Androgen Levels In Patients Research Articles

Galanin-Like Peptide and its' Correlation With Androgen Levels in Patients with Polycystic Ovary Syndrome

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Galanin-like peptide and its correlation with androgen levels in patients with polycystic ovary syndrome.

We aimed to investigate serum galanin-like peptide (GALP) levels and their correlation with hormonal and metabolic parameters in patients with polycystic ovary syndrome (PCOS). The study included 48 women (age range, 18-44 years) with a diagnosis of PCOS, and a control group that included 40 healthy females (age range, 18-46 years). Waist circumference, body mass index (BMI), and Ferriman-Gallwey score were evaluated and plasma glucose, lipid profile, oestradiol, progesterone, total testosterone, prolactin, insulin, dehydroepiandrosterone sulphate (DHEA-S), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), 25-hydroxyvitamin D (25(OH)D), fibrinogen, d-dimer, C-reactive protein (CRP), and GALP levels were measured in all study subjects. Waist circumference (p = 0.044) and Ferriman-Gallwey score (p = 0.002) were significantly higher in patients with PCOS compared to the control group. Among the metabolic and hormonal parameters studied, only total testosterone was significantly higher in patients with PCOS (p = 0.002). Also, the serum 25(OH)D level was significantly lower in the PCOS group (p = 0.001). CRP, fibrinogen, and D-dimer levels were all similar between the 2 groups. Serum GALP level was significantly higher in PCOS patients (p = 0.001). GALP was negatively correlated with 25(OH)D (r = -0.401, p = 0.002) and positively correlated with total testosterone values (r = 0.265, p = 0.024). Multiple regression analysis revealed that both total testosterone and 25(OH)D significantly contributed to GALP levels. Our study is the first in the literature to evaluate serum GALP levels in patients with PCOS. Increased GALP levels in PCOS and its association with total testosterone levels might show that GALP can act as an intermediary in increased GnRH-mediated LH release, which is one of the underlying pathogenetic mechanism of PCOS.

Polikistik Over Sendromu Olan Adölesanlarda Hipoksiyle İndüklenen Faktör (HIF) 1-Alfanın Değerlendirilmesi ve Önemi

It was aimed at investigating the place of serum hypoxia inducible factor (HIF)-1 alpha level in the diagnosis of adolescent polycystic ovary syndrome (PCOS), its clinical significance and whether or not it can be used as a biomarker. 30 patients with PCOS and 30 healthy adolescent and young adult women with ages ranging between 15 and 22 were recruited in a grade III Women’s Health Education and Research Hospital. A general physical examination, pelvic examination and ultrasonographic evaluation was carried out on each patient. Serum fasting glucose and insulin levels, lipid profile, HIF-1 alpha levels were recorded as the main parameters of patients. No statistically significant differences were found in serum HIF-1 alpha levels between groups. While the mean HIF-1 alpha levels in PCOS patients was higher as compared to the healthy population, this difference was not statistically significant. Waist/hip circumference ratio, serum LH level, LH/FSH ratio and serum androgen levels in patients with PCOS were significantly higher as compared to control cases. The small number of patients included in the study and the age range covering the adolescence, which is the period that PCOS symptoms and findings have not become clear yet constitute the limitations of our study, and it is possible that they have affected out study results. Place of HIF-1 alpha level in the diagnosis of PCOS must be supported with studies including larger patient groups.

Differences in the spectrum of steroidogenic enzyme inhibition between Osilodrostat and Metyrapone in ACTH-dependent Cushing syndrome patients.

