Risk factors for accelerated atherosclerosis in young women with hyperprolactinemia.

Prolactin is a metabolic hormone. The hypothesis is that hyperprolactinemia can cause metabolic and inflammatory changes which are associated with accelerated atherosclerotic process, but the treatment of hyperprolactinemia with dopamine agonists, leads to reversibility of these processes. The first aim of this study was to determine whether hyperprolactinemia in premenopausal women is accompanied with the increase in body mass index (BMI), changes in body composition, lipid disturbances, the presence of inflammation and changes in systolic and diastolic blood pressure as risk factors for the development of early atherosclerosis. The second aim was to know whether the therapy of hyperprolactinemia and prolactin normalization lead to improvement of the observed parameters. Twenty female patients with prolactinomas, before and during treatment with dopamine agonists and 16 healthy controls were evaluated. Prolactin, BMI, total body fat, free fat mass, total body water, total cholesterol, triglycerides, high density lipoprotein (HDL), low density lipoprotein (LDL) and fibrinogen as well as systolic and diastolic blood pressure were measured at baseline and during the therapy. Hyperprolactinemic patients had pathologic and significantly higher levels of prolactin (PRL) than the controls (p=0.000). The BMI, body fat, total body water (TBW), total cholesterol, triglycerides, LDL were in normal range and higher in the patients than in the controls. HDL was lower in hyperprolactinemic females than controls. The difference was significant only for body fat (fat % p=0.006; fat kg p=0.009). Fibrinogen was slightly increased in patients compared with the controls. Hyperprolactinemic patients had normal, but increased levels of systolic and diastolic blood pressure compared with the controls. The difference with border significance was found in diastolic blood pressure (p=0.065). The correlation of PRL with all the observed parameters was positive apart from HDL, but relatively significant only with diastolic blood pressure (r=0.31). The therapy with dopamine agonists caused the decrease of all the observed parameters, but significant decreases was achieved only in BMI (p=0.028), total cholesterol levels (p<0.001) and LDL (p<0.002). Changes in BMI, body composition, serum lipids and lipoproteins, fibrinogen level and blood pressure confirm our hypothesis about the possible role of hyperprolactinemia in developing adverse metabolic disturbances which are reversible after treatment.

[Disturbances of lipid and lipoprotein metabolism in hypeprolactinemia and acromegaly].

The synthesis and metabolism of lipids and lipoproteins are regulated by a number of hormones, among which are prolactine and growth hormone. The levels of triglycerides, total cholesterol and LDL, although within normal range, were higher in hypeprolactinemia than after the therapy with dopamine agonists in hypeprolactinemic females. This is confirmed by the results of our research and other studies. The changes of total, LDL and non HDL-cholesterol were significant. No significant differences in the level of HDL-cholesterol was confirmed. The mechanisms of the onset of this disturbance has not yet been explained. Recent studies suggest that prolactin has not only the indirect, but also the direct impact on metabolism of lipids and lipoproteins. Acromegaly is also associated with a higher prevalence of a disbalanced metabolism of lipids and lipoproteins. The hypersecretion of GH is often associated with hypertriglyceridaemia. The levels of total cholesterol and HDL cholesterol were normal, higher or lower in these studies. The LDL cholesterol showed higher levels. The level of lipoprotein (a), apoprotein (A, E) were higher in 30% of the patients with acromegaly. The hypersecretion of GH and PRL can increase cardiovascular risk due to their association with disturbances of lipid metabolism.