Lipid profile in women of reproductive age with various polycystic ovary syndrome phenotypes

Cover Page


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription Access

Abstract

Hypothesis/Aims of study. Dyslipidemia is a common metabolic disorder and is an atherogenic factor in the development of cardiovascular disease in women with polycystic ovary syndrome. Currently, four phenotypes of polycystic ovary syndrome are distinguished, associated in varying degrees of severity with dyslipidemia, insulin resistance, impaired glucose tolerance, and diabetes mellitus on one hand and chronic inflammation and oxidative stress on the other. Hyperandrogenic phenotypes (A, B, C) in polycystic ovary syndrome are associated with the development of adverse metabolic disorders and associated complications. The aim of this study was to evaluate the lipid profile in the serum of women of reproductive age with various polycystic ovary syndrome phenotypes.

Study design, materials and methods. The study included 86 women of reproductive age from 22 to 37 years old (average age was 26.6 ± 4.3 years), who, in accordance with polycystic ovary syndrome phenotypes (A, B, C, D), were divided into four groups. We studied the levels of anti-Müllerian hormone, follicle-stimulating and luteinizing hormones, prolactin, estradiol, and androgens from days 2 to 5 of the menstrual cycle. The levels of progesterone in the blood serum were determined by the enzyme immunoassay on days 20 to 23 of the menstrual cycle for three consecutive cycles. We also used echographic methods for diagnosing polycystic ovaries. All women underwent a biochemical blood test with an assessment of the lipid profile parameters (total cholesterol, triglycerides, high-density lipoproteins (HDL), and low-density lipoproteins, LDL). Besides, an oral glucose tolerance test was assessed with the study of plasma glucose and insulin levels on an empty stomach and two hours after ingestion of 75 g of glucose, the HOMA-IR index being used to assess insulin resistance.

Results. Phenotype A was found in 40 (46.5%) women with polycystic ovary syndrome, phenotype B in 22 (25.6%), phenotype C in 10 (11.6%), and phenotype D (non-androgenic) in 14 (16.3%) patients with PCOS. Of those 42 (48.8%) individuals had changes in carbohydrate metabolism (impaired glucose tolerance), of whom 39 (92.8%) women had androgenic polycystic ovary syndrome phenotypes (A, B, C). Both non-androgenic phenotype D and impaired glucose tolerance were found in 7.2% of cases. In women with hyperandrogenic polycystic ovary syndrome phenotypes, both the fasting and stimulated insulin levels were increased significantly comparing to the non-androgenic anovulatory phenotype (p < 0.05). The HOMA-IR index in women with phenotypes A, B and C was significantly (p < 0.05) higher than in patients with non-androgenic phenotype D. When evaluating the lipid profile parameters, no significant differences in cholesterol level and atherogenic coefficient in women with various polycystic ovary syndrome phenotypes were found. The levels of triglycerides and LDL were significantly (p < 0.05) higher in women with androgenic phenotype B compared to those in patients with non-androgenic phenotype D and they correlated significantly (p < 0.05) with the serum levels of androgens and sex hormone-binding globulin (SHBG). Patients with androgenic polycystic ovary syndrome phenotypes (A and B) had significantly (p < 0.05) decreased HDL levels that correlated negatively (r = –0.29; p < 0.05) with the levels of free testosterone and SHBG, when compared to the same parameters in women with non-androgenic phenotype D. In women with androgenic polycystic ovary syndrome phenotypes (A, B, C), a significant correlation (r = 0.27; p < 0.05) between the levels of stimulated insulin and SHBG were found, and a direct relation (r = 0.32; p < 0.05) between those parameters and increased levels of triglycerides and LDL was also revealed.

Conclusion. In women with hyperandrogenic and anovulatory polycystic ovary syndrome phenotypes A and B, atherogenic dyslipidemia and impaired carbohydrate metabolism were significantly more pronounced, when compared with patients with non-androgenic phenotype D. A differential and personalized approach to the examination of patients with various polycystic ovary syndrome phenotypes is an important step in the prevention of the risks of developing cardiovascular diseases in women of reproductive age.

