Abstract
Early identification and treatment of active tuberculosis disease among high risk household contacts could limit new transmission and better clinical outcome, thus decreasing TB burden. Host iron homeostasis is an important yet underevaluated factor in pathophysiology of tuberculosis (TB). One such protein is hepcidin which internalizes ferroportin (membrane iron transporter), thus inhibiting iron export from macrophages which is utilised by bacteria leading to disease severity. Iron homeostasis markers were evaluated in 50 pulmonary tuberculosis patients (PTB) and their household contacts to assess their utility as biomarkers for TB development. Altered iron homeostasis with significantly lower haemoglobin levels despite optimum serum iron levels was observed in PTB compared to household contacts and healthy controls pointing towards anaemia of inflammation. Higher serum hepcidin with lower ferroportin expression and hence higher ferritin levels was seen in PTB compared to both household contacts and healthy controls due to IL-6 induced hepcidin production in TB. Transferrin levels were found to be significantly lower in PTB and household contacts as compared to healthy controls owing to higher ferritin levels in PTB group. Upon infection, regulation of iron absorption is disturbed via increased hepcidin levels leading to ferroportin internalization and thus inhibition of iron export from macrophages which may lead to favourable M.tb. survival and multiplication leading to tuberculosis. Some of these markers could be assessed for early identification and treatment of active tuberculosis among high risk household contacts limiting new transmission and better clinical outcome, thus decreasing TB burden.