Different Effects of Atorvastatin on Cardiometabolic Risk Factors in Young Women With and Without Hyperprolactinemia

Abstract

Long-term prolactin excess is often accompanied by numerous metabolic complications. No previous study has compared the effect of statin therapy on circulating levels of cardiometabolic risk factors in patients with elevated and normal prolactin levels. The study population consisted of 3 age-, weight-, and lipid-matched groups of young women: 19 women with untreated hyperprolactinemia (group A), 20 normoprolactinemic women receiving bromocriptine treatment (because of previous hyperprolactinemia) (group B), and 20 untreated women with prolactin levels within the reference range (group C). Because of elevated total and low-density lipoprotein cholesterol levels, all women were then treated with atorvastatin (40 mg daily). Apart from measuring plasma lipids, glucose homeostasis markers, and hormone levels at the beginning of the study and 12 weeks later, we measured circulating levels of uric acid, high-sensitivity C-reactive protein, homocysteine, and fibrinogen. Despite similar baseline levels of plasma lipids, levels of uric acid, high-sensitivity C-reactive protein, homocysteine, and fibrinogen as well as the degree of insulin resistance were higher in group A than in the remaining 2 groups. Atorvastatin reduced total and low-density lipoprotein cholesterol levels in all study groups. However, only in normoprolactinemic women (groups B and C) did atorvastatin reduce circulating levels of nonlipid cardiometabolic risk factors, whereas only in group A did the drug slightly impair insulin sensitivity. The results of the study suggest that cardiometabolic effects of atorvastatin depend on the prolactin status of patients.

Cardiometabolic Risk Factors in Men with Elevated Macroprolactin Content: A Pilot Study

“…Unfavorable changes in cardiometabolic risk factors induced by prolactin excess were reversed by dopaminergic agents, particularly by cabergoline [21]. Finally, the impact of hypolipidemic agents on cardiometabolic risk factors did not differ between patients with monomeric hyperprolactinemia effectively treated with dopamine agonists and subjects in whom prolactin levels were within the reference range [19,20].…”

“…Monomeric hyperprolactinemia make subjects more susceptible to the development of insulin resistance, prediabetes, atherogenic dyslipidemia, weight gain, subclinical atherosclerosis and endothelial dysfunction [12][13][14][15][16][17][18]. Moreover, untreated monomeric hyperprolactinemia in dyslipidemic subjects exerted a negative impact on cardiometabolic effects of atorvastatin [19] and fenofibrate [20]. Unfavorable changes in cardiometabolic risk factors induced by prolactin excess were reversed by dopaminergic agents, particularly by cabergoline [21].…”

Cardiometabolic risk factors in young women with macroprolactinaemia

“…Dopamine agonists, the drugs of choice in the treatment of monomeric hyperprolactinaemia, reduced plasma levels of cardiometabolic risk factors [14]. Moreover, cardiometabolic effects of atorvastatin [15] and fenofibrate [16] depended on the prolactin status of patients, being much less pronounced (or even absent) in women with untreated hyperprolactinaemia than in women with bromocriptine-treated hyperprolactinaemia and drug-naïve women with normal prolactin levels. These results suggest that the presence of elevated levels of monomeric prolactin eliminates the beneficial effect of atorvastatin on plasma levels of cardiometabolic risk factors.…”

The impact of vitamin D status on cardiometabolic effects of fenofibrate in women with atherogenic dyslipidemia

“…These pleiotropic effects partially explain why fibrate treatment may bring cardiovascular benefits, which are observed mainly in subjects with atherogenic dyslipidaemia 4,5 . Unfortunately, some endocrine disorders may negatively affect extra‐lipid properties of hypolipidaemic agents 6‐11 . Previous studies showed that pleiotropic effects of fenofibrate were attenuated by thyroid hypofunction, 9 elevated levels of monomeric prolactin 10 and macroprolactinemia, 11 despite the fact that these studies included only patients with mild or moderate forms of these disorders (for ethical reasons subjects with overt hypothyroidism and severe prolactin excess were excluded).…”