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Hepatitis B

SNOMED: 81665004889 words•Updated 03/03/2026
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Exam Tips

  • Core serology pattern: acute HBV = HBsAg positive with IgM anti-HBc positive; chronic HBV = HBsAg persists at least 6 months.
  • Vaccination causes anti-HBs positivity without anti-HBc; prior natural infection usually gives anti-HBc positivity.
  • Always link infectivity to viral replication markers (HBeAg and HBV DNA), not ALT alone.
  • In OSCE counselling, include partner/household testing and vaccination, safer sex, and no needle-sharing.
  • Perinatal transmission is the highest-risk route for chronicity; this is a frequent SBA theme.
  • See Figure: phase-based interpretation of chronic HBV (HBeAg status, HBV DNA, ALT, fibrosis risk).

Definition

Hepatitis B is a blood-borne and sexually transmissible infection caused by hepatitis B virus (an enveloped DNA hepadnavirus) that primarily targets the liver. Infection may present as acute hepatitis or persist as chronic infection (HBsAg positivity for at least 6 months), with chronic immune-mediated liver injury predisposing to fibrosis, cirrhosis, and hepatocellular carcinoma.

Pathophysiology

HBV enters hepatocytes and forms a stable nuclear template (cccDNA), allowing persistent viral replication. Most hepatocyte damage is immune mediated rather than directly cytopathic: host T-cell responses drive necroinflammation, ALT elevation, and progressive fibrosis in susceptible patients. Clinical phases are defined by HBeAg status, HBV DNA level, and ALT (HBeAg-positive infection, HBeAg-positive hepatitis, HBeAg-negative infection, HBeAg-negative hepatitis, and HBsAg loss/occult phase). Perinatal acquisition has high chronicity because of relative immune tolerance in infancy, whereas adult-acquired infection is usually self-limiting. See Figure: HBV serology timeline (HBsAg, anti-HBc IgM/IgG, HBeAg, anti-HBs) and Figure: natural history of chronic HBV phases.

Risk Factors

  • Birth in or migration from high/intermediate HBV prevalence regions
  • Perinatal exposure (mother-to-child transmission)
  • Injecting drug use and sharing injecting equipment
  • Unprotected sex, multiple partners, men who have sex with men, sex work
  • Household or sexual contact with a person with HBV
  • Occupational blood exposure (healthcare/laboratory/tattoo/piercing/mortuary work)
  • Haemodialysis, blood product exposure, solid organ transplantation
  • Prison residence or work in custodial settings
  • Travel to high-endemic regions
  • Immunosuppression (higher risk of chronicity/reactivation)

Clinical Features

Symptoms

  • Often asymptomatic (especially children and chronic infection)
  • Prodrome in acute infection: fever, malaise, profound fatigue, anorexia, nausea
  • Arthralgia and urticarial or maculopapular rash (pre-icteric immune-complex phase)
  • Right upper quadrant abdominal pain
  • Jaundice with dark urine and pale stools in cholestatic presentations
  • Pruritus (if cholestatic)
  • Symptoms of chronic liver disease when advanced (abdominal distension, oedema, encephalopathy features)

Signs

  • Jaundice and scleral icterus
  • Hepatomegaly or right upper quadrant tenderness
  • Stigmata of chronic liver disease in long-standing infection (spider naevi, palmar erythema, splenomegaly)
  • Signs of decompensated cirrhosis (ascites, asterixis, muscle wasting)
  • Extrahepatic signs: vasculitic rash, oedema/hypertension with glomerulonephritis

Investigations

HBsAg:Positive in current infection; persistence for 6 months or more indicates chronic HBV
IgM anti-HBc:Positive in acute/recent infection
Total anti-HBc (IgG predominant):Marker of previous or ongoing natural infection (not vaccine response)
Anti-HBs:Appears after recovery or vaccination; indicates immunity
HBeAg and anti-HBe:HBeAg suggests high infectivity/active replication; anti-HBe suggests partial immune control
Quantitative HBV DNA PCR:Defines viral replication level; guides treatment eligibility and monitoring
Liver blood tests (ALT/AST, bilirubin, ALP, albumin), coagulation (INR), FBC, U&Es:ALT elevation in active hepatitis; synthetic failure (low albumin/high INR) indicates severe disease
Liver fibrosis assessment (transient elastography or biopsy when needed):Stages fibrosis/cirrhosis and informs urgency of antiviral therapy
Liver ultrasound +/- AFP surveillance in high-risk chronic HBV:Screens for hepatocellular carcinoma and cirrhotic change
Tests for coinfection and differentials (HCV, HDV, HIV, HAV/HEV serology, autoimmune and metabolic liver screen):Identifies coinfections and alternative causes of hepatitis

