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Viral Hepatitis Dept. of Infectious Diseases SunYat-sen University Q.F.XIE Introduction • Viral hepatitis are a group of diseases, Caused by A、B、C、D and E 5 hepatitis virus • Hepatitis A and E Transmitted by fecal-oral route, present acute and self-limited course • Hepatitis B ,C and D Spread parenterally easily lead to chronic hepatitis • Clinical characters including fatigue, intestinal symptoms tender and enlarged liver abnormal LFTs jaundice in some cases very variable in severity Significance Highly endemic Wide clinical spectrum High fatality rate in severe cases No specific pathogenic therapy available now Chronic hepatitis B and C very common, some may develop to cirrhosis even HCC Successful vaccination for HBV and HAV Etiology-HAV Heparnavirus Appeared in bile and feces, spreaded via feces No chronic carrier status observed Anti-HAV antibody to HAV Anti-HAV IgM indicative of current or recent infection appeared very early, disappear in about 3months most useful for confirm the diagnosis Anti HAV IgG current or previous infection a protective antibody, conferring immunity persist for life long time Etiology-HBV • Orthohepadnavirus, Dane particle • 4 open reading frame: S,C,P,X • 8 genotypes A-H, B and C predominantly in China • Strong ability against to environment • 3 antigen and antibody system • HBsAg found in serum and other body fluid not infectious itself suggesting current infection and infectivity Anti-HBs a protective antibody to HBsAg an indicator of past infection and immunity to HBV reinfection suggesting non-infectious • HBeAg suggesting HBV replication and high infectivity negative when pre-C mutation but with high level of replication useful for evaluation of anti-HBV therapy Anti-HBe antibody to HBeAg HBe seroconversion HBeAg(+) →(-)and anti-HBe(-) →(+) • HBcAg existing in the core of virion a marker of replication and infectivity Anti-HBc IgM a marker of acute primary HBV infection Anti-HBc IgG appeared in almost all HBV present and past infection host body • HBVDNA the genome of HBV suggesting active virus replication and infectivity useful for diagnosis and evaluation of anti-HBV therapy Hepatitis B Virus Etiology-HCV • RNA virus, 6genotypes, mainly 1b in the country • Molecular heterogeneity driven by high mutation rate usually proceed to chronic course • Anti-HCV IgM and IgG types antibody to HCV suggesting HCV infection • HCVRNA the genome of HCV suggesting replication and infectivity of HCV useful for the diagnosis and evaluation of antivirus treatment Etiology-HDV • An incomplete RNA virus • Causes hepatitis only patients with either acute(coinfection) or chronic (superinfection) hepatitis B • HDVAg and anti-HDV • both the markers of HDV infection • HDVRNA • the genome of HDV • a marker of existing HDV infection • suggesting virus replication and infectivity Etiology-HEV Nonenveloped RNA virus Appeared in bile and feces, spreaded via feces No chronic carrier status observed Anti-HEV IgM and IgG both appeared in acute infection useful for the diagnosis of HEV infection • HEVRNA the genome of the virus suggesting existing of HEV infection not available for routine clinical diagnosis Epidemiology • Source of infection Patients with acute or chronic viral hepatitis Carriers of hepatitis virus, particularly asymptomatic carriers • Transmission Hepatitis A and E transmitted by the fecal- oral route, water-borne and food-transmitted infection in epidemics Hepatitis B transmitted parenterally mother-to-infant play a key role in China blood ,blood products and body fluid others Hepatitis C and D similar to hepatitis B intravenous drug abusers most common hepatitis C for the time being Prevalence rate in China 1992 • Hepatitis • Hepatitis A B • Hepatitis • Hepatitis • Hepatitis C D E anti-HAV+ 80.90% HBsAg + 9.75% (2006) 7.18% anti-HCV+ 3.20% anti-HDV+ 1.15% anti-HEV+ 17.2% Pathogenesis • Hepatocellular damage produced by viral replication directly only in hepatitis D • Other types of viral hepatitis induced mainly by immunemediated attack on the liver Pathology • The