Osilodrostat is a new 11β-hydroxylase inhibitor with a mode of action analogous to Metyrapone. The objective of this study was to compare steroidogenic profiles in patients treated with either Osilodrostat or Metyrapone for adrenocorticotrophic hormone (ACTH)-dependent Cushing's syndrome (CS). Patients followed up at Cochin hospital Endocrinology department between March 2019 and December 2021 for an ACTH-dependent CS, controlled by either Osilodrostat or Metyrapone, were included. A serum profile of five steroids (cortisol, 11-deoxycortisol, 17-hydroxyprogesterone, androstenedione and testosterone) was determined using UPLC- tandem mass spectrometry (UPLC-MS/MS). Nineteen patients treated with Osilodrostat, eight patients treated with Metyrapone and six patients treated with consecutive Metyrapone then Osilodrostat were included. Hypocortisolism (basal cortisol <100 nmol/L) was found in 48% of patients treated with Osilodrostat and 7% of patients treated with Metyrapone. 11-deoxycortisol and androstenedione levels were higher in patients treated with Metyrapone (80.9 (2.2-688.4) and 14.9 (2.5-54.3) nmol/L, respectively) than in patients treated with Osilodrostat (10.3 (0.5-71.9) and 4.0 (0.3-13.3) nmol/L) (P = 0.0009 and P = 0.0005). Testosterone level in women was also higher in Metyrapone group (3.3 (0.93-4.82) nmol/L vs 1.31(0.13-5.09) nmol/L, P = 0.0146). CYP11B1 activity (11-deoxycortisol/cortisol) was not significantly different between the two groups. CYP21A2 activity (17OHprogesterone/11-deoxycortisol) and CYP17A1 activity (17OHprogesterone/androstenedione) were significantly decreased in Osilodrostat group (P < 0.0001). In patients with ACTH-dependent CS, the use of CYP11B1 inhibitors in routine care suggests that Osilodrostat has a less specific effect on the inhibition of steroidogenic enzymes than Metyrapone. This might explain a smaller increase in 11-deoxycortisol and androgen levels in patients treated with Osilodrostat.

The association between triglycerides/high-density lipoprotein cholesterol ratio, insulin resistance, and serum androgen levels in patients with polycystic ovary syndrome

Objectives: Insulin resistance and dyslipidemia are common comorbidities of polycystic ovary syndrome. We aim to evaluate the association between triglycerides/high-density lipoprotein cholesterol ratio, insulin resistance, and serum androgen levels in patients with polycystic ovary syndrome. Methods: We enrolled a total of 40 polycystic ovary syndrome patients and 20 healthy control subjects in this cross-sectional study. The polycystic ovary syndrome patients were divided into two subgroups obese and non-obese. The triglycerides/high-density lipoprotein cholesterol ratio and homeostatic model assessment of insulin resistance were calculated for all individuals. Demographic characteristics, serum levels of metabolic parameters, and androgens were compared between the study subgroups. P-value &amp;lt; 0.05 was accepted as statistically significant. Results: The triglycerides/high-density lipoprotein cholesterol ratio was higher in obese polycystic ovary syndrome patients than in other groups (3.64 ± 3.06 vs. 1.07 ± 0.36 in control and 1.18 ± 0.53 in non-obese group, p &amp;lt; 0.005). The triglycerides/high-density lipoprotein cholesterol ratio was positively correlated with homeostatic model assessment of insulin resistance (r=0.546, p &amp;lt; 0.001), total testosterone (r=0.402, p = 0.010), and free androgen index (r=0.609, p &amp;lt; 0.001) while was negatively correlated with sex hormone-binding globulin (r=-0.497, p = 0.001). Obese polycystic ovary syndrome patients had higher serum total testosterone levels, higher free androgen index, and lower sex hormone-binding globulin than non-obese polycystic ovary syndrome patients (0.71 ± 0.49 ng/mL vs. 0.45 ± 0.16 ng/mL, p = 0.006; 3.1 ± 1.91 vs. 1.01 ± 0.49, p &amp;lt; 0.005; and 26 ± 10.3 nmol/L vs. 59.6 ± 43.7 nmol/L, p &amp;lt; 0.005, respectively). Obese polycystic ovary syndrome patients had also worse lipid parameters, including high triglycerides and low high-density cholesterol when compared with other groups. Conclusions: The triglycerides/high-density lipoprotein cholesterol ratio was correlated with the homeostatic model assessment of insulin resistance, and androgenic hormonal profiles including total testosterone and free androgen index in patients with polycystic ovary syndrome.

Differential activity of the corticosteroidogenic enzymes in normal cycling women and women with polycystic ovary syndrome.

