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The comparison of free androgen index and serum free testosterone levels in women with hirsutism or polycystic ovary syndrome  [PDF]
Oya Güng?r,G?nül Erden,Ceylan Bal,Nihal U?uz1
Journal of Clinical and Experimental Investigations , 2011,
Abstract: In many laboratories free testosterone can not be measured, so that free androgen index is suggested instead. The aim of this study was to compare free androgen index and serum free testosterone levels measured by radioimmunoassay in women with hirsutism or polycystic ovary syndrome.Materials and methods: Totally 94 women referred to the polyclinics of Ankara Numune Hospital were retrospectively included. Three patient groups were composed; 55 of hirsutism, 20 of polycystic ovary syndrome and 19 of both hirsutism and polycystic ovary syndrome. Total testosterone and sex hormone binding globuline levels were measured by chemiluminescence method and free testosterone levels were measured by radioimmunoassay. Free androgen index was calculated from total testosterone and sex hormone binding globuline.Results: There was a significant positive correlation between free testosterone and free androgen index in patients with hirsutism, in patients with polycystic ovary syndrome, in patients with hirsutism and polycystic ovary syndrome, and in total patient group [r(hirsutism)=0,597, r(PCOS)=0,617, r(hirsutism and PCOS)=0,779, r(total patient group)=0,649, P<0,01].Receiver operating characteristics curves were drawn to assess the diagnostic power of parameters for all patient groups [For hirsutism (n=55) auROC (FT)=0,431 auROC (FAI)=0,485] [For PCOS (n=20) auROC (FT)=0,431 auROC (FAI)=0,359] [For hirsutism and PCOS (n=19) auROC (FT)=0,676 auROC (FAI)=0,669]. In our study, free testosterone and free androgen index were found useful to diagnose ‘hirsutism and polycystic ovary syndrome’ but not others.Conclusion: Free androgen index can be used instead of free testosterone in hirsutism and polycystic ovary syndrome for diagnosis. J Clin Exp Invest 2011;2(2):152-6
Investigating Risk Factors for Cardiovascular Disease Based on Polycystic Ovary Syndrome phenotypes in the 18-14 year Old High School Girls in Shiraz 2009
M Akbarzadeh,T Naderi,MH Dabbaghmaneh,HR Tabatabaee
Journal of Shahid Sadoughi University of Medical Sciences , 2012,
Abstract: Introduction: In patients with polycystic ovary syndrome hyperinsulinaemia, insulin resistance, dyslipidemia and hyperglycemia may represent an increased risk for coronary cardiovascular disease .This study aimed to investigate risk factors for cardiovascular disease based on polycystic ovary syndrome phenotypes in Shiraz. Methods: This Cross-sectional study was performed on 3200 students aged 18-14. Demographic survey, clinical signs of androgen excess (acne, hirsutism, alopecia), Ultrasound were applied in order to find the cyst. Tests included prolactin, dehydroepiandrodion sulfate, and oral glucose tolerance test, fasting blood glucose, blood sugar two hours later, triglycerides, cholesterol, high density lipoprotein. Data were submitted to SPSS software, version 11.5 and then analyzed by chi-square tests. Results: The serum cholesterol mean in four phenotypes had a statistically significant relationship with non-PCOS patients(p<0.05). Mean of serum cholesterol in oligomenorrhea, Hyperandrogenism and polycystic ovary phenotype (195.09±30.28) was higher than the other phenotypes. Mean of serum cholesterol and low density lipoprotein(LDL-C) were significantly higher in patients with Hyperandrogenism and polycystic ovarian phenotype(130.046±26.27) and oligomenorrhea, Hyperandrogenism and polycystic ovary syndrome phenotype(138.58±28.34) compared with non-infected individuals. Serum glucose mean in all phenotype was higher than non-infected after two hours and it showed a significant relation in oligomenorrhea and also polycystic ovarian phenotype(98.03 ± 20.98 versus 87.5±12.97) with non-infected individuals. Conclusion: Biochemical factors that lead to increased risk of cardiovascular diseases is increased in patients with polycystic ovary syndrome. Therefore, it should be attended in prevention programs
The Pancreas Is Altered by In Utero Androgen Exposure: Implications for Clinical Conditions Such as Polycystic Ovary Syndrome (PCOS)  [PDF]
Mick Rae, Cathal Grace, Kirsten Hogg, Lisa Marie Wilson, Sophie L. McHaffie, Seshadri Ramaswamy, Janis MacCallum, Fiona Connolly, Alan S. McNeilly, Colin Duncan
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056263
