PCOS患者子宫内膜厚度与血清AMH、糖脂代谢的相关性研究

目的 探究多囊卵巢综合征(PCOS)患者子宫内膜厚度与血清抗缪勒管激素(AMH)、糖脂代谢相关性.方法 选择2018年3月至2020年8月于本院接受检查的PCOS女患132例,选择同期本院体检门诊进行健康体检女性47例,比较两组患者的子宫内膜厚度、血清AMH、糖脂代谢指标[空腹血糖(FPG)、空腹胰岛素(FINS)、胰...     

Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

The increased prevalence of non-insulin-dependent diabetes mellitus (NIDDM) among women with polycystic ovary syndrome (PCOS) has been ascribed to the insulin resistance characteristic of PCOS. This study was undertaken to determine the role of defects in insulin secretion as well as familial factors to the predisposition to NIDDM seen in PCOS. We studied three groups of women: PCOS with a family history of NIDDM (PCOS FHx POS; n = 11), PCOS without a family history of NIDDM (PCOS FHx NEG; n = 13), and women without PCOS who have a family history of NIDDM (NON-PCOS FHx POS; n = 8). Beta cell function was evaluated during a frequently sampled intravenous glucose tolerance test, by a low dose graded glucose infusion, and by the ability of the beta cell to be entrained by an oscillatory glucose infusion. PCOS FHx POS women were significantly less likely to demonstrate appropriate beta cell compensation for the degree of insulin resistance. The ability of the beta cell to entrain, as judged by the spectral power for insulin secretion rate, was significantly reduced in PCOS FHx POS subjects. In conclusion, a history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. The risk of developing NIDDM imparted by insulin resistance in PCOS may be enhanced by these defects in insulin secretion.     

Serum levels of leptin and homocysteine in women with polycystic ovary syndrome and its relationship to endocrine, clinical and metabolic parameters

We examined the relationship between endocrine, clinical and metabolic parameters in 35 women (mean age 27.3 years) with polycystic ovary syndrome (PCOS) and 30 age- and body mass index-matched normal ovulatory women. In PCOS women, serum leptin, homocysteine, insulin, insulin-like growth factor-1, insulin-like growth factor binding protein-3 levels and the insulin resistance index (HOMA-IR) were significantly higher, while sex hormone-binding globulin and high-density lipoprotein cholesterol levels were lower compared with healthy women. Serum luteinizing hormone (LH), estradiol (E(2)), androstenedione, testosterone and dehydroepiandrosterone sulphate levels were found to be significantly higher in PCOS women compared with healthy women. The levels of E(2), LH and testosterone were positively correlated with leptin levels in PCOS women. Similarly, androstenedione levels and HOMA-IR were positively correlated with homocysteine levels and insulin levels were positively correlated with LH. We conclude that increased homocysteine levels, hyperandrogenaemia, insulin resistance and impaired lipid metabolism contribute to the risk of premature atherosclerosis in PCOS women.     

Insulin sensitivity and beta-cell function in women with polycystic ovary syndrome

OBJECTIVE: To evaluate insulin sensitivity (IS) and beta-cell function (beta F) in lean and obese women with polycystic ovary syndrome (PCOS), either separately or by using a disposition index (DI). RESEARCH DESIGN AND METHODS: A total of 64 women with PCOS and 20 healthy women were examined by anthropometry, oral glucose tolerance tests (OGTTs), and insulin tolerance tests. Statistical analysis used one-way ANOVA, Kruskal-Wallis, and Mann-Whitney U tests, as appropriate. RESULTS: A significantly higher waist-to-hip ratio (P < 0.0001) was found in both lean and obese women with PCOS. Higher basal blood glucose (P < 0.004) and blood glucose values at 3 h of OGTT (P < 0.008) were found in lean and obese PCOS subjects in comparison with control subjects. Insulin resistance by homeostasis model assessment (P < 0.007) was significantly higher in obese PCOS than in control or lean PCOS subjects. Early-phase insulin secretion (insulinogenic index [Delta I/Delta G(30-0), where I is insulin and G is glucose]; P < 0.0007) was significantly higher in both lean and obese PCOS subjects than in healthy women. All tested combinations of parameters of IS and beta F (DIs) followed a physiological hyperbolic relationship. Significantly lower values of the fasting state-derived DIs were found (all P < 0.05) in obese PCOS subjects. Significantly higher values of all of these indexes derived from nonfasting values were found in lean PCOS as compared with control and obese PCOS subjects (all P < 10(-3)). CONCLUSIONS: Increased beta F was found even in lean individuals with PCOS. Insulin hypersecretion is thus probably connected to the pathogenesis of PCOS.     

