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About one‐third of patients with chronic hepatitis B (CHB) have hepatic steatosis, and cardiometabolic risk factors are increasingly prevalent. This review examines what metabolic dysfunction does to the measurements on which the elimination cascade depends, from prevention through diagnosis, treatment eligibility, on‐treatment risk control, and functional cure to postcure surveillance. Metabolic dysfunction lowers the response to adult vaccination, enters three of the four routes to treatment eligibility in the World Health Organization criteria, contributes to the hepatocellular carcinoma risk that persists during antiviral therapy, and is absent from most risk scores and surveillance rules used before and after hepatitis B surface antigen loss. Its two components diverge: hepatic steatosis and cardiometabolic burden appear to additively increase the probability of hepatitis B surface antigen loss, but act in opposite directions on cirrhosis, hepatocellular carcinoma, and mortality. Assessing and correcting metabolic dysfunction as part of CHB care, and including patients with CHB in trials of metabolic therapy, would allow success to be defined by liver outcomes rather than by the virus alone.
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Huang et al. (2026) studied this question.
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