Abstract

Introduction: Thyroid hormones modulate the lipoprotein and glucose metabolisms. In hyperthyroidism, insulin resistance is a frequent finding. The aim of our study was to assess the interrelationships between thyroid function, autoimmunity, lipid profile, glucose metabolism and other cardiovascular risk factors in patients with Graves’ disease. Material & Methods: We recorded free T3, free T4, TSH, TSH receptor antibodies, parameters of the lipid profile, glucose metabolism (including insulin resistance markers like homeostasis model assessment for insulin resistance - HOMA-IR), C reactive protein and homocysteine in 126 patients with Graves’ disease in the first cycle of treatment with methimazole (92.9% females, mean age 44.9 ± 15.2 years). Patients were divided in subgroups according to: TSH receptor antibodies [positive (n = 57) or negative (n = 69)] and thyroid function [euthyroidism (n = 74), subclinical (n = 29) or clinical hyperthyroidism (n = 22)]. Spearman correlations, t-tests and Mann-Whitney tests were performed for statistical analysis. Results: Comparing the positive and negative TSH receptor antibodies groups, significantly lower apolipoprotein B (80.3 ± 23.9 vs 89.7 ± 23.8 mg/dL; p = 0.047) and TSH [0.180 (0.002-1.080) vs 1.020 (0.235-2.055) μUI/mL; p < 0.001] were found in the positive TSH receptor antibodies group. Comparing with the normal thyroid function group, patients in the clinical hyperthyroid group presented significantly lower apolipoprotein B (70.9 ± 25.8 vs 89.8 ± 24.0 mg/dL; p = 0.007] and higher fasting glucose (96.0 ± 24.4 vs 86.4 ± 10.0 mg/dL; p = 0.019), insulin [10.4 (6.2-15.8) vs 7.5 (4.8-9.7) μUI/mL; p = 0.021], HOMA-IR [2.09 (1.29-4.53) vs 1.55 (0.96-2.13); p = 0.023] and C reactive protein [0.57 (0.20-0.93) vs 0.20 (0.07-0.38) mg/L; p = 0.005]. No significant differences were found between the subclinical hyperthyroid and the normal groups. There was a negative correlation between TSH and the TSH receptor antibodies (r = -0.386; p < 0.001). Apolipoprotein B was positively correlated with TSH (r = 0.236; p = 0.016), and negatively with the TSH receptor antibodies (r = -0.211; p = 0.030). Both free T3 and free T4 were positively correlated with fasting insulin (r = 0.268; p = 0.008 and r = 0.226; p = 0.025, respectively) and HOMA-IR (r = 0.258; p = 0.010 and r = 0.259; p = 0.010, respectively). Free T4 was also positively correlated with fasting glucose (r = 0.269; p = 0.008). Conclusion: In patients with Graves’ disease, the interrelationships between thyroid function, autoimmunity, insulin resistance and lipid profile may contribute to the increased cardiovascular risk. The lipid profile suggests a hypolipidemic effect.

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