The phenotypic complex of patients with definitive diagnosis of polycystic ovary syndrome may include patients with normal and high serum androgen levels. Patients with hyperandrogenemia seem to present higher risk of changes to the glucose and lipid metabolism and, eventually, of earlier development of cardiovascular diseases than normoandrogenemic patients or healthy women. From a laboratory and clinical point of view, it is important to check androgen levels in patients with polycystic ovary syndrome. The identification of partial insufficiency of a given corticosteroidogenic enzyme is also relevant to understand the physiopathology of androgen increase in polycystic ovary syndrome. Therefore, the present review analyzes the functions of the different enzymes involved in the ovary and adrenal steroidogenesis in normal cycling women and in patients with polycystic ovary syndrome. In addition, it emphasizes appropriate reason for investigating eventual enzyme deficiency to provide rationale for prescription and follow-up of women with polycystic ovary syndrome.

Baicalin inhibits recruitment of GATA1 to the HSD3B2 promoter and reverses hyperandrogenism of PCOS.

High androgen levels in patients suffering from polycystic ovary syndrome (PCOS) can be effectively reversed if the herb Scutellaria baicalensis is included in traditional Chinese medicine prescriptions. To characterize the effects of baicalin, extracted from S. baicalensis, on androgen biosynthesis in NCI-H295R cells and on hyperandrogenism in PCOS model rats and to elucidate the underlying mechanisms. The optimum concentration and intervention time for baicalin treatment of NCI-H295R cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and enzyme-linked immunosorbent assays. The functional genes affected by baicalin were studied by gene expression profiling (GEP), and the key genes were identified using a dual luciferase assay, RNA interference technique, and genetic mutations. Besides, hyperandrogenic PCOS model rats were induced and confirmed before and after baicalin intervention. As a result, Baicalin decreased the testosterone concentrations in a dose-and time-dependent manner in NCI-H295R cells. GEP revealed that 3β-hydroxysteroid dehydrogenase type II (HSD3B2) was the key enzyme of androgen biosynthesis, and baicalin inhibited the expression of HSD3B2 by regulating the binding of transcription factor GATA-binding factor 1 (GATA1) to the HSD3B2 promoter. Hyperandrogenic PCOS model rats treated with baicalin significantly reversed the high androgen levels of serum and the abnormal ovarian status, restored the estrous cyclicity, and decreased the expression of HSD3B2 in ovarian. In summary , our data revealed that GATA1 is an important transcription factor activating the HSD3B2 promoter in steroidogenesis, and baicalin potentially be an effective therapeutic agent for hyperandrogenism in PCOS by inhibiting the recruitment of GATA1 to the HSD3B2 promoter in ovarian tissue.

Aggressiveness of Localized Prostate Cancer: the Key Value of Testosterone Deficiency Evaluated by Both Total and Bioavailable Testosterone: AndroCan Study Results.

Failure rates after first-line treatment of localized prostate cancer (PCa) treatment remain high. Improvements to patient selection and identification of at-risk patients are central to reducing mortality. We aimed to determine if cancer aggressiveness correlates with androgen levels in patients undergoing radical prostatectomy for localized PCa. We performed a prospective, multicenter cohort study between June 2013 and June 2016, involving men with localized PCa scheduled to undergo radical prostatectomy. Clinical and hormonal patient data (testosterone deficiency, defined by total testosterone (TT) levels < 300ng/dL and/or bioavailable testosterone (BT) levels < 80ng/dL) were prospectively collected, along with pathological assessment of preoperative biopsy and subsequent radical prostatectomy specimens, using predominant Gleason pattern (prdGP) 3/4 grading. Of 1343 patients analyzed, 912 (68%) had prdGP3 PCa and 431 (32%) had high-grade (prdGP4, i.e., ISUP ≥ 3) disease on prostatectomy specimens. Only moderate concordance in prdGP scores between prostate biopsies and prostatectomy specimens was found. Compared with patients with prdGP3 tumors (i.e., ISUP ≤ 2), significantly more patients with prdGP4 cancers had demonstrable hypogonadism, characterized either by BT levels (17.4% vs. 10.7%, p < 0.001) or TT levels (14.2% vs. 9.7%, p = 0.020). BT levels were also lower in patients with prdGP4 tumors compared to those with prdGP3 disease. Testosterone deficiency (defined by TT and/or BT levels) was independently associated with higher PCa aggressiveness. BT is a predictive factor for prdGP4 disease, and evaluating both TT and BT to define hypogonadism is valuable in preoperative assessment of PCa (AndroCan Trial: NCT02235142).