Management

Lifestyle Modifications

  • Advise strict avoidance of alcohol and review hepatotoxic medicines/supplements
  • Counsel on transmission reduction: condoms, do not share razors/toothbrushes/needles, cover bleeding wounds
  • Screen and vaccinate household/sexual contacts; offer STI screening where relevant
  • Notify acute HBV cases through appropriate public health pathways and arrange contact tracing
  • Regular follow-up for chronic HBV with liver function, HBV DNA, fibrosis assessment, and HCC surveillance where indicated

Pharmacological Treatment

First-line nucleos(t)ide analogues for chronic HBV (specialist-led)

  • Tenofovir disoproxil 245 mg orally once daily
  • Entecavir 0.5 mg orally once daily on an empty stomach (1 mg once daily in selected resistant/decompensated cases)

Preferred long-term suppressive therapy in active chronic HBV. Monitor renal function with tenofovir; adjust dose in renal impairment for tenofovir/entecavir. Do not stop abruptly without specialist input due to risk of severe hepatitis flare.

Finite-course immunomodulatory therapy

  • Peginterferon alfa-2a 180 micrograms subcutaneously once weekly (typically 48 weeks)

Consider in selected non-cirrhotic patients with favorable predictors. Contraindications/cautions include decompensated cirrhosis, significant psychiatric illness, uncontrolled autoimmune disease, and pregnancy risk; monitor for cytopenias, thyroid dysfunction, and mood change.

Post-exposure and prevention pharmacotherapy

  • Hepatitis B vaccine (e. g, adult monovalent schedule 20 micrograms IM at 0, 1, and 6 months)
  • Hepatitis B immunoglobulin (HBIG) for high-risk exposures and neonates of infected mothers, given urgently with vaccine

Use occupational/sexual/perinatal PEP pathways urgently (ideally within 48 hours after significant exposure). Vaccine is contraindicated only with prior anaphylaxis to a vaccine component; HBIG dosing is protocol-based (age/weight/exposure type).

Acute hepatitis B supportive care

  • Symptomatic antiemetics/analgesia as needed

Most acute infections are self-limiting; admit urgently if encephalopathy, coagulopathy, rapidly rising bilirubin/INR, or suspected fulminant hepatic failure.

Surgical / Interventional

  • Liver transplantation for fulminant hepatic failure or end-stage/decompensated HBV cirrhosis despite optimal medical therapy

Complications

  • Fulminant hepatic necrosis/acute liver failure (rare but high mortality)
  • Chronic hepatitis with progressive fibrosis and cirrhosis
  • Decompensated cirrhosis (ascites, variceal bleeding, encephalopathy, jaundice)
  • Hepatocellular carcinoma
  • HBV reactivation during immunosuppression
  • Immune-complex extrahepatic disease (e. g, glomerulonephritis, polyarteritis nodosa-like vasculitis)
  • Increased risk of selected extrahepatic malignancies (e. g, lymphoma, gastric, cervical associations)

Prognosis

Prognosis is strongly age-dependent at acquisition: about 90% of perinatally infected infants, 20-50% of children infected at 1-5 years, and around 5% of immunocompetent adults progress to chronic infection. Most adults with acute HBV recover, but a minority develop severe acute liver failure. In chronic HBV, persistent inflammation and replication increase risk of cirrhosis and HCC; sustained viral suppression with antivirals markedly improves long-term liver outcomes.

Sources & References

🏥BMJ Best Practice(1)

💊BNF Drug References(8)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 740)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 738, 739)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1488)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1488)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1513, 1514)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1488)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 732)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 736, 737)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1738)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 736)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 739)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1492)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 769, 770)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 416)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 415, 416)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 1435)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 181)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 230, 231)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 180, 181)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 181, 182)[context]

Sources

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