多囊卵巢综合征糖脂代谢异常筛查及管理

多囊卵巢综合征（PCOS）是一种常见的妇科内分泌紊乱疾病,常伴发糖脂代谢紊乱,远期易并发糖尿病及心血管疾病。一经诊断PCOS,应及时进行糖脂代谢筛查,做到早期发现,早期干预,降低并发症发生风险。因该病表型不同,所以其糖脂代谢紊乱的管理应根据相应特点并结合患者需求进行,给予患者个体化综合治疗。     

多囊卵巢综合征患者胰岛素抵抗与脂代谢的关系

目的:探讨多囊卵巢综合征(PCOS)患者胰岛素抵抗(IR)、肥胖及血脂代谢的关系。方法:把PCOS病人分成IR组(15例),非IR组(25例),另设正常育龄妇女为对照组(20例)三组,检测空腹血甘油三脂(TG)、总胆固醇(TC)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、葡萄糖耐量试验(OGTT)、胰岛素(INS)释放试验,并计算体重指数(BMI)和腰臀比(WHR)。结果:(1)BMI、WHR三组间差别有显著意义(P<0.05,P0.05),后者三组间差别有显著意义(P<0.05)。结论:PCOS病人的IR与肥胖及脂代谢关系密切,使发生心血管疾病风险增加。     

血浆抵抗素与多囊卵巢综合征患者胰岛素抵抗的关系

目的 :探讨血浆抵抗素 (resistin)水平与多囊卵巢综合征 (PCOS)胰岛素抵抗的关系。方法 :采用ELISA方法检测 30例PCOS患者及 35例正常对照组空腹血浆抵抗素浓度 ,并采用放射免疫法检测黄体生成激素 (LH)、卵泡刺激素(FSH)及空腹胰岛素 (FIN) ,用氧化酶法检测空腹血浆葡萄糖 (FPG)浓度 ,计算胰岛素抵抗指数 (HOMA IR)。结果 :①PCOS组血浆抵抗素、LH、LH/FSH、FIN、HOMA IR均显著高于对照组 (均P <0 0 5 ) ;②PCOS组血浆抵抗素与FPG、FIN、HOMA IR、LH及LH/FSH呈显著正相关 (r分别为 0 5 8、0 6 1、0 6 4、0 4 7、0 4 1)。结论 :抵抗素参与了PCOS胰岛素抵抗的发生过程 ;血浆抵抗素浓度可能作为一种新的敏感指标在评价PCOS胰岛素抵抗程度方面具有一定的临床价值     

多囊卵巢综合征与代谢综合征的关系

代谢综合征（metabolic syndrome，MS）的概念最早是由Reaven在1993年提出的，当时称为X综合征。其主要临床表型为胰岛素抵抗（insulin resistance，IR），高胰岛素血症，糖耐量异常（impaired glucose tolerance，IGT），高血压与致粥样脂质代谢异常。由于代谢综合征是高血压、血糖异常、血脂紊乱和肥胖症等多种疾病在人体内集结的一种状态，可直接导致严重心血管疾病的发生，并造成死亡，对人类健康危害巨大。因此，该综合征的诊断、治疗和预防受到医学界的广泛重视。[第一段]     