A gonadotropin-releasing hormone antagonist reduces serum adrenal androgen levels in prostate cancer patients

BackgroundAdrenal androgens play an important role in the development of castration-resistant prostate cancer therapeutics. The effect of gonadotropin-releasing hormone (GnRH) antagonists on adrenal androgens has not been studied sufficiently. We measured testicular and adrenal androgen levels in patients treated with a GnRH antagonist.MethodsThis study included 47 patients with histologically proven prostate cancer. All of the patients were treated with the GnRH antagonist degarelix. The mean patient age was 73.6 years. Pre-treatment blood samples were collected from all of the patients, and post-treatment samples were taken at 1, 3, 6, and 12 months after starting treatment. Testosterone (T), dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), 17β-estradiol (E2), and androstenedione (A-dione) were measured by liquid chromatography-mass spectrometry. Dehydroepiandrosterone-sulfate (DHEA-S), luteinizing hormone, and follicle-stimulating hormone levels were measured by electro-chemiluminescence immunoassays.ResultsA significant reduction in T level (97.3% reduction) was observed in the patients 1 month after initiating treatment. In addition, levels of DHT, E2, DHEA-S, and A-dione decreased 1 month after initiating treatment (93.3, 84.9, 16.8, and 35.9% reduction, respectively). T, DHT, E2, DHEA-S, and A-dione levels remained significantly suppressed (97.1, 94.6, 85.3, 23.9, and 40.5% reduction, respectively) 12 months after initiating treatment. A significant decrease in DHEA level (15.4% reduction) was observed 12 months after initiating treatment.ConclusionsSerum adrenal androgen levels decreased significantly in patients treated with a GnRH antagonist. Thus, long-term GnRH antagonist treatment may reduce serum adrenal androgen levels.

Effects of a hyperandrogenaemic state on the proliferation and decidualization potential in human endometrial stromal cells

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women, involving hyperandrogenaemia and insulin resistance. Treatment options include dexamethasone, as well as the off-label use of metformin. To evaluate the impact of those drugs on cyclic changes in endometrial development, we tested possible effects of metformin and dexamethasone on endometrial stromal cells decidualisation, proliferation, and gene regulation in a hyperandrogenaemic microenvironment in vitro. Ten endometrial biopsies (of which five were decidualized in vitro) were used from regularly cycling women. Cells were treated with testosterone, dexamethasone, and metformin in different concentrations. Thereafter, cells were assessed for proliferation and decidualization capacity, as well as mTor and MMP-2 gene regulation. Metformin showed a dose-dependent negative effect on prolactin secretion, a known decidualization marker. This effect was stronger in a hyperandrogenaemic condition and could not be compensated by dexamethasone. Testosterone had a dose dependent negative effect on proliferation in decidualized endometrial stromal cells. Dexamethasone slightly compensated the negative proliferative effect only in low-dose testosterone. High-dose metformin also showed a dose-dependent reduction in endometrial stromal cell proliferation without a major impact by testosterone or dexamethasone in decidualized and non-decidualized cells. High-dose metformin significantly reduced the expression of matrix metalloproteinase-2 (MMP-2) and mechanistic Target of Rapamycin (mTor), regardless of the concentration of dexamethasone and testosterone. The strongest effect could be observed for the combination with high-dose dexamethasone. When therapies, such as metformin and dexamethasone, are used to normalize peripheral androgen levels in patients with PCOS, their effect on the endometrial microenvironment should be taken into consideration as well, especially metformin has to be used with caution because of its dose dependent, possibly inhibiting effect at the endometrial proliferation.

