The relationship between hepcidin and anemia in controlled and uncontrolled Type-2 Diabetes Mellitus (T2DM) patients at Sanglah Hospital, Bali, Indonesia

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Background: Anemia in patients with diabetes mellitus (DM) is often associated with anemia of chronic disease caused by inflammation or iron metabolism disorders. Hepcidin is known to function in initiating the internalization and degradation of ferroportin. It can inhibit the release of iron from cells where an increase in hepcidin levels will reduce iron absorption in the intestine, resulting in a decrease in serum iron levels. This study aims to determine the relationship between serum hepcidin levels and anemia in patients with Type-2 Diabetes Mellitus (T2DM).Methods: This cross-sectional study was conducted on 77 consecutive T2DM patients who met the inclusion and exclusion criteria and received health services at Sanglah Hospital, Bali, Indonesia, during the study period. The variables assessed in this study included T2DM status (controlled and uncontrolled), anemia, hemoglobin, HbA1c, erythrocyte sedimentation rate, and hepcidin. Data were analyzed with SPSS version 20 for Mac.Results: There was no significant difference in age, sex, disease duration, SGOT, SGPT, leukocytes, platelets, and ESR between controlled and uncontrolled T2DM groups (p>0.05). However, there was a significant difference in eGFR and hemoglobin levels between controlled and uncontrolled T2DM groups (p<0.05). Mann-Whitney U test found a significant difference in hepcidin levels between controlled and uncontrolled T2DM groups (MD=138.14; 95%CI=10.65-286.94; p=0.046). A weak significant negative correlation was found between hemoglobin and hepcidin levels by the Spearman correlation test (r=-0.259; p=0.043).Conclusion: There was a significant difference between the mean hemoglobin and hepcidin levels in the controlled T2DM group compared to uncontrolled T2DM group patients. A weak statistically significant negative correlation was found between hepcidin levels and anemia in T2DM patients.