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Hepcidin inhibits ferroportin-mediated iron efflux, leading to intracellular macrophage iron retention, possibly favoring Mycobacterium tuberculosis iron acquisition and tuberculosis (TB) pathogenesis. Plasma hepcidin was measured at human immunodeficiency virus (HIV) diagnosis in a retrospective HIV-prevalent, antiretroviral-naïve African cohort to investigate the association with incident pulmonary and/or extra-pulmonary TB. One hundred ninety-six participants were followed between 5 August 1992 and 1 June 2002, with 32 incident TB cases identified. Greater hepcidin was associated with significantly increased likelihood of TB after a median time to TB of 6 months. Elucidation of iron-related causal mechanisms and time-sensitive biomarkers that identify individual changes in TB risk are needed.

Original publication

DOI

10.5588/ijtld.14.0143

Type

Journal article

Journal

Int J Tuberc Lung Dis

Publication Date

11/2014

Volume

18

Pages

1337 - 1339

Keywords

Adult, Biomarkers, Cohort Studies, Female, Follow-Up Studies, Gambia, HIV Infections, Hepcidins, Humans, Longitudinal Studies, Male, Retrospective Studies, Time Factors, Tuberculosis, Tuberculosis, Pulmonary, Young Adult