Features of the hormonal status in patients with temporomandibular joint dysfunction and class II malocclusion

The article presents data on androgen levels in female patients with temporomandibular joint (TMJ) dysfunction of varying degree and class II malocclusion. The study revealed significant correlation between degenerative and inflammatory TMJ changes and androgens level in patients with stigmas of connective tissue dysplasia (p<0.05), probably due to indirect proinflammatory action of androgens as they stimulate inflammatory mediators expression.

The effect of ezetimibe on androgen production in hypercholesterolemic women with polycystic ovary syndrome.

Statin therapy was found to reduce circulating androgen levels in patients with polycystic ovary syndrome (PCOS). No similar data are available for ezetimibe. The study included 14 women with PCOS and hypercholesterolemia, intolerant to statins or having contraindications to this treatment, who were treated with ezetimibe (10mg daily). They were compared with 14 matched women with both of these disorders receiving simvastatin (40mg daily). Plasma lipids, glucose homeostasis markers, and serum levels of androgens, sex hormone-binding globulin, and gonadotropins were assessed at baseline and after 3months of treatment. Both simvastatin and ezetimibe decreased plasma levels of total and LDL cholesterol. Ezetimibe, but not simvastatin, slightly reduced insulin resistance. Simvastatin decreased serum levels of total testosterone (-23%, P<0.001), free testosterone (-32%, P<0.001), androstendione (-20%, P<0.01), and dehydroepiandrosterone sulfate (-17%, P<0.05), as well as tended to reduce the luteinizing hormone/follicle-stimulating hormone ratio (-23%, P=0.095). Ezetimibe only insignificantly reduced serum levels of free testosterone (-14%, P=0.098). There were no differences in the effects of simvastatin on circulating hormone levels between insulin-resistant and insulin-sensitive subjects. In turn, the effect of ezetimibe on free testosterone levels was stronger in insulin-resistant patients. Although ezetimibe and simvastatin are equipotent in lowering lipid levels in hypercholesterolemic patients with coexisting PCOS, simvastatin exhibits a more pronounced effect on circulating androgen levels in this group of patients.

Testosterone Modulates the Expression of Molecules Linked to Insulin Action and Glucose Uptake in Endometrial Cells

Polycystic ovary syndrome (PCOS) is a common hyperandrogenic disorder associated with insulin resistance. Insulin exerts its metabolic function by activating the PI3K/Akt pathway and favoring glucose uptake. Caveolin-1 is a scaffolding protein which increases insulin receptor (IR) stability. Alternatively, activation of IR increases caveolin-1 phosphorylation on tyrosine-14. Furthermore, endometrial tissue from PCOS patients is proposed to be insulin resistant; however, the particular role of testosterone in modulating the metabolic effects of insulin remains unexplored in endometrial stromal cells. To evaluate whether androgens modulate the response to insulin, T-HESCs cells were stimulated with 100 nM testosterone for 24 h and changes in the protein levels of caveolin-1, IR, and Akt were determined by Western blotting (WB). After testosterone treatment, the consequences of acute insulin stimulation were evaluated by WB analysis of phospho-S473Akt and phospho-Y14Caveolin-1, as well as by measuring glucose incorporation analyzing 2-deoxyglucose (2-DOG) uptake. For cells pretreated with testosterone, higher IR, IRS-1, and caveolin-1 protein levels compared with control conditions were detected. However, in testosterone treated cells acute insulin stimulation did not increase phospho-S473Akt and phospho-Y14caveolin-1 levels and reduced 2-DOG uptake was observed compared to control cells. Our results suggest that testosterone may have a detrimental role on the metabolic effects of insulin in endometrial stromal cell cultures. Thus, the high androgen levels in patients with PCOS may favor insulin resistance observed in endometria from these women.

Evaluation of Androgen Levels in Patients with Acute Coronary Syndrome

Objectives: To determine plasma levels of free Testosterone (fT) and dehydroepiandrosterone sulphate (DHEA-S) in male patients with acute coronary syndrome. Methods: We checked the serum fT and DHEA-S levels of 30 healty male subjects and 64 male patients with acute coronary syndrome whose coronary artery diseases were confirmed by coronary angiography. Results: We observed no difference between two groups on the level of fT while DHEA-S level was significantly lower (p = 0.01). No correlation had existed between lipid parameters and levels of fT and DHEA-S. Conclusion: More comprehensive studies are needed about whether lower levels of DHEAS in patients are contributed to acute coronary syndrome or are the effect of disease.

