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article · Suez Canal University Medical Journal

Correlation between Iron Overload and Glycemic Abnormalities among Thalassemia Patients Attending Suez Canal University Hematology Outpatient - Clinic

2024Open accessSuez Canal University

Abstract

Background: Thalassemia is one of the commonest hemoglobinopathies in the world. Frequent blood transfusions are recommended for transfusion-dependent thalassemia. The human body lacks a physiological mechanism to eliminate excess iron load following a blood transfusion. Excess iron accumulates particularly in the liver, heart, and endocrine organs. Diabetes mellitus is one of the endocrine complications. Three main processes—insulin resistance, insulin insufficiency, and hepatic dysfunction—are thought to be involved in its development. Aim: early detection of glycemic abnormalities in patients with thalassemia to prevent its complications and start early and proper management. Subjects and Methods: This was an analytical cross-sectional study conducted over 67 patients attending the hematology outpatient clinic of Suez Canal University Hospital, Ismailia, Egypt, in the period between March 1 and June 10, 2022. Additionally, the patients included were all thalassemic patients of both sexes aged more than 12 years old with exclusion of type 1 Diabetes Mellitus patients and chronic liver disease patients. Results: Our study demonstrated that 19.4% were diabetic and 35.8% were prediabetic among thalassemia patients according to fasting glucose. On the other hand, regarding assessment of insulin resistance using homeostatic model assessment (HOMA-IR), 3 % of our study sample was within the border line range and 14.9% has HOMA IR more than 2. Conclusion: Our study concluded that iron overload is considered a risk factor for developing glycemic abnormalities in thalassemia patients which is most probably caused by inadequate chelation that led to hemosiderosis of the pancreas and other organs

Research topics

  • Hemoglobinopathies and Related Disorders
  • Iron Metabolism and Disorders
  • Erythrocyte Function and Pathophysiology

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DOI: 10.21608/scumj.2024.436571

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