Increased hepcidin expression in multibacillary leprosy

Iron is essential for all organisms and its availability can control the growth of microorganisms; therefore, we examined the role of iron metabolism in multibacillary (MB) leprosy, focusing on the involvement of hepcidin. Erythrograms, iron metabolism parameters, pro-inflammatory cytokines and urinary hepcidin levels were evaluated in patients with MB and matched control subjects. Hepcidin expression in MB lesions was evaluated by quantitative polymerase chain reaction. The expression of ferroportin and hepcidin was evaluated by immunofluorescence in paucibacillary and MB lesions. Analysis of hepcidin protein levels in urine and of hepcidin mRNA and protein levels in leprosy lesions and skin biopsies from healthy control subjects showed elevated hepcidin levels in MB patients. Decreases in haematologic parameters and total iron binding capacity were observed in patients with MB leprosy. Moreover, interleukin-1 beta, ferritin, soluble transferrin receptor and soluble transferrin receptor/log ferritin index values were increased in leprosy patients. Hepcidin was elevated in lepromatous lesions, whereas ferroportin was more abundant in tuberculoid lesions. In addition, hepcidin and ferroportin were not colocalised in the biopsies from leprosy lesions. Anaemia was not commonly observed in patients with MB; however, the observed changes in haematologic parameters indicating altered iron metabolism appeared to result from a mixture of anaemia of inflammation and iron deficiency. Thus, iron sequestration inside host cells might play a role in leprosy by providing an optimal environment for the bacillus.

role of hepcidin level in iron overload in children with beta-thalassemia

Thalassemias are a group of inherited blood disorders with defective production of hemoglobin. Patients with beta-thalassemia develop iron overload due to increased iron absorption and transfusion therapy. Hepcidin is a hepatic hormone released in case of iron overload to regulate systemic iron homeostasis by inhibiting iron absorption from diet and recycling of iron by macrophages. To determine role of hepcidin in the pathogenesis of iron overload in 6-thalassemia. 20 Patients with beta thalassemia major [TM] included 10 males and 10 females, 20 patients with beta thalassemia intermedia [TI] included 10 males and 10 females and twenty healthy children of matched age and sex were included in this study. We assessed iron overload by measuring serum ferritin, assessed erythropoietic activity by measuring serum erythropoietin levels, and correlated these with urinary hepcidin measurements. We found severe urinary hepcidin deficiency in TI with strong inverse relationship between urinary hepcidin and serum erythropoietin levels in comparison with control group. In contrast, urinary hepcidin levels were elevated in TM with decrease of erythropoietin levels. In addition, serum ferritin level was significantly higher in TM than TI and significantly higher in TM and TI compared with normal control. Hepcidin deficiency may be the key factor allowing excessive iron absorption and iron overload in TI while in TM, chronic hemolysis and frequent blood transfusions may be the main factors that increase iron load