钙蛋白酶10基因多态性与多囊卵巢综合征患者糖耐量及脂代谢异常的相关性

目的 探讨钙蛋白酶10(CAPN-10)基因56位点单核苷酸多态性(SNP-56)与多囊卵巢综合征(PCOS)患者糖耐量及脂代谢异常的相关性.方法 选取山东地区PCOS患者334例(PCOS组),健康妇女304例(对照组),采用熔解温度不同的基因分型法检测CAPN-10基因SNP-56,并采用免疫化学发光法测定泌乳素、卵泡刺激素(FSH)、黄体生成素(LH)、雌二醇、睾酮水平.PCOS组同时测定血糖、血脂、血清胰岛素水平.结果 (1)基因型及等位基因频率分布两组比较,差异均无统计学意义(P＞0.05).(2)在PCOS组,口服葡萄糖耐量试验(OGTF)180 min血糖水平AA基因型者为(5.7±2.2)mmol/L,GA基因型者为(4.9±1.2)mmol/L,GG基因型者为(4.9±1.4)mmol/L,分别比较,差异均有统计学意义(P均＜0.01);总胆固醇(TC)水平AA基因型者为(4.9±1.0)mmol/L,GA基因型者为(4.5±0.9)mmol/L,两者比较,差异也有统计学意义(P＜0.05).(3)在PCOS组,有糖尿病家族史者共44例,AA基因型频率为22.7%(10/44),GA+GG基因型频率为77.3%(34/44),GG基因型频率为34.1%(15/44);无糖尿病家族史者共290例,AA基因型频率为11.0%(32/290),GA+GG基因型频率为89.0%(258/290),GG基因型频率为47.2%(137/290),有无糖尿病家族史者AA与GA+GG基因型频率比较及AA与GG基因型频率比较,差异均有统计学意义(x2=4.751,x2=5.697;P均＜0.05).在PCOS组,有肿瘤家族史者共21例,AA基因型频率为33.3%(7/21),GA+GG基因型频率为66.7%(14/21),GG基因型频率为19.0%(4/21);无肿瘤家族史者共313例,AA基因型频率为11.2%(35/313),GA+GG基因型频率为88.8%(278/313),GG基因型频率为47.3%(148/313).结论 (1)CAPN-10基因SNP-56与PCOS的遗传易感性无明显相关性,但与PCOS患者糖、脂代谢异常有明显相关性.(2)CAPN-10基因SNP-56与PCOS患者糖尿病家族史及肿瘤家族史相关,应重视对高危PCOS个体的随访.     

多囊卵巢综合征的基因多态性研究进展

多囊卵巢综合征(PCOS)是育龄期妇女的常见疾病,具有高雄激素、高胰岛素和胰岛素抵抗等特征。PCOS是妇科内分泌疾病中最具争议的疾病之一,其家族遗传特性已被证明,但目前可能参与其发病的基因尚未完全阐明,并且没有广为接受的PCOS基础致病基因。PCOS的异质性使研究更加困难,目前研究的基因主要是影响雄激素生物合成、转运、作用和调节的基因,与胰岛素抵抗和相关异常有关的基因以及与慢性炎症相关的基因。     

多囊卵巢综合征患者的血脂代谢异常及与胰岛素抵抗的关系分析

目的:探讨多囊卵巢综合征(PCOS)患者血脂代谢异常及与胰岛素抵抗(IR)的关系,以期为血脂代谢异常PCOS患者的临床管理提供参考。方法:回顾性分析507例PCOS患者的临床资料,分析血脂代谢异常及其与腰臀比、体重指数(BMI)、IR指数、性激素水平等指标的相关关系。结果:PCOS患者IR的发生率为38.1%;与非IR的患者相比,伴有IR的患者具有较高的甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)和较低的高密度脂蛋白(HDL)(1.83±1.19vs1.12±0.70mmol/L、5.23±1.06vs4.91±0.90mmol/L、3.25±0.98vs2.88±0.79mmol/L、1.41±0.40vs1.64±0.36mmol/L,P<0.001)。总体血脂异常的发生率为24.7%,IR组显著高于非IR组(39.9%vs15.3%,P<0.001);TG、TC、LDL水平与胰岛素稳态模型-IR指数(HOMA-IR)值呈正相关,HDL水平与HOMA-IR值呈负相关。在控制BMI的影响后,TG与HDL水平仍与HOMA-IR值呈显著相关性。总体上,随着HOMA-IR值的增大,血脂异常的发生率逐渐增加。结论:PCOS患者胰岛素抵抗和血脂异常的发生率均较高,血脂异常与胰岛素抵抗呈相关性,推测临床上使用胰岛素增敏剂可能通过改善IR进而改善PCOS患者的血脂代谢异常。     

