Effects of levothyroxine treatment on insulin sensitivity, endothelial function and risk factors of atherosclerosis in hypothyroid women.

OBJECTIVES: Contradictory results are encountered in literature regarding the effects of hypothyroidism on the risk factors of atherosclerosis. We aimed to explore the changes in atherosclerotic risk factors and insulin sensitivity before and after levothyroxine replacement therapy in women with primary hypothyroidism and compare with that of healthy controls. PATIENTS AND METHODS: Twelve patients (mean age of 34±11.7years) without an evident disease except for primary hypothyroidism (TSH≥20mIU/L) and eleven euthyroid, age-matched (33.8±8.4years) female volunteers as controls were included. Baseline thyroid hormones, lipid parameters, homocysteine, fibrinogen levels were measured in both groups. Flow-mediated endothelial-dependent vasodilatation (FMD) method was used to evaluate endothelial dysfunction. Insulin sensitivity was assessed by M values based on euglycemic hyperinsulinemic clamp technique. The same measurements were performed after 6months of levothyroxine treatment and recovery of euthyroid state in hypothyroid patients. RESULTS: Treatment reduced total cholesterol (P<0.005), LDL-cholesterol (P<0.005), lipoprotein(a) (P<0.01), fibrinogen (P<0.0001) and homocysteine (P<0.0005) levels. Treatment significantly improved M values of hypothyroid patients (3.68±1.53mg/kg.min vs 6.02±1.21mg/kg.min, P<0.0001) and FMD (9.1±3.7% vs 16.4±4.4%, hypothyroid vs euthyroid, P<0.0001). Significant correlations were found between M values and TSH (r=-0.6, P<0.005), fibrinogen (r=-0.53, P<0.01) measurements, free T3 (r=0.51, P<0.02) and free T4 (r=0.49, P<0.02) levels. FMD was significantly correlated with fibrinogen levels (r=-0.49, P<0.05). CONCLUSION: Insulin resistance, endothelial dysfunction, atherosclerotic risk markers improves with treatment of hypothyroidism.

Somatostatin receptor 2 expression determined by immunohistochemistry in cold thyroid nodules exceeds that of hot thyroid nodules, papillary thyroid carcinoma, and Graves' disease.

BACKGROUND: There is a plethora of partly contradictory reports on somatostatin receptor (SSTR) expression in thyroid tumors. Therefore, our goal was to systematically determine SSTR2 expression in benign cold thyroid nodules (CNs), hot thyroid nodules (HNs), papillary carcinomas (PCs), and Graves' disease (GD) in comparison with intraindividual control tissues by means of immunohistochemistry. METHODS: Tissue sections from 19 HNs, 10 CNs, 17 PCs and their surrounding tissues, and 8 GD thyroids were immunostained for SSTR2. Membranous SSTR2 staining was quantitated by evaluating 10 high-power fields (HPFs) systematically distributed along the largest diameter of the tissue section. RESULTS: The area covered by thyroid epithelial cells in 10 HPFs expressed as median (in mm(2)) was 0.53 for CNs, 0.44 for HNs, 1.5 for PCs, 1.3 for GD, and 0.3 for the surrounding tissues. The SSTR2 staining density determined by dividing the area of SSTR2 positively stained thyroid epithelial cells (in mm(2)) by the area of all thyroid epithelial cells (in mm(2)) in 10 HPFs was 0.1662 for CNs, 0.0204 for HNs, 0.0369 for PCs, and 0.0386 for GD. CONCLUSIONS: SSTR2 expression is inhomogeneous in thyroid disease, with the highest density detected in CNs. It remains to be determined whether this finding could be of pathophysiologic or therapeutic relevance. The high SSTR2 density in CNs should be considered in the interpretation of SSTR scintigraphy-positive findings.