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Hepatitis B

DNA hepatitis virus causing acute hepatitis, chronic infection, cirrhosis, and hepatocellular carcinoma, with diagnosis based on serologic patterns

Gastroenterology & Hepatologycommonlong-term-condition
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Gastroenterology & Hepatology
common
8 min read
reviewed 2026-05-04
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About This Page

This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.

Key points

  • HBsAg = current infection; anti-HBs = immunity; anti-HBc IgM = acute infection; anti-HBc IgG = prior exposure
  • Chronic HBV = HBsAg positive for >6 months
  • First-line chronic therapy: tenofovir alafenamide, tenofovir disoproxil fumarate, or entecavir
  • Infants born to HBsAg-positive mothers need vaccine plus HBIG within 12 hours
  • HBV can cause HCC without cirrhosis

Overview

HBV is a partially double-stranded DNA virus transmitted by blood, sex, and perinatally. Adult acute infection usually clears; perinatal infection often becomes chronic. HBV directly increases HCC risk, and serology interpretation is central.

Epidemiology

US risk is concentrated among people born in endemic regions, injection drug use, MSM, household/sexual contacts, incarcerated persons, and hemodialysis patients. Universal adult screening and vaccination are increasingly emphasized.

Clinical Features

Symptoms
Fatigue, anorexia, nausea, RUQ discomfort
Jaundice, dark urine, pale stools
Often asymptomatic chronic infection
Fulminant hepatitis: encephalopathy or coagulopathy
Cirrhosis symptoms: ascites, GI bleeding, confusion
Signs
Jaundice and hepatomegaly
RUQ tenderness
Stigmata of chronic liver disease if cirrhosis
Asterixis or altered mental status in acute liver failure

Investigations

First-line
HBV serologiesHBsAg, anti-HBs, total anti-HBc, IgM anti-HBc, HBeAg/anti-HBe
ALT/AST, bilirubin, INR, albumin, plateletsAssess hepatic injury and synthetic function
HBV DNAQuantifies viral replication
Second-line
HIV, HCV, HDV testingCoinfections alter prognosis and treatment
Fibrosis assessmentElastography or noninvasive markers
Pregnancy testing and HBV DNA in pregnancyHigh viral load may require tenofovir
Specialist
HCC surveillanceUltrasound with or without AFP every 6 months when indicated
Transplant/hepatology evaluationAdvanced fibrosis, decompensation, or early HCC
1
Acute HBV
  • Supportive care for most adults
  • Antiviral therapy for acute liver failure or protracted severe acute hepatitis
2
Chronic HBV
  • Treat immune-active disease or cirrhosis with detectable HBV DNA
  • Preferred agents: entecavir, TDF, or TAF
  • Monitor untreated inactive carriers
3
Prevention
  • Vaccinate susceptible patients
  • Post-exposure prophylaxis with vaccine +/- HBIG
  • Newborn: HBV vaccine + HBIG within 12 hours

Complications

  • Cirrhosis/portal hypertension: Ascites, varices, encephalopathy.
  • HCC: Risk rises with cirrhosis and chronic HBV.
  • Acute liver failure: Severe hepatitis can cause coagulopathy and encephalopathy.
  • Extrahepatic disease: Vasculitis, renal disease, metabolic complications depending on etiology.
USMLE Step 2 CK Exam Tips
  • 1HBsAg positive means current infection
  • 2Anti-HBs positive means immunity
  • 3Anti-HBc IgM = acute infection or flare
  • 4Window period: anti-HBc IgM only
  • 5Vaccination gives anti-HBs only
  • 6Chronic HBV = HBsAg >6 months
  • 7Neonate of HBV-positive mother gets vaccine plus HBIG

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Verified Sources & References

AASLD 2018 Hepatitis B Guidance
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