目的 探讨多囊卵巢综合征(PCOS)的病因、发病机理及寻找最佳的治疗方案提供依据.方法 通过放射免疫(RIA)法测患者胰岛素释放试验,酶法测糖耐量试验,电化学发光免疫分析(ECLIA)法测血清LH、FSH、E2、P、T水平.结果 表明28.2%患者有胰岛素抵抗(IR),13.1%有IR和糖耐量受损,5.5%糖耐量受损.单纯IR患者中,肥胖者占35.7%;单纯糖耐量受损者中,肥胖者占36.3%;IR伴糖耐量受损者中,肥胖者占34.6%;肥胖组LH、LH/FSH、E2、T水平与非肥胖组之间无显著性差异(P>0.05);而肥胖组与非肥胖的空腹血糖及空腹胰岛素水平有显著性差异(P<0.05);肥胖者与非肥胖者月经周期及卵泡数目两指标有显著性差异(P<0.05).结论 有较多PCOS患者存在IR或糖耐量受损;在IR和糖耐量受损的患者中,肥胖者占有较高的比重,肥胖可促进IR形成;肥胖可加重IR和生殖功能障碍.%Objective To explore the etiology and mechanisms of polycystic ovarian syndrome (PCOS). Methods The levels of serum LH, FSH, E2, P and T in patients with PCOS were detected by ECLIA. The insulin release test was detected by RIA and the glucose tolerance test by enzymatic method. Results It showed that 28.2% patients only insulin resistance (IR) , 13. 1% patients also existed of IR and glucose tolerance damage, 5.5% patients only had glucose tolerance damage. Pure IR in the obese accounted for 35. 7% ; Pure impaired glucose tolerance, fat person accounted for 36. 3% ; IR with impaired glucose tolerance, fat person accounted for 34. 6%. There were no significant differences on LH, LH/FSH, E2, T levels between the obese group and the non-obese group (P > 0. 05) , but there was a significant difference on fasting blood glucose and fasting insulin levels between them ( P < 0. 05 ). The menstrual cycle and follicular number between the obese group and the non-obese group had significantly differences (P <0. 05). Conclusion There exist different degrees of IR and glucose tolerance damage in most of PCOS patients. The obese people account for higher proportion in patients with IR and glucose tolerance. The obesity can promote the formation of IR and increase reproductive dysfunction.
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