Endocrine Abstracts (2006) 11 P401

The effect of hyperthyroidia on glycemic control in patients with diabetes mellitus

S Fica1, C Barbu1, A Lazar2, M Grigorescu2, A Albu2 & R Bunghez2


1Endocrinology, Carol Davila University, Bucharest, Romania; 2Endocrinology and Metabolism Department, Elias Hospital, Bucharest, Romania.


The aim of the study was to evaluate the effects of hyperthyroidia on glycemic control in patients with diabetes mellitus.

Research design and methods: We retrospectively evaluated the patients with diabetes and hyperthyroidism. We analysed clinical data, thyroid ultrasound exploration, laboratory analyses (glycosylated hemoglobin, free thyroxin FT4, triiodothyronine T3, thyroid stimulating hormone TSH).

Results: We evaluated 48 patients (42 women/ 6 men), mean age was 55.7±15.3 years and duration of diabetes 8.8±7.9 years; 24 patients with Graves diseases (50%), 14 with toxic multinodular goiter (29%), 7 with autonomous hyperfunctioning adenoma (14.5%), and 3 with amiodarona induced hyperthyroidism (6.5%). The treatment used for diabetes: insulin 30 (62.5%) patients, antidiabetic oral agents 11 (23%), diet 7 patients (14.5%). In the context of hyperthyroidism mean value of glycosylated hemoglobin was 9.4%±2.2% (poor glycemic control) versus 7.1%±1.6% after the treatment of hyperthyroidism. Among insulin-treated patients, the average needs of insulin in the context of hyperthyroidism was 0.72 u/kg versus 0.55 u/kg in the context of stable thyroid function (P<0.01). We found a significant association between type 1 diabetes mellitus and Graves disease compared to toxic multinodular goiter (80% vs 50%, P<0.01)

Conclusions: The presence of hyperthyroidism aggravates glycemic control of the patients with diabetes and increases insulin need in insulin-treated patients. Once the thyroid function was stable, the insulin need decreased significantly (P<0.01). Hypethyroidism must be treated radical to obtain a good glycemic control. Type 1 diabetes is significant associated to Graves disease by autoimmune mechanism.

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