Introduction: Thyrotoxicosis has been shown to cause deterioration of glucose levels in patients with DM 2 while return to euthyroidism results in better glycaemic control. Studies in normal subjects suggest that increased thyroid hormones may aggravate insulin resistance and decrease pancreatic secretion of insulin but the exact underlying mechanisms have not been completely elucidated. The purpose of this study was to investigate if this also occurs in subclinical hyperthyroidism as in the case of thyroxin suppression therapy in women with simple goiter.
Patients and methods: We prospectively studied 32 premenopausal women with simple goiter: 16 normal cycling women (Group A) and 16 women with polycystic ovary syndrome (PCOS) (Group B) matched for age and weight. We measured T3, T4, TSH, Insulin, C-peptide and glucose levels, before and 3 months after suppression treatment with thyroxin 2 μg /kg per day. For the assessment of insulin resistance HOMA-IR was calculated. Comparisons between groups were made with Wilcoxon matched pairs test.
Results: As expected, there was a significant increase in T4 and a significant decrease in TSH in both groups (P<0.0001). In Group A, glucose and C-peptide levels and HOMA-IR were significantly decreased after thyroxin therapy while insulin levels remained unchanged (glucose 94.4±3.0 vs 80.8±2.4 mg/dl P<0.004, C-peptide 2.92±0.27 vs 1.76±0.14 ng/dl, P<0.0004, HOMA-IR 4.1±0.27 vs 3.5±0.1, P<0.004). In Group B, only insulin levels and HOMA-IR were significantly reduced (insulin 20.1±10.6 vs 11.1±4.2 μIU/ml, P<0.02, HOMA-IR 4.8±1.2 vs 2.5±0.25, P<0.05) after thyroxin therapy. No significant change was noted in body weight as well in T3 levels during the study.
Conclusions: In contrast to primary hyperthyroidism, suppression thyroxin therapy in women with simple goiter as well as women with simple goiter and PCOS results in reduction of insulin resistance and better glucose tolerance.