Effect of adiponectin gene polymorphisms on circulating adiponectin and insulin resistance indexes in women with polycystic ovary syndrome

BACKGROUND: We examined the possible association of adiponectin gene polymorphisms with polycystic ovary syndrome (PCOS) and their influence on serum adiponectin and insulin resistance indexes in Greek women with PCOS. METHODS: We genotyped samples from 100 women with PCOS characterized with respect to body mass index (BMI), glucose and insulin concentrations during an oral glucose tolerance test (OGTT), lipid profile, and serum adiponectin concentrations and from 140 healthy controls for the 45T>G and 276G>T polymorphisms in the adiponectin gene. RESULTS: The distributions of genotypes and alleles of both polymorphisms were no different in women with PCOS and controls, indicating that the individual polymorphisms are not associated with increased risk for PCOS. However, the two polymorphisms were found to be associated with insulin resistance indexes among women with PCOS and to influence adiponectin production. In particular, carriers of the TG genotype at position +45 had greater hyperinsulinemia, as estimated by the area under the curve for insulin (AUC(insulin)) during the OGTT, than those with the TT genotype (P <0.05), and this was independent of age and BMI. In addition, women with PCOS with the GG or GT genotypes at position +276 had a higher BMI (P = 0.01) and greater AUC(insulin) (P = 0.01) than carriers of the TT genotype. The latter genotype was found less frequently among overweight/obese women with PCOS than in normal-weight individuals (P = 0.002). In addition, the presence of the GG or GT genotype was associated with lower serum adiponectin than the TT genotype, independent of age, BMI, and insulin concentrations (P = 0.03). Serum adiponectin was negatively correlated with serum triglycerides and insulin resistance indexes and positively with HDL-cholesterol. CONCLUSIONS: Adiponectin gene polymorphisms at positions +45 and +276 are not associated with PCOS. However, these genomic variants may influence production of adiponectin and the metabolic variables related to insulin resistance/metabolic syndrome in patients with PCOS.     

胰岛素抵抗对多囊卵巢综合征育龄妇女生育能力的影响

目的探讨胰岛素抵抗对多囊卵巢综合征(PCOS)育龄妇女生育的影响。方法选择PCOS患者143例,分成3组:PCOS患者曾有1次或1次以上自然流产史并无正常妊娠65例作为流产组,PCOS患者正常妊娠且无不良妊娠史42例作为正常妊娠组,另选择仅因PCOS因素来我院行辅助生育治疗的不孕患者36例作为不孕组;并选择同时期仅因为输卵管因素或男方因素不孕的正常育龄妇女44例作为对照组,于月经期第3~7天、闭经者任一时期早晨空腹抽血测卵泡刺激素(FSH)、黄体生成素(LH)、睾酮(T)、泌乳素(PRL)及血糖、胰岛素。观察胰岛素抵抗与PCOS患者的相关性。结果 PCOS流产组与不孕组的空腹血浆胰岛素≥20 m U/L的发生率、空腹血糖:空腹血浆胰岛素(4.5)发生率均高于对照组,差异有统计学意义(P0.05),PCOS流产组、不孕组的空腹血浆胰岛素≥20 m U/L的发生率、空腹血糖:空腹血浆胰岛素4.5发生率高于PCOS正常妊娠组,但差异无统计学意义(P0.05);PCOS的流产组HOMA-IR4.5的发生率高于PCOS正常妊娠组与对照组,且差异有统计学意义(P0.05),PCOS不孕组HOMA-IR4.5的发生率与PCOS正常妊娠组及对照组,差异无统计学意义(P0.05)结论胰岛素抵抗可能参与多囊卵巢综合征育龄妇女流产与不孕的发生。     

Altered D-chiro-inositol urinary clearance in women with polycystic ovary syndrome