多囊卵巢综合征胰岛素抵抗与瘦素关系的探讨

目的　探讨多囊卵巢综合征 (PCOS)妇女血清瘦素 (leptin)水平与胰岛素抵抗 (IR)的关系 ,为研究PCOS的发病机制和治疗新途径提供理论依据。方法　 5 1例PCOS患者及 2 3例正常妇女均测定体重指数(BMI)、腰臀比 (WHR)、血清生殖激素及leptin水平 ,同期行口服糖耐量 (OGTT)及胰岛素 (Ins)释放试验 ,OGTT示IR者给予二甲双胍 (1 5 g/d)治疗 3个月后复测上述指标。 结果　PCOS患者血清leptin水平高于相应对照组 ,且IR组显著高于NIR组 ;PCOS患者经二甲双胍治疗后血清Ins水平显著下降 ,胰岛素敏感指数 (ISI)显著上升 ,同时leptin水平下降。相关分析表明 ,PCOS患者血清leptin与BMI、WHR及T显著正相关 ,与ISI负相关 (r=0 6 7,P <0 0 1) ,多元回归显示leptin中有BMI、ISI引入。结论　PCOS患者血清leptin水平升高与胰岛素敏感性相关 ;二甲双胍治疗PCOS患者可提高其胰岛素敏感性 ,降低血清leptin水平。     

多囊卵巢综合征的分型探讨

目的探讨不同分型方法用于多囊卵巢综合征(PCOS)分型时,其临床、内分泌、糖和脂代谢紊乱的特征,以指导临床治疗。方法将192例PCOS患者按鹿特丹修订的分型标准分为A组110例[长期无排卵;具有雄激素水平升高的临床和(或)生化依据;卵巢增大,单侧卵巢体积大于10ml或超声下至少有直径2~9mm的小卵泡≥12个;并排除其他疾病所致的雄激素增多症];B组46例[长期无排卵;具有雄激素水平升高的临床和(或)生化依据,并排除其他疾病所致的雄激素增多症];C组36例(长期无排卵;卵巢增大,单侧卵巢体积>10ml或超声下至少有直径2~9mm的小卵泡≥12个;并排除其他疾病所致的雄激素增多症)。又按肥胖与否将192例患者分为肥胖型PCOS70例(OB-PCOS组)和非肥胖型PCOS122例(NOB-PCOS组)。以同期就诊、年龄及体重匹配、基础体温(BBT)双相的输卵管因素不孕症患者104例为对照组。采用多毛评分及痤疮评分法对192例患者进行评分并测定其血清生殖激素、胰岛素、血脂及血糖的水平。采用空腹胰岛素(FINS)及胰岛素曲线下面积(IAUC)评估高胰岛素血症;采用稳态模型的胰岛素抵抗指数(HOMA-IR)评估胰岛素抵抗;糖耐量试验(OGTT)及葡萄糖曲线下面积(GAUC)评估糖代谢状态。采用游离雄激素指数(FAI)评估雄激素增多症及雄激素生物学活性。结果(1)评分:多毛评分A组为(7·1±1·8)分,B组为(6·9±1·9)分,均明显高于C组的(3·9±1·5)分,差异有统计学意义(P<0·01);痤疮评分A组为(0·9±1·1)分,B组为(0·7±1·1)分,均高于C组的(0·2±0·4)分,差异也有统计学意义(P<0·01);OB-PCOS组与NOB-PCOS组多毛评分及痤疮评分比较,差异均无统计学意义(P>0·05)。(2)黑棘皮症:A组的发生率为21·8%(20/110),B组的发生率为19·6%(9/46),C组的发生率为0(0/36),A、B组黑棘皮症的发生率均明显高于C组,差异有统计学意义(P<0·01);OB-PCOS组黑棘皮症的发生率为35·0%(25/70),NOB-PCOS组为6·0%(8/122),两组比较,差异有统计学意义(P<0·01)。(3)生殖激素:①FAI:A组为2·6±1·8,B组为2·2±1·4,均明显高于C组的1·2±0·6,差异有统计学意义(P<0·01);OB-PCOS组FAI为3·4±1·8,NOB-PCOS组为1·8±1·2,两组比较,差异也有统计学意义(P<0·01)。②黄体生成素(LH)与卵泡刺激素(FSH)的比值:NOB-PCOS组LH/FSH为2·4±1·1,明显高于OB-PCOS组的1·5±0·8,差异有统计学意义(P<0·01),A、B、C3组比较,差异无统计学意义(P>0·05)。(4)生化指标:OB-PCOS组FINS、HOMA-IR、IAUC、GAUC、甘油三酯(TG)分别为(17±11)mIU/L、1·0±0·6、(249±128)mIU·h·L-1、(19·6±7·8)mmol·h·L-1和(1·9±1·0)mmol/L,均明显高于NOB-PCOS组的(8±10)mIU/L、0·1±0·8、(132±81)mIU·h·L-1、(16·7±3·4)mmol·h·L-1和(1·1±0·7)mmol/L,分别比较,差异均有统计学意义(P均<0·01);A、B、C3组间上述生化指标比较,差异均无统计学意义(P>0·05)。结论鹿特丹修订的PCOS分型方法可反映疾病的基本特征;而肥胖分型不仅能反映病情的基本特征和严重程度,而且对代谢并发症的风险评估具有重要意义。     

