Viral

-lepati

Trans

Transmission: fecal-oral route: contaminated food, water, shellfish: day-care ctr outbreaks

• Incubation: 2-6 wks, no chronicity

• Diagnosis: acute hepatitis © IgM anti-HAV; past exposure » © IgG anti-HAV (© IgM)

• Prevention: vaccinate children ( -2 y) and those at high risk (2 doses at 0.6-12 mos)

• Postexposure prophylaxis: IG 0.02 ml kg IM » start vaccine w in 2 wks of exposure

Hepatitis B (Lancet 2003362:2089)

• Transmission: blood, sexual, perinatal

• Extrahepatic syndromes: PAN (• 1%). MPGN. arthritis, dermatitis. PMR

• Natural history acute infection: 70% subclinical. 30% jaundice. • 1% fulminant hepatitis chronic: <5% (adult-acquired). -90% (perinatally-acquired)

• Serologic and virologic tests

HBsAg: appears before symptoms; used to screen blood donors HBeAg: evidence of viral replication and t infectivity IgM anti-HBc: first Ab to appear; indicates acute infection window period HBsAg become . anti-HBs not yet anti-HBc only clue to infection IgG anti-HBc: indicates previous (HBsAg ©) or ongoing (HBsAg ©) HBV infection anti-HBe: indicates waning viral replication. 1 infectivity anu-HBs: indicates resolution of acute disease & immunity (sole marker after vaccination) HBV DNA: presence in serum correlates with active viral replication in liver

Figure 3-8 Serologic court* of acute HBV «ifection with resolution

I TALT 1 |Symptomsj [ Jaundice 1

-window period'

IgM anti-HBc

-window period'

IgM anti-HBc

45678

Months alter exposure

45678

Months alter exposure

(Adapted from Friedman LS & Keeffe EB. Serolopc course of HBV. Handbook of Utvr Dncoic 1998.38. Hoofnagle JH & DiBiiceglic AM. Serologic diagnosis of acute and chronic viral hepatitis. Semin Liver Oil 1991:11:73.)

Diagnosis

HbsAg

anti-HBs

anti-HBc

HBeAg

anti-HBe

HBV DNA

Acute hepatitis

©

IgM

©

8

®

Window period

e

0

IgM

-

-

®

Recovery

e

©

IgG

6

i

e

Immunisation

e

©

8

e

0

HBeAg ©

©

e

IgG

©

0

HBeAg 3

®

e

IgG

0

©

"Prccore mutant HBeAg not generated, but inu-HBe can develop due to cross-reactivity with HEkAg. high »«rum HBV DNA leveh

"Prccore mutant HBeAg not generated, but inu-HBe can develop due to cross-reactivity with HEkAg. high »«rum HBV DNA leveh

• Treatment for acute HBV: supportive

• Treatment for chronic HBV (© HBsAg & DNA) if: HBeAg © and DNA -10s copies ml;

HBeAg © and DNA -104 copies ml; ALT 2 x ULN; or inflammation on bx options: IFNi*-2b (n£jm 1990:323 295). peg IFN-«-2a (nejm 2005:3512682) for 48 wks. lamivudine (nejm 1999:341 1256) (development of resist at t rates), adefovir (nejm 2003;348:800&806) (30% resist. at 5 y). telbivudine (some X-resist w lamivudine). or entecavir (nejm 2006:354.1001); oral agents preferred b c 1 tox.; entecavir most potent Rx endpoinc if HBeAg t) - HBeAg © + anti-HBe ©; if HBeAg © — ALT nl 4 HBV DNA © liver transplantation: HBIG and or nucleoside analog effective in preventing reinfection

• Risk of hepatocellular carcinoma: 10-390 x 1 risk (highest: perinatal acquired and high

HBV DNA level; jama 2006:295 65); screen with serum AFP and hepatic U S q6mos

• Prevention: vaccinate if at high risk (3 doses at 0. 1. and 6 mos)

• Postexposure ppx: HBIG : vaccine (if unvaccinated or known nonresponder) Hepatitis C (Lancet 2003:362 2095)

. • Transmission: blood » sexual; 20% without a clear precipitant

• Extrahepatic syndromes: cryoglobulinemia, porphyria cutanea tarda. MPGN. lymphoma

• Natural history acute infection: 75% subclinical; 25% jaundice; fulminant hepatitis very rare chronic: 50-80% chronic hepatitis. 20-30% of whom develop cirrhosis (after -20 y), hepatocellular carcinoma develops in 2-5% of cirrhotics y (usually after 20-30 y)

• Serologic and virologic tests anti-HCV (ELISA): © in 6 wks. does not imply recovery, may become © after recovery HCV RNA: © within 2 wks. marker of active infection

HCV RIBA: used to confirm ► anti-HCV ELISA in Pts with undetectable HCV RNA HCV genotype: used to guide duration and predict response to Rx (genotype 2,3 >1,4)

• Diagnosis acute hepatitis - © HCV RNA, • anti-HCV resolved hepatitis » 0 HCV RNA. • anti-HCV chronic hepatitis © HCV RNA. © anti-HCV

consider liver biopsy to assess grade of inflammation and stage of fibrosis

Indications: HCV RNA ©, bx w fibrosis stage >1, and compensated liver disease (for genotype 2 or 3, may proceed to Rx w o biopsy due to high response rate - 80%) Contraindications: decompensated cirrhosis, pregnancy, psych illness, active substance abuse, severe cardiac pulm disease, uncontrolled DM. seizure d o. autoimmune dis. PEG-IFNa-2a ribavirin —55% sustained virologic response rate (NEJM 2006355:2444) genotypes 2 or 3: Rx 24 wks. ? 12 wks total if HCV RNA at 4 wks (NEJM 20053512609) genotypes 1 or 4: Rx 48 wks if HCV RNA 1 2 log by 12 wks Predictors of response: low HCV RNA. absence of cirrhosis, female, age - 40 y. wt <75 kg. nongenotype 1. white Hispanic, adherence, absence of HIV coinfection

• Postexposure ppx: none (IG not effective); if HCV RNA ©, consider Rx w in 3 mo Hepatitis D

• Transmission: blood or sexual

• Pathogenesis: requires HBV to cause either simultaneous or superimposed infection

• Natural history: more severe hepatitis, faster progression to cirrhosis

• Serologic virologic tests: anti-HDV; follow HDV RNA during Rx (high relapse rate)

Hepatitis E

• Transmission: fecal-oral; travelers to Pakistan, India. SE Asia. Africa, and Mexico s • Natural history: acute hepatitis with t mortality (10-20%) during pregnancy

• Diagnosis: IgM anti-HEV (through CDC) Other viruses (cmv. ebv, hsv.vzv)

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