Prevalence of metabolic syndrome in four phenotypes of PCOS and its relationship with androgenic components among Iranian women: A cross-sectional study


Background: Polycystic ovary syndrome (PCOS) increases the risk of metabolic syndrome (MetS). Insulin resistance (IR) plays a major role in the pathophysiology of both PCOS and MetS.

Objective: This study was designed to compare the prevalence of MetS among different phenotypes of PCOS and its relationship with androgenic components.

Materials and Methods: 182 participants eligible for this five-group comparative study were selected by convenience sampling method. They were classified according to the Rotterdam criteria: clinical and/or biochemical hyperandrogenism (H) + PCOS on ultrasound (P) + ovulation disorders (O) (n = 41), clinical and/or biochemical H + PCOS on P (n = 33), PCOS on P + O (n = 40), clinical and/or biochemical H + O (n = 37), and control (without PCOS) (n = 31). MetS was measured based on the National Cholesterol Education Program Adult Treatment Panel III criteria. Androgenic components included free androgen- index (FAI), total-testosterone (TT) level and sex-hormone-binding-globulin (SHBG).

Results: A significant difference was observed between the study groups in terms of MetS prevalence (p = 0.01). In phenotype H+P+O, there was a statistically significant positive association between TG and TT, and a significant negative association between SBP and DBP with SHBG. In phenotype O+P, WC was inversely associated with SHBG. In phenotype H+O, FBS and TG were positively associated with FAI but HDL was inversely associated with FAI. Moreover, WC and DBP were positively associated with TT in phenotype H+O. No associations were detected between MetS parameters and androgenic components in other PCOS subjects (phenotype H+P) and in the control group. TT was significantly higher in the PCOS group suffering from MetS (p = 0.04).

Conclusion: According to the research results, hyperandrogenic components are potent predictors of metabolic disorders. Thus, we suggest that MetS screening is required for the prevention of MetS and its related complications in PCOS women.

Key words: Polycystic ovary syndrome, Metabolic syndrome, Hyperandrogenism.

[1] Mehrabadi S, Jahanian Sadatmahalleh Sh, Kazemnejad A. Association of depression and anxiety with cognitive function in patients with polycystic ovary syndrome. J Mazandaran Univ Med Sci 2017; 27: 159–170.

[2] Tehrani FR, Simbar M, Tohidi M, Hosseinpanah F, Azizi F. The prevalence of polycystic ovary syndrome in a community sample of Iranian population: Iranian PCOS prevalence study. Reprod Biol Endocrinol 2011; 9: 39.

[3] Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004; 19: 41–47.

[4] Huang R, Zheng J, Li S, Tao T, Ma J, Liu W. Characteristics and contributions of hyperandrogenism to insulin resistance and other metabolic profiles in polycystic ovary syndrome. Acta Obstet Gynecol Scand 2015; 94: 494–500.

[5] Sharma S, Majumdar A. Prevalence of metabolic syndrome in relation to body mass index and polycystic ovarian syndrome in Indian women. J Hum Reprod Sci 2015; 8: 202–208.

[6] Madani T, Hosseini R, Ramezanali F, Khalili G, Jahangiri N, Ahmadi J, et al. Metabolic syndrome in infertile women with polycystic ovarian syndrome. Arch Endocrinol Metab 2016; 60: 199–204.

[7] Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; American heart association; world heart federation; international atherosclerosis society; and international association for the study of obesity. Circulation 2009; 120: 1640–1645.

[8] Carmina E, Napoli N, Longo RA, Rini GB, Lobo RA. Metabolic syndrome in polycystic ovary syndrome (PCOS): lower prevalence in southern Italy than in the USA and the influence of criteria for the diagnosis of PCOS. Eur J Endocrinol 2006; 154: 141–145.

[9] Nandi A, Chen Z, Patel R, Poretsky L. Polycystic ovary syndrome. Endocrinol Metab Clin North Am 2014; 43: 123– 147. [10] Lazic M, Aird F, Levine JE, Dunaif A. Prenatal androgen treatment alters body composition and glucose homeostasis in male rats. J Endocrinol 2011; 208: 293–300.

[11] Yang R, Yang S, Li R, Liu P, Qiao J, Zhang Y. Effects of hyperandrogenism on metabolic abnormalities in patients with polycystic ovary syndrome: a meta-analysis. Reprod Biol Endocrinol 2016; 14: 67.

[12] Vaggopoulos V, Trakakis E, Chrelias C, Panagopoulos P, Basios G, Makridima S, et al. Comparing classic and newer phenotypes in Greek PCOS women: the prevalence of metabolic syndrome and their association with insulin resistance. J Endocrinol Invest 2013; 36: 478–484.

[13] Zahiri Z, Sharami SH, Milani F, Mohammadi F, Kazemnejad E, Ebrahimi H, et al. Metabolic syndrome in patients with polycystic ovary syndrome in Iran. Int J Fertil Steril 2016; 9: 490–496.

[14] 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: 194–200.