抑制素与多囊卵巢综合征

多囊卵巢综合征(PCOS)是育龄妇女常见的复杂的内分泌及糖代谢异常的病理状态.患者卵泡选择受阻,早卵泡期FSH相对缺乏,雄激素过多,病理过程中是否存在卵泡抑制素自分泌和旁分泌的异常尚有争议.对抑制素的理化性质、分子量、生物活性等予以综述,探讨其在PCOS病因和病理生理中的作用.     

多囊卵巢综合征患者父母亲遗传表型的探讨

目的 探讨多囊卵巢综合征（ＰＣＯＳ）患者父母亲的遗传表型。方法 采用问卷表收集１３９例ＰＣＯＳ患者的父母亲和１３７名对照者父母亲的临床资料,比较母亲月经不规律、父亲早秃和父母亲高血压在两者间的发生频率,χ＾２检验差异显著的因素选入多因素Ｌｏｇｉｓｔｉｃ回归模型分析。结果 ＰＣＯＳ患者中,母亲月经不规律者占３８．１％、父亲早秃１９．４％、父亲高血压３０．９％,均明显高于对照者（分别为３．６％、５．１     

多囊卵巢综合征患者血栓调节蛋白水平变化的研究

目的通过检测多囊卵巢综合征（PCOS）患者血清血栓调节蛋白（TM）的水平变化,探讨TM与PCOS发生血管病变的关系。方法选择PCOS患者80例为研究组,其中胰岛素抵抗（IR）组43例和非IR组37例,正常妇女30例为对照组,采用酶联免疫吸附法检测血清TM水平;生化法检测血清总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL—C）、高密度脂蛋白胆固醇（HDL—C）、空腹血糖（FSG）、载脂蛋白A1（ApoAl）和载脂蛋白B（ApoB）;放射免疫法检测内分泌激素和空腹胰岛素（FINS）。结果非IR组、氓组TM水平与对照组比较,差异有显著性（P〈0．05）,非IR组和氓组TG、ApoB高于对照组（P〈0．01）,而HDL—C、ApoAl低于对照组（P〈0．01）。结论伴胰岛素抵抗的PCOS患者TM水平增高,可能与其发生血管病变有关。     

