leading to HV&IVC thrombophlebitis, metabolic cause (Wilson disease)• Congestive causes like ( HVOO,IVC disease , CHF)• HBV can lead to cirrhosis and liver cancer.
  • 3. Introduction• Hepatitis is an inflammation of the liver.• It is usually caused by viral & non viral infections also due to toxins (alcohol) & drugs (mostly ATT)• In our setup it maybe due to bacterial infection but may be an autoimmune response as well.• It is characterized by anorexia , jaundice, abdominal pain, liver enlargement and sometimes fever.• Others , usually bacterial infections leading to HV&IVC thrombophlebitis, metabolic cause (Wilson disease)• Congestive causes like ( HVOO,IVC disease , CHF)• HBV can lead to cirrhosis and liver cancer.
  • 4. Viral hepatitis• The different types of viral hepatitis A,E,(virus transmitted through the faces of an infected person.• Hepatitis B,C,D are serum hepatitis• Hepatitis F,G, cryptogenic ( caused by a virus as not identified)• More hepatitis viruses are less common yellow fever, epstien barr virus(EBV), cytomegalovirus(CMV),
  • 5. Hepatitis B virus• HBV is a serious disease ,can cause lifelong infection , liver cirrhosis ,liver cancer , and liver failure ,death.• HBV is 100 times more infectious than HIV and 10 times more infectious than HCV.• HBV is a blood borne transmitted ( body fluids , semen, saliva,vaginal fluid (high titers in the blood and lower titer in body fluids)
  • 6. Hepatitis B virus introductions• HBV is a 42 nm,double-shelled DNA virus of the class Hepadnaviridae.• The outer surface membrane contains HBV surface antigen (HBsAg) which also circulates in blood as 22 nm spherical and tubular particles.
  • 7. HBV virus
  • 8. Continu…• The inner core of the virus contains HBV core antigen (HBcAg) (HBeAg)• HBV is a single molecule of partially double – stranded DNA, and DNA- dependent DNA polymerase.
  • 9. Continu…
  • 10. Risk groups• 1, I/V drug users Health workers• 2, Multiple sex partners• 3,Homosexuals• 4,Infant born to HBV infected mothers• 5,Hemodialysis patients• 6, Areas with high rates of HBV infections• 7,Tatooing
  • 11. HBV transmitted• HBV is transmitted by the exchange of blood & body fluids ,eg . Blood, semen, breast milk ,saliva and vaginal secretor fluids , tears.
  • 12. Epidemiology• Globally• 50 million new cases per year• 350-400 million chronic carriers 75% in Asia• 520,000 deaths per year
  • 13. Epidemiology in Nepal• One epidemiology study in done in nepal• Group;1, Population No. HBsAg• a, Soldiers 922 20 (2.2%)• b, healthy people 232 2 (0.8%) from districts• c, pregnant women 81 1 (1.2%)• d, blood donors 624 5 (0.8%)• blood donors 168 1 (0.6%)
  • 14. Continu…….• Group 2,• Hospital staff 792 7 (0.8%)• Student nurses 122 0• Relatives of CLD 388 12 (3.1%)• Patients• Group 3,• Hemophilia 4 1 (25%)• Drug addicts 72 2(3%)• Hemodialysis 41 1(2%)• HBV carriers 49 49(100%)
  • 15. Continu…• Group 4,• Chronic liver disease 145 57 (39%)• Acute hepatitis 150 14 (9.3%)
  • 16. Clinical course of hepatitis B infection Death Recovery 1% 99% Transient Acute 100% Subclinical hepatitis infection 25% 65% Acute HBV infection 10% 10-30% Chronic HBV 70-90% Infection Chronic Healthy Hepatitis ? HBsAg Carrier Cirrhosis Hepatocellular Carcinoma ?
  • 17. HBsAg True Positive Negative ALT Search for other virus Raised Normal Anti-HbcIgM Positive HbcAb Negative F/u after 6 months Positive Negative F/U HBeAg HBvDNA F/UPositive Negative >105ml <105mlLiver biopsy HBcAb Rx F/U HBvDNA Negative Positive Rx Liver biopsy HBvDNA HBvDNA Absent Raised Search for other causes of ALT
  • 18. Infection• Acute hepatitis B develops in approximately 30% to 50% of adults at the time of initial infection and is characterized by anorexia, nausea , vomiting and jaundice.• SGPT raises 2 ½ times• The risk of progression to chronic infection varies with age , being highest among young children and infants (30%-90%) and lowest among adolescents and adults (2%-6%).• Rates of progression to cirrhosis and HCC vary according to age at acquisition of chronic infections ,HBeAg status , co infection with HGV,HIV,HCV, and alcohol abuse.
