补肾调冲方对肥胖型多囊卵巢综合征不孕患者疗效及对子宫内膜容受性的影响

目的:探讨补肾调冲方对肥胖型多囊卵巢综合征(polycystic ovarian syndrome,PCOS)不孕患者疗效及对子宫内膜容受性的影响。方法:2014年6月—2016年7月新疆维吾尔自治区中医医院共收治147例肥胖型PCOS不孕患者,以该批患者为研究对象,按随机数字表法分为治疗组(73例),对照组(74例)。对照组PCOS不孕患者给予达英-35+来曲唑治疗,治疗组在此基础上给予补肾调冲方,两组均进行3个月经周期的治疗,结束后对两组患者疗效、生殖内分泌激素水平、身体质量指数(body mass index,BMI),脂肪细胞因子以及子宫内膜容受性进行比较。结果:治疗组患者总有效率为90.41%,对照组为79.73%,治疗组优于对照组(P0.05);经过治疗后两组患者均较治疗前促黄体生成激素(luteotropic hormone,LH),卵泡刺激素(follicle-stimulating hormone,FSH),LH/FSH水平明显降低,雌二醇(estradiol,E2)水平明显升高,且治疗组患者效果优于对照组(P0.05);通过治疗,两组患者均较治疗前内脂素(visfatin,VF),瘦素(leptin,LEP),BMI水平明显降低,脂联素(adiponectin,APN)水平明显升高,且治疗组患者明显优于对照组(P0.05);经过治疗,两组患者均较治疗前子宫内膜厚度明显升高,子宫内膜螺旋动脉搏动指数(pulsatility index,PI)与阻力指数(resistance index,RI)明显降低,且治疗组效果优于对照组(P0.05)。结论:补肾调冲方对肥胖型PCOS不孕患者具有积极的治疗效果,可以调节患者生殖内分泌激素水平,降低患者体质量,改善子宫内膜容受性,治疗不孕安全有效,值得在临床上推广。     

达英-35联合二甲双胍治疗38例多囊卵巢综合征

目的:观察达英-35联合二甲双胍治疗多囊卵巢综合征(PCOS)的临床疗效。方法:38例临床患者,口服达英-35和二甲双胍3个周期,观察治疗前后临床症状、性激素水平、瘦素(Lp)、胰岛素抵抗指数(HOMA-IR)、性激素结合球蛋白(SHBG)、体重指数(BMI)和卵巢形态学等指标,比较生殖内分泌指标及糖代谢指标的变化。结果:用药后LH/FSH比值、雄激素水平、瘦素和胰岛素抵抗指数较治疗前均降低,性激素结合球蛋白较治疗前显著升高(P<0.01)。治疗后BMI下降(P<0.05),卵巢体积较治疗前明显缩小(P<0.05)。结论:达英-35联合二甲双胍可有效改善多囊卵巢综合征患者的胰岛素抵抗状态,降低血中雄激素水平并恢复生育功能,治疗多囊卵巢综合征安全有效。     

Therapeutic effects of puerarin on polycystic ovary syndrome: A randomized trial in Chinese women

Background:This study aims to assess the therapeutic effects of a well-known component (puerarin) obtained from a Chinese herb root in patients with polycystic ovary syndrome (PCOS).Methods:Women with premature ovarian failure (POF) were assigned to the obese group (body mass index [BMI] ≥24 kg/m² and waist hip ratio [WHR] >0.85) or non-obese group (group 3, n = 21). Obese patients were further randomly assigned to the obese treatment group (group 1, n = 15) and obese control group (group 1, n = 15). All patients received standard treatment (Diane-35, 1 tablet/d, orally, plus metformin, 1.5 g/d, orally). In addition to the standard modality, patients in group 1 and group 3 also orally received 150 mg/d of puerarin tablets for 3 months. Venous blood was drawn before and after treatment. Then, the metabolic and antioxidant biomarkers were measured. The normality of distribution of the data was tested using the Kolmogorov–Smirnov method. The baseline characteristics were analyzed using one-factor analysis of variance (ANOVA), and post-hoc was performed using the least significance difference (LSD)-t test.Results:Significantly improved blood levels of sex hormone binding globulin (SHBG) and superoxide dismutase (SOD) were observed in patients who received the additional treatment of puerarin, regardless of their lean or obese status, while these were not observed in patients who did not receive puerarin. Furthermore, obese patients with PCOS had significantly lower systolic blood pressure, total cholesterol, and testosterone blood levels, when compared with before treatment.Conclusion:The addition of puerarin to the present treatment protocol can be considered for the management of metabolic disorders and hyperandrogenism in PCOS patients.     

