Factor analysis of hepcidin on cardiac iron overload and fibrosis among thalassemia major children

Abstract

Cardiac iron overload is a common cause of death in thalassemia major and is associated with hepcidin, which is primary iron homeostasis. Therapeutics that could increase hepcidin levels or act as hepcidin agonists might help treat the abnormal iron absorption in individuals with β-thalassemia and related disorders. We aimed to verify the structure and study the relationship of release variables, hepcidin, cardiac iron overload, or fibrosis. A cross-sectional study was conducted among thalassemia majors, aged 6–18 years at Rumah Sakit Anak dan Bunda Harapan Kita Indonesia, between January 2019 and May 2020. Clinical data, hepcidin-25, interacting variables laboratory test, MRIT2* used to assess cardiac iron overload, late gadolinium enhancement (LGE), and soluble suppression of tumoregenicity2 (ST2) to assess fibrosis were studied. The correlation test was performed with SPSS version 20, Amos 22 was used to assess confirmatory factor analysis (CFA), and squared multiple correlation (SMC) was used to determine the proportion of total variation explained by the model. We recruited 80 patients, of those 8 (10%) were cardiac iron overload, 5 (5.25%) were fibrosis, and 3 (3,75%) were ST2 > 35 mg/dL. CFA showed variables that interact with hepcidin release were Hb, reticulocyte-He (Re-He), HIF-1α, Immature granulocyte (IG), hs-CRP, IL-6, ferritin, and transferrin saturation. There was no direct hepcidin role in cardiac iron overload and fibrosis. No interacting variable role on hepcidin. SMC of hepcidin on cardiac iron overload was 20%. Factor analysis of hepcidin was Hb, Ret-He, HIF-1α, IG, hs-CRP, IL-6, ferritin, and transferrin saturation. No direct hepcidin role in cardiac iron overload and fibrosis. Hepcidin explains approximately 20% of the total variation in cardiac iron overload.