Abstract: Using an ovine model of polycystic ovary syndrome (PCOS), (pregnant ewes injected with testosterone propionate (TP) (100 mg twice weekly) from day (d)62 to d102 of d147 gestation (maternal injection – MI-TP)), we previously reported female offspring with normal glucose tolerance but hyperinsulinemia. We therefore examined insulin signalling and pancreatic morphology in these offspring using quantitative (Q) RT-PCR and western blotting. In addition the fetal pancreatic responses to MI-TP, and androgenic and estrogenic contributions to such responses (direct fetal injection (FI) of TP (20 mg) or diethylstilbestrol (DES) (20 mg) at d62 and d82 gestation) were assessed at d90 gestation. Fetal plasma was assayed for insulin, testosterone and estradiol, pancreatic tissue was cultured, and expression of key β-cell developmental genes was assessed by QRT-PCR. In female d62MI-TP offspring insulin signalling was unaltered but there was a pancreatic phenotype with increased numbers of β-cells (P<0.05). The fetal pancreas expressed androgen receptors in islets and genes involved in β-cell development and function (PDX1, IGF1R, INSR and INS) were up-regulated in female fetuses after d62MI-TP treatment (P<0.05–0.01). In addition the d62MI-TP pancreas showed increased insulin secretion under euglycaemic conditions (P<0.05) in vitro. The same effects were not seen in the male fetal pancreas or when MI-TP was started at d30, before the male programming window. As d62MI-TP increased both fetal plasma testosterone (P<0.05) and estradiol concentrations (P<0.05) we assessed the relative contribution of androgens and estrogens. FI-TP (commencing d62) (not FI-DES treatment) caused elevated basal insulin secretion in vitro and the genes altered by d62MI-TP treatment were similarly altered by FI-TP but not FI-DES. In conclusion, androgen over-exposure alters fetal pancreatic development and β-cell numbers in offspring. These data suggest that that there may be a primary pancreatic phenotype in models of PCOS, and that there may be a distinct male and female pancreas.
Digit ratios by computer-assisted analysis confirm lack of anatomical evidence of prenatal androgen exposure in clinical phenotypes of polycystic ovary syndrome
Marla E Lujan, Amanda J Podolski, Donna R Chizen, Denis C Lehotay, Roger A Pierson
Reproductive Biology and Endocrinology , 2010, DOI: 10.1186/1477-7827-8-156
Abstract: Ninety-six women diagnosed with PCOS according to the 2003 Rotterdam criteria had their finger lengths measured with computer-assisted analysis. Participants were categorized into four recognized phenotypes of PCOS and their 2D:4D compared to healthy female controls (n = 48) and men (n = 50).Digit ratios assessed by computer-assisted analysis in women with PCOS did not differ from female controls, but were significantly lower in men. When subjects were stratified by PCOS phenotype, 2D:4D did not differ among phenotypes or when compared to female controls.Computer-assisted measurements validated that digit ratios of women with PCOS do not show anatomical evidence of increased prenatal androgen exposure.Polycystic ovary syndrome (PCOS) is a complex endocrine disorder, having no single diagnostic trait [1,2]. Much controversy has surrounded the diagnosis of this condition but in 2003 experts proposed that a diagnosis of PCOS be based on the presence of two of three symptoms: 1) oligo or chronic anovulation (amenorrhea), 2) biochemical and/or clinical hyperandrogenism and 3) polycystic ovaries on ultrasonography [1,2]. These criteria recognized the broad clinical spectrum of PCOS including, the manifestation four unique phenotypes [3]. Frank PCOS represents the most severe form of this condition and is characterized by the presence all three symptoms. Non-PCO PCOS is characterized by oligoanovulation, hyperandrogenism, but normal ovarian morphology. Ovulatory PCOS describes the presence of hyperandrogenism, polycystic ovaries and normal menstrual cycles, whereas Mild PCOS describes the presence of oligoamenorrhea and polycystic ovaries, but no hyperandrogenism. While the validity of these phenotypes is still being debated [4,5], there is consensus among experts that PCOS imparts serious consequences for the long-term health and quality of life of patients and therefore should invite early identification and intervention [1-6].Despite familial clustering, the diverse man
Androgen Receptor CAG Repeat Polymorphism and Epigenetic Influence among the South Indian Women with Polycystic Ovary Syndrome  [PDF]
Shilpi Dasgupta,Pisapati V. S. Sirisha,Kudugunti Neelaveni,Kathragadda Anuradha,Alla G. Reddy,Kumarasamy Thangaraj,B. Mohan Reddy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012401
Abstract: The present study was carried out to assess the role of androgen receptor CAG repeat polymorphism and X chromosome inactivation (XCI) pattern among Indian PCOS women and controls which has not been hitherto explored and also to test the hypothesis that shorter CAG alleles would be preferentially activated in PCOS. CAG repeat polymorphism and X chromosome methylation patterns were compared between PCOS and non-PCOS women. 250 PCOS women and 299 controls were included for this study. Androgen receptor CAG repeat sizes, XCI percentages, and clinical and biochemical parameters were measured. The mean CAG repeat number is similar between the cases (18.74±0.13) and controls (18.73±0.12). The obese PCOS women were significantly more frequent in the <18 and >20 CAG repeat category than the lean PCOS women, yielding a highly significant odds (p = 0.001). Among the women with non-random X-inactivation, alleles with <19 repeats were more frequently activated among cases than controls (p = 0.33). CAG repeat polymorphism by itself cannot be considered as a useful marker for discriminating PCOS. We observed a trend of preferential activation of the shorter allele among the PCOS cases with non random XCI pattern. In the obese PCOS women, this microsatellite variation may account for the hyperandrogenicity to a larger extent than the lean PCOS women.