Gonadotropin releasing hormone analogs induce apoptosis by extrinsic pathway involving p53 phosphorylation in primary cell cultures of human prostatic adenocarcinomas

Gonadotropin-releasing-hormone (GnRH) analogs are widely used to block hypothalamic-pituitary-gonadal axis and inhibit blood androgen levels in patients with prostate cancer (PCa). In addition, GnRH analogs induce proliferation arrest and apoptosis through GnRH receptors expressed on the membrane of PCa cells. Possible molecular mechanisms involved in GnRH-mediated apoptosis on prostate cancer cells were studied. Primary cultures from PCa and benign prostatic hyperplasia (BPH) (non-malignant control) were derived from samples provided by our Institutional Hospital. Cell cultures were incubated for 24 hr with 20 ng/ml of GnRH agonist Leuprolide (Lp) or antagonist Cetrorelix (Cx). Apoptosis was evaluated by studying the expression of Bax and Bcl-2 and the activation of caspase-9 (intrinsic pathway), caspase-8 (extrinsic pathway), and caspase-3. Also, mRNA level, protein expression and phosphorylation of p53 were studied. Cleaved caspase-8 and -3, but not -9, increased in presence of Lp and Cx in PCa cell cultures. Bax and Bcl-2 mRNA levels showed no changes after GnRH-analog treatments. Only Bax protein showed an increase after Cx treatment in PCa cell cultures. p53 mRNA level was higher in PCa than in BPH cell cultures. Lp and Cx increased p53 expression and phosphorylation in PCa cell cultures. Apoptosis induced by GnRH analogs seems to be mediated by extrinsic pathway involving p53 phosphorylation. Phosphorylated-p53 might be associated with the increase in apoptotic NGF receptor, p75, previously reported by our laboratory. These findings reinforce the concept of clinical use of GnRH analogs for PCa suggesting that intraprostatic treatment may be more effective.

Effects of testosterone and metformin on glucose metabolism in endometrium

To investigate the effects of testosterone and metformin on glucose metabolism in endometrium. In vitro experiment. Reproductive and Genetic Center, Obstetrics and Gynecology, The First Hospital of Peking University, Beijing, China. Premenopausal women undergoing total abdominal hysterectomy for uterine myoma or adenomyosis. Endometrial glandular epithelial cell culture. Insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT-4) expression in endometrial glandular epithelial cell. After the action of testosterone solution, the protein expressions of IRS-1mRNA, IRS-1, and GLUT-4 in endometrial glandular epithelial cells all decreased significantly. Metformin may reverse this effect. The high androgen levels in patients with polycystic ovary syndrome could induce insulin resistance in endometrial glandular epithelial cell, whereas metformin has an antagonizing effect.

Impact of glycemic variations on the regulation of androgen metabolism in obese women with polycystic ovary syndrome

To assess the influence of alterations in glucose concentrations on androgen levels in patients with polycystic ovary syndrome (PCOS) and in healthy controls. Prospective, controlled study. Tertiary care center. Seven patients with PCOS and 20 healthy controls. Hyperinsulinemic glucose clamp study with stepwise reduction of the plasma glucose level from hyperglycemia to hypoglycemia. Concentrations of insulin, C-peptide, cortisol, T, androstenedione, 17-hydroxyprogesterone, DHEA, and DHEAS during hyperglycemia, euglycemia, and hypoglycemia. Total T levels and the free androgen index were significantly higher in the PCOS group at baseline and throughout the clamp. The levels of T, androstenedione, DHEAS, and 17-hydroxyprogesterone were not influenced by short-term changes of plasma glucose concentrations in both groups. However, hypoglycemia led to a significant increase in DHEA levels in PCOS patients as well as in controls. Cortisol levels were not increased during hypoglycemia in either group. In contrast to men, androgen levels are not influenced by short-term changes of plasma glucose levels in PCOS patients and in healthy women. However, DHEA concentrations increase with decreasing glucose levels independently from an activation of the hypothalamic-pituitary-adrenal axis. This supports a gender difference regarding the counterregulatory hormone response to hypoglycemia.

