1. HEPATITIS B Dr. Situ Oladele South Atlantic Petroleum Medical Centre, Nasarawa State University, Keffi, Nasarawa State, Nigeria

2. WORLD HEPATITIS DAYJuly 28 3. INTRODUCTION Viral hepatitis refers to a group of inflammatorydiseases of the liver caused by viruses that haveaffinity for the liver. Clinically relevant ones are typed A, B, C, D and E.Hepatitis B and C are the most clinically importantones. DNA hepadnavirus (retrovirus). 3.2 kilobase pairsvirus discovered in 1965 however it was first seenin 1970. HBV is 50 -100 times more infectious than HIV 4. EPIDEMIOLOGY: WORLD 5. EPIDEMIOLOGY HBV affects about 2 billion (about 1/3 worldpopulation) worldwide (past or present infections)and of those affected, 600,000 die annually. About 300-350 million are lifelong carriersworldwide Low prevalence areas (0.1-2%): New Zealand,Australia, USA, Canada and Western Europe. Intermediate prevalent areas (3-5%) Japan,Middle East, Latin and South America, central Asia high prevalence areas (10-20%) China, Indonesia,Pacific Islands, south East Asia, sub-Saharan Africa 6. EPIDEMIOLOGY: NIGERIA 7. EPIDEMIOLOGY: NIGERIA 70% of population showing evidence of pastinfection. 7.3-24% (average 13.7%) of the populationhas serological evidence of currentinfection. Going by the 2006 national census, 19million Nigerians are currently infected andabout 5 million of these are expected to dieas a consequence of the disease. 8. MODES OF INFECTION: Perinatal (high prevalence area), early childhood household contact, unsafe injections (intermediate and highprevalence areas), blood transfusion, sex (low, intermediate and high prevalenceareas).Sex is the overall most common mode. 9. Concentration of HBVin Various Body FluidsHIGH MODERATE LOW/UNDETECTABLEBloodsemenUrineSerumVaginal secretions FaecesWound exudates saliva SweatTearsbreast milk 10. NATURAL HISTORY AND RISK OFCHRONICITY The virus can survive at least 7 days (up to15yrs at 20oC) outside human body The incubation period is 90 days (30-180days). Virus becomes detectable 30-60days post infection Up to 90-95% of adults recover fully within 6 months of infection. Infected Infants: have a 70-90% risk ofchronicity Childhood infections (1-4years) have a30-50% risk of chronicity. 11. NATURAL HISTORY AND RISK OFCHRONICITY Estimated 10-30% of patients are expectedto progresses to cirrhosis without treatment.25% of adult who were chronicallyinfected from childhood die from HBVcancer or cirrhosis. Adults and adolescent have a 1-3% risk ofchronicity. Elderly individuals have about 25% risk ofchronicity and only about 0.1-0.5% of adultshave fulminant hepatic failure 12. Relative Risk of Chronic hepatitis B forHepatocellular carcinoma (HCC) is100 and 10 year risk of HCC may beas high as 15% Hepatocellular carcinoma usually 25-30years after initial HBV 13. Acute Hepatitis B Virus InfectionTypical Serologic Course SymptomsHBeAg anti-HBe Total anti-HBcTiter IgM anti-HBcHBsAganti-HBs0 48 12 16 20 24 28 32 36 52100Weeks after Exposure 14. Chronic Hepatitis B Virus InfectionTypical Serologic Course Acute Chronic(6 (Years)months)HBeAganti-HBeHBsAgTotal anti-HBcIgM anti-HBc0 4 8 12 16 20 24 28 32 36 52Weeks after Exposure 15. OUTCOMES Infection Symptomatic Asymptomatic acute hepatitisB95% 95% Resolved ChronicResolvedChronic Immuneinfection Immune infectionCirrhosisCirrhosis AsymptomaticAsymptomaticLiver cancer Liver cancer 16. OUTCOMES Improvement and Resolution Fulminant Hepatic Failure Chronic Hepatitis Cirrhosis Hepatocellular Carcinoma 17. OUTCOME BY AGE OF INFECTION 100100808060Chronic Infection6040402020 Symptomatic Infection0 0 18. SYMPTOMS Hyperacute: hepatic encephalopathy Acute(nonspecific symptoms): anorexia, nausea,vomiting, low grade fever, myalgia, fatigability,aversion for food