Polycystic ovary syndrome and hirsuti
Turk Pediatri Ar?ivi , 2011,
Abstract: Polycystic ovary syndrome is a multi-factorial heterogenous disorder characterized by chronic anovulation and hyperandrogenism. Diagnosis is based on clinical or laboratory evidence of hyperandrogenism. For diagnosis at least two of the three Rotterdam criteria (oligo/anovulation, clinical or biochemical signs of hyperandrogenism, polycystic ovaries) should be ensured. Clinical symptoms usually begin around menarche. Oligomenorrhea, amenorrhea, hirsutism, acne , alopecia can be associated with central obesity. nsulin resistance, hyperandrogenism, LH excess, and sonographic appearance of polycystic ovaries are the laboratory findings. Functional ovarian and adrenal hyperandrogenism can be demonstrated in the majority of the patients. Although pathogenesis is multifactorial, insulin resistance seems to play a central role. rrespective of obesity there is insulin resistance in 50-70% of the patients. Adolescents presenting with hirsutism, menstrual irregularities and central obesity should be evaluated for differential diagnosis of hyperandrogenism and the etiology be determined. Treatment depends on the clinical signs and the source of hyperandrogenism. In the patients with menstrual disorders and/or functional ovarian hyperandrogenism, oral contraceptives are the first line drugs. Antiandrogens are prefered in patients with hirsutism and functional hyperandrogenism. If insulin resistance is the heading symptom insulin sensitizers can be used.Hirsutism is defined as excessive terminal hair growth at androgen dependent sites and is the most frequent symptom of hyperandrogenism. Treatment consists of androgen decreasing drugs related to the etiology of androgen excess and locally epilation of the hair. In patients presenting with polycystic ovary syndrome and hirsutism, initially the etiology of hyperandrogenism should be identified and treatment planned appropriate to the reason. (Turk Arch Ped 2011; 46 Suppl: 97-102)
Large effects on body mass index and insulin resistance of fat mass and obesity associated gene (FTO) variants in patients with polycystic ovary syndrome (PCOS)
Susanne Tan, André Scherag, Onno Janssen, Susanne Hahn, Harald Lahner, Tiina Dietz, Susann Scherag, Harald Grallert, Carla Vogel, Rainer Kimmig, Thomas Illig, Klaus Mann, Johannes Hebebrand, Anke Hinney
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-12
Abstract: We conducted an association study in 386 patients with PCOS (defined by the Rotterdam-criteria) using single nucleotide polymorphisms (SNPs) in or in proximity to the fat mass and obesity associated gene (FTO), insulin-induced gene-2 (INSIG2), transcription factor 7-like 2 gene (TCF7L2) and melanocortin 4 receptor gene (MC4R). To compare the effect of FTO obesity risk alleles on BMI in patients with PCOS to unselected females of the same age range we genotyped 1,971 females from the population-based KORA-S4 study (Kooperative Gesundheitsforschung im Raum Augsburg, Survey 4).The FTO risk allele was associated with IR traits and measures of increased body weight. In addition, the TCF7L2 SNP was associated with body weight traits. For the SNPs in the vicinity of INSIG2 and MC4R and for the other examined phenotypes there was no evidence for an association. In PCOS the observed per risk allele effect of FTO intron 1 SNP rs9939609 on BMI was +1.56 kg/m2, whereas it was +0.46 kg/m2 in females of the same age range from the general population as shown previously.The stronger effect on body weight of the FTO SNP in PCOS might well have implications for the etiology of the disease.The polycystic ovary syndrome (PCOS) is a common endocrinopathy affecting about 6% of women of child-bearing age [1]. It is classically characterised by chronic anovulation, hyperandrogenism and polycystic ovarian morphology on ultrasonography [2]. In addition, a close relationship exists between obesity, insulin resistance (IR) and PCOS [3,4]. Despite a growing body of evidence demonstrating a substantial heritability of PCOS and the intrinsic impact of IR on the development of PCOS, its etiology and underlying pathophysiology still remains elusive.To date, multiple genetic studies in PCOS have been performed examining genes coding for enzymes of steroid biosynthesis like CYP11, CYP17, CYP19, androgen receptor, insulin, insulin receptor and enzymes in the post-receptor signal cascade of insulin. H
Gabriela Dum?chi?ǎ-?argu,Voichi?a Mogo?,Florentina Pricop
Jurnalul de Chirurgie , 2010,