Metabolic syndrome in adolescents with polycystic ovary syndrome

The aim of the presented study is to evaluate metabolic features in adolescents with polycystic ovary syndrome (PCOS) in comparison with age- and BMI-matched subjects. Forty-three adolescents with PCOS according to ESHRE criteria were prospectively evaluated and compared with 48 control subjects. Blood sampling was done in the early follicular phase of menstrual cycle, between 1st and 5th day, for plasma glucose, total and high-density lipoprotein (HDL)-cholesterol, triglycerides, insulin and C peptide. The diagnosis of metabolic syndrome was done according to IDF adolescent criteria. Adolescents with PCOS have increased low-density lipoprotein (LDL)-cholesterol (p?<?0.002), decreased HDL-cholesterol (p <0.0007) and increased C peptide levels (p?<?0.02) in comparison with healthy adolescents. Total cholesterol, triglycerides, fasting blood glucose, fasting insulin, HOMA-IR, waist-to-hip ratio, systolic and diastolic blood pressure did not differ between the groups. There was no difference when we compared the prevalence of adolescents with at least one feature of metabolic syndrome between PCOS (17 from 43) and healthy controls (27 from 48). In conclusion, adolescents with PCOS have less favourable blood lipid profiles with higher LDL-cholesterol and lower levels of HDL-cholesterol and are more insulin resistant than their healthy counterparts having higher fasting C peptide levels.     

Metabolic syndrome in women with polycystic ovary syndrome

The prevalence of the metabolic syndrome in polycystic ovary syndrome (PCOS) is high across all age groups. Dyslipidemia, particularly a decreased high-density lipoprotein cholesterol level, also is common in women with PCOS.     

Insulin resistance and lipid profile in women with polycystic appearing ovaries: implications with regard to polycystic ovary syndrome

The aim of this study was to investigate carbohydrate and lipid profiles in women with polycystic appearing ovaries (PCO) on ultrasound examination who did not fulfill the criteria for polycystic ovary syndrome (PCOS). We sonographically evaluated and biochemically diagnosed 35 patients with PCO, 31 women with PCOS and 23 healthy controls. We performed oral glucose tolerance tests (OGTT) and calculated the quantitative insulin sensitivity check index (QUICKI) and the homeostatic model assessment (HOMAIR) scores. Serum fasting insulin levels, 1-h insulin response, HOMAIR and QUICKI scores were significantly higher in the PCO and PCOS groups than in the controls. However, serum fasting glucose levels, fasting insulin levels, HOMAIR and QUICKI scores were similar in women with PCO and PCOS. In women with PCO, high-density lipoprotein (HDL) levels were higher, and very-low-density lipoprotein (VLDL) and triglyceride levels were lower compared with women with PCOS. Furthermore, insulin responses to OGTT, HOMAIR and QUICKI scores and lipid values correlated with serum androgen levels and body mass index (BMI) in PCO patients. In conclusion, women with PCO who do not fulfill the criteria for PCOS have abnormal insulin sensitivity and insulin resistance. The finding of similar insulin abnormalities in women with PCO to those in women with PCOS confirms that women with PCO have similar metabolic characteristics to those with PCOS.     

Preptin in women with polycystic ovary syndrome

Introduction: Polycystic ovary syndrome (PCOS) patients, frequently develop metabolic complications, such as insulin resistance (IR), impaired carbohydrate metabolism, dyslipidemia, obesity. Among the new markers responsible for metabolic disorders, preptin seems to be of great significance.

Material: One hundred and thirty-four women aged 17–45 were enrolled. PCOS was diagnosed in 73 women on the basis of ESHRE-ASRM criteria. Non-PCOS group consisted of 61 women with regular menstruation matched for nutritional status.

Methods: All women underwent anamnesis, physical examination, anthropometric measurements, the abdominal ultrasound examination, and dual energy X-ray absorptiometry (DXA). Serum adropin levels were determined by ELISA. Biochemical and hormonal (testosterone, androstenedione, LH, FSH, estradiol) measurements were also performed. Insulin resistance indices (HOMA, QUICKI, Matsuda) and free androgen index (FAI) were calculated with the test results according to the standard formula. For all comparisons, statistical significance was defined by p?≤?.05.

