ECE2009 Poster Presentations Diabetes and Cardiovascular (103 abstracts)
Background & aims: Impaired glucose tolerance and diabetes as well as cardiac dysfunction are known complications in homozygous beta-thalassemic transfused patients due to iron overload. We aimed to study pancreatic alpha and beta-cell function in regularly transfused patients with homozygous beta-thalassemia and to investigate if cardiac dysfunction may correlate with the development of impaired glucose metabolism.
Methods: An oral glucose tolerance test (OGTT) with 75 g was performed in 38 beta-thalassemic patients (1745 years old), 28 with normal and 10 with impaired fasting glucose. All patients were receiving two blood units every 1520 days and were on iron chelation therapy. Glucose, insulin, C-peptide and glucagon plasma levels were assayed every thirty minutes up to 2 h. Patients were divided according to the American Diabetes Association criteria into those with diabetes mellitus, impaired glucose tolerance and those with normal glucose tolerance. A division concerning cardiac dysfunction was also made according to Doppler Echocardiograph and myocardium MRI results.
Results: Diabetes mellitus was diagnosed in eight patients, and impaired glucose tolerance was observed in ten patients, giving a prevalence of total impaired glucose metabolism of 47.3% in our patient population. After OGTT, the area under insulin plasma concentrations versus time curve (AUC02 hInsulin) was lower for patients with impaired glucose metabolism compared to those with normoglycaemia (3936 (μIU/ml) min versus 6549 (μIU/ml) min, P<0.01). Similarly, AUC02 hInsulin was lower in patients with cardiac dysfunction compared to those with normal cardiac function (3079 (μIU/ml) min versus 6189 (μIU/ml) min, P<0.05). The area under the curve for glucagon after OGTT was similar in normoglycemic and hyperglycemic patients.
Conclusions: The significant decrease of AUC02 hInsulin in thalassemic patients with impaired glucose metabolism is consistent with pancreatic beta-cell failure while alpha-cell function does not seem to be influenced. In thalassemic patients with normal fasting glucose, cardiac dysfunction may be a prognostic factor for impaired glucose metabolism.