Viral Hepatitis — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Nguyen is a 54-year-old Vietnamese-born man referred with abnormal liver enzymes found on insurance bloods. He migrated to Australia at age 30 and works as a mechanic. He has chronic hepatitis B diagnosed at age 25 but has never been treated. He has type 2 diabetes and obesity. [1]

His main problems are: [1] [5] [6]

1. Chronic hepatitis B in the HBeAg-negative immune active phase — HBV DNA 45,000 IU/mL, ALT 118
2. Compensated cirrhosis — FibroScan 18 kPa, platelets 110, small oesophageal varices
3. Hepatocellular carcinoma risk — requires 6-monthly surveillance
4. Metabolic syndrome — type 2 diabetes and obesity with overlapping MASLD

My integrated plan is to start tenofovir to suppress HBV, institute 6-monthly ultrasound and AFP surveillance, manage his portal hypertension with carvedilol, address his metabolic risk, and test and vaccinate his family." [1] [5] [6]

Examiner probing questions and model answers

Q1: "His HBV DNA is 45,000 IU/mL and ALT is 118. He is HBeAg negative. Why is he not in the immune tolerant phase?" [1]

"The immune tolerant phase requires HBeAg positivity, very high HBV DNA — typically above one million IU/mL — and a persistently normal ALT. Mr Nguyen is HBeAg negative with anti-HBe positive, his DNA is 45,000 IU/mL, and his ALT is elevated at 118. This is the HBeAg-negative immune active, or reactivation, phase, caused by precore or basal core promoter mutants that stop producing HBeAg but continue to replicate. This is a treatment indication because there is active immune-mediated liver injury and progressive fibrosis — and his FibroScan of 18 kPa confirms he already has cirrhosis." [1]

Q2: "Why tenofovir and not pegylated interferon?" [1]

"Tenofovir is first-line here for three reasons. First, he has cirrhosis, and pegylated interferon is contraindicated in decompensated cirrhosis and relatively contraindicated in significant fibrosis because of the risk of a flare precipitating decompensation. Second, tenofovir has a very high barrier to resistance — essentially zero resistance at eight years in the registration trials — which matters because HBV therapy is long-term. Third, he prefers a daily tablet over 48 weeks of weekly injections with interferon's substantial side-effect profile. Tenofovir DF 300 mg daily is appropriate; if he develops renal impairment or bone density concerns, I would switch to tenofovir alafenamide 25 mg daily, which has superior renal and bone safety." [1]

Q3: "He achieves viral suppression on tenofovir. Does his hepatocellular carcinoma surveillance stop?" [1] [5]

"No. Once cirrhosis is established, the HCC risk persists despite viral suppression. HBV causes HCC through a combination of chronic inflammation, regenerative drive, and direct viral DNA integration into the host genome — integration is not fully reversed by suppressing replication. AASLD guidance recommends 6-monthly liver ultrasound plus AFP for all patients with cirrhosis from chronic HBV, and for HBV patients without cirrhosis in defined high-risk groups. The surveillance continues indefinitely. The interval is six months because the tumour doubling time is roughly four to six months — annual is too long, and more frequent adds little." [5]

Q4: "His wife is HBsAg negative and anti-HBs negative. What do you do?" [1]

"She is susceptible to hepatitis B. I would vaccinate her with the full three-dose schedule and check anti-HBs one to two months after the final dose to confirm seroprotection, defined as a level above 10 mIU/mL. Non-responders may need a repeat course. I would also test his children — if they were born before his diagnosis was established, they may have acquired HBV perinatally, and I must not assume they were vaccinated. Each family member gets HBsAg, anti-HBs, and anti-HBc to determine their status: susceptible, immune, or infected." [1]

Q5: "His pregnant niece has just been found to be HBsAg positive and HBeAg positive with HBV DNA of 6 million IU/mL. How would you advise on preventing transmission to her baby?" [2]

