Background and Objectives: Metabolic and bariatric surgery improves obesity and metabolic dys-function-associated steatotic liver disease (MASLD), but its effect on the residual risk of hepatocellu- lar carcinoma (HCC) is less clearly defined. This narrative review examines the relationship between postoperative metabolic improvement, fibrosis regression, and HCC risk, with particular attention to surveillance. Materials and Methods: A targeted literature search identified clinical studies, mechanistic investigations, and professional guidance relevant to bariatric surgery, MASLD, and HCC. Results: Randomized and paired-biopsy studies support improvement in steatohepatitis, whereas observational cohorts associate surgery with lower HCC occurrence and fewer major adverse liver outcomes. These findings address different endpoints and should not be treated as interchangeable evidence of cancer prevention. Advanced fibrosis can persist despite substantial weight loss and resolution of steatohepatitis. Conversely, the absolute postoperative HCC risk among patients with documented fibrosis regression remains insufficiently characterized. The available evidence does not establish a postoperative biochemical, elastographic, or histological threshold at which surveillance can safely be stopped in patients with established cirrhosis. Conclusion: Surveillance decisions should therefore remain anchored to the underlying liver disease, treatment eligibility, and applicable guidance rather than weight loss alone. Noncirrhotic advanced fibrosis requires individualized assessment because professional recommendations differ and evidence is limited. Future studies should report HCC separately from composite liver outcomes and evaluate risk according to baseline and postoperative fibrosis, metabolic trajectories, and surveillance exposure. Bariatric surgery may modify the course of liver disease, but metabolic improvement should not be equated with elimination of carcinogenic risk.

Bariatric surgery is often presented as cancer-preventive, but its association with colorectal cancer (CRC) is less clear than for other obesity-related cancers. This critical narrative review examined epidemiological studies, evidence syntheses, human mechanistic studies and guidance identified through targeted searches updated to 31 October 2026, separating comparisons with nonsurgical obesity care from comparisons with the general population. Most meta-analyses report inverse associations, but results depend on the estimator and study selection: two largely overlapping reviews reported a nonsignificant pooled hazard ratio (HR) of 0.88 (95% confidence interval [CI] 0.69–1.12), and HRs of 0.81 and 0.75 only after excluding one study. Persistent excess colon cancer risk relative to the general population does not by itself indicate harm from surgery. The Swedish Obese Subjects study found no significant adjusted association after a median 22.2 years, and an October 2026 Nordic cohort found none for colon or rectal cancer. Human mucosal findings diverge, and experimental data offer hypotheses rather than clinical proof. The magnitude and causality of any association remain uncertain, and no late postoperative hazard is established. Screening after surgery should follow established risk factors, prior colonoscopy findings and symptoms rather than the operation alone.

It is essential to assess not only the hematologic outcomes but also the immunologic and inflammatory consequences of RBC transfusion in preterm infants. T