and cigar, dark coloured urine. Sub-acute: gynaecomastia, hair changes,testicular atrophy. Chronic: peripheral stigmata of chronic liverdisease Reactivation of chronic hepatitis: mixedsymptomsJAUNDICE Starts 10days post onset of constitutionalnonspecific symptoms. Lasts 1-3months 19. DIAGNOSIS AND LIVER DISEASESTAGINGPhase one: Liver function tests (ALT, AST, ALP, PT,Total protein and Albumin) and viral markersof possible hepatotoxic viruses (HDV, HEV,HAV, HIV) Full blood count and platelets & Urinalysis Hepatic ultrasound and other liver imagingtechniquesPhase two: Molecular biology: HBV DNA Liver biopsy and staging: 20. HBsAg AntiAnti Interpretation of ResultsHBs HBe+ve -ve -veCharacteristic of early acute HBV infection+ve +ve/-ve +veImplies either acute or chronic HBV infection which may be differentiated with respect to IgM anti HBc-ve +ve +veCharacteristic of previous HBV infection and current immunity to the virus-ve -ve +veNo clear interpretationCould be due past HBV infectionLow level of HBV infectionFalse +ve /non specific reaction-ve -ve -veSuggests liver toxicity due to other agents other than HBV-ve +ve -veTypical of vaccinated individual 21. OTHER TESTS Thyroid function test Body mass index Fasting blood sugar and insulin assayfor resistance Neropsychiatric evaluation Alcohol and drug abuse evaluation 22. CLINICAL STATES Acute, Sub-acute, Chronic active, Chronic asymptomatic carrier state Decompensated end-stage liverdisease 23. WHO TO SCREEN? 24. WHO TO SCREEN? All Nigerians HBsAg and HBcAg are used forsreening: every new visit to the clinic, pre-school, pre-employment, pre-insurance, pre-blood donation, pre-marriage and pregnancy, sexual history, STI, illegal drug users, healthcare workers, morgue works, chronic alcoholics, 25. WHO TO SCREEN? Children or spouses of HBsAg positiveindividuals All HIV positive patients Cirrhosis patients or nodular liver or big liver Jaundiced patients especially after bloodtransfusion Patients with bleeding problems especially ifit started after blood transfusion. Chronic Renal Failure patients especiallyafter haemodialysis. 26. TREATMENTS Generally, there is no specific treatment forHBV infection. Comfort, nutritional balance,avoidance of hepatotoxic drugs, etc., areessential. HBV drugs are expensive and not readilyavailable Chronically infected people respond lessand patient with significant cirrhosis respondless with increased chance for serious sideeffects. 27. DRUGS pegylated IFN, lamivudine, telbivudine, adefovi, entecavir, tenofovir. 28. INTERFERONS IFN (PEGYLATED) IFN is given as S/C injection, 180mcgweekly for 4months (up to 12months inpatients with high viral loads and patientswith negative HBeAG). 30-40% on treatedpatients sustained suppression of HBV.Some will also lose their HBsAg. There yet no known resistance to the drug Marketed as PEGASYS Avoid in advanced stage (decompensateddisease) 29. LAMIVUDINE Use when PEGASYS is not available or affordable Taken as Tab 100mg daily and is well tolerated orally Can be used in decompensated patients DISADVANTAGE High rate of drug resistance (15-30% in 1yr, 50% in 3yrs, 70% in 5yrs). Infinite duration of treatment (cannot stop until at least 1yr after HBeAg seroconversion occurs) 30. DIETARY LIMITATIONS 31. DIETARY LIMITATIONS Patients with acute or chronic HBV infectionwithout cirrhosis have NO dietaryrestrictions. For individuals with decompensatedcirrhosis (portal hypertension,encephalopathy), a low sodium/salt diet(1.5gm/d), high protein diet (i.e. white meatlike pork, turkey, fish), and, in cases ofhyponatremia, fluid restriction (1.5L/d) areindicated. 