Viral Hepatitis — Written Clinical Reasoning

Model answer — Part A: HBsAg-positive patient starting R-CHOP

Frame the problem first. An HBsAg-positive patient starting anti-CD20-containing chemotherapy sits in the highest reactivation risk tier — anti-CD20 agents such as rituximab deplete the B-cell immunity that keeps HBV suppressed, and reactivation in this setting can be fulminant, can interrupt curative chemotherapy, and is almost entirely preventable [1] [2].

Assessment: characterise the HBV first — HBeAg/anti-HBe status, HBV DNA, ALT, and a fibrosis assessment (elastography or APRI/FIB-4) because cirrhosis raises the stakes of any flare; screen HDV (every HBsAg-positive patient earns an anti-HDV), HCV and HIV; document baseline liver function; and involve hepatology early [1] [3].

The plan — prophylaxis, not rescue. Start a high-barrier nucleos(t)ide analogue — entecavir or tenofovir — before or with the first chemotherapy cycle; prophylaxis is superior to pre-emptive monitoring in the high-risk tier because waiting for a DNA rise leaves the window in which hepatitis declares [1] [2]. Choose the agent on renal function (tenofovir alafenamide or entecavir over tenofovir disoproxil if eGFR is reduced), and continue it for at least 12 months after the last rituximab dose — B-cell reconstitution lags treatment by many months, and late reactivation after premature cessation is well described [2].

Monitoring and communication: HBV DNA and ALT every 1–3 months during immunosuppression and through the post-treatment year; educate the patient that interrupting the antiviral risks a flare; write the antiviral plan into the chemotherapy order set so it cannot be lost between teams; and note that a reactivation flare during treatment means continuing the antiviral, supporting the liver, and discussing chemotherapy timing with oncology — not stopping everything [1] [2].

Discriminating points for full marks: name the risk tier explicitly (anti-CD20 in an HBsAg-positive patient is above 10% reactivation risk); state that even HBsAg-NEGATIVE, anti-HBc-positive (resolved) patients receive prophylaxis under anti-CD20 therapy; and reject lamivudine for prophylaxis on resistance grounds [1] [2].

Model answer — Part B: newly diagnosed anti-HCV-positive patient

Confirm viraemia. Anti-HCV is an exposure marker, not an infection marker — about a quarter of acutely infected people clear spontaneously. The mandatory next test is HCV RNA: RNA-positive means current infection; RNA-negative means resolved infection or false-positive antibody, and neither needs antiviral therapy [4].

Pre-treatment assessment in the RNA-positive patient: quantify RNA (genotyping is no longer required before pangenotypic regimens); stage fibrosis with transient elastography or APRI/FIB-4 because cirrhosis changes regimen choice and aftercare; screen HBV (HBsAg, anti-HBc — DAAs can unmask HBV replication) and HIV; check renal function; review medications for interactions (acid suppression reduces velpatasvir absorption; strong CYP3A/P-gp inducers are incompatible with glecaprevir/pibrentasvir); and address alcohol and metabolic cofactors [4].

Treatment selection. If non-cirrhotic: glecaprevir/pibrentasvir for 8 weeks or sofosbuvir/velpatasvir for 12 weeks — both pangenotypic with SVR12 rates in the high 90s in their pivotal trials [5] [6]. If compensated cirrhosis: sofosbuvir/velpatasvir 12 weeks, or glecaprevir/pibrentasvir 12 weeks. Decompensated cirrhosis, prior DAA failure, transplant and significant CKD are referred to specialist care — protease-inhibitor regimens are contraindicated in decompensation [4].

Post-treatment plan: check HCV RNA at 12 weeks after completing therapy — SVR12 is durable cure, with late relapse around 1% in long-term follow-up [8]. Then the two aftercare decisions that earn marks: cirrhosis keeps 6-monthly ultrasound HCC surveillance for life — cure removes the virus, not the scar — and counsel on reinfection if exposure risks continue, since SVR confers no immunity [7] [4].

Closing sentence for full marks: in Australia this pathway sits inside a national elimination commitment — nurse-led and primary-care models treat most non-cirrhotic patients, and the physician's value is in staging, interactions, coinfections and the post-SVR surveillance frame [4].