Documento de consenso de poliquistosis renal autosómica dominante del grupo de trabajo de enfermedades hereditarias de la Sociedad Española de Nefrología. Revisión 2020

Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent cause of genetic renal disease and accounts for 6–10% of patients on kidney replacement therapy (KRT).Very few prospective, randomized trials or clinical studies address the diagnosis and management of this relatively frequent disorder. No clinical guidelines are available to date. This is a revised consensus statement from the previous 2014 version, presenting the recommendations of the Spanish Working Group on Inherited Kidney Diseases, which were agreed to following a literature search and discussions. Levels of evidence mostly are C and D according to the Centre for Evidence-Based Medicine (University of Oxford). The recommendations relate to, among other topics, the use of imaging and genetic diagnosis, management of hypertension, pain, cyst infections and bleeding, extra-renal involvement including polycystic liver disease and cranial aneurysms, management of chronic kidney disease and KRT and management of children with ADPKD. Recommendations on specific ADPKD therapies are provided as well as the recommendation to assess rapid progression.     

Imaging-Based Diagnosis of Autosomal Dominant Polycystic Kidney Disease

The clinical use of conventional ultrasonography (US) in autosomal dominant polycystic kidney disease (ADPKD) is currently limited by reduced diagnostic sensitivity, especially in at-risk subjects younger than 30 years of age. In this single-center prospective study, we compared the diagnostic performance of MRI with that of high-resolution (HR) US in 126 subjects ages 16–40 years born with a 50% risk of ADPKD who underwent both these renal imaging studies and comprehensive PKD1 and PKD2 mutation screening. Concurrently, 45 healthy control subjects without a family history of ADPKD completed the same imaging protocol. We analyzed 110 at-risk subjects whose disease status was unequivocally defined by molecular testing and 45 unaffected healthy control subjects. Using a total of >10 cysts as a test criterion in subjects younger than 30 years of age, we found that MRI provided both a sensitivity and specificity of 100%. Comparison of our results from HR US with those from a previous study of conventional US using the test criterion of a total of three or more cysts found a higher diagnostic sensitivity (approximately 97% versus approximately 82%) with a slightly decreased specificity (approximately 98% versus 100%) in this study. Similar results were obtained in test subjects between the ages of 30 and 40 years old. These results suggest that MRI is highly sensitive and specific for diagnosis of ADPKD. HR US has the potential to rival the diagnostic performance of MRI but is both center- and operator-dependent.     

The Future of Polycystic Kidney Disease Research—As Seen By the 12 Kaplan Awardees

Polycystic kidney disease (PKD) is one of the most common life-threatening genetic diseases. Jared J. Grantham, M.D., has done more than any other individual to promote PKD research around the world. However, despite decades of investigation there is still no approved therapy for PKD in the United States. In May 2014, the University of Kansas Medical Center hosted a symposium in Kansas City honoring the occasion of Dr. Grantham''s retirement and invited all the awardees of the Lillian Jean Kaplan International Prize for Advancement in the Understanding of Polycystic Kidney Disease to participate in a forward-thinking and interactive forum focused on future directions and innovations in PKD research. This article summarizes the contributions of the 12 Kaplan awardees and their vision for the future of PKD research.     

Endocrine Disruptors and Polycystic Ovary Syndrome: Phthalates

Objective:We aimed to investigate a possible role of the endocrine disruptors phthalates, di-2-ethylhexyl phthalate (DEHP) and mono (2-ethylhexyl) phthalate (MEHP), in polycystic ovary syndrome (PCOS) aetiopathogenesis. We also wished to evaluate the relationship between phthalates and metabolic disturbances in adolescents with PCOS.Methods:A total of 124 adolescents were included. Serum MEHP and DEHP levels were determined by high-performance liquid chromatography. Insulin resistance was evaluated using homeostasis model assessment-insulin resistance, quantitative Insulin Sensitivity Check Index, fasting glucose/insulin ratio, Matsuda index, and total insulin levels during oral glucose tolerance test. Participants were further subdivided into lean and obese subgroups according to body mass index (BMI).Results:Sixty-three PCOS and 61 controls, (mean age 15.2±1.5; range: 13-19 years) were enrolled. Serum DEHP and MEHP concentrations were not significantly different between PCOS and control groups. The mean (95% confidence interval) values of DEHP and MEHP were 2.62 (2.50-2.75) μg/mL vs 2.71 (2.52-2.90) μg/mL and 0.23 (0.19-0.29) μg/mL vs 0.36 (0.18-0.54) μg/mL in PCOS and the control groups respectively, p>0.05. Correlation analysis, adjusted for BMI, showed that both phthalates significantly correlated with insulin resistance indices and serum triglycerides in adolescents with PCOS.Conclusion:Serum DEHP and MEHP concentrations were not different between adolescents with or without PCOS. However, these phthalates are associated with metabolic disturbances such as dyslipidemia and insulin resistance, independently of obesity, in girls with PCOS.     

