Dyslipidemia involvement in the development of polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is widely accepted as the most common endocrine abnormality in women of childbearing age and may be accompanied by dyslipidemia, hyperandrogenism, hyperinsulinemia, oxidative stress and infertility. Dyslipidemia is now known to play an important role in the development of PCOS. Lipid abnormalities, including elevated low-density lipoprotein and triglyceride levels and reduced high-density lipoprotein levels, are often found in women with PCOS and play an important role in PCOS; therefore, we summarize the effect of lipid abnormalities on hyperandrogenism, insulin resistance, oxidative stress and infertility in PCOS and review the effects of common lipid-lowering drugs on patients with PCOS. The purpose of this article is to elucidate the mechanisms of lipid metabolism abnormalities in the development of PCOS.     

达英-35治疗多囊卵巢综合征的临床观察

目的观察达英-35治疗多囊卵巢综合征（PCOS）并胰岛素抵抗患者的临床效果。方法选取20例合并胰岛素抵抗的PCOS患者,均进行达英-35口服治疗,对治疗前、后的临床症状以及内分泌生化指标统计分析。结果患者治疗后与治疗前比较,在体质量指数（BMI）、腰围与臀围比（WHR）方面无明显差异;睾酮（T）、黄体生成素（LH）、空腹血糖/空腹胰岛素（GIR）明显降低及性激素结合蛋白（SHBG）显著升高（P〈0.05）,卵泡刺激素（FSH）、三酰甘油（TG）、血清胰岛素样生长因子-1（IGF-1）、C反应蛋白（CRP）无明显变化。结论达英-35治疗多囊卵巢综合征,能有效控制高雄激素血症,明显改善临床症状,不能提高胰岛素敏感性。     

在育龄期不孕的高雄激素血症女性中筛查先天性肾上腺皮质增生症

目的致不孕的原因复杂多样,在不孕原因的筛查中,先天性肾上腺皮质增生症(CAH)常被忽视。本研究在育龄期不孕的高雄激素血症女性中筛查CAH,并探讨拟妊娠女性CAH的诊治。方法纳入2016年12月至2019年4月因"不孕"就诊于南京医科大学第一附属医院生殖医学中心后转诊至内分泌科的育龄期高雄激素血症女性20例。完善血激素水平、糖脂代谢指标的检测,并行ACTH兴奋试验、子宫及双侧卵巢B超、肾上腺计算机断层扫描(CT)等检查,必要时行基因测序。结果20例不孕的高雄激素血症女性中CAH 7例(35.0%),其中基因测序确诊21-羟化酶缺陷症(21-OHD)6例、多囊卵巢综合征(PCOS)10例、特发性高雄激素血症(IHA)3例。性激素结果显示,CAH组睾酮水平显著高于PCOS组、IHA组[(4.4±2.0对2.9±0.4,2.8±0.8)nmol/L,P<0.05];ACTH兴奋试验结果显示,CAH组基础17-羟孕酮(17-OHP)显著高于PCOS组[(101.0±100.8对1.4±0.8)ng/ml,P<0.05],而与IHA组相比差异无统计学意义[(101.0±100.8对3.0±1.8)ng/ml,P>0.05];CAH组60 min 17-OHP显著高于PCOS组、IHA组[(200.1±80.8对3.1±1.2,3.4±0.2)ng/ml,P<0.05]。给予CAH患者糖皮质激素治疗后,4例成功妊娠并分娩。随访已分娩患者的后代,均未发现CAH临床症状及外生殖器畸形。结论ACTH兴奋试验在CAH特别是21-OHD的鉴别诊断中具有重要意义,基因检测有助于进一步明确CAH的突变类型。糖皮质激素治疗可提高CAH患者的妊娠率,也有助于降低母体高雄激素状态、避免女性后代出现男性化表现。     

Polycystic ovary syndrome with feasible equivalence to overweight as a risk factor for non-alcoholic fatty liver disease development and severity in Mexican population

Introduction and objectivesPolycystic ovary syndrome (PCOS) is the most common endocrinology disorder in women of reproductive age; these patients have a higher risk of suffering from non-alcoholic fatty liver disease (NAFLD). We determine the frequency of NAFLD in Mexican patients with PCOS and matched-controls.Patients and methodsCross-sectional study, with 98 women of 18–44 years old. Rotterdam 2003 criteria integrated PCOS diagnosis. Those with significant alcohol consumption, chronic liver disease, use of steatogenic drugs, and pharmacological PCOS treatment or fertility protocol were excluded. Controls were matched in a 1:1 ratio by age and body mass index (BMI). The presence of NAFLD was determined by transient elastography performed by a single experienced operator.ResultsA total of 98 female volunteers at reproductive age were recruited. NAFLD denoted markedly higher in patients with than without PCOS at 69.3% vs. 34.6%, respectively. Compared to controls, PCOS patients had a significantly higher risk of NAFLD (OR = 4.26, 95% CI 1.83–9.93). Severe steatosis was the most frequent NAFLD stage between women with PCOS and NAFLD. Patients with hyperandrogenism have a significantly higher mean CAP 277.83 dB/m than controls without hyperandrogenism 191.57 dB/m. NAFLD prevalence was 84.3% in PCOS patients with phenotype A, while in another phenotype, it was 41.1%.ConclusionsPCOS is an independent risk factor for NAFLD development. NAFLD screening needs to be considered in all PCOS patients independently of BMI, except in PCOS patients without hyperandrogenism and BMI < 25.     

