Hepatitis

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Hepatitis:

Praveen Sreekumar Hepatitis

Causes of Acute hepatitis:

Causes of Acute hepatitis Viral hepatitis Other infections –eg: Malaria Alcoholic hepatitis Drug induced hepatitis – eg: following ATT – INH, Rif AutoImmune Hepatitis (AIH) Hemochromatosis Wilson’s disease Ischemic hepatitis Cholestastic hepatitis – eg: with anabolic steroids Post transplant HIV

Viruses causing hepatitis:

Viruses causing hepatitis Hepatitis viruses – A,B,C,D,E,G Ebstein Barr virus CMV Herpes simplex virus Coxsackie Enteroviruses Adenovirus TT virus, SEN-V – Transfusion hepatitis Other infectious agents causing hepatitis Salmonella, Leptospira Amoebiasis Malarial hepatitis

Hepatitis A:

Hepatitis A HAV is a 27 nm RNA hepatovirus, picorna virus Epidemics, institutional outbreaks Feco-oral transmission Spread favoured by crowding & poor sanitation Source: contaminated water or food IP- 15 -50 days HAV is excreted in feces for up to 2 weeks before the onset of clinical illness Starts with fever, fever subsides and then jaundice appears.By this time viral shedding stops & infectivity is lost.

Hepatitis A:

Hepatitis A Mortality is low, subsides in one week time Fulminant hepatic failure rare occurs in pts with previous chronic hepatitis C Chronic hepatitis do not occur No carrier state In children less severe, often asymptomatic IgM anti HAV detectable in first week of illness & disappear in 3-6 months so useful for diagnosis. IgG anti HAV not useful IgG anti HAV indicates previous exposure to HAV, non infectivity & immunity to recurring infection.

Hepatitis B:

Hepatitis B 42 nm DNA virus, Australia antigen is Dane particle Core Protein (HBcAg), Surface Ag(HBsAg) Transmission by inoculation, sexual contact, secretions, perinatal (risk of chronic hepatitis in neonates is 90%) Clinical features similar to hep A, IP – 50 -150 days Course – a/c hepatitis, c/c hepatitis, cirrhosis, HCC (25-40%) A/w – Arthritis, Glomerulonephhritis, FSGS, Polyarteritis nodosa

Hepatitis B:

Hepatitis B HBsAg- first evidence of hepatitis B infection before SGPT rise Anti -HBs – appears after clearence of HBsAg, so indicates previous infection, non infectivity & also indicates immunity. Seen after succesful vaccination Anti HBc – IgM anti HBc appear shortly after HBsAg appear If + in a/c hepatitis indicates recent hepatitis B hepatitis Persists for 3-6 months Useful in HBsAg negative patients Reappear during flare up of inactive chronic hepatitis

Hepatitis B:

Hepatitis B HBeAg – secretory form of HBcAg – indicates viral replication & infectivity. HBeAg + after 3 months  likelihood of chronic hepatitis HBsAg + , HBeAg - , with high infectivity  precore mutants HBV DNA by PCR or rtPCR – precise marker of infectivity & viral replication Pre core mutants appear in chronic hepatitis pts , which stop secreting HBeAg still remain infective, High HBV DNA levels  rapid progression to cirrhosis

Hepatitis C:

Hepatitis C Single stranded RNA virus, Flavivirus like, 6 genotypes Responsible for 90% of transfusion related hepatitis Intravenous drug use No transmission via breast feeding IP – 6-7 weeks, mild illness, usually asymptomatic Waxing & waning levels of transaminases > 80% chance of chronic hepatitis

Hepatitis C:

Hepatitis C Associations – Cryoglobulinemia Glomerluonephritis Autoimmune thyroiditis lymhocytic sialadeniitis idiopathic pulmonary fibrosis sporadic porphyria cutanea tarda monolconal gammopathies lymphoma Risk of type 2 Diabetes is increased in pts with hepatitis C

Hepatitis C:

Hepatitis C Anti HCV Ab, non protective, diagnostic by Recombinant Immunoblo Assay (RIBA) HCV RNA by PCR , Rx if > 50,000 RNA /mm 3 RIBA +, HCV PCR +  infective & requires Rx RIBA + , HCV PCR negative  recovery from HCV infection in past

Hepatitis D(Delta agent):

Hepatitis D(Delta agent) Defective RNA virus, Causes hepatitis only with Hep B Clears when HBsAg is cleared from blood In chronic hepatitis B, HDV superinfection may carry worse P/G Such cases often progress rapidly to Fulminant hepatitis or severe chronic hepatitis  cirrhosis Endemic in mediterraneans 3 times risk of HCC Prevented by Hepatitis B vaccination

Hepatitis E:

Hepatitis E 29 – 32 nm Calcivirus Waterborne outbreaks in India Feco oral transmission Self limited May cause fulminant hepatic failure in pregnancy Hepatitis G – Flavivirus, 10 years viremia, does nt cause significant liver disease / damage

Course of hepatitis:

Course of hepatitis Prodromal phase- malaise, myalgia, arthralgia, abd pain Icteric phase Convalescent phase Compliactions – complete clinical & lab. recovery by 9 weeks in hepatitis A & 16 weeks in hepatitis B, 1% may have a Fulminant course hepatitis B, D, C may become chronic hepatitis

Clinical Findings:

Clinical Findings Patient has jaundice usually Patient in hepatic encephalopathy without jaundice indicates rapidity of liver damage  poor prognosis Right hypochondrial pain Fever – usually low grade fever O/E – Tender soft liver, If liver span < 7  Poor P/G Asterixis, altered sleep pattern indicates encephalopathy Look for KF ring esp in young nonalcoholic pts with r/c jaundice skin hyperpigmentation, hypogonadism s/o hemochromatosis Tremor, cerebellar signs etc. s/o alcoholic hepatitis

Investigations:

Investigations Urine bile salts & bile pigments Serum bilirubin (T & CB), SGOT & SGPT, ALP, A/G ratio, PT/INR Hb, TC, DC, platelet count, Reticu. Count if CB is less ESR – ( for AIH), if high ANA & if required AMA Sickling test in endemic areas Peripheral smear to exclude Malaria as a cause of hepatitis and also if there are atypical lymphocytes, do a Paul Bunnel test VIRAL MARKERS – anti HAV, HBSAg, anti HCV, anti HEV In suspected cases – Serum Ferritin(>1000 s/o), S.Ceruloplasmin Widal test – esp. if there is a preceding h/o fever 3 weeks prior

Treatment:

Treatment Supportive care Avoid unnecessary blood transfusions ‘Do not’ recap needles Proper screening of blood & blood products Vaccination – HAV, HBV HAV – Ig – 0.02 mL/kg i.m HBIg – 0.06 mL/kg given within 7 days of exposure followed by routine Hepatitis B vaccination Hep B – Lamivudine, Tenofovir tried Hep C – IFN + Ribavirin – problem is cost & r/c once Rx is Stopped

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