A liver mass, an AFP of 1,240 and only money for one more test

Diagnosis Hepatocellular carcinoma arising in a cirrhotic liver with chronic hepatitis B. His age, male sex, chronic HBsAg carriage, family history, nodular liver with portal hypertension (platelets 78, splenomegaly, ascites) and a focal mass in the right lobe all fit.

Pathology HCC is a malignant tumour of hepatocytes that develops along a pathway of chronic injury, hepatocyte necrosis and regeneration, fibrosis, cirrhosis, dysplastic nodules and early carcinoma. Histologically it shows trabecular, pseudoglandular or solid patterns with eosinophilic cells, raised nuclear-to-cytoplasmic ratio, loss of the reticulin framework, and often bile production. Vascular invasion into portal radicles is common and is the main driver of recurrence after resection.

Molecular basis

• HBV DNA integrates into the host genome, causing insertional mutagenesis and genomic instability, for example near the TERT promoter.
• The HBx protein is a transactivator that binds and inactivates p53 and interferes with apoptosis, Wnt/beta-catenin and PI3K-Akt signalling.
• Chronic inflammation generates reactive oxygen species and sustained NF-kappa-B signalling with telomere shortening.
• Aflatoxin B1 from mouldy maize and groundnuts is activated to an epoxide that forms DNA adducts and produces a characteristic p53 codon 249 G to T transversion. Combined with HBV, the risk multiplier is large, which is directly relevant to this farmer's storage practices.

Why AFP is not proof AFP is also raised in hepatitis flares, cirrhosis, pregnancy and germ cell tumours, so a high value is not specific. Sensitivity is at best around 60% at conventional cut-offs, so a normal value never excludes HCC. A value above 400 ng/mL with a mass in a cirrhotic liver is highly predictive, but it is not the same as a histological or radiological diagnosis, and it says nothing about stage or respectability.

Spend the money on imaging, not on a needle The single most informative test is a multiphase contrast-enhanced CT of the liver (or MRI if available). In a cirrhotic liver, arterial hyperenhancement with washout in the portal venous or delayed phase is diagnostic of HCC without histology. A CT also shows the number of lesions, segmental location, portal or hepatic vein invasion, extrahepatic spread and the size of the future liver remnant, so it answers the staging question at the same time. Ultrasound cannot characterise a lesion.

If his hospital genuinely cannot provide CT, refer him to a centre that can, and ask a social worker or the hospital's welfare unit to help with cost. Contrast-enhanced ultrasound is a cheaper alternative in expert hands. Serial AFP alone is not a substitute for imaging.

Staging Score him formally: Child-Pugh class from bilirubin, albumin, INR, ascites and encephalopathy, plus performance status. His albumin 29 g/L and bilirubin 62 µmol/L already suggest at least Child-Pugh B, which has major implications for surgery. Then apply the Barcelona (BCLC) system: a solitary tumour without macrovascular invasion in a patient with preserved performance status is potentially amenable to resection or ablation (BCLC A in the 2022 revision, intermediate B in older versions), but only if liver function is adequate.

Would I biopsy? No, if the imaging is characteristic. Biopsy carries a bleeding risk in a man with platelets of 78 × 10⁹/L and an INR of 1.6, has a needle-track seeding rate of roughly 1-3%, risks sampling error, and is unnecessary when non-invasive criteria are met. Reserve biopsy for indeterminate imaging or where a different tumour, such as cholangiocarcinoma or metastasis, would change management.

Primary and secondary prevention that was missed

• Hepatitis B vaccination, including a birth dose within 24 hours, which Nigeria provides through the pentavalent vaccine; he was born before this and was never immunised.
• Prevention of mother-to-child transmission: screen every pregnant woman for HBsAg, and give tenofovir in the third trimester to those with high viral loads, plus vaccine and immunoglobulin at birth.
• Antiviral suppression: tenofovir or entecavir would have reduced his HBV DNA, slowed fibrosis and lowered (though not abolished) his HCC risk. He was known HBsAg-positive since 2011 and never treated - a major system failure.
• Six-monthly ultrasound with or without AFP surveillance in chronic hepatitis B and cirrhosis, imperfect but recommended.
• Aflatoxin control: drying and storing maize and groundnuts properly, discarding mouldy nuts, and avoiding damp storage.
• Alcohol avoidance and screening and vaccination of his household contacts, who are at real risk.

What is realistic now

• Refer to a tertiary hepatobiliary multidisciplinary team. If he is Child-Pugh A with an adequate future remnant and no portal hypertension, surgical resection offers the only realistic chance of cure; his platelet count and albumin make that uncertain.
• If not resectable but liver function is preserved, locoregional therapy - radiofrequency or microwave ablation for a single lesion in expert hands, or transarterial chemoembolisation for intermediate disease.
• Sorafenib or lenvatinib for advanced disease, usually unaffordable out of pocket, with no realistic prospect of cure.
• Whatever is decided, offer good palliative care: analgesia by the WHO ladder, sodium restriction with spironolactone and furosemide for ascites, lactulose for encephalopathy, avoidance of NSAIDs and hepatotoxins, and an honest conversation with him and his family about prognosis and preferences.
• Start tenofovir for his hepatitis B if renal function permits, to reduce decompensation, and screen and vaccinate his family.