"Prevention is layered. First, every infant receives the hepatitis B birth-dose vaccine within 24 hours of birth. Second, because she is HBeAg positive with a high viral load, the infant also receives hepatitis B immune globulin, 100 to 200 IU intramuscularly, within 12 hours of birth. Third, because her viral load is above 200,000 IU/mL, I would start maternal tenofovir 300 mg daily, ideally from 28 to 32 weeks and continued to delivery. The Pan trial showed this significantly reduces mother-to-child transmission beyond what vaccine and HBIG alone achieve. Breastfeeding is safe and encouraged once the infant is immunised." [2]

Q6: "How would your management change if he were also found to be anti-HDV positive with detectable HDV RNA?" [4]

"That would fundamentally change his prognosis. HDV coinfection is the most severe form of chronic viral hepatitis, with faster fibrosis, higher cirrhosis and HCC rates. I would still give tenofovir for the HBV if his HBV DNA is detectable, because suppressing HBV provides the surface antigen substrate but the priority is the delta virus. The treatment options for HDV are pegylated interferon — with poor response rates around 25 to 30 percent — or bulevirtide, an entry inhibitor given as 2 mg subcutaneously daily, which the MYR301 phase 3 trial showed reduces HDV RNA and normalises ALT. I would refer to a specialist centre with HDV expertise, intensify HCC surveillance, and consider transplant assessment earlier, because HDV accelerates decompensation." [4]

Short Case Discussion

Scenario: "Examine this patient's abdominal system"

Candidate presentation (model): [1] [6]

"I examined Mr Nguyen's abdominal system. He is thin, with several spider naevi over the anterior chest wall in the superior vena cava distribution, and loss of axillary hair. On the hands there is palmar erythema sparing the central palm. There is no asterixis. [1]

The abdomen is soft. The liver edge is firm and irregular, palpable 3 cm below the costal margin. The spleen is enlarged 4 cm below the left costal margin. There is no ascites. There is peripheral oedema to the ankles bilaterally. [6]

These findings are consistent with chronic liver disease complicated by portal hypertension. The spider naevi and palmar erythema indicate chronic liver disease; the splenomegaly indicates portal hypertension. I would like to take a full viral hepatitis and alcohol history, organise liver function tests, a viral hepatitis screen, a FibroScan, and screening endoscopy." [1] [6]

Examiner: "Why is the spleen enlarged?" [6]

"Splenomegaly in this context reflects portal hypertension from cirrhosis. Increased portal venous pressure causes congestive splenomegaly over time. Splenomegaly is one of the most specific clinical indicators of portal hypertension — its presence, alongside the firm irregular liver, confirms the portal-hypertensive phenotype and explains his thrombocytopenia, which is from hypersplenism." [6]

Examiner: "How would you grade his liver disease if he were confused?" [7]

"I would use the West Haven classification for hepatic encephalopathy — grade 1 mild confusion and sleep disturbance, grade 2 lethargy with asterixis, grade 3 somnolent but arousable, grade 4 coma. I would also calculate his Child-Pugh score using bilirubin, albumin, INR, ascites and encephalopathy to estimate prognosis, and his MELD-Na to determine transplant priority if he were being assessed. Encephalopathy would push his Child-Pugh toward class C and indicate decompensation, which would change the management urgency." [7]

Examiner: "What viral causes of chronic liver disease should you screen for?" [1] [3]

"The chronic bloodborne hepatotropic viruses — hepatitis B and hepatitis C — are the priority. For HBV I would test HBsAg, anti-HBs, and anti-HBc. For HCV I would screen with anti-HCV and confirm with HCV RNA if positive. If HBsAg is positive, I would add HBeAg, anti-HBe, HBV DNA, and screen for hepatitis D with anti-HDV, because HDV coinfection changes management entirely. I would also check immune status for hepatitis A so I can vaccinate if non-immune, since superimposed HAV in cirrhosis is dangerous." [1] [3]