Viral Hepatitis — Written Clinical Reasoning

SAQ 1 — Integrated Management of Chronic Hepatitis B with Cirrhosis (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, including interpretation of his serology, the phase of chronic HBV, antiviral selection with dose and monitoring, complications surveillance, and the public-health obligations to his family. Justify each decision with reference to evidence [1].

Model Answer

Serology interpretation and phase (4 marks): [1]

• HBsAg positive with anti-HBc positive confirms chronic hepatitis B infection (not vaccination, which would be anti-HBs positive and anti-HBc negative).
• HBeAg negative with anti-HBe positive and HBV DNA 45,000 IU/mL (above 2000 IU/mL threshold) plus raised ALT places him in the HBeAg-negative immune active (reactivation) phase — this is a treatment indication.
• Liver stiffness of 18 kPa and thrombocytopenia (platelets 110) indicate compensated cirrhosis with clinically significant portal hypertension (small varices present).

Antiviral therapy (4 marks):

• Two indications converge: immune active disease and cirrhosis with detectable HBV DNA — both are absolute treatment indications [1].
• First-line: tenofovir disoproxil fumarate 300 mg daily (or tenofovir alafenamide 25 mg daily, or entecavir 0.5 mg daily). He has no renal impairment or bone disease, so TDF is appropriate; if renal function declines, switch to TAF.
• Therapy is long-term (effectively lifelong) because the barrier to HBsAg loss (functional cure) is low with oral agents. Stopping risks a severe flare.
• Monitoring: HBV DNA at 12 weeks to confirm suppression, then 6-monthly; renal function and phosphate annually (tenofovir nephrotoxicity); LFTs and INR.

Cirrhosis complications surveillance (5 marks): [5] [6]

• Hepatocellular carcinoma surveillance — 6-monthly liver ultrasound plus AFP, indefinitely. Chronic HBV with cirrhosis is a high-risk group; HBV causes HCC even without cirrhosis, but cirrhosis amplifies the risk further.
• Variceal management — small varices already identified; reassess risk. If high-risk features (red wale signs, Child-Pugh B/C), start carvedilol 6.25 mg daily or endoscopic band ligation as primary prophylaxis. Repeat endoscopy as per guidelines.
• Decompensation prevention — avoid hepatotoxins, ensure HAV vaccination (superimposed HAV in cirrhosis is dangerous), counsel on alcohol abstinence.
• Calculate Child-Pugh and MELD-Na to stage prognosis and determine transplant timing. Currently compensated (Child-Pugh A, approximately 6 to 7).

Cofactors and comorbidity (3 marks): [1]

• Address metabolic syndrome: his type 2 diabetes and obesity represent overlapping MASLD, which accelerates fibrosis and independently increases HCC risk. Weight loss, glycaemic control, and statin therapy as appropriate.
• Screen for and vaccinate against hepatitis A if non-immune.

Public-health obligations to family (2 marks): [1]

• Test spouse and children for HBsAg, anti-HBs, and anti-HBc. Vaccinate all susceptible contacts. For an HBsAg-negative, anti-HBs-negative partner, give the full vaccine course and confirm seroconversion.
• His children, if born before his diagnosis was known, may have perinatally acquired HBV — they must be tested, not assumed vaccinated.

Prognosis and transplant (2 marks): [1] [5]

• With viral suppression, the risk of decompensation and HCC falls substantially but does not reach zero. Currently compensated; transplant is not indicated now but is the safety net if he decompensates or develops HCC beyond Milan criteria.

SAQ 2 — HCV Diagnosis and DAA Therapy Planning (10 marks)

Prompt: A 48-year-old woman with a history of injecting drug use (last use 3 years ago) is found to have anti-HCV antibody positive and HCV RNA 2.4 million IU/mL, genotype 1. Her ALT is 78 U/L. FibroScan shows liver stiffness 9.5 kPa (F3, advanced fibrosis, no cirrhosis). She is hepatitis B surface antigen negative. Outline the diagnostic reasoning, the treatment plan, and the post-treatment surveillance [3].

Model Answer

Diagnostic confirmation (2 marks):

• Anti-HCV positive is a screening result indicating exposure. HCV RNA positive confirms active infection — this is the indication for treatment, not the antibody alone [3].
• Genotype 1 confirmed. Fibrosis staging shows F3 (advanced fibrosis) without cirrhosis — important because it determines regimen safety (protease inhibitors are safe in compensated disease) and post-treatment surveillance intensity.

Treatment plan (4 marks): [3]

• Treat all patients with active HCV regardless of fibrosis stage per AASLD/IDSA and EASL guidance.
• Two pangenotypic options: sofosbuvir-velpatasvir 400/100 mg daily for 12 weeks or glecaprevir-pibrentasvir 300/120 mg daily for 8 weeks (8 weeks is acceptable for treatment-naive genotype 1 without cirrhosis).
• Since she has no cirrhosis, glecaprevir-pibrentasvir for 8 weeks is appropriate and shorter. Protease inhibitors are safe in compensated liver disease.
• Confirm SVR12 (undetectable HCV RNA 12 weeks after therapy completion) — SVR equals cure, with relapse risk below 1 percent.

Post-treatment management (2 marks): [3] [5]

• Because she has F3 fibrosis (not cirrhosis), she does not require ongoing HCC surveillance after SVR — advanced fibrosis without cirrhosis carries a much lower HCC risk, and fibrosis may regress. Discharge from hepatology with counselling.
• Counsel on re-infection risk: anti-HCV will remain positive for life but is not protective. If she returns to injecting drug use, re-test with HCV RNA (not antibody) periodically.

Special considerations (2 marks): [3]

• Screen for HBV coinfection before DAA therapy — HBV reactivation can occur during HCV DAA therapy in HBsAg-positive patients. She is HBsAg negative, so no prophylaxis needed, but document anti-HBc status for occult HBV risk if future immunosuppression.
• Harm reduction: link to opioid substitution therapy and needle exchange if any ongoing risk; DAAs are explicitly recommended for people who inject drugs.