Clinical and laboratory indicators of polycystic ovary syndrome in Chinese Han nationality with different Rotterdam criteria-based phenotypes. (1st February 2016)

• Record Type: Journal Article
• Authors: Zhao, Yue; Ruan, Xiangyan; Mueck, Alfred O.
• Is Part Of: Gynecological endocrinology. Volume 32:Number 2(2016:Feb.)
• Page Start: 151
• Page End: 156
• Publication Date: 2016-02-01
• Subjects: Insulin resistance -- phenotype -- polycystic ovary syndrome -- rotterdam criteria -- testosterone; Endocrine gynecology -- Periodicals; Generative organs, Female -- Diseases -- Periodicals; 618.1
• DOI: 10.3109/09513590.2015.1107895
• Languages: English
• ISSNs: 0951-3590

Abstract

Abstract: The aim of this study was to investigate the clinical, endocrinic and metabolic indicators in polycystic ovary syndrome (PCOS) with different Rotterdam criteria (RC)-based subtypes, thus to guide the treatments. Six hundred and forty-seven PCOS cases were divided into four groups, with 60 cases set as the control group, the clinical and endocrinic indicators of different subtypes were evaluated. Group A was the most common and the most serious (63.2%), while group B was the least (9%). The clinical signs, as well as the endocrinic and metabolic characteristics, of the two groups were similar, but group A exhibited higher androgen level and hirsutism score. The phenotypes of group C (15.6%) and group D (12.9%) were mild, but compared with the control group, luteinizing hormone (LH) and LH/follicle stimulating hormone (FSH) were significantly increased. Insulin resistance in these four subtypes were positively correlated with apolipoprotein B (ApoB)/apolipoprotein A1 (ApoA1), while only positively correlated with serum total testosterone, and negatively correlated with LH/FSH in group A. RC-PCOS typing could reflect the basic characteristics of the disease. Hyperandrogenism was the main basis for distinguishing PCOS, although the non-hyperandrogenism group could represent a relatively mild phenotype of PCOS, there might exist different pathogenic pathways.