Nonalcoholic fatty liver disease and polycystic ovary syndrome

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the Western world comprising a spectrum of liver damage from fatty liver infiltration to end-stage liver disease, in patients without significant alcohol consumption. Increased prevalence of NAFLD has been reported in patients with polycystic ovary syndrome (PCOS), one of the most common endocrinopathies in premenopausal women, which has been redefined as a reproductive and metabolic disorder after the recognition of the important role of insulin resistance in the pathophysiology of the syndrome. Obesity, in particular central adiposity and insulin resistance are considered as the main factors related to NAFLD in PCOS. Moreover, existing data support that androgen excess, which is the main feature of PCOS and is interrelated to insulin resistance, may be an additional contributing factor to the development of NAFLD. Although the natural history of NAFLD remains unclear and hepatic steatosis seems to be a relatively benign condition in most patients, limited data imply that advanced stage of liver disease is possibly more frequent in obese PCOS patients with NAFLD. PCOS patients, particularly obese patients with features of the metabolic syndrome, should be submitted to screening for NAFLD comprising assessment of serum aminotransferase levels and of hepatic steatosis by abdominal ultrasound. Lifestyle modifications including diet, weight loss and exercise are the most appropriate initial therapeutic interventions for PCOS patients with NAFLD. When pharmacologic therapy is considered, metformin may be used, although currently there is no medical therapy of proven benefit for NAFLD. Long-term follow up studies are needed to clarify clinical implications and guide appropriate diagnostic evaluation, follow-up protocol and optimal treatment for PCOS patients with NAFLD.     

Elevated fasting insulin is associated with cardiovascular and metabolic risk in women with polycystic ovary syndrome

AimsPCOS is associated with various immediate and long term health complications. The aim of this study was to investigate the association of serum fasting insulin concentration with cardiovascular and metabolic risk factors in women with polycystic ovary syndrome.MethodsA total of 349 women, 249 women with polycystic ovary syndrome and 100 age-matched healthy controls, were recruited in this case-control study. Fasting insulin and various other biochemical, hormonal and clinical parameters were measured in all participants. The correlation of insulin with cardiometabolic risk factors was evaluated in PCOS women with normal and high serum insulin concentration.ResultsFasting Insulin, BMI, WHR, FAI, LH: FSH, HOMA, QUICKI were significantly higher in PCOS women compared with healthy controls (p < 0.01). Fasting insulin showed a positive correlation with more cardiovascular and metabolic risk factors in PCOS compared to controls. The BMI, BAI, LAP, HOMA IR, QUICKI and FAI were significantly higher (all p < 0.05) in PCOS patients with higher insulin levels than with PCOS women with normal levels.ConclusionFasting insulin is an important determinant in the pathogenesis of obesity and hyperandrogenism in PCOS. It is associated with an increased risk of cardiovascular and metabolic disorders in women with PCOS.     

Longer anogenital distance in female fetus of diabetic and obese pregnant women

ObjectivePrevious studies revealed that prenatal exposure to androgen excess such as polycystic ovary syndrome (PCOS) is associated with offspring's anogenital distance (AGD) length, and AGD is a biomarker of intrauterine androgen exposure. This study aims to investigate a possible relationship of fetal AGD with maternal diabetes and obesity, and to evaluate whether AGD predicts the fetal androgen exposure related to diabetes and obesity in female fetus. This study is the first to focus on the relationship between offspring's AGD and maternal diabetes and obesity.Materials and methodsThis is a prospective study investigating 218 pregnant women (125 in control group and 93 in study group). Fetal AGD was measured from the center of anus to the posterior convergence of the fourchette by ultrasound. Multivariate linear regression analysis was applied to assess the association of the fetal AGD length with maternal diabetes and obesity.ResultsThe control patients had significantly shorter fetal AGD (mean:10.7 mm, P < 0.001) compared to diabetic, obese and diabetic obese patients (mean: 12.6 mm, 12.8 mm and 12.9 mm, respectively). The results of regression analysis showed that both maternal diabetes and obesity were significantly correlated with longer AGD in female fetus. The results confirmed also that offspring's AGD measurement in utero by ultrasound is feasible and reliable.ConclusionThe study findings suggest that both maternal diabetes and obesity are associated with intrauterine androgenic milieu during pregnancy, and fetal AGD may be used as a biomarker to predict this effect. This may provide important advantages in terms of early detection of reproductive system abnormalities related to prenatal androgen exposure.     

Long-term testosterone administration affects the number of paracervical ganglion ovary-projecting neurons in sexually mature gilts

The influence of testosterone (T) overdose on the number and distribution of ovarian neurons in the paracervical ganglion (PCG) in pigs was examined. To identify the ovarian neurons, on day 3 of the estrous cycle, the ovaries of both the control and experimental gilts were injected with retrograde neuronal tracer Fast Blue. From next day to the expected day 20 of the second studied cycle, experimental gilts were injected with T, while control gilts received oil. The PCG was then collected and processed for double-labeling immunofluorescence. T injections increased the T (∼3.5-fold) and estradiol-17β (∼1.6-fold) levels in the peripheral blood, and reduced the following in the PCG: the total number of Fast Blue-positive neurons, the number of perikarya in the lateral part of the PCG, the numbers of VAChT⁺/SOM⁺, VAChT⁺/VIP⁺, VAChT⁺/nNOS⁺, VAChT⁺/VIP⁻, VAChT⁺/DβH⁻, VAChT⁻/SOM⁻, VAChT⁻/VIP⁻, VAChT⁻/nNOS⁻ and VAChT⁻/DβH⁻ perikarya, In the T-affected PCG, the populations of ovarian perikarya coded VAChT⁻/SOM⁺, VAChT⁻/VIP⁺ and VAChT⁻/DβH⁺, and expressing androgen receptor were increased. After T treatment within the PCG dropped the density of nerve fibers expressing VAChT and/or SOM, VIP, DβH. Obtained data suggest that elevated androgen levels occurring during pathological processes may regulate ovary function(s) by affecting the PCG gonad-supplying neurons.