https://orcid.org/0000-0003-0111-9030
Polycystic ovary syndrome (PCOS) still represents one of the greatest challenges in medicine due to its complexity, progression aspects, and the consequences it entails for women’s lives: from adolescence to the postmenopausal stage [Citation1]. In fact, its prevalence and etiology remain a dilemma and a concern. After more than 80 years since Stein and Leventhal described the features of the syndrome [Citation2], its definition has been based on Rotterdam criteria with four phenotypes, which rises doubts if women who regularly ovulate or without hyperandrogenism should be considered affected with PCOS.
The description of the clinical picture had been reported in the literature before the twentieth century, but it has been recognized since 1935 as PCOS by the work of two American surgeons, Stein and Leventhal [Citation2]. After that, several publications have been made seeking for a single pathophysiological mechanism to justify PCOS. However, the interaction between genetic, environmental, behavioral and psychological factors is, to date, the best way to understand this condition and its various phenotypes [Citation1]. The syndrome affects globally a large number of women, ranging from 5 to 15% of the women during their reproductive years [Citation3,Citation4]. Although the PCOS has hyperandrogenic anovulation as a central feature, its diagnosis is also based on the exclusion of other conditions that may present a similar clinical picture [Citation1]. Thus, the diagnosis is based on criteria of expert consensus, including panels promoted by the US National Institute of Health (NIH) in 1990 [Citation5] and the Rotterdam consensus, organized by the American Society for Reproductive Medicine (ASRM) and the European Society of Human Reproduction and Embryology (ESHRE), in 2003 [Citation5–7]. The latest consensus is the one issued by the Androgen Excess and Polycystic Ovary Syndrome Society (AE-PCOS), which recommends that women should have clinical or laboratory hyperandrogenism associated with chronic anovulation and/or polycystic ovaries images [Citation6,Citation7].
Currently, it is considered an endocrine-metabolic disorder diagnosed in adults and it is based on Rotterdam Criteria with the presence of at least two of three clinical features: polycystic ovary morphology, oligoamenorrhea, and hyperandrogenism (clinical and/or biochemical) [Citation8,Citation9]. Other concerns are carbohydrate or lipid metabolic disorders, which are not part of the diagnosis, but are important factors for prognosis, mainly due to cardiovascular risk. In fact, PCOS is considered an independent factor for the development of diabetes mellitus [Citation8,Citation9].
In 2020, we performed a retrospective study that analyzed clinical and laboratory data of 462 women with PCOS treated at an outpatient clinic in a tertiary hospital in southeastern Brazil [Citation10]. Women with PCOS had a median age of 25.0 years (range: 21.0–29.0) and a median body mass index of 28.7 kg/m2 (23.9–34.0). The prevalence of insulin resistance was 55.0%, glucose intolerance 28.1%, and type 2 diabetes 4.1%. Dyslipidemia due to low HDL‐C levels occurred in 60.5%, hypertriglyceridemia in 25.9%, and central obesity in 61.3%. In our study, the metabolic syndrome was present in 27.4% of women, and hypertension in 10.9%. Interestingly, the prevalence of the metabolic syndrome in normal weight, overweight, and obese women with PCOS was 17.6%, 22.6%, and 33.9%, respectively [Citation10]. The therapy may focus on these metabolic disorders [Citation1].
In general, currently used therapies do not address the cause, but ameliorate the effects or complications associated with the syndrome such as: a) menstrual dysfunction; b) hyperandrogenism; c) infertility; d) metabolic changes; and e) prevention of cardiovascular diseases and cancer [Citation1]. Although stimulation of ovulation is effective, pregnancy rates are not high, thus more complex assisted reproductive techniques are required. Perhaps the genetic and morphological changes observed in the endometrium are crucial for the fertility of PCOS women. Nonetheless, based on recent data, the comprehensive endometrial molecular mechanisms related to PCOS that may result in subfertility, are still unclear [Citation11,Citation12].
Regardless of being treated, phenotypes and the clinical progress of these women are major concerns. In the first case, phenotypes C and D are dilemmas due to the ovulatory state and anovulation without hyperandrogenism, respectively. In fact, in 2006, the AE-PCOS did not consider women without hyperandrogenism as real PCOS patients [Citation3–7]. After that, the members of the society decided not to consider hyperandrogenism as a mandatory parameter to confirm the diagnosis of PCOS. Despite this, the question remained.
Regarding management, first line treatment may differ depending on phenotypes. For instance, oral combined contraceptives may not be appropriate as a first line of treatment for phenotype D or letrozol for phenotype C. Therefore, concerns still remain.
In conclusion, the PCOS remains a great puzzle with a number of questions to be answered. In our view, anovulation and hyperandrogenism are required to confirm the diagnosis of PCOS.
, Maria C.P. Baracat
, and José M. Soares Jr
Disciplina de Ginecologia, Departmento deObstetrícia e Ginecologia, Hospital das Clínicas,Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
[email protected]
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References
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