Analysis of gene mutations in PKD1/PKD2 by multiplex ligation-dependent probe amplification: some new findings

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a serious genetic disorder that can lead to chronic renal disease. Protein dysfunction caused by mutations in the genes polycystic kidney disease 1 (PKD1) and polycystic kidney disease 2 (PKD2) is an important factor in the pathogenesis of ADPKD. In the present study, 30 Chinese patients with confirmed diagnosis of ADPKD, based on ultrasound or computerized tomography (CT) findings were selected, and the exon copy numbers of PKD1 and PKD2 were determined using multiplex ligation-dependent probe amplification (MLPA). MLPA identified exon deletion in 1 case, suspected exon deletion in 4 cases, and suspected duplications in 3 cases. One case of suspected exon deletion was confirmed using quantitative real-time polymerase chain reaction (q-PCR) and sequencing (PKD2 exon 8). A missense mutation was observed in 1 case of exon deletion using q-PCR and sequencing (PKD1 exon 40, c.11333 C>A). The cases of suspected duplications were verified by q-PCR, and the copy number of exon 6 of PKD1 in 1 case of suspected duplication was 3.8 times greater than that in normal controls. Our findings provide new insights into ADPKD screening and mark a possibly meaningful step toward improved diagnosis and treatment of patients with ADPKD.     

Improvement of Endothelial Dysfunction with Simvastatin in Patients with Autosomal Dominant Polycystic Kidney Disease

Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Endothelial dysfunction (ED), which is an early manifestation of vascular injury, has been shown in patients with ADPKD. Statins have a beneficial effect in the reversal of ED. The aim of this study was to investigate the effects of a statin, simvastatin, on ED in patients with ADPKD. Sixteen patients with ADPKD having well-preserved renal function were included in the study. Endothelial function of the brachial artery was evaluated by using high-resolution vascular ultrasound. Endothelial-dependent dilatation (EDD) was expressed as the percentage change in the brachial artery diameter from baseline to reactive hyperemia. After the baseline evaluations of EDDs, patients were started treatment with simvastatin at a dose of 40 mg/day and were treated for six months. EDDs were recalculated after one and six months of therapy. Interleukin-6 (IL-6) and high-sensitivity C-reactive protein were also measured as markers of inflammation. Baseline EDD was 11.3 ± 6.9% in patients with ADPKD. After one month of simvastatin treatment, EDD increased significantly to 14.6 ± 4.6 % (P = 0.016 versus baseline). Endothelial-dependent dilatation further increased significantly to 18.9 ± 7.5 % (P = 0.011 versus baseline, P = 0.048 versus first month) after six months of therapy. There was also a significant decrease in the level of IL-6 from 21.6 ± 21.7 pg/mL to 9.1 ± 3.5 pg/mL (P= 0.002).

Six months of simvastatin therapy resulted in a significant improvement of ED in patients with ADPKD. This finding may be in part related to the pleiotropic effects of simvastatin.     

The effects of polycystic ovary syndrome on gestational diabetes mellitus

The aim of this study was to explore the inter-relationship between polycystic ovary syndrome and gestational diabetes mellitus, and demonstrate maternal and fetal outcomes. This was a case-control study in 1360 pregnant women who received a diagnosis of gestational diabetes mellitus between 24 and 28 weeks of gestational age. Among all diagnosed with gestational diabetes mellitus, 150 pregnant women had received a polycystic ovary syndrome, and 160 women who did not have polycystic ovary syndrome were designated as controls. The incidence of pregnancy-induced hypertension was 26.3% and 12% in the case and control groups, respectively. Preeclampsia was seen at an incidence of 12% and 6% in case and in control groups, respectively. The difference in neonatal hypoglycemia between the two groups was statistically significant, with an incidence of 17% and 5% in the case and in control groups, respectively. This study demonstrated that the presence of polycystic ovary syndrome along with gestational diabetes mellitus increases the risk of pregnancy induced hypertension by 2.4 fold, preeclampsia by 2 fold and neonatal hypoglycemia by 3.2 fold, compared to gestational diabetes mellitus alone.