Context Data on prevalence of metabolic risk factors in hyperandrogenic postmenopausal women are limited. Also, the correlation between metabolic disorders and androgen excess in this scenario is poorly understood. Objectives We aimed to assess the prevalence of obesity, hypertension, type 2 diabetes (T2D), and dyslipidemia (DLP) in postmenopausal women with hyperandrogenism of ovarian origin before and after surgical normalization of testosterone (T) levels, as well as the impact of androgen normalization on body mass index (BMI), glucose, and lipid metabolism. Design Retrospective study. Setting Tertiary health center. Participants Twenty-four Brazilian women with postmenopausal hyperandrogenism who underwent bilateral oophorectomy between 2004 and 2014 and had histologically confirmed virilizing ovarian tumor (VOT) or ovarian hyperthecosis (OH) and T-level normalization after surgery were selected. Main Outcome Measures FSH, LH, total and calculated free T, BMI, fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) serum levels were accessed before (n = 24) and 24 months after (n = 19) bilateral oophorectomy. Results At baseline, the overall prevalence rates of obesity, T2D, DLP, and hypertension were 58.3%, 83.3%, 66.7%, and 87.5%, respectively. No significant difference in prevalence was found between patients with OH and VOTs. At follow-up, FSH, LH, and total and free T levels had returned to menopausal physiologic levels, but mean BMI and mean FPG, HbA1c, LDL-C, HDL-C, and TG levels did not differ from baseline. Conclusions Postmenopausal hyperandrogenism is associated with adverse metabolic risk. Long-term normalization of testosterone levels did not improve BMI, glucose, or lipid metabolism.
Purpose Polycystic ovary syndrome (PCOS) etiology remains to be elucidated but familial clustering and twin studies have shown a strong heritable component. The purpose of this study was to identify rare genetic variants that are associated with the etiology of PCOS in a preselected cohort. Methods This prospective study was conducted among a selected group of women with PCOS. The study's inclusion criteria were PCOS patients diagnosed by Rotterdam criteria with the following phenotypes: severe insulin resistance (IR), normoandrogenic-normometabolic phenotype, adrenal hyperandrogenism, primary amenorrhea, and familial PCOS. Forty-five patients were studied by target sequencing while 8 familial cases were studied by whole exome sequencing. Results Patients were grouped according to the inclusion criteria with the following distribution: 22 (41.5%) with severe IR, 13 (24.5%) with adrenal hyperandrogenism, 7 (13.2%) with normoandrogenic phenotype, 3 (5.7%) with primary amenorrhea and 8 (15.1%) familial cases. DNA sequencing analysis identified one pathogenic variant in LMNA, three likely pathogenic variants in INSR, PIK3R1 and DLK1 and six variants of uncertain significance level with interesting biologic rationale in 5 genes (LMNA, GATA4, NR5A1, BMP15 and FSHR). LMNA was the most prevalent affected gene in this cohort (3 variants). Conclusions Several rare variants in genes related to IR were identified in women with PCOS. Although IR is a common feature of PCOS, patients with extreme or atypical phenotype should be carefully evaluated to rule out monogenic conditions.
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