The Jean Hailes Foundation for Women's Health, Monash Institute of Health Services Research, Monash University, Melbourne, Victoria, Australia.
Fertil Steril. 2010 Jan;93(1):184-91. doi: 10.1016/j.fertnstert.2008.09.034. Epub 2008 Nov 18.
To assess the interaction between insulin resistance and endothelial function and the optimal treatment strategy addressing cardiovascular risk in polycystic ovary syndrome.
Randomized controlled trial.
Controlled clinical study.
PATIENT(S): Overweight age- and body mass index-matched women with polycystic ovary syndrome.
INTERVENTION(S): Six months metformin (1 g two times per day, n = 36) or oral contraceptive pill (OCP) (35 microg ethinyl E(2)-2 mg cytoproterone acetate, n = 30).
MAIN OUTCOME MEASURE(S): Fasting and oral glucose tolerance test glucose and insulin levels, endothelial function (flow-mediated dilation, asymmetric dimethylarginine, plasminogen activator inhibitor-1, von Willebrand factor), inflammatory markers (high-sensitivity C-reactive protein), lipids, and hyperandrogenism.
RESULT(S): The OCP increased levels of glucose and insulin on oral glucose tolerance test, high-sensitivity C-reactive protein, triglycerides, and sex-hormone binding globulin and decreased levels of low-density lipoprotein cholesterol and T. Metformin decreased levels of fasting insulin, oral glucose tolerance test insulin, high-density lipoprotein cholesterol, and high-sensitivity C-reactive protein. Flow-mediated dilation increased only with metformin (+2.2% +/- 4.8%), whereas asymmetric dimethylarginine decreased equivalently for OCP and metformin (-0.3 +/- 0.1 vs. -0.1 +/- 0.1 mmol/L). Greater decreases in plasminogen activator inhibitor-1 occurred for the OCP than for metformin (-1.8 +/- 1.6 vs. -0.7 +/- 1.7 U/mL).
CONCLUSION(S): In polycystic ovary syndrome, metformin improves insulin resistance, inflammatory markers, and endothelial function. The OCP worsens insulin resistance and glucose homeostasis, inflammatory markers, and triglycerides and has neutral or positive endothelial effects. The effect of the OCP on cardiovascular risk in polycystic ovary syndrome is unclear.
评估胰岛素抵抗与内皮功能之间的相互作用，以及针对多囊卵巢综合征心血管风险的最佳治疗策略。
随机对照试验。
对照临床试验。
超重、年龄和体重指数匹配的多囊卵巢综合征患者。
二甲双胍（每天 2 次，每次 1 克，n = 36）或口服避孕药（OCP）（35 微克炔雌醇 E(2)-2 毫克环丙孕酮醋酸酯，n = 30）治疗 6 个月。
空腹和口服葡萄糖耐量试验血糖和胰岛素水平、内皮功能（血流介导的扩张、不对称二甲基精氨酸、纤溶酶原激活物抑制剂-1、血管性血友病因子）、炎症标志物（高敏 C 反应蛋白）、脂质和高雄激素血症。
OCP 增加了口服葡萄糖耐量试验时的血糖和胰岛素水平、高敏 C 反应蛋白、甘油三酯和性激素结合球蛋白水平，降低了低密度脂蛋白胆固醇和 T 水平。二甲双胍降低了空腹胰岛素、口服葡萄糖耐量试验胰岛素、高密度脂蛋白胆固醇和高敏 C 反应蛋白水平。仅二甲双胍可使血流介导的扩张增加（+2.2% +/- 4.8%），而 OCP 和二甲双胍均可使不对称二甲基精氨酸降低（-0.3 +/- 0.1 对 -0.1 +/- 0.1 mmol/L）。OCP 降低纤溶酶原激活物抑制剂-1 的程度大于二甲双胍（-1.8 +/- 1.6 对 -0.7 +/- 1.7 U/mL）。
在多囊卵巢综合征中，二甲双胍可改善胰岛素抵抗、炎症标志物和内皮功能。OCP 可加重胰岛素抵抗和葡萄糖稳态紊乱、炎症标志物和甘油三酯，并具有中性或正向的内皮功能效应。OCP 对多囊卵巢综合征心血管风险的影响尚不清楚。
