Abstract
Insulin-dependent diabetes mellitus (IDDM) is a frequent complication in patients with β-thalassaemia major. It is believed to be a consequence of the damage inflicted by iron overload to the pancreatic β-cell. Liver disorders and genetic influences seem to be additional predisposing factors to diabetes mellitus in patients with β-thalassaemia. Ethnic variations are frequently reported on prevalence and complications of diabetes mellitus in the β-thalassaemia patients. We investigated 50 Saudi children (<15 years) with β-thalassaemia major and 50 β-thalassaemia minor, and age- and sex-matched controls for the prevalence of diabetes mellitus, and its relation to hitherto claimed predisposing factors. Fasting blood glucose, plasma insulin level, liver function tests, plasma ferritin, iron, and transferrin were assessed in each patient and glucose tolerance was evaluated. Results in patients with β-thalassaemia major were compared with those obtained for β-thalassaemia minor and the controls. The results showed moderate elevation of ferritin level in the majority of the β-thalassaemia major despite desferroxamine therapy. Either hyperinsulinaemia or hypoinsulinaemia was encountered in the majority of these patients. The prevalence of diabetes mellitus was 6 per cent compared to 2 per cent in the β-thalassaemia minor and normal children. Impaired glucose tolerance (IGT) occurred at a significantly higher (24 per cent) frequency in the β-thalassaemia major compared to 2 and 0 per cent in the β-thalassaemia minor patients and normal controls, respectively. The prevalence of diabetes mellitus was significantly lower in the Saudi thalassaemic patients compared to the results obtained from patients of other ethnic groups reported in literature. Liver function abnormalities were more frequent in this group than in the β-thalassaemia minor and the controls. It appears from the inference of our results that combinations of factors including iron overload and liver damage, predispose the β-thalassaemia major patients to β-cell damage and, hence, to impaired glucose tolerance.