About the authors

Elena I. Abashova

The Research Institute of Obstetrics, Gynecology, and Reproductology named after D.O. Ott

Email: abashova@yandex.ru
ORCID iD: 0000-0003-2399-3108
SPIN-code: 2133-0310
Scopus Author ID: 36503679200
ResearcherId: J-5436-2018

MD, PhD, Senior Researcher of the Department of Gynecology and Endocrinology, Head of the Ovulation Induction Center

Russian Federation, Saint Petersburg

Maria I. Yarmolinskaya

The Research Institute of Obstetrics, Gynecology, and Reproductology named after D.O. Ott; North-Western State Medical University named after I.I. Mechnikov

Email: m.yarmolinskaya@gmail.com
ORCID iD: 0000-0002-6551-4147
SPIN-code: 3686-3605
Scopus Author ID: 7801562649
ResearcherId: P-2183-2014.

MD, PhD, DSci (Medicine), Professor, Professor of the Russian Academy of Sciences, Head of the Department of Gynecology and Endocrinology, Head of the Diagnostics and Treatment of Endometriosis Center; Professor. The Department of Obstetrics and Gynecology

Russian Federation, Saint Petersburg

Olga L. Bulgakova

The Research Institute of Obstetrics, Gynecology, and Reproductology named after D.O. Ott; North-Western State Medical University named after I.I. Mechnikov

Author for correspondence.
Email: o.bulgakova1310@gmail.com
ORCID iD: 0000-0002-1007-4543
ResearcherId: AAS-1434-2020

MD, Post-Graduate Student

Russian Federation, Saint Petersburg

Elena V. Misharina

The Research Institute of Obstetrics, Gynecology, and Reproductology named after D.O. Ott; North-Western State Medical University named after I.I. Mechnikov

Email: mishellena@gmail.com
ORCID iD: 0000-0002-0276-7112
SPIN-code: 7350-5674
Scopus Author ID: 57200069538
ResearcherId: К-2720-201

