Metabolic profile and functional state of vascular endothelium in women with various forms of premature ovarian insufficiency

• Published in: Ginekologiâ (Moskva. Online) Vol. 20; no. 3; pp. 36 - 41
• Main Authors: Pozdnyakova, A A, Marchenko, L A, Runikhina, N K, Sharashkina, N V, Ivanets, T Yu
• Format: Journal Article
• Language: English; Russian
• Published: IP Berlin A.V 15.06.2018
• Subjects: functional markers of endothelial dysfunction; lipid profile; premature ovarian insufficiency
• ISSN: 2079-5696; 2079-5831
• DOI: 10.26442/2079-5696_2018.3.36-41

Objective. Compare levels of biochemical and functional markers of cardiovascular risk in the molecular-genetic and autoimmune forms of premature ovarian insufficiency (POI). Materials and methods. The study included 68 women with POI, 49 of them - with molecular-genetic form (a subgroup IA), 16 women with autoimmune form (a subgroup IB), 3 women - idiopathic form (a subgroup IC), and 85 women with regular periods (group II - control). Hormonal profile, levels of biochemical and functional markers of endothelial dysfunction [total cholesterol (TC), triglycerides, low density lipoproteins (LDL), high density lipoproteins, atherogenic index, apolipoproteins A1 and B, uric acid, high-sensitivity C-reactive protein (hsCRP), glucose, insulin, insulin resistance index HOMA, right and left carotid intima-media thickness (cIMT), brachial artery flow-mediated dilatation (FMD)] were assessed in all the participants. Results. The levels of cholesterol, LDL, cIMT were statistically significantly increased in subgroups IA and IB compared to group II. The patients with autoimmune form of POI (subgroup IB) had statistically increased levels of cholesterol and LDL compared to group with molecular-genetic form (subgroup IA). The women in subgroup IA also had significantly increased levels of uric acid, a highly sensitive CRP, endothelin-1 and decreased brachial artery FMD in comparison with the control group. Conclusion. Molecular-genetic POI is associated with more pronounced adverse changes in the profile of cardiovascular disease risk markers.