OBJECTIVE: Evidence suggests that some actions of insulin are effected by inositolphosphoglycan (IPG) mediators. We hypothesize that a deficiency in D-chiro-inositol (DCI) and/or a DCI-containing IPG (DCI-IPG) may contribute to insulin resistance in humans. RESEARCH DESIGN AND METHODS: To assess this possibility in polycystic ovary syndrome (PCOS), we determined insulin sensitivity (Si by frequently sampled intravenous glucose tolerance test), plasma and urinary DCI and myo-inositol (MYO) levels (by gas chromatography/mass spectrometry), and the release of insulin and DCI-IPG during the oral glucose tolerance test (area under the curve [AUC]) in 23 women with PCOS and 26 normal women. RESULTS: Women with PCOS were heavier than control subjects (P = 0.002 for BMI), but also had decreased Si (P < 0.001) and increased AUC(insulin) (P < 0.001) compared with normal women, even when corrected for BMI. The urinary clearance of DCI (uCl(DCI)) was increased almost sixfold in PCOS compared with normal women (P = 0.001), but not MYO clearance (P = 0.10). uCl(DCI) correlated inversely with Si when all women were analyzed together (n = 49, r = -0.50, P < 0.001) and was one of the three best independent parameters predicting Si. Finally, the ratio of AUC(DCI-IPG) to AUC(insulin) was decreased threefold in women with PCOS (P < 0.001). CONCLUSIONS: uCl(DCI) is inversely correlated with insulin sensitivity in women and is a strong independent predictor of insulin resistance in multivariate models. PCOS, which is characterized by insulin resistance, is associated with a selective increase in uCl(DCI) and impaired DCI-IPG release in response to insulin. These findings are consistent with a defect in tissue availability or utilization of DCI in PCOS that may contribute to the insulin resistance of the syndrome.     

Women with polycystic ovary syndrome are sensitive to the TNF-alpha-lowering effect of glucose-induced hyperinsulinaemia

BACKGROUND: Restoration of near-euglycaemia by intensive insulin therapy results in decreased serum levels of inflammatory mediators. The authors investigated whether the anti-inflammatory effect of insulin was independent of its glucose-lowering action and if this effect was intact in insulin-resistant women with the polycystic ovary syndrome (PCOS) characterized by low-grade chronic inflammation. MATERIALS AND METHODS: Blood was drawn on the third and sixth days after progestin-induced withdrawal bleeding in 20 young non-diabetic women with PCOS and once between the third and sixth days of the menstrual cycle in 21 age-matched lean healthy control women during a 75-g oral glucose tolerance test (oGTT). Serum insulin, glucose and tumour necrosis factor alpha (TNF-alpha) concentrations were measured after 0, 30, 60, 90 and 120 min. RESULTS: The increase in insulin and glucose concentrations during the oGTT was significantly more pronounced in patients with PCOS (one patient with impaired fasting glucose, one patient with impaired glucose tolerance, three patients with both) compared with healthy controls. The TNF-alpha serum concentrations decreased in patients with PCOS (mean of both days, P = 0.004). In patients and in controls, there was an inverse correlation between the serum concentrations of insulin and of TNF-alpha during oGTT (for patients, a mean of both days, P = 0.009; for controls, P = 0.047), but not between the serum concentrations of glucose and TNF-alpha. CONCLUSIONS: The decrease in TNF-alpha concentrations during oGTT and the inverse correlation between endogenous hyperinsulinaemia and serum TNF-alpha concentrations suggested an anti-inflammatory effect of moderately-high insulin concentrations. This occurred despite the presence of moderate hyperglycaemia. These findings also demonstrated a preserved responsiveness of inflammatory mediators to insulin in PCOS.     

Insulin resistance in polycystic ovarian disease

The classic polycystic ovarian syndrome (PCOS) was originally described by Stein and Leventhal as the association of amenorrhea with polycystic ovaries and, variably, hirsutism and/or obesity. It is estimated that 5 to 10% of women of reproductive age have PCOS. Although insulin resistance is not part of the diagnostic criteria for PCOS, its importance in the pathogenesis of PCOS can not be denied. PCOS is associated with insulin resistance, independent of total or fat-free body mass. Postreceptor defects in the action of insulin have been described in PCOS that are similar to those found in obesity and type 2 diabetes. Treatment with insulin sensitizers, metformin, and thiazolidinediones (TZDs) improve both metabolic and hormonal patterns and also improve ovulation in PCOS. Recent studies have shown that women who have PCOS have higher circulating levels of inflammatory mediators such as C-reactive protein, tumor necrosis factor, tissue plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1). It is possible that the beneficial effect of insulin sensitizers in PCOS may be partly due to a decrease in inflammation.     

