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Significance of cardiac and iron profile alteration in diabetic patients

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Abstract

Diabetes mellitus is a major health problem around the world. Iron overload is one of the causes of the disease and its complications. Iron is one of the elements which participate in the production of reactive oxygen species which causes oxidative stress and diabetic complications such as cardiac dysfunctions. The current study aims to access the cardiac and iron profile in type 2 diabetic patients. This study was conducted on 120 subjects. Subjects were divided into two main groups (80 diabetic patients and 40 healthy controls); diabetic subjects were subdivided into two subgroups (G-IIa and G-IIb) according to fasting blood glucose and glycosylated hemoglobin (HbA1c). Serum iron profile (iron, total iron binding capacity, and percentage transferrin saturation) is calculated as the index of iron. Lactate dehydrogenase (LDH), total creatine kinase (CK), and creatine kinase-MB (CK-MB) activities are measured as an index of cardiac functions. Also, fasting blood glucose and HbA1c were assayed. Diabetic patients were characterized by a significant elevation in the fasting blood glucose, HbA1c, cardiac enzyme activities, iron level, and percentage transferrin saturation as compared to normal healthy control, while diabetic patients showed a significant decrease in the total iron binding capacity as compared to normal healthy subjects. Our current study suggests that iron is one of the causative factors for diabetes and diabetic complications.

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Correspondence to Nabil A. Hasona.

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All participants provided informed consent for our study. Our study was carried out in accordance with the Helsinki Declaration, and institutional ethics committee approval was obtained from the College of Medicine, Hail University, KSA.

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The author declares that he has no conflict of interest.

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The author declares that he has received no funding for the research reported.

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Hasona, N.A. Significance of cardiac and iron profile alteration in diabetic patients. Comp Clin Pathol 26, 951–954 (2017). https://doi.org/10.1007/s00580-017-2470-y

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  • DOI: https://doi.org/10.1007/s00580-017-2470-y

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