[15] Tripathy P, Sahu A, Sahu M, Nagy A. Metabolic risk assessment of Indian women with polycystic ovarian syndrome in relation to four Rotterdam criteria based phenotypes. Eur J Obstet Gynecol Reprod Biol 2018; 224: 60–65.

[16] Kim MJ, Lim NK, Choi YM, Kim JJ, Hwang KR, Chae SJ, et al. Prevalence of metabolic syndrome is higher among non-obese PCOS women with hyperandrogenism and menstrual irregularity in Korea. PLoS One 2014; 9: e99252.

[17] Das BP, Alakananda, Goel I. A Study on Prevalance of Metabolic Syndrome in Polycystic Ovarian Syndrome and its Phenotypes. Int J Sci Res 2017; 6: 11–19.

[18] Moghetti P, Tosi F, Castello R, Magnani CM, Negri C, Brun E, et al. The insulin resistance in women with hyperandrogenism is partially reversed by antiandrogen treatment: evidence that androgens impair insulin action in women. J Clin Endocrinol Metab 1996; 81: 952–960.

[19] Zhang HY, Zhu FF, Xiong J, Shi XB, Fu SX. Characteristics of different phenotypes of polycystic ovary syndrome based on the rotterdam criteria in a large-scale chinese population. BJOG 2009; 116: 1633–1639.

[20] Hashemi S, Ramezani Tehrani F, Noroozzadeh M, Azizi F. Normal cut-off values for hyperandrogenaemia in Iranian women of reproductive age. Eur J Obstet Gynecol Reprod Biol 2014; 172: 51–55.

[21] Ferriman D, Gallwey JD. Clinical assessment of body hair growth in women. J Clin Endocrinol Metab 1961; 21: 1440–1447.

[22] Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement: Executive Summary. Crit Pathw Cardiol 2005; 4: 198–203.

[23] Azizi F, Khalili D, Aghajani H, Esteghamati A, Hosseinpanah F, Delavari A, et al. Appropriate waist circumference cut-off points among Iranian adults: the first report of the Iranian National Committee of Obesity. Arch Iran Med 2010; 13: 243–244.

[24] Kavardzhikova S, Pechlivanov B. [Clinical, hormonal and metabolic characteristics of different phenotypes of polycystic ovary syndrome, in Bulgarian population]. Akush Ginekol 2010; 49: 32–37.

[25] Goverde AJ, van Koert AJ, Eijkemans MJ, Knauff EA, Westerveld HE, Fauser BC, et al. Indicators for metabolic disturbances in anovulatory women with polycystic ovary syndrome diagnosed according to the Rotterdam consensus criteria. Hum Reprod 2009; 24: 710–717.

[26] Jamil AS, Alalaf SK, Al-Tawil NG, Al-Shawaf T. A casecontrol 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.

[27] Hosseinpanah F, Barzin M, Keihani S, Ramezani Tehrani F, Azizi F. Metabolic aspects of different phenotypes of polycystic ovary syndrome: Iranian PCOS prevalence study. Clin Endocrinol 2014; 81: 93–99.

[28] Diamanti-Kandarakis E, Christakou C, Kandarakis H. Polycystic ovarian syndrome: the commonest cause of hyperandrogenemia in women as a risk factor for metabolic syndrome. Minerva Endocrinol 2007; 32: 35–47.

[29] Pehlivanov B, Orbetzova M. Characteristics of different phenotypes of polycystic ovary syndrome in a Bulgarian population. Gynecol Endocrinol 2007; 23: 604–609.

[30] Lerchbaum E, Schwetz V, Rabe T, Giuliani A, Obermayer- Pietsch B. Hyperandrogenemia in polycystic ovary syndrome: exploration of the role of free testosterone and androstenedione in metabolic phenotype. PLoS One 2014; 9: e108263.

[31] Sung YA, Oh JY, Chung H, Lee H. Hyperandrogenemia is implicated in both the metabolic and reproductive morbidities of polycystic ovary syndrome. Fertil Steril 2014; 101: 840–845.

[32] Demirel F, Bideci A, Cinaz P, Camurdan MO, Biberoglu G, Yesilkaya E, et al. Serum leptin, oxidized low density lipoprotein and plasma asymmetric dimethylarginine levels and their relationship with dyslipidaemia in adolescent girls with polycystic ovary syndrome. Clin Endocrinol 2007; 67: 129–134.

[33] Fruzzetti F, Perini D, Lazzarini V, Parrini D, Genazzani AR. Adolescent girls with polycystic ovary syndrome showing different phenotypes have a different metabolic profile associated with increasing androgen levels. Fertil Steril 2009; 92: 626–634.

[34] Dreno B, Poli F, Pawin H, Beylot C, Faure M, Chivot M, et al. Development and evaluation of a Global Acne Severity Scale (GEA Scale) suitable for France and Europe. J Eur Acad Dermatol Venereol 2011; 25: 43–48.

[35] Fruzzetti F, Perini D, Lazzarini V, Parrini D, Genazzani AR. Hyperandrogenemia influences the prevalence of the metabolic syndrome abnormalities in adolescents with the polycystic ovary syndrome. Gynecol Endocrinol 2009; 25: 335–343.