Serum leptin as an additional possible pathogenic factor in polycystic ovary syndrome

OBJECTIVES: Recent data raised the possibility that high leptin levels may contribute to infertility in some women with PCOS. DESIGN AND METHODS: To assess changes in leptin levels and its relationship to some hormonal changes (insulin, testosterone, SHBG, FSH, LH, and prolactin) associated with PCOS in obese (n = 27) and nonobese (n = 18) patients when compared to obese and nonobese normal controls (n = 20). RESULTS: Leptin concentration were significantly higher in PCOS than in controls, p < 0.05, with 81% sensitivity and 50% specificity. Whereas, high serum insulin levels were found in obese and nonobese women with PCOS, high serum leptin, FAI together with reduced SHBG were found in obese rather than nonobese PCOS women. Moreover, hyperleptinemia in PCOS women was not correlated to hyperinsulinemia (r = -0.13 and -0.4 in obese and nonobese PCOS women, respectively). In the patient's group correlation analysis between fasting serum leptin and different studied variables showed some correlation with body mass index (BMI) only (r = 0.413) suggesting that high leptin levels could be a characteristic of the obese PCOS. However, multiregression analysis showed that together with testosterone, leptin can successfully predict the presence or absence of PCOS. CONCLUSION: The potential significance of leptin for the pathophysiology of PCOS will await direct studies of the effects of exogenous leptin and/or its inhibitors on the reproductive axis of women, including those with PCOS.     

Polycystic ovarian syndrome: diagnosis and management

Polycystic ovarian syndrome (PCOS) affects 4% to 12% of women of reproductive age. The lack of well-defined diagnostic criteria makes identification of this common disease confusing to many clinicians. Also, with the varied manifestations of the disorder a patient may present to any one of several providers: an internist, family practitioner, nurse practitioner, pediatrician, gynecologist, dermatologist, or endocrinologist. Furthermore, the most distressing aspect of PCOS for any given patient may change over time, from hirsutism as a teenager to infertility as a young adult--potentially requiring several different providers along the way. It is important, therefore, that those caring for these patients understand not only the management issues pertinent to their specialty, but also appreciate the other potential health risks in these women. Recent insights into the pathophysiology of PCOS have shown insulin resistance to play a substantial role and as such have brought the long-term issues of type 2 diabetes mellitus and its resultant increased risk of coronary artery disease to the forefront. No longer can irregular menses and/or hirsutism be thought of as benign nuisances. This review will focus on the two most confusing aspects of PCOS for the practicing provider--diagnosis/differential diagnosis and treatment options. Special attention is given to the role of insulin resistance and the potential utility of insulin sensitizers in management. The benefit and utmost importance of lifestyle modification for the long-term health of these women is stressed as well. It is hoped that some clarity in this regard will allow more women to not only be diagnosed and managed properly for their presenting symptoms (hirsutism, irregular menses, etc.), but also to be educated and managed for the continuing health risk of insulin resistance throughout their lives.     

多囊卵巢综合征子宫内膜病变相关因素分析

目的探讨多囊卵巢综合征（PCOS）子宫内膜病变相关因素。方法用组织学方法检测109例P-COS患者子宫内膜病理状态,同时测量人体学指标,检测内分泌激素、胰岛素、血糖,60例正常妇女为对照组,比较各组间的差异。结果子宫内膜的组织病理学诊断结果：A组50例,以子宫内膜单纯型增生为主;B组59例,以增生期为主。LH/FSH值、TI、R者A组、B组分别与对照组比较,BMI A组与对照组比较,差异均有统计学意义（P〈0.01）。结论 PCOS子宫内膜病理改变以单纯型增生为主,肥胖、胰岛素抵抗、高睾酮是子宫内膜异常增生及癌变的重要因素。     

糖耐量及胰岛素水平在多囊卵巢综合征中的临床意义

目的探讨多囊卵巢综合征(PCOS)患者糖代谢和胰岛素分泌的特征。方法比较84例PCOS患者组和30例对照组的糖耐量及胰岛素水平。结果体重指数(BMl)<25的PCOS患者与对照组比较,空腹和口服葡萄糖后,1小时、2小和3小时的血糖均无显著性差异(P>0.05),胰岛素水平均显著升高(p<0.05)。BMI≥25的PCOS患者空腹及口服葡萄糖后1小时、2小时和3小时的血糖和胰岛素水平均显著高于对照组和BMI<25的PCOS患者(p<0.05)。结论BMI>25的PCOS患者更易出现糖代谢异常,肥胖可能促进胰岛素抵抗形成。检测糖耐量及胰岛素水平可用于指导PCOS患者的治疗。     

