Viral, autoimmune and metabolic hepatitis — formative SAQs

SAQ 1 — The perinatally infected school-age child with chronic hepatitis B (20 marks, ~15 minutes)

A ten-year-old boy is referred because his mother, who is hepatitis B surface antigen positive, has just been diagnosed. The boy is well and growing normally. His serology shows a positive hepatitis B surface antigen, a positive e antigen, an HBV DNA of two hundred million international units per millilitre, and persistently normal alanine aminotransferase. ^[2]

Questions

1. Give the diagnosis, the phase of chronic hepatitis B, and the clinical reasoning that distinguishes it. (5 marks) ^[3]
2. Outline the management and explain why antiviral treatment is not started at this point. (5 marks) ^[3]
3. Describe the perinatal prevention that should have been offered and why perinatal chronicity is so high. (4 marks) ^[3]
4. Explain the hepatocellular carcinoma surveillance the child now needs. (3 marks) ^[2]
5. Describe the trigger that would change the management to active treatment. (3 marks) ^[3]

Model answer (must-hit)

1. The diagnosis is chronic hepatitis B acquired perinatally. The phase is the immune-tolerant phase, defined by the positive surface antigen and e antigen, the very high HBV DNA and the persistently normal alanine aminotransferase, which shows that the immune system is not yet attacking the infected hepatocytes. The low inflammation despite the high viral load is the hallmark that separates it from the immune-active phase. ^{[2] [3]}
2. The management is surveillance without antiviral treatment, because the immune-tolerant phase carries minimal histological inflammation and the risk of treatment is not justified by the benefit; treating here risks antiviral resistance without halting meaningful disease. The child is monitored with six-monthly transaminases and liver function, and hepatocellular carcinoma surveillance is begun. ^[3]
3. Perinatal prevention is the hepatitis B vaccine plus hepatitis B immunoglobulin given within twelve hours of birth, followed by the full vaccine course, with post-vaccination serology at nine to twelve months. For a mother with a high viral load, maternal tenofovir prophylaxis from twenty-eight weeks further reduces the residual risk. Perinatal chronicity is around ninety per cent without immunoprophylaxis, because the immature neonatal immune system tolerates rather than clears the virus. ^[3]
4. The child needs six-monthly abdominal ultrasound with alpha-fetoprotein for hepatocellular carcinoma surveillance, because chronic hepatitis B carries a risk of hepatocellular carcinoma that begins in childhood and is independent of cirrhosis. ^[2]
5. The trigger for active treatment is the transition to the immune-active phase, signalled by a persistently rising alanine aminotransferase with active inflammation, at which point a nucleoside analogue such as entecavir or tenofovir is started to suppress replication. ^[3]