[Clinical features, hormonal profile, and metabolic abnormalities of obese women with obese polycystic ovary syndrome].
OBJECTIVE
To investigate and analyze the clinical presentation, hormonal profile, and metabolic abnormalities of obese women with polycystic ovary syndrome (PCOS).


METHODS
The data of the anthropometric measurements, clinical manifestations of hyperandrogenism, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E(2)), testosterone (T), prolactin (PRL), dehydro-epiandrosterone sulfate (DHEAS), sex-hormone-binding globulin (SGBG), and 17-oxyhydroprogesterone (17-OHP), fasting plasma glucose (FPG) and fasting insulin (FINS) detected after oral glucose tolerance test (OGTT), serum lipid levels, including total cholesterol (Chol), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL), homeostasis model assessment (HOMA) and area under curve (AUC) so as to assess the insulin resistance (IR), free androgen index (FAI) to estimate the extent of hyperandrogenism, HOMA IS and DeltaI(30)/DeltaG(30) used to assess the function of islet beta cells, were collected from 192 women with PCOS, aged 24 +/- 6, that were divided into 2 groups according to the body mass index (BMI): Group A (n = 70) with the BMI > or = 25 kg.m(-2) and Group B (n = 122) with the BMI < 2 5 kg.m(-2), and 65 age-matched bilateral tubal block factor infertile women served as controls that were divided into 2 groups as well: Group C (n = 25) with the BMI > or = 25 kg.m(-2); and Group D (n = 79) with the BMI < 25 kg.m(-2), and underwent a cross-sectional study.


RESULTS
(1) Clinical phenotype: The presence of obesity was 36.46% (70/192) of which 80.00% (56/70) was central obesity. The incidence of acanthosis nigricans was 17.18% (33/192), 35.71% in Group A and 6.56% in Group B. (P < 0.01). Groups A and C showed increased frequency of acanthosis nigricans compared with Group B. The value of FAI of Group A was 3.40 +/- 1.84, significantly higher than those of Group B (1.75 +/- 1.20) and Group C (1.65 +/- 0.90), (both P < 0.01). The LH/FSH ratio of Group B was 2.41 +/- 1.13, significantly higher than those of Groups A, C, and D (all P < 0.01). (2) Hormonal profile: The IR rate was 43.23% in the 192 patients, 82.86% in Group A and 20.49% in Group B. The LH and LH/FSH ratio were significantly higher in Group B than in Groups A, C, and D (all P < 0.01); T level was higher in Groups A and B than in Group C and D (all P < 0.05). SHBG was lower in Group A (108.70 +/- 81.35 nmol.L(-1)) and Group C (150.34 +/- 106.23 nmol.L(-1)) compared with Group B (192.49 +/- 98.30 nmol.L(-1)) and Group D (231.84 +/- 90.09 nmol.L(-1)) (P < 0.01 and P < 0.05). FAI level was 3.40 +/- 1.84 in Group A, significantly higher than those of Groups B (1.75 +/- 1.20), C (1.65 +/- 0.90), and D (0.84 +/- 0.45) (all P < 0.01). The FINS, TG, and HOMA IR of Groups A and C were all significantly higher than those of Groups B and D (all P < 0.01). The OGTT GAUC was significantly higher than those of Groups B, C, and D (P = 0.006, 0.028, and 0.031 respectively). (3) Metabolic profile: The prevalence of IR was 43.23% (83/192) with a higher prevalence rate in Group A (82.76%, 58/70) compared with Group B (20.49%, 25/122). The values of FINS, HOMA IR, GAUC, IAUC, and TG were all higher in Group A than in Group B (all P < 0.01). BMI and WHR were positively correlated with FAI and HOMA-IR (all P < 0.01), whereas negatively correlated with LH/FSH ratio (r = -0.345, -0.260, P < 0.01). There were no significant differences in HOMA-IS and DeltaI(30)/DeltaG(30) among these groups (all P > 0.05).


CONCLUSIONS
Obese PCOS women have more severe hyperandrogenism, IR and hyperinsulinism than normal-weight PCOS women, which may have some health implications later in life.
Li
Xin
X
The Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, China.
Lin
Jin-fang
JF
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006728:Hormones / Q000097:blood*; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood / Q000209:etiology / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000378:metabolism; D008055:Lipids / Q000097:blood; D007986:Luteinizing Hormone; D008599:Menstruation Disturbances; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000150:complications / Q000378:metabolism*; D011388:Prolactin / Q000097:blood; D013739:Testosterone / Q000097:blood
D001786:Blood Glucose; D006728:Hormones; D007328:Insulin; D008055:Lipids; D013739:Testosterone; D004958:Estradiol; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone