Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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