varying lesion could be seen in entire liver, but variable in severity and in different stages of the disease • No specific lesion suggesting etiologic type of hepatitis virus Clinical manifestations • Wide clinical spectrum from asymptomatic form to fatal outcome such as liver failure • Similar clinical course in different etiological type of viral hepatitis The clinical types viral hepatitis Acute hepatitis Chronic hepatitis Liver failure (severe hepatitis) Cholestatic viral hepatitis Hepatitis cirrhosis Asymptomatic virus carrier status (usually only in HBV) Incubation period Hepatitis A Hepatitis E 2---6w 2---9w Hepatitis B Hepatitis C Hepatitis D 1---6m 2w---6m 4---20w ~4w ~6w ~3m ~ 6w Acute hepatitis 3 phases of the icteric hepatitis • • • • Prodromal phase sudden or insidious onset, lasting 3-7d constitutional symptom: malaise, fatigue, mild fever some time, dark urine gastrointestinal symptoms: anorexia, nausea, vomiting serum ALT level rise deeply Jaundice phase jaundice appeared and peak level often in 2 weeks after the onset other symptoms subside after jaundice tender liver palpable serum bilirubin elevated lasting for 2—6 weeks Convalescent phase symptoms and jaundice gradual resolution liver return to normal size serum ALT and bilirubin decreased 1 to 2 months needed Anicteric acute viral hepatitis more common, mild manifastation Chronic hepatitis Seen only in hepatitis B,C and D, virus infection over 6 months Severity variable, 3 subtypes: mild, typical and advanced Common manifestations: malaise, fatigue, poor appetite, nausea, distension of abdomen • Jaundice seen in some cases • Enlargement of liver and/or spleen • Spider naevi, hepatic palms in cases with long history • Abnormal LFTs: transaminase, bilirubin A/G Prognosis different: stable, breakthrough or flare, develop to Cir or Ca Liver failure (severe hepatitis) Bad prognosis Pathological basis: extensive necrosis of hepatic cells 4 subtypes: acute liver failure, subacute acute-on-chronic, chronic Clinical syndrome including: jaundice deepen rapidly liver size become smaller bleeding, prolonged prothrombin time, PTA less than 40% cerebral edema, high intracranial pressure complicated infection: SBP hepatic encephalopathy toxic abdominal distension and ascites hepatic-renal syndrome Cholestatic viral hepatitis acute and chronic mild manifestation but deepen jaundice Hepatitis cirrhosis hepatic fibrosis compensated cirrhosis decompensated cirrhosis Asymptomatic HBV carrier HBV infection more than 6 months have no symptoms and signs normal LFTs 70%-80%have no pathologic change in liver biopsy Diagnosis Clinical Data Epidemiological evidences Laboratory investigations Ultrasound Biopsy Differential diagnosis Jaundice caused by other etiological agents Hepatitis caused by other etiological agents Treatment Basic principles of management guideline for daily living, physical activity , food and drink intake of the patients supportive and symptomatic treatment Hepatic function protective agents Anti-virus therapy most important treatment for chronic hepatitis B、acute and chronic hepatitis C hepatitis B indication: HBVDNA ≥105copies/ml for HBeAg~, HBVDNA ≥104copies/ml for HBeAg+; ALT ≥2ULN, or biopsy ≥G2S2 Drugs: interferon-α(typical or pegylated) or, nucleotide analogues:3TC,adfovir, entecavir,Ldt… Hepatitis C indication: HCVRNA+ drugs: interferon-α(typical or pegylated) +ribavirin Traditional Chinese medicine Management for liver failure basic supportive therapy treatment of complications bleeding infection complications encephalopathy renal failure Hepatic transplantation Management of asymptomatic HBV carrier medical check up periodically no any alcohol intake liver biopsy when patient’s age more than 40 years and HBV replication in high level Prevention Improvement of sanitation Blood screening of donors Anti-virus treatment for hepatitis B and hepatitis C Immunoprophylaxis active immunization vaccines for hepatitis A and B are available around world, very successful for pre-exposure prevention passive immunization IG for hepatitis A, HBIG for hepatitis B; post-exposure Thanks !