Viral Hepatitis, Potential Aflatoxin B1 Exposure, and Projected Metabolic Risk Factors for Hepatocellular Carcinoma in Somalia: A Call for Integrated Prevention, Surveillance, and Research

This commentary is a narrative synthesis of Somali, regional, and global evidence on hepatocellular carcinoma (HCC) risk in Somalia; it does not report new epidemiological data, and claims are graded according to whether they are directly demonstrated in Somalia or inferred from broader African or global literature. Hepatocellular carcinoma (HCC) is a major cause of cancer mortality globally and presents a particularly difficult challenge in sub-Saharan Africa, where chronic hepatitis B virus (HBV) infection, hepatitis C virus (HCV), food-borne aflatoxin exposure, limited surveillance, and restricted access to curative treatment intersect. Somalia has no mature population-based cancer registry, yet available hospital-based evidence indicates that liver cancer is an important component of the national cancer burden. Directly documented Somali evidence is limited to hospital case series and to donor-, hospital-, and laboratory-based HBV studies: a Somali series of 268 patients with HCC documented a predominantly male population, a relatively young mean age, large tumors, and portal-vein thrombosis associated with poor prognostic features, and recent Mogadishu studies have shown continuing HBV transmission and important gaps in vaccination, testing, and linkage to care. By contrast, the contribution of aflatoxin B1 exposure and of metabolic dysfunction-associated steatotic liver disease (MASLD) to HCC in Somalia is not directly documented. No Somali biomonitoring, dietary-exposure, or MASLD-prevalence data exist; the discussion of these pathways in this commentary is therefore inferred from regional and global literature and should be read as a precautionary, hypothesis-generating projection of future risk rather than an established local driver of current disease. This commentary argues that Somalia should nonetheless not address viral, toxic, and metabolic exposures through isolated programs. An integrated, phased HCC prevention strategy should combine timely HBV birth-dose vaccination, maternal screening and antiviral prophylaxis, adult testing and treatment, HCV diagnosis and cure, precautionary food-safety surveillance for aflatoxins, metabolic-risk assessment embedded in liver care, risk-based liver ultrasound surveillance with alpha-fetoprotein (AFP) used only as an adjunct, strengthened diagnostic imaging and pathology, and a national liver-cancer registry. Locally led epidemiological and implementation research, including population-attributable-fraction scenario modelling and representativeness analyses of existing hospital series, is urgently needed to quantify the relative contribution of viral, toxic, and metabolic pathways and to identify feasible models for surveillance and referral in a resource-constrained setting.