Alicja Filus

Serum leptin concentrations in pre- and postmenopausal women on sex hormone therapy

Aim. The aim of the present study was to investigate the influence of endogenous estradiol and estrogen and estrogen–progestin therapies on concentration in pre- and postmenopausal women. Materials and methods. The study groups consisted of 26 women with surgical menopause (mean±standard deviation (SD): age 51.8±2.6 years, body mass index (BMI) 26.45±4.56 kg/m2), 54 with natural menopause (mean±SD: age 50.5±3.0 years, BMI 25.75±4.09 kg/m2) and 40 premenopausal controls (mean±SD: age 48.3±2.3 years, BMI 26.23±4.12 kg/m2). The group with surgical menopause received estradiol transdermally (50 μg/day) and those with natural menopause received additionally medroxyprogesterone acetate (5 mg/day) for the last 12 days of the cycle. Before and after 4 months of therapy, body weight, waist and hip circumferences and blood pressure were measured, and BMI and waist-to-hip ratio (WHR) were calculated. Serum leptin, follicle-stimulating hormone (FSH), estradiol (E2), testosterone, prolactin and dehydroepiandrosterone sulfate (DHEAS) were measured prior to and after treatment. Results. Leptin concentrations did not differ statistically among the groups. No correlations between leptin and E2, FSH, prolactin, testosterone and DHEAS concentrations were found in any of the groups before and after treatment. Leptin level correlated positively with body mass, BMI and hip and waist circumferences in all groups. There were no correlations between leptin and WHR in the pre- and postmenopausal groups. In the premenopausal group and in some postmenopausal groups, serum leptin level correlated with blood pressure. Conclusions. Endogenous E2 and androgens in premenopausal women and estrogen and estrogen–progestin therapies in postmenopausal subjects do not influence serum leptin concentrations. Leptin level is related to body mass and BMI, but not to sex hormone status. The distribution of adipose tissue and the type of obesity (android or gynoid) have no influence on serum leptin concentration. The correlation between serum leptin level and blood pressure requires further investigation.

Gonadotroph adenoma causing ovarian hyperstimulation syndrome in a premenopausal woman

ABSTRACT Introduction: Gonadotroph adenomas occur commonly in middle-aged adults without any specific endocrinological symptoms. To date, only 30 cases of gonadotropinoma causing ovarian hyperstimulation syndrome in pre-menopausal women have been reported. Case report: A 37-year old woman with pituitary macroadenoma and hyperprolactinaemia was admitted to the Department of Endocrinology, Diabetology and Isotope Therapy. She presented with recurrent ovarian cysts, menstrual disturbances, headaches, visual impairment and galactorrhea. Her endocrine profile showed normal values of FSH, elevated concentrations of estradiol and suppressed LH levels. Transsphenoidal resection of the tumor tissue resulted in normalization of the hormone values and improvement in the clinical picture. Conclusions: Gonadotroph adenomas should be considered in the differential diagnosis in premenopausal women with OHSS. Chinese abstract 引言：促性腺激素腺瘤常见于中年人且没有任何特殊的内分泌相关症状。目前为止，也只有30例绝经前妇女促性腺激素腺瘤引起卵巢过度刺激综合征的报道。 个案报道：一名37岁妇女因垂体大腺瘤和高泌乳素血症到妇科内分泌、糖尿病及同位素门诊就诊。她叙述自己所患的卵巢囊肿已复发，同时还有月经紊乱、头痛、视力减退和溢乳的症状。其性激素检查显示FSH水平正常、雌激素浓度升高、LH水平降低。经蝶骨切除垂体腺瘤术后激素水平恢复正常，同时临床症状也得到改善。 结论：绝经前妇女发生卵巢过度刺激综合征时应考虑与促性腺激素腺瘤相鉴别。

Androgen receptor polymorphism and platelet reactivity in healthy men

There is established evidence of gender differences in the prevalence and severity of vascular thrombosis and mortality, with men having onset of coronary artery disease earlier in the life thanwomen, andwith first symptoms more often being myocardial infarction [1]. The impact of sex hormones on gender differences in platelet activity (one of the main factors in atherothrombosis) is also being increasingly recognized [2]. One of the “culprit” hormoneswhich could play a role in that setting is testosterone, which seems to have an influence on platelet activity, although the available data are conflicting. Some experimental studies show that in castrated rats given testosterone to physiological levels, enhanced platelet aggregation present after castration [3,4] and atherosclerotic plaque growth are inhibited [5]. Testosterone deprivation can also be harmful in men with prostate cancer treated with anti-androgenic therapy [6]. By contrast, in another study, exogenously administered testosterone up-regulated the population of thromboxane A2 (TXA2) receptors onplatelets in healthy youngmale volunteers, and this was concomitant with an enhanced aggregation response to TXA2mimetic I-BOP [7]. In yet another study, the reduction in circulating testosterone concentration following castration was associated with a significant reduction in platelet TXA2 receptor density and maximum aggregation response to TXA2-mimetic I-BOP[8]. Available data therefore suggest that testosterone influences platelet aggregation through increasing or decreasing TXA2 receptor density on the platelet surface. The mechanism for this action is largely obscure. A recent study has suggested the presence of androgen receptors (ARs) within platelets. In this study ADP-induced platelet aggregation was associated with platelet cytosolic binding to radiolabeled testosterone [9]. What is more, humanmegakaryocytes generated ex vivo expressed RNA for AR, confirmed by Western immunoblotting to be present in humanplatelets in another study [10]. These in vitro effects of testosteroneonplatelet aggregation suggestnon-genomic actionsonplatelets, or the presence of functional AR within platelets, which modulate the response to TXA2-induced platelet aggregation [10]. One possible pathway could involve testosterone linking to ARs in platelet cytosol, which in turn up-load TXA2 receptors onto the platelet surface, enhancing aggregation induced by I-BOP (TXA2-receptor agonist). The strength of the testosterone action in vivo is dependent on testosterone level and AR density and structure. ARs are expressed in vascular endothelium, in smooth muscle cells, and presumably within platelets.Genetically, theyareencodedonchromosomeX(locusq11–12). The polyglutaminic sequence coding region is the mostly polymorphic one in that gene and accounts for the transcript activity of the final product. It consists of a periodically repeating nucleotide triplet, the socalled CAG (cytosine, adenine, guanine) repeats [11]. Genetic variations of the AR gene – principally fewer CAG repeats in the amino-terminal domain – has been associated with higher testosterone levels in women

Treatment with statins and testosterone levels in men

INTRODUCTION Statins belong to the most commonly used medicines worldwide. They affect cholesterol synthesis and thus they may suppress steroidogenesis. Our aim was to evaluate whether the use of statins is associated with the concentration of sex hormones.Material and methods/Results: In a population sample of men (n = 237) we found that subjects receiving statins had significantly lower concentrations of: total testosterone (14.9 vs. 16.35 nmol/L, p = 0.008 after correction for body mass), free testosterone (32 vs. 39 pmol/L, p = 0.004), calculated free testosterone (0.32 vs. 0.36 nmol/L, p < 0.001) and bioavailable testosterone (6.10 vs. 7.56 nmol/L, p < 0.001) than age-matched controls. CONCLUSIONS We conclude that the use of statins may have an impact on the diagnosis of age-related testosterone deficiency in men.