32. WHY TREAT THE HBV PATIENT? To limit active liver disease and prevent liverdisease progression to cirrhosis, liver failureor cancer To prevent transmission of HBV infection To improve quality of life To limit active viral replication and achievesustained virological response 33. GENERAL INDICATIONS FORTREATMENT/MANAGEMENTChronic HBeAgChronic HBeAgpositive patientsnegative patientsHBV DNA >20,000 I.U/ml (105 HBV DNA >2000 I.U/ml (104copies/ml and when ALT is for copies/ml and when ALT is3-6months (>20 U/L in females; 30 U/L inmales ) for 3-6monthsAll patients with histologic All patients with histologicevidence of active liver evidence of active liverdisease/inflammation disease/inflammation 34. PREVENSION AND VACCINE: HBV vaccine has been available since 1982 and isabout 95% effective. In 1992 31 countries haveHBV vaccination schedule. In 2011, the numberhas increased to 179 countries. protects for 5-10 yrs. Use HB Ig for suddenneedle pricks. Rate of HBV transmission after an occupationallyrelated needle stick injury is 30% in unvaccinatedhealth worker (unlike 0.3 % in HIV, 3% in HCVinfection) 35. PREVENSION AND VACCINE: Take at birth, 6weeks and 10 weeks of life Uninfected and unvaccinated adults will take3 subcutanous injections at intervalsunmissed or would start again. A booster dose in 10yrs 36. PATIENT MORNITORING ANDEVALUATION FBC: every 4-8 weeks ALT (LFT): every 4-8weeks HBV DNA: at 12, 24 and 48 weeks HBeAg and anti-HBeAg: every 6months tillseroconversion Liver histology: NOT CURRENTLYRECOMMENDED FOR ROUTINEMONITORING 37. TREATMENT RESPONSE Primary response: viral load more than 10 foldsafter 12 weeks of treatment. Primary non-response: viral load less than 10folds after 12 weeks of treatment. Complete response: undetectable viral load after24 weeks of treatment Partial response: detectable but viral load10,000copies/ml after 24 weeks of treatment Sustained virological response (Virologicalbreakthrough): undetectable virus for >6months Treatment failure 38. CONTRAINDCATION TOTREATMENT Pregnancy* continued alcohol abuse sever cardiac disease uncontrolled psychiatric illness uncontrolled seizure disorder untreated thyroid disorder 39. DRUD SIDE EFFECTS flu-like syndrome fatigue, weight loss, anorexia, diarrhoea, alopecia haematological derangements: PCV, WBC,platelets, neutrophils neuropsychiatric disorders: mood swings,depression, suicidal ideation, insomnia, psychosis metabolic abnormalities: diabetes, thyroid disorders lung complications: pneumonitis, pneumonia dermatological problems: rashes eye complications: retinal vessels occlusion, retinalhemorrhages 40. SPECIAL CATEGORIES 41. SPECIAL CATEGORIES Pregnancy and newborns: Those born tomothers with active HBV infection must bevaccinated with HBIG within 12hrs of birthand the vaccinated with HBV vaccine HIV/HBV co-infection: both diseases mustbe treated together. Tenofovir +emtricitabine (Truvada)/Lamivudine with aNNRTI or PI is preferred. Diabetes: current guideline recommendsthat all patients with diabetes (type 1 or 2)from 19-59 yrs should be vaccinated withHBV vaccine. 42. OTHER SIDE EFFECTS OF HBVINFECTION Pleural effusion, hepatopulmonary andportopulmonary syndrome may occure in patientswith cirrhosis Myocarditis and pericarditis and arrhythmias mayoccur primarily in patients with fulminant hepatitis DIC may occur in patients with fulminant hepatitis. Athralgias and arthritis (serum sickness) withsubcutaneous nodules may occur, but are very rare Encephalitis, aseptic meningitis, Guillain-Barresyndrome and mononeuritis complex may occur inpatients with acute hepatitis B 43. OTHER SIDE EFFECTS OF HBVINFECTION Aplastic anaemia is uncommon andagranulocytosis is very rare Pancreatitis Chronic renal failure Polyarteritis nodosa Fleeting rash and hives (common in women) Popular acrodermatitis may be seen in acuteinfection in children (Gianotti-Crosti syndrome) 44. THANK YOU