Department of Internal Medicine and Clinical Pharmacology.
Department of Pediatrics in Bytom, School of Health Sciences in Katowice, Medical University of Silesia, Katowice, Poland.
Coron Artery Dis. 2021 Dec 1;32(8):706-712. doi: 10.1097/MCA.0000000000001031.
Hypothyroidism, hyperprolactinemia, macroprolactinemia and low vitamin D status were found to impair pleiotropic effects of hypolipidemic agents. The aim of the current study was to investigate whether cardiometabolic effects of atorvastatin in men are determined by endogenous testosterone.
We studied three groups of men matched for age, BMI, plasma lipids and blood pressure: 19 untreated subjects with low testosterone levels (group A), 19 normotestosteronemic men receiving testosterone preparations (group B) and 21 untreated men with testosterone levels within the reference range (group C). Because of coexistent hypercholesterolemia, all subjects were managed with atorvastatin (40 mg daily) for 6 months. Glucose homeostasis markers, plasma lipids, as well as circulating levels of testosterone, uric acid, high-sensitivity C-reactive protein (hsCRP), fibrinogen, homocysteine and 25-hydroxyvitamin D were determined at the beginning and at the end of the study.
At baseline, group A was more insulin-resistant and was characterized by higher levels of hsCRP, fibrinogen and homocysteine, and lower levels of 25-hydroxyvitamin D than the remaining groups of patients. Despite reducing total and low-density lipoprotein cholesterol and hsCRP levels in all treatment groups, this effect was stronger in groups B and C than in group A. In groups B and C, atorvastatin use was also associated with a decrease in uric acid, fibrinogen and homocysteine concentrations and with an increase in 25-hydroxyvitamin D levels. In group A, but not in the remaining groups, the drug decreased insulin sensitivity.
The obtained results suggest that untreated hypotestosteronemia may attenuate cardiometabolic effects of atorvastatin in men.
甲状腺功能减退症、高催乳素血症、巨泌乳素血症和维生素 D 状态低下会损害降脂药物的多效性。本研究旨在探讨阿托伐他汀在男性中的心脏代谢作用是否由内源性睾酮决定。
我们研究了三组年龄、BMI、血浆脂质和血压匹配的男性：19 名未接受治疗且睾酮水平较低的患者（A 组）、19 名接受睾酮制剂治疗的正常睾酮男性（B 组）和 21 名未接受治疗且睾酮水平在参考范围内的男性（C 组）。由于合并高胆固醇血症，所有患者均接受阿托伐他汀（40mg/日）治疗 6 个月。在研究开始和结束时，测定葡萄糖稳态标志物、血浆脂质以及睾酮、尿酸、高敏 C 反应蛋白（hsCRP）、纤维蛋白原、同型半胱氨酸和 25-羟维生素 D 的循环水平。
基线时，A 组胰岛素抵抗更严重，且 hsCRP、纤维蛋白原和同型半胱氨酸水平较高，25-羟维生素 D 水平较低，与其余两组患者相比。尽管所有治疗组均降低了总胆固醇和低密度脂蛋白胆固醇及 hsCRP 水平，但 B 组和 C 组的降低幅度强于 A 组。在 B 组和 C 组中，阿托伐他汀的使用还与尿酸、纤维蛋白原和同型半胱氨酸浓度降低以及 25-羟维生素 D 水平升高相关。但在 A 组而非其余两组中，药物降低了胰岛素敏感性。
研究结果表明，未治疗的低睾酮血症可能会减弱阿托伐他汀在男性中的心脏代谢作用。