育龄期多囊卵巢综合征患者的糖代谢异常和胰岛素抵抗

目的探讨育龄期多囊卵巢综合征（PCOS）患者的糖代谢异常和胰岛素抵抗。方法选择育龄期PCOS患者168例,分为肥胖PCOS组78例和非肥胖PCOS组90例,正常对照组100例,对比临床表现及检测内分泌激素、空腹血糖、空腹胰岛素、服糖后2h血糖及2h胰岛素。结果育龄期PCOS患者的月经周期、多毛、痤疮、B超提示卵巢增大、卵巢多囊性改变、有不孕史与对照组比较,差异均有显著性（P〈0．05）,育龄期PCOS组的血清LH、T与对照组比较,差异有显著性（P〈0．05）。育龄期肥胖P-COS组的空腹血糖、服糖后2h血糖、空腹胰岛素、服糖后2h胰岛素与对照组比较,差异均有显著性（P〈0．05）。结论早期出现月经稀发、BMI升高的患者是否存在PCOS,值得重视。育龄期PCOS患者尤其肥胖型要高度重视糖代谢异常及胰岛素抵抗,以决定是否采取干预措施,避免出现远期并发症而对PCOS患者造成健康威胁。     

可溶性晚期糖基化终末产物受体在多囊卵巢综合征中的表达及其意义

[目的]探讨血清可溶性晚期糖基化终末产物受体 (sRAGE)水平在多囊卵巢综合(PCOS)患者中的表达及临床意义.[方法]选取2015年1月至2016年4月于本院生殖中心就诊的PCOS患者80例,依据伴或不伴高雄激素血症(HA)/胰岛素抵抗(IR),将PCOS患者分为四组.A组:PCOS+不伴高雄激素血症(NHA)+不伴高胰岛素抵抗(NIR);B组:PCOS+IR;C组:PCOS+HA;D组:PCOS+HA+IR,每组20例.另选20名健康女性为正常对照组(E组).采用电化学发光法检测各组黄体生成激素(LH)、睾酮(T)和空腹胰岛素(fasting blood insulin,FINS)、己糖激酶法检测空腹血糖(fasting blood glucose,FBG)、ELISA法检测血清sRAGE水平,用稳态模式胰岛素抵抗指数(HOMA-IR)评价IR程度.分析sRAGE与各指标的相关性.[结果]sRAGE值由高到底分别是E组、A组、C组、B组、D组(P<0.05),组间比较差异有统计学意义(P<0.05);sRAGE与LH、T、FBG、FINS、HOME-IR呈负相关.[结论]sRAGE可通过竞争性结合RAGE的配体,减弱其所导致的病理作用,在PCOS中起潜在保护作用.     

Oxidative stress in polycystic ovary syndrome and its contribution to the risk of cardiovascular disease

OBJECTIVES: To determine oxidant and antioxidant status in women with polycystic ovary syndrome (PCOS) and its contribution to the risk of cardiovascular disease. DESIGN AND METHODS: 27 women with PCOS were compared with regard to oxidant and antioxidant status with 18 age- and body mass index (BMI)-matched healthy. Oxidant status was evaluated by determination of erythrocyte malondialdehyde (MDA) concentration, while antioxidant status was evaluated by determination of erythrocyte reduced glutathione (GSH) concentration, and glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities. Area under curve (AUC) for glucose, AUC for insulin and the insulin sensitivity index (ISI) were calculated from two-hour OGTT. RESULTS: Women with PCOS were found to have higher AUC for glucose (p = 0.01), AUC for insulin (p < 0.001), MDA level (p = 0.009) and SOD activity (p = 0.04), and lower ISI (p < 0.001) and GSH level (p = 0.03) than the controls. In correlation analysis, a significant relationship was found between MDA levels and age (p < 0.01), BMI (p < 0.001), waist-to-hip ratio (p < 0.01), systolic and diastolic blood pressures (both p < 0.05), AUCs for glucose and insulin (both p < 0.05), ISI (r = -0.42, p < 0.05) and triglyceride (p < 0.01). CONCLUSIONS: An increase in oxidant status was found in women with PCOS, and this increase was related to central obesity, age, blood pressure, serum glucose, insulin and triglyceride levels and insulin resistance. In contrast, antioxidant status was observed to be insufficient. These findings suggest that increased oxidative stress may contribute to the increased risk of cardiovascular disease in women with PCOS.     