Abstract: The polycystic ovary syndrome (PCOS) is defined by a chronic anovulation, clinical and/or biochemical evidence of hyperandrogenism, in the presence of polycystic ovaries and the absence of the other causes. The aim of the study is to estimate the prevalence of thyroid pathology in women with polycystic ovary syndrome. Methods: This study is a retrospective one and was made from January 2003 to December 2009 in the Endocrinology Clinic of “Saint Spiridon” Hospital and included a number of 483 women with polycystic ovary syndrome. The study includes: anamnesis dates, clinical exams, hormonal determinations, and echographic examinations of the thyroid and ovaries. Results From this group, were taken in evidence for thyroid malfunctions 179 women: 74 autoimune thyroiditis, 88 goiters, 8 congenital mixedems, 6 Basedow diseases, 1 thyroid neoplasm, 1 toxic adenoma and 1 struma ovarii. Women with polycystic ovary syndrome have a high prevalence of thyroid pathology (37,6%). This raises the possibility that female hormones might play a pathogenic role in such diseases. Conclusions: Evaluation of the thyroid gland with a blood test for thyroid stimulating hormone (TSH), antithyroglobulin and antithyroid peroxidase antibody plus an echographic examination, should be a part of the investigation of polycystic ovary syndrome. Likewise, PCOS should be evaluated in patient with under-active thyroid gland.
Association between Fat Mass- and Obesity- Associated (FTO) Gene Polymorphism and Polycystic Ovary Syndrome: A Meta-Analysis  [PDF]
Xianli Cai, Chibo Liu, Sihua Mou
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086972
Abstract: Aims Many studies have investigated the relationship between FTO gene polymorphism and polycystic ovary syndrome (PCOS) susceptibility but revealed mixed results. In this study, we aimed to perform a meta-analysis to clarify this association. Methods Published literature from PubMed, Embase and CNKI was retrieved. Meta-analysis was performed to calculate pooled odds ratio (OR) with 95% confidence interval (CI) using the random- or fix- effects model. Results A total of 5 studies (4778 cases and 4272 controls) were included in our meta-analysis. The results suggested that FTO rs9939609 polymorphism (or its proxy) was marginally associated with PCOS risk after adjustment for body mass index (BMI) (OR = 1.26; 95%CI: 1.02–1.55). However, the marginal association was not stable after sensitivity analysis. In the subgroup analysis by ethnicity, the association was significant in East Asians (OR = 1.43, 95%CI = 1.30–1.59) but not in Caucasians (OR = 1.04, 95%CI = 0.85–1.29). Conclusions Our present meta-analysis indicated that FTO rs9939609 polymorphism (or its proxy) might not be associated with risk of PCOS in overall population. However, in East Asians, there might be a direct association between FTO variant and PCOS risk, which is independent of BMI (adiposity).
Frequency of facial and body acne in 14- to 18- year-old female high school students and its relationship to polycystic ovary syndrome
Tahereh Naderi,Marzieh Akbarzadeh,Mohammad Hossein Dabagh Manesh,Hamidreza Tabatabaei
Dermatology and Cosmetic , 2011,
Abstract: "nBackground and Aim: Adolescents with polycystic ovary syndrome concern about weight gain, menstrual irregularities, acne and hirsutism. The aim of this study was to determine the frequency of facial and trunkal lesions of acne in 14- to 18-year-old high school students with polycystic ovary syndrome in Shiraz in 2009."n"nMethods: In this cross-sectional study, 3189 14- to 18-year-old female students were enrolled. Using questionnaires, data on personal information, clinical features and laboratory findings of hyperandrogenism and results of ultrasound examination were collected. Severity of acne was classified as mild, moderate and severe, based on the type and number of the lesions. Chi-squared and independent t tests were used for comparing proportions and means, respectively."n"nResults: The prevalence of severe acne was 5%. Mean total testosterone in individuals with severe acne was higher in comparison with those without acne. Severity of facial and trunkal acne were associated with polycystic ovaries (P<0.05). Mean level of luteinizing hormone (LH) was higher in those without acne than in those with severe acne (P >0.05)."n"nConclusion: Associations between severity of facial and trunkal acne lesions and polycystic ovaries were observed. Considering the undesirbale effects of acne on quality of life, hormonal screening and ultrasound examination in girls with moderate acne is recommended.
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