BCLC Staging and Treatment Principles for Hepatocellular Carcinoma

Alpha-fetoprotein is the marker primarily elevated in hepatocellular carcinoma. CA19-9 comes primarily from the biliary system and can rise somewhat in cirrhotic patients, but not to a high degree, so it remains the more specific marker for cholangiocarcinoma.

After HCC resection on a normal liver, patients are generally placed on lenvatinib long-term. After transplant, there is no separate adjuvant chemotherapy; instead, immunosuppression is adjusted to tacrolimus plus everolimus rather than the standard tacrolimus and mycophenolate, since everolimus is associated with a lower recurrence risk. For cholangiocarcinoma with nodal or vascular invasion, patients are referred to medical oncology for cisplatin or gemcitabine-based adjuvant therapy, usually once they have recovered, six to twelve weeks later, from preoperative jaundice and cholangitis.

No, this is not typical of the Pringle manoeuvre itself. Needing a stent afterwards points to bile duct involvement: a narrowed biliary confluence after a right hepatectomy, a bile leak that progressed to a stricture after a hepaticojejunostomy, or compromised duct vascularity following preoperative radiotherapy. The Pringle manoeuvre alone may raise liver enzymes, but it should not cause obstructive jaundice.

For HCC after resection or an interventional procedure, MRI is favoured over repeated CT scans, both to limit cumulative radiation and contrast exposure and because MRI catches smaller lesions earlier, while they are still resectable or eligible for salvage transplant. Cholangiocarcinoma follow-up similarly relies on CT or MRI rather than ultrasound, alongside tumour markers, AFP and PIVKA-II for HCC, CA19-9 for cholangiocarcinoma.

Intent comes first. Even in India, transplant is offered at only a handful of government centres, with growth coming mainly from the private sector. Beyond intent, a new programme needs mentorship from teams already trained in transplant so that skills transfer gradually, buy-in across radiology, anaesthesia, critical care and hepatology rather than a purely surgeon-driven effort, and infrastructure including a strong interventional radiology service, phasic CT and MRI, and an apheresis machine for ABO-incompatible transplants. Management has to be fully behind the programme, because it takes far more time and effort than routine GI or hepatobiliary surgery.

The decision rests on liver function as much as tumour size. Small, early tumours in a liver with no cirrhosis, or with normal portal pressure (Child A status), can be resected. Where portal pressure or bilirubin is elevated, signalling reduced liver function, transplant is the better option instead of resection.

In a cirrhotic liver, a large resection is not an option. A small but deep-seated tumour, one that would require removing a disproportionate amount of liver tissue to reach, is better managed with microwave or radiofrequency ablation than with surgery.

When the main portal vein is involved in a cirrhotic patient, surgery is no longer possible. Radiotherapy options such as stereotactic body radiotherapy (SBRT) or transarterial radioembolisation (TARE) become the treatment, sometimes combined with TACE, where TACE controls the primary tumour and SBRT addresses the portal vein tumour thrombus.

Where disease has spread beyond what locoregional treatment can address, systemic options include sorafenib, lenvatinib, and increasingly the combination of atezolizumab and bevacizumab. Emerging evidence also points to using these therapies as downstaging tools to bring patients back within transplant or resection criteria.