Baldness, benign prostate hyperplasia, prostate cancer and androgen levels

Introduction. We evaluated the pattern of baldness and serum androgen levels in patients with benign prostate hyperplasia (BPH) and prostate cancer. BPH, prostate cancer and androgenic alopecia (AA) were somehow androgen dependent and affect large population of elderly men.Material and method. A total of 152 patients, 108 patients with BPH and 44 patients with prostate cancer were included in the study. We measured serum total, free and bioavailable testosterone, FSH, LH, prolactin, estradiol, albumin and SHBG levels. Baldness classification was based on Norwood's classification and we categorised baldness as vertex and frontal baldness.Result. The frequency of AA in BPH and prostate cancer groups were not different. We looked for some correlation between the two groups with respect to AA and hormone levels. We did not find any correlation between AA and total testosterone, free testosterone, bioavailable testosterone or SHBG levels in both groups.Conclusion. This prospective study with selected small group of patients showed that there is no difference of male pattern baldness in BPH and prostate cancer patients and also there is no correlation between pattern of baldness and serum androgen levels.

Ovarian Steroidogenesis and Serum Androgen Levels in Patients with Premature Ovarian Failure

Women with premature ovarian failure (POF) have been reported to have lower serum androgen levels compared with normal women. We reviewed the androgen profiles of 143 POF patients and found androgen levels above normal for postmenopausal women in 16% of these subjects. To determine the source of androgens in those women, we studied the available ovarian biopsy samples of 15 POF patients with increased androgen levels using immunohistochemistry, with a panel of antibodies directed against the main steroidogenic enzymes. Five of the ovarian biopsies exhibited abnormal follicles characterized by hypertrophied theca interna expressing steroidogenic enzymes involved in androgen synthesis. In five other biopsies, the steroidogenic activity was scarce and confined to a small number of ovarian stromal cells, sometimes situated in the proximity of follicular remnants. Finally, in five patients, we found no histological evidence of present or past follicular development beyond the quiescent follicular stage, and no steroidogenic cells were detected by immunohistochemistry. Our findings suggest that ovarian theca-derived cells are a source of androgens in some women with POF, whereas in others, as in most postmenopausal patients, the adrenals or the ovarian hilus cells may synthesize a significant quantity of androgens under LH stimulation.

Serum androgen levels in patients undergoing controlled ovarian hyperstimulation for in vitro fertilization cycles

Aim. To investigate androgen behavior during controlled ovarian hyperstimulation (COH) for in vitro fertilization (IVF).Design. A prospective, observational study.Setting. An IVF unit of an academic medical center.Patients and methods. Blood was drawn three times during the COH cycle from 17 consecutive patients undergoing the long gonadotropin-releasing hormone-analog protocol: the day on which adequate suppression was obtained (Day-S); the day of or prior to administration of human chorionic gonadotropin (Day-hCG); and (3) the day of ovum pick-up (Day-OPU).Results. There was a significant increase in serum sex steroid levels during gonadotropin treatment. After hCG administration, there was a significant increase in levels of serum 17-hydroxyprogesterone (17-OHP) and ovarian androgens (total and free testosterone and androstenedione), with no significant change in adrenal androgen (dehydroepiandrosterone sulfate). Significant correlations were observed between plasma estradiol (E2) and androgen levels during COH and until hCG administration, but not after hCG administration. The E2/testosterone ratio increased significantly during COH and until hCG administration, and then decreased significantly. The number of oocytes retrieved correlated significantly with serum 17-OHP, E2 and E2/testosterone ratio. The number of gonadotropin ampoules used correlated inversely only with serum E2 levels.Conclusion. In patients undergoing COH for IVF, androgen levels increase in response to gonadotropin, and then again after hCG administration. Although the E2/testosterone ratio correlates with the number of oocytes retrieved, androgen levels do not.