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Endocrine Abstracts (2015) 37 GP06.03 | DOI: 10.1530/endoabs.37.GP.06.03

1CHC Bezanijska Kosa, Belgrade, Serbia; 2Clinic of Endocrinology, Diabetes and Metabolic Diseases and Faculty of Medicine, University of Belgrade, Belgrade, Serbia; 3IBISS, University of Belgrade, Belgrade, Serbia; 4Clinic of Gynecology and Obstetrics, and Faculty of Medicine, University of Belgrade, Belgrade, Serbia; 5Faculty of Medicine, Institute of Physiology, University of Belgrade, Belgrade, Serbia.

Introduction: Dyslipidaemia is a common metabolic derangement in polycystic ovary syndrome (PCOS) and may be represented with different lipid alterations. The aim of this study was to evaluate lipid profile in different PCOS phenotypes.

Methods: We evaluated 365 PCOS women (PCOS: 25.05±6.24 kg/m2; 25.48±5.21 years) diagnosed using ESHRE/ASRM criteria and 125 BMI-matched healthy women (controls: 25.41±5.16 kg/m2; 30.35±5.62 years). PCOS group was divided into four phenotypes: a (anovulation (ANOV), hyperandrogenism (HA), polycystic ovary morphology (PCOM)), B (ANOV, HA), C (HA, PCOM) and D (ANOV, PCOM). Phenotype D had lower BMI in comparison to all other phenotypes (P<0.05). Blood samples were collected in follicular phase of menstrual cycle for determination of total cholesterol (TC), LDL, HDL, triglycerides, apolipoprotein-A1 and apolipoprotein-B. Ratios TC/HDL, LDL/HDL, TG/HDL, apoliporotein-B/apolipoprotein-A1 were calculated.

Results: PCOS women in comparison to controls had higher levels of TC (5.07±1.09 vs 4.89±0.97 mmol/l, P<0.001), LDL (3.16±0.97 vs 3.09±0.82 mmol/l, P=0.012), TG (1.20±0.85 vs 0.98±0.54 mmol/l, P<0.001), apolipoprotein-B (0.88±0.29 vs 0.83±0.25, P=0.021), while there were no differences in HDL, apoliporpotein-A1 (P>0.05). PCOS women had higher ratios: TC/HDL (3.94±1.36 vs 3.68±1.03, P=0.001), LDL/HDL (2.46±1.07 vs 2.36±0.89, P=0.019), TG/HDL (1.02±1.20 vs 0.78±0.61, P<0.001), apoliporotein-B/apolipoprotein-A1 (0.59±0.33 vs 0.52±0.19, P=0.011). Comparisons between PCOS phenotypes revealed that phenotype D had lower levels of triglycerides and the ratio TG/HDL than other three phenotypes (P<0.05 for all comparisons), while there was no difference in other lipid concentrations and ratios. Phenotype A, B and C had higher TC, TG, TC/HDL, TG/HDL, and apoliporotein-B/apolipoprotein-A1 in comparison with controls, while there were no differences between phenotype D and controls.

Conclusion: In our group of women with PCOS, only phenotype D was characterised with less deteriorated lipid profile than other PCOS phenotypes.

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