Excessive insulin receptor serine phosphorylation in cultured fibroblasts and in skeletal muscle. A potential mechanism for insulin resistance in the polycystic ovary syndrome.

We investigated the cellular mechanisms of the unique disorder of insulin action found in the polycystic ovary syndrome (PCOS). Approximately 50% of PCOS women (PCOS-Ser) had a significant increase in insulin-independent beta-subunit [32P]phosphate incorporation (3.7-fold, P < 0.05 vs other groups) in skin fibroblast insulin receptors that was present in serine residues while insulin-induced tyrosine phosphorylation was decreased (both P < 0.05 vs other groups). PCOS skeletal muscle insulin receptors had the same abnormal phosphorylation pattern. The remaining PCOS women (PCOS-n1) had basal and insulin-stimulated receptor autophosphorylation similar to control. Phosphorylation of the artificial substrate poly GLU4:TYR1 by the PCOS-Ser insulin receptors was significantly decreased (P < 0.05) compared to control and PCOS-n1 receptors. The factor responsible for excessive serine phosphorylation appeared to be extrinsic to the receptor since no insulin receptor gene mutations were identified, immunoprecipitation before autophosphorylation corrected the phosphorylation defect and control insulin receptors mixed with lectin eluates from affected PCOS fibroblasts displayed increased serine phosphorylation. Our findings suggest that increased insulin receptor serine phosphorylation decreases its protein tyrosine kinase activity and is one mechanism for the post-binding defect in insulin action characteristic of PCOS.     

No association between common Gly972Arg variant of the insulin receptor substrate-1 and polycystic ovary syndrome in Southern Chilean women

BACKGROUND: Previously studies have indicated that the insulin receptor substrate-1 (IRS-1) Gly972Arg (G972R) polymorphism is associated with polycystic ovary syndrome (PCOS). We examined the possible association between G972R common variant of the IRS-1 gene and PCOS in Southern Chilean women with PCOS and controls. METHODS: A total of 50 women with PCOS (29.1+/-8.1 yr) and 75 healthy women (29.3+/-9.3 yr) were included. Serum lipids, glucose and uric acid concentrations were determined by enzymatic-colorimetric methods. The G972R variant of the IRS-1 gene was detected by PCR-RFLP. RESULTS: Women with PCOS exhibited a higher concentrations of total testosterone, glucose, insulin, total cholesterol, triglycerides, LDL-C and uric acid, and lower HDL-C concentrations than controls (P<0.05). The presence of G972R polymorphism in PCOS and control women was not significantly different (16% vs. 6.6%, P=0.276). The OR for PCOS associated to 972R variant was 2.67 (95% CI: 0.82-8.69, P=NS). Moreover, neither association between G972R genotypes and metabolic parameters were observed in PCOS women or controls. CONCLUSION: Our data do not support an association between G972R variant of the IRS-1 with PCOS or its metabolic parameters in Southern Chilean women.     

Polycystic ovary syndrome: new perspective on an old problem

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. New treatment approaches resulting from a refined understanding of the pathophysiology are evolving. The literature shows that PCOS is an endocrinopathy resulting from insulin resistance and the compensatory hyperinsulinemia. This results in adverse effects on multiple organ systems and may result in alteration in serum lipids, anovulation, abnormal uterine bleeding, and infertility. In addition, PCOS may place the patient at long-term risk for the development of type 2 diabetes, hypertension, endometrial cancer, and cardiovascular disease. Oral contraceptives, progestins, antiandrogens, and ovulation induction agents remain standard therapies. However, insulin-sensitizing agents are now being shown to be useful alone or combined with standard therapies. Early identification of patients at risk and prompt initiation of therapies, followed by long-term surveillance and management, may promote the patient's long-term health.     

Troglitazone for treatment of polycystic ovary syndrome

Polycystic ovary syndrome(PCOS) is characterized by clinical symptoms such as menstrual dysfunction, unovulatory infertility, masculinization, obesity, polycystic ovary by ultrasound, and endocrine abnormalities such as hyperandrogenism, and elevated LH to FSH ratio. Recent reports suggest that insulin resistance plays an important role in the pathogenesis of PCOS, and several insulin sensitizing agents have been used for the treatment of PCOS. Troglitazone, one of the thiazolidinediones, improves not only insulin sensitivity but also hyperandrogenism and ovulatory function. Troglitazone appears to be useful in treating women with PCOS. Further investigations are needed to assess the effectiveness and safety.