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GI & hepatology

Viral hepatitis

HAV: fecal-oral, self-limited, vaccine preventable, no chronicity. Post-exposure: vaccine ± IG.

Rahul Gupta & Dan Rubin5 min6 questions1 trials

Hepatitis A — fecal-oral, no chronicity

Personal contact, food/water, travel. Incubation weeks. Abrupt nausea, anorexia, malaise, fever, jaundice, RUQ pain; ALT > AST often >1000; ↑ bili/ALP. Symptoms in 70% of adults, 2–8 weeks, self-limited. Jaundice peaks after ~2 weeks (CDC 2020).

  • Dx: IgM anti-HAV (persists 3–6 months). IgG from week 2–3 = lifelong immunity.
  • Treatment is supportive; ALF is rare (<1%).
  • Vaccinate: MSM, PWID, chronic liver disease, HIV, international travel, homelessness, selected exposures. Havrix/Vaqta 2 doses; Twinrix 3 doses (HAV+HBV, age ≥18).
  • Post-exposure: one HAV vaccine ± immune globulin within 2 weeks if non-immune.

Hepatitis B — serologies you must be able to recite

Screen HBsAg / anti-HBs / anti-HBc once in all adults and every pregnancy; repeat if HIV, PWID, MSM, household contact, unexplained LFT rise, or B-cell–depleting therapy (: Hepatology 2025; CDC 2023/2024; USPSTF: ; ).

HBsAgAnti-HBsAnti-HBcMeaningNext
+−+Infected (acute or chronic)IgM anti-HBc (acute vs chronic), HBV DNA, HBeAg
−++Resolved infectionReactivation risk with chemo / immunosuppression
−−+Isolated core: remote recovery with waned anti-HBs, occult chronic, window, or false positiveIgM anti-HBc, anti-HBe, HBV DNA, repeat. Occult HBV = DNA+ with HBsAg−
−+−VaccinatedNothing
−−−Uninfected, non-immuneVaccinate (Engerix-B 3 doses; Heplisav-B 2 doses if ≥18, not for HD)
  • Acute: 70% subclinical, 30% jaundiced, <1% ALF. ALT > AST in the thousands. Chronic = HBsAg >6 months (<5% of adults; 40% of those → cirrhosis).
  • Extrahepatic: PAN, membranous / MPGN, aplastic anemia, serum-sickness arthritis.
  • First-line treatment: tenofovir or entecavir. Treat ALF, F2–F4 fibrosis/cirrhosis, HIV/HCV/HDV coinfection, immunosuppression, DM/MASLD comorbidity; otherwise HBeAg / ALT / DNA thresholds (Hepatology 2025).
  • HCC screen: all HBsAg+ with cirrhosis, plus high-risk noncirrhotic (Asian/Black men >40, Asian women >50, HDV, family HCC).
  • Reactivation: 1-log DNA or LFT rise, or HBsAg seroreversion from isolated core. HBsAg+ needs prophylaxis; isolated core is lower risk but not zero with rituximab. Entecavir or tenofovir.

Hepatitis C — treat almost everyone

Universal one-time HCV antibody at age ≥18 (USPSTF: ); each pregnancy; annually if PWID or MSM with HIV (/: CID 2023). Antibody+ needs RNA — there is often no reflex.

  • Ab+ RNA+ = current infection. Ab+ RNA− = cleared or treated (can reinfect; antibody is not immunity).
  • Acute: 75% subclinical; fulminant rare. Chronic in ~80%; 20% → cirrhosis (higher if male, alcohol, obesity, HIV). HCC 1–13%/yr once cirrhotic.
  • Extrahepatic: mixed cryoglobulin, PCT, lichen planus, thyroiditis, Sjögren, MPGN, NHL.
  • Before DAA: FIB-4 / elastography / FibroSure; HIV (start ART first); HAV IgG; full HBV panel (reactivation risk); CBC, LFTs, GFR.
  • Simplified first treatment, no cirrhosis: glecaprevir/pibrentasvir × 8 weeks or sofosbuvir/velpatasvir × 12 weeks. Compensated cirrhosis: pathway. Decompensated: hepatology.
  • SVR = undetectable RNA ≥12 weeks after therapy. Cirrhosis still needs HCC and variceal screening after cure.

D and E

  • HDV needs HBsAg (). Coinfection is more severe than HBV alone, often biphasic ALT. Superinfection is worse: 90% chronic, cirrhosis in 80% within 5–10 , 3× HCC vs HBV mono-infection. PWID, MSM, HIV, Mediterranean / Mongolia / Moldova / West and Middle Africa. Anti-HDV → HDV RNA. Peg-IFN is the imperfect option.
  • HEV: contaminated food/water, vertical, transfusion (; ). Usually mild. Extrahepatic: arthritis, neuro, pancreatitis, renal, thyroid. Fulminant risk in pregnancy (). Chronic in transplant / immunocompromised. IgM/IgG + RNA. Supportive if acute; ribavirin if chronic.