Autoimmune Thyroiditis Attenuates Cardiometabolic Effects of Cabergoline in Young Women With Hyperprolactinemia

Abstract

AbstractBoth prolactin excess and autoimmune (Hashimoto) thyroiditis may predispose to the development of cardiometabolic disorders. The aim of this study was to investigate whether autoimmune thyroiditis determines cardiometabolic effects of cabergoline. The study population consisted of 2 groups of young women: 32 women with euthyroid Hashimoto thyroiditis (group A) and 32 individuals without thyroid disorders (group B). Both groups were matched for age, body mass index, blood pressure, and prolactin levels. Plasma prolactin, thyroid antibodies, glucose homeostasis markers, plasma lipids, circulating levels of uric acid, high‐sensitivity C‐reactive protein (hsCRP), fibrinogen and homocysteine, and the urinary albumin‐to‐creatinine ratio were assessed before and after 6 months of cabergoline treatment. All women completed the study. Both groups differed in thyroid antibody titers, insulin sensitivity, high‐density lipoprotein cholesterol, hsCRP, homocysteine, and the albumin‐to‐creatinine ratio. Although cabergoline treatment reduced prolactin levels, improved insulin sensitivity, decreased glycated hemoglobin, increased high‐density lipoprotein cholesterol, decreased hsCRP, and reduced the albumin‐to‐creatinine ratio in both treatment groups, these effects (except for glycated hemoglobin) were more pronounced in group B than in group A. Only in group B, the drug decreased triglycerides, uric acid, fibrinogen, and homocysteine. In group A, hsCRP levels correlated with both baseline thyroid antibody titers and with other cardiometabolic risk factors. The impact of cabergoline on cardiometabolic risk factors depended on the degree of reduction in prolactin levels, while in group A additionally correlated with the effect of treatment on hsCRP. The obtained results suggest that coexisting autoimmune thyroiditis attenuates cardiometabolic effects of cabergoline in young women with hyperprolactinemia.