Results: Serum preptin levels were significantly higher in the PCOS group. No significant correlations between preptin level and metabolic and hormonal markers were observed. The logistic regression analysis demonstrated that serum preptin level was an independent factor differentiating the two groups.

Conclusions: Serum preptin levels were significantly higher in women with PCOS compared with controls. This peptide might be an independent predictor of PCOS in the future.     

Insulin resistance and lipid profile in women with polycystic appearing ovaries: implications with regard to polycystic ovary syndrome.

The aim of this study was to investigate carbohydrate and lipid profiles in women with polycystic appearing ovaries (PCO) on ultrasound examination who did not fulfill the criteria for polycystic ovary syndrome (PCOS). We sonographically evaluated and biochemically diagnosed 35 patients with PCO, 31 women with PCOS and 23 healthy controls. We performed oral glucose tolerance tests (OGTT) and calculated the quantitative insulin sensitivity check index (QUICKI) and the homeostatic model assessment (HOMAIR) scores. Serum fasting insulin levels, 1-h insulin response, HOMAIR and QUICKI scores were significantly higher in the PCO and PCOS groups than in the controls. However, serum fasting glucose levels, fasting insulin levels, HOMAIR and QUICKI scores were similar in women with PCO and PCOS. In women with PCO, high-density lipoprotein (HDL) levels were higher, and very-low-density lipoprotein (VLDL) and triglyceride levels were lower compared with women with PCOS. Furthermore, insulin responses to OGTT, HOMAIR and QUICKI scores and lipid values correlated with serum androgen levels and body mass index (BMI) in PCO patients. In conclusion, women with PCO who do not fulfill the criteria for PCOS have abnormal insulin sensitivity and insulin resistance. The finding of similar insulin abnormalities in women with PCO to those in women with PCOS confirms that women with PCO have similar metabolic characteristics to those with PCOS.     

Hyperinsulinaemia and polycystic ovary syndrome

Over the past 20 years, it has been established that hyperinsulinaemia is a fundamental disturbance in many women with polycystic ovary syndrome (PCOS). A subgroup of women with this syndrome have ‘metabolic PCOS’ which can be considered to be a pre-diabetic state. Clinically, this subgroup is most easily identified in obese women with a strong family history of diabetes in whom menstrual disturbance is the predominant feature. There is an urgent need to define the more subtle features in young lean women with PCOS, in whom the metabolic syndrome is yet to emerge, which would enable the prediction of future health risks. The molecular mechanisms of insulin resistance leading to hyper-insulinaemia are now being elucidated. Abnormalities of both insulin secretion and intracellular insulin signalling have both been proposed in women with PCOS. Strategies to lower serum insulin concentrations include diet, exercise and possibly, oral insulin sensitizing agents such as metformin. Although the short-term efficacy of reducing hyperinsulinaemia in women with PCOS is clear, the best method to prevent the progression to diabetes later in life has not been defined.     

Myeloperoxidases and polycystic ovary syndrome

New biological markers are emerging trying to identify earlier cardiovascular high risk subjects. Myeloperoxidases have been involved in the role of atherosclerosis process, by the beginning of the endothelial dysfunction up to the plaque rupture and clinical manifestation, and it has been demonstrated that this enzyme has also a prognostic value. We aimed to assess myeloperoxidases levels in patients with polycystic ovary syndrome (PCOS) with insulin resistance (IR), considering that these women represent a high risk group for cardiovascular disease. We developed a transversal study, comprising 26 patients with PCOS and IR and 30 controls (PCOS without IR). IR was considered with HOMA-IR?≥3.0. IR absence was considered when HOMA-IR?<3.0, triglycerides?<200, BMI?<28.7, and BMI<27.8 in patients with familial history of type 2 diabetes. All patients went through anamnesis, physical examination, transvaginal ultrasound, and blood samples. IR PCOS patients had higher levels of myeloperoxidase (22.3?×?18.1, p?=?0.047), and also higher BMI. Myeloperoxidase levels correlated directly with insulin. In conclusion, IR PCOS young patients have higher myeloperoxidase levels.