MD, PhD, Senior Researcher. The Department of Endocrinology of Reproduction

Russian Federation, Saint Petersburg

References

  1. Письмо Минздрава РФ от 10 июня 2015 г. № 15-4/10/ 2-2814 «Синдром поликистозных яичников в репродуктивном возрасте (современные подходы к диагностике и лечению)». Клинические рекомендации (протокол лечения). [Letter of the Ministry of health of the Russian Federation No. 15-4/10/2-2814 “Sindrom polikistoznykh yaichnikov v reproduktivnom vozraste (sovremennye podkhody k diagnostike i lecheniyu)”. Klinicheskie rekomendatsii (protokol lecheniya); dated 2015 June 10. (In Russ.)]. Доступно по: https://rulaws.ru/acts/Pismo-Minzdrava-Rossii-ot-10.06.2015-N-15-4_10_2-2814/. Ссылка активна на 15.10.2020.
  2. Teede HJ, Misso ML, Costello MF, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Hum Reprod. 2018;33(9):1602-1618. https://doi.org/10.1093/humrep/dey256.
  3. Dejager S, Pichard C, Giral P, et al. Smaller LDL particle size in women with polycystic ovary syndrome compared to controls. Clin Endocrinol (Oxf). 2001;54(4):455-462. https://doi.org/10.1046/j.1365-2265.2001.01245.x.
  4. Kim JJ, Choi YM. Dyslipidemia in women with polycystic ovary syndrome. Obstet Gynecol Sci. 2013;56(3):137-142. https://doi.org/10.5468/ogs.2013.56.3.137.
  5. González F, Rote NS, Minium J, Kirwan JP. Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome. J Clin Endocrinol Metab. 2006;91(1):336-340. https://doi.org/10.1210/jc.2005-1696.
  6. Lambert EA, Teede H, Sari CI, et al. Sympathetic activation and endothelial dysfunction in polycystic ovary syndrome are not explained by either obesity or insulin resistance. Clin Endocrinol (Oxf). 2015;83(6):812-819. https://doi.org/10.1111/cen.12803.
  7. Kaplan M, Ates I, Yüksel M, et al. The role of oxidative stress in the etiopathogenesis of gluten-sensitive enteropathy disease. J Med Biochem. 2017;36(3):243-250. https://doi.org/10.1515/jomb-2017-0017.
  8. Papalou O, Victor VM, Diamanti-Kandarakis E. Oxidative stress in polycystic ovary syndrome. Curr Pharm Des. 2016;22(18):2709-2722. https://doi.org/10.2174/1381612822666160216151852.
  9. Final Report National Institute of Health. Evidence-based Methodology Workshop on Polycystic Ovary Syndrome December 3-5, 2012. Available from: http://prevention.nih.gov/workshops/2012/pcos/resourc-es.aspx.
  10. Panidis D, Tziomalos K, Misichronis G, et al. Insulin resistance and endocrine characteristics of the different phenotypes of polycystic ovary syndrome: A prospective study. Hum Reprod. 2012;27(2):541-549. https://doi.org/10.1093/humrep/der418.
  11. Huang R, Zheng J, Li S, et al. Characteristics and contributions of hyperandrogenism to insulin resistance and other metabolic profiles in polycystic ovary syndrome. Acta Obstet Gynecol Scand. 2015;94(5):494-500. https://doi.org/ 10.1111/aogs.12612.
  12. Дедов И.И., Мельниченко Г.А. Синдром поликистозных яичников. – М.: МИА, 2007. – 192 с. [Dedov II, Mel’nichenko GA. Sindrom polikistoznykh yaichnikov. Moscow: MIA; 2007. 192 р. (In Russ.)]
  13. Kakoly NS, Khomami MB, Joham AE, et al. Ethnicity, obesity and the prevalence of impaired glucose tolerance and type 2 diabetes in PCOS: A systematic review and meta-regression. Hum Reprod Update. 2018;24(4):455-467. https://doi.org/10.1093/humupd/dmy007.
  14. Rubin KH, Glintborg D, Nybo M, et al. Development and risk factors of type 2 diabetes in a nationwide population of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2017;102(10):3848-3857. https://doi.org/10.1210/jc.2017-01354.
  15. Kar S. Anthropometric, clinical, and metabolic comparisons of the four Rotterdam PCOS phenotypes: A prospective study of PCOS women. J Hum Reprod Sci. 2013;6(3):194-200. https://doi.org/10.4103/0974-1208.121422.
  16. Jamil AS, Alalaf SK, Al-Tawil NG, Al-Shawaf T. A case-control observational study of insulin resistance and metabolic syndrome among the four phenotypes of polycystic ovary syndrome based on Rotterdam criteria. Reprod Health. 2015;12:7. https://doi.org/10.1186/1742-4755-12-7.
  17. Talbott E, Guzick D, Clerici A, et al. Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol. 1995;15(7):821-826. https://doi.org/10.1161/01.atv.15.7.821.
  18. Blagojević IP, Ignjatović S, Macut D, et al. Evaluation of a summary score for dyslipidemia, oxidative stress and inflammation (the Doi Score) in women with polycystic ovary syndrome and its relationship with obesity. J Med Biochem. 2018;37(4):476-485. https://doi.org/10.2478/jomb-2018-0008.
  19. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and Pcos Society Disease State Clinical Review: Guide to the best practices in the evaluation and treatment of polycystic ovary syndrome. Part 2. Endocr Pract. 2015;21(12):1415-1426. https://doi.org/10.4158/EP15748.DSCPT2.
  20. Azziz R, Carmina E, Chen Z, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2016;2:16057. https://doi.org/10.1038/nrdp.2016.57.
  21. Bil E, Dilbaz B, Cirik DA, et al. Metabolic syndrome and metabolic risk profile according to polycystic ovary syndrome phenotype. J Obstet Gynaecol Res. 2016;42(7):837-843. https://doi.org/10.1111/jog.12985.
  22. Zaeemzadeh N, Sadatmahalleh SJ, Ziaei S, et al. Prevalence of metabolic syndrome in four phenotypes of PCOS and its relationship with androgenic components among Iranian women: A cross-sectional study. Int J Reprod Biomed. 2020;18(4): 253-264. https://doi.org/10.18502/ijrm.v13i4.6888.

Supplementary files

Supplementary Files
Action
1. JATS XML
2. Frequency of polycystic ovary syndrome phenotypes

Download (65KB)

Copyright (c) 2021 Abashova E.I., Yarmolinskaya M.I., Bulgakova O.L., Misharina E.V.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies