PMID- 25595199 OWN - NLM STAT- MEDLINE DCOM- 20160405 LR - 20220330 IS - 1742-4755 (Electronic) IS - 1742-4755 (Linking) VI - 12 DP - 2015 Jan 16 TI - A case-control observational study of insulin resistance and metabolic syndrome among the four phenotypes of polycystic ovary syndrome based on Rotterdam criteria. PG - 7 LID - 10.1186/1742-4755-12-7 [doi] LID - 7 AB - BACKGROUND: Polycystic ovary syndrome (PCOS) is associated with an increased risk of insulin resistance (IR), metabolic syndrome (MetS), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). Metabolic aspects of the four PCOS phenotypes remain to be fully defined. The aim of this study was to compare metabolic parameters and insulin resistance among the four PCOS phenotypes defined according to the Rotterdam criteria and to determine predictors of these complications. METHODS: A total of 526 reproductive-aged women were included in this observational case-control study. Of these, 263 were diagnosed as a PCOS based on Rotterdam criteria and 263 infertile women with no evidence of PCOS were recruited as controls. Biochemical, metabolic and insulin resistance parameters were compared in the two groups and the frequency of MetS and IR were compared among the four phenotypes. Data were analyzed for statistical significance using Student's t-test and one way analysis of variance followed by a post-hoc test (least significant difference). Chi-square tests were used to compare proportions. Univariate and multivariate logistic regression analyses were also applied. RESULTS: IR was identified in 112 (42.6%) of the PCOS women and 45 (17.1%) of the control (P <0.001). There were no significant differences in the frequency of IR and MetS between the four PCOS phenotypes. Homeostatic model assessment for IR (HOMA-IR) >/=3.8 was the most common IR parameter in PCOS and control groups. Women with oligo-anovulation (O) and PCO morphology (P) had a significantly lower level of 2-h postprandial insulin compared to women with O, P and hyperandrogenism (H) phenotypes. Logistic regression analysis showed that body mass index, waist circumference, triglyceride/high-density lipoprotein ratio (cardiovascular risk), HOMA-IR and glucose abnormalities (T2DM) were associated with increased risk of having MetS (P < 0.05). CONCLUSIONS: PCOS women with (O + P) show milder endocrine and metabolic abnormalities. Although, there were no significant differences in IR, MetS and glucose intolerance between the four PCOS phenotypes, women with PCOS are at higher risk of impaired glucose tolerance and undiagnosed diabetes. FAU - Jamil, Avin S AU - Jamil AS AD - Department of Obstetrics and Gynecology, College of Medicine, Hawler Medical University, P.O. Box 383-65, Erbil, Iraq. avinsadiq_2008@yahoo.com. FAU - Alalaf, Shahla K AU - Alalaf SK AD - Department of Obstetrics and Gynecology, College of Medicine, Hawler Medical University, P.O. Box 383-65, Erbil, Iraq. shahla_alaf@yahoo.com. FAU - Al-Tawil, Namir G AU - Al-Tawil NG AD - Department of Community Medicine, College of Medicine, Hawler Medical University, Erbil, Iraq. namiraltawil@yahoo.com. FAU - Al-Shawaf, Talha AU - Al-Shawaf T AD - Women's Health Research Unit, Centre for Primary Care and Public Health, Barts and The London Medical College, Queen Mary University, London, UK. talhayas@aol.com. AD - Department of Primary Care and Public Health, Imperial College, London, UK. talhayas@aol.com. LA - eng PT - Journal Article PT - Observational Study PT - Research Support, Non-U.S. Gov't DEP - 20150116 PL - England TA - Reprod Health JT - Reproductive health JID - 101224380 RN - 0 (Blood Glucose) RN - 0 (Lipids) SB - IM MH - Adolescent MH - Adult MH - Anthropometry/methods MH - Blood Glucose/metabolism MH - Case-Control Studies MH - Female MH - Humans MH - Insulin Resistance/*physiology MH - Iraq/epidemiology MH - Lipids/blood MH - Metabolic Syndrome/blood/epidemiology/*etiology/physiopathology MH - Phenotype MH - Polycystic Ovary Syndrome/blood/*complications/epidemiology/physiopathology MH - Young Adult PMC - PMC4417246 EDAT- 2015/01/18 06:00 MHDA- 2016/04/06 06:00 PMCR- 2015/01/16 CRDT- 2015/01/18 06:00 PHST- 2014/10/14 00:00 [received] PHST- 2015/01/09 00:00 [accepted] PHST- 2015/01/18 06:00 [entrez] PHST- 2015/01/18 06:00 [pubmed] PHST- 2016/04/06 06:00 [medline] PHST- 2015/01/16 00:00 [pmc-release] AID - 1742-4755-12-7 [pii] AID - 364 [pii] AID - 10.1186/1742-4755-12-7 [doi] PST - epublish SO - Reprod Health. 2015 Jan 16;12:7. doi: 10.1186/1742-4755-12-7.