| Literature DB >> 25299867 |
P A Minchella1, A E Armitage2, B Darboe3, M W Jallow3, H Drakesmith2, A Jaye3, A M Prentice4, J M McDermid1.
Abstract
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.Entities:
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Year: 2014 PMID: 25299867 DOI: 10.5588/ijtld.14.0143
Source DB: PubMed Journal: Int J Tuberc Lung Dis ISSN: 1027-3719 Impact factor: 2.373