Niacin deficiency in carcinoid syndrome: Definitions, biomarkers, and a pragmatic framework for clinical assessment

Niacin deficiency has been recognized for decades in patients with carcinoid syndrome, but its prevalence, biological meaning, and optimal assessment remain uncertain because definitions and biomarkers vary across studies. We conducted a scoping review, in accordance with PRISMA-ScR guidance, to map how niacin deficiency has been conceptualized and assessed in carcinoid syndrome, including mechanistic hypotheses, biochemical and functional measures, and overt clinical pellagra. PubMed was searched from inception to February 2026, with additional citation chasing. Twenty-four sources were included, comprising primary studies, case reports/series, and narrative syntheses. The literature shows marked heterogeneity across biological levels of assessment. Upstream markers such as urinary 5-hydroxyindoleacetic acid and plasma tryptophan provide context on serotonin burden and substrate availability, but they do not define niacin status. Biochemical depletion has most often been assessed using urinary niacin metabolites, particularly 24-h N1-methylnicotinamide, whereas functional depletion has been evaluated with whole-blood NAD/NADP-based indices. Overt pellagra is uncommon and represents a late clinical endpoint that is insensitive for subclinical depletion. Differences in biomarkers and operational definitions largely explain why results are difficult to compare across studies. Niacin deficiency in carcinoid syndrome cannot be reduced to a single marker or phenotype. A non-prescriptive framework that separates mechanistic context, biochemical and functional depletion, and clinical manifestations may improve reporting and interpretation across studies. Because the evidence base is dominated by small observational studies and case-based reports, the conclusions remain hypothesis-generating and point to the need for prospective validation of biomarkers against patient-relevant outcomes.