  • 19. Clinical features• The first serologic marker to appear following acute infection is HBsAg, which can be detected as early as 1 or 2 weeks and as late as 11 or 12 weeks (mode 30-60 days) after exposure to HBV• HBeAg is generally detectable in patients with acute infections, the presence of HBeAg in serum correlates with higher titers of HBV and greater infectivity.
  • 20. Continu….• A diagnosis of acute HBV infection can be made on the basis of the detection of IgM class antibody to HBV core antigen (IgM ,anti- HBc) in serum ,It is generally detectable at the time of clinical onset.
  • 21. Serological markers ; HBV• HBsAg: Marker of infection,presence >6months=chronic• HBeAg: active viral replication,• Anti-HBsAg: indicates recovery and /or immunity (after vaccine)• Anti-Hbe: inactive viral replication• Anti-HBc: infection or immunity
  • 22. HBV genotypes• HBV classified into 7 genotypes (A-G)• -a: north america and western europe• B&C: asia• D: southern europe and india• E:&G: africa• F:central and south america and alaska• H: central america• B associated with less HCC, less active and more slowly progressive liver disease than C• A&B respond better to Interferon than C&D• Genotype does not predict response to oral agents
  • 23. HBV infection• Chronic HBV: chronic necroinflammatory liver disease >6month,ALT^,HBeAg-postive or – negative, HBV DNA> 10 x4-5• Inactive HBsAg carrier : Persistent infection without necroinflammatory disease, ALT normal , HBeAg -negative HBV DNA<10 x 4-5• Resolved HBV: previous infection without virological ,biochemicalor histological evidence of active disease.
  • 24. Continu…• Acute exacerbation HBV: elevated ALT>10 x ULN or >2 x baseline• Reactivation of HBV: reappearance of necroinflammatory disease in person known to be inactive carrier or resolved HBV
  • 25. Liver histology ≥ Phases of chronic HBV• Immunotolerant phase: HBeAg- postive; HBV DNA high (10 x 5-10) ALT normal -candidates for therapy.Immunoactive phase: HBeAg-postive or HBeAg – negative,HBV DNA high (10 x4-10) ,ALT elevated, symptoms +/-Non replicative phase :(inactive HBV carrier)HBeAg –negative HBV DNA low(<10 x4 ) ALT normal, HBsAg may later become undectable.
  • 26. Routine HBV carriers exam• Follow-up interval 6 months : Tests : ALT and AST; AFP. USG,• Inactive HBsAg carrier: If ALT/AST increase , re evaluate• Chronic hepatitis B: CBC,LFT,HBeAg, anti-HBe
  • 27. HBV infected mothers• Hepatitis B immunoglobulin (HBIG 0.5 ml , I/M to new born.• Hepatitis B vaccination should have been given 12 hours of birth.
  • 28. Post exposure prophylaxis• 1, HBIG is required• 2,the first dose of hepatitis B vaccine immediately, 0 – 1 – 6 months.
  • 29. Hepatitis B vaccine• The standard regimen for adult is 10-20mcg initially ( depending on the formulations ) .• Schedules; 0 -1 -6 months.• Alternative schedules have been approved• 0 -1 -2 -12 months• 0- 7 and 21 days ,plus 12 months• Preferred site vaccine deltoid muscles
  • 30. Treatment of chronic HBV• Nucleoside/nucleotide analogues: - Entecavir : 0.5-1.0 mg/d• -Lamivudine : 100 mg/d• -Adefovir dipivoxil :10mg/d• -Tenoforvir : 300mg/d• Interferon: interferon alfa-2b 5MU/d or 10MU tiw x 4 months.• Peginterferon alfa-2a (Pegasys) 180 mcg/week x 24-48 weeks.• Liver transplantation ( decompensated chronic HBV with cirrhosis.
  • 31. Reference• Davidson principal and practice of medicine• C.M.D.T• Oxford hand book of medicine• Liver unit, Bir hospital
  • 32. Thank youThank you