**1.2. Epidemiology**

Globally, PCOS affects 5–20% of women of reproductive age [9]. One report summarized the incidence of PCOS as 6–13% in Hispanic women, 3–9% in African American women, and 2–9% in Asian women [10]. The prevalence of PCOS in different geographical regions ranges from

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Around 27% of premenopausal women with PCOS have type II DM [17]. Dyslipidemia may be up to 70% in women with PCOS [18, 19]. In a large study of European and American women with PCOS, the total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels increased significantly, up to 29 and 16 mg/dl, respectively, in non-Hispanic white, obese women with PCOS compared to obese women without PCOS [19]. This study also noted that the total cholesterol and LDL-C levels were elevated significantly, up to 32 and 32 mg/dl, respectively, in nonobese women with PCOS compared to nonobese women without PCOS [19]. Another worldwide systematic review and meta-analysis demonstrated that triglycerides (TG) and LDL-C levels were 26 and 12 mg/dl higher, and high-density lipoprotein cho-

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lesterol (HDL-cholesterol) concentration was 6 mg/dl lower than that of controls [20].

(CHD) and stroke for women with PCOS compared to those without PCOS [23].

cancer and for ovarian cancer (OR up to 2.52), but stable for breast cancer [26].

**2. Etiology**

(INSR and HMGA2) dysfunction in PCOS [31].

One clinical study demonstrated that nearly 26% of women with PCOS have hypertension [21]. The metabolic imbalances in patients with PCOS cause chronic low-grade inflammation and cardiovascular disturbances, which increase the risk of cardiovascular disease [22]. One systematic review and meta-analysis showed a 2-fold increased risk of coronary heart disease

Women with PCOS account for around 80% of women with anovulatory infertility [24, 25]. A recently systematic review and meta-analysis showed that women of all ages with PCOS were at a significantly increased risk [odds ratio (OR) up to 2.79] for endometrial cancer [26]. Moreover, this study also revealed that when women over 54 years of age were excluded from the analysis, the risk for women with PCOS increased more (OR up to 4.05) for endometrial

The etiology of PCOS is still not clear. A systematic review suggested that post-natal exposure to androgens results in reprogramming of the hypothalamic-pituitary-ovarian-axis [27]. Recently, some clinical studies have confirmed that human fetal androgen excess promotes PCOS development after birth by checking infant blood levels at term [28]. The circulating androgen levels of the human female fetus in the second trimester can increase into the male range and mid-gestational amniotic testosterone levels in female fetuses of PCOS mothers may be higher than those in normal mothers, which might influence fetal development [28]. Another review article mentioned that the fetal ovary is more likely to produce an excess of androgens in response to maternal human chorionic gonadotropin (hCG) in subjects genetically predisposed to PCOS [29]. Furthermore, some genetic variations are associated with PCOS. For example, DENND1A is found in the cytoplasm and nuclei of ovarian theca cells. Over expression of DENND1A variant 2 results in a PCOS-like phenotype, and knock-down of DENND1A variant 2 in PCOS theca cells reversed this phenotype [30]. In addition, a recent review showed that genome-wide association studies (GWAS) have identified some loci containing genes with clear roles in reproductive (LHCGR, FSHR, and FSHB) and metabolic

**Table 1.** Diagnostic criteria for PCOS.

5 to 10% according to the NIH 1990 criteria, from 10 to 15% according to the AE-PCOS 2006 criteria, and from 6 to 21% when the Rotterdam criteria are applied [7]. East Asian subjects (Korean, Chinese, and Thai) appear to have a lower prevalence of PCOS (about 5%) compared to Caucasian women (11–20%) [11].

One systematic review and meta-analysis showed the incidence of PCOS phenotypes using the 2012 NIH criteria was 50% for phenotype A, 13% for phenotype B, 14% for phenotype C, and 17% for phenotype D [12].

#### **1.3. Comorbidities**

Patients with PCOS often have comorbidities such as obesity, insulin resistance/type II diabetes mellitus (Type II DM), dyslipidemia, hypertension/cardiovascular disease, infertility/subfertility, or cancer. One systematic review and meta-analysis demonstrated that women with PCOS had a pooled prevalence of 61% for overweight [body mass index (BMI) > 25], 49% for obesity (BMI > 30), and 54% for central obesity [13]. Insulin resistance (IR) is present in 50–80% of these women, which is associated with obesity [14, 15]. Both lean (30%) and obese women (70%) with PCOS show decreased insulin sensitivity [16].

Around 27% of premenopausal women with PCOS have type II DM [17]. Dyslipidemia may be up to 70% in women with PCOS [18, 19]. In a large study of European and American women with PCOS, the total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels increased significantly, up to 29 and 16 mg/dl, respectively, in non-Hispanic white, obese women with PCOS compared to obese women without PCOS [19]. This study also noted that the total cholesterol and LDL-C levels were elevated significantly, up to 32 and 32 mg/dl, respectively, in nonobese women with PCOS compared to nonobese women without PCOS [19]. Another worldwide systematic review and meta-analysis demonstrated that triglycerides (TG) and LDL-C levels were 26 and 12 mg/dl higher, and high-density lipoprotein cholesterol (HDL-cholesterol) concentration was 6 mg/dl lower than that of controls [20].

One clinical study demonstrated that nearly 26% of women with PCOS have hypertension [21]. The metabolic imbalances in patients with PCOS cause chronic low-grade inflammation and cardiovascular disturbances, which increase the risk of cardiovascular disease [22]. One systematic review and meta-analysis showed a 2-fold increased risk of coronary heart disease (CHD) and stroke for women with PCOS compared to those without PCOS [23].

Women with PCOS account for around 80% of women with anovulatory infertility [24, 25]. A recently systematic review and meta-analysis showed that women of all ages with PCOS were at a significantly increased risk [odds ratio (OR) up to 2.79] for endometrial cancer [26]. Moreover, this study also revealed that when women over 54 years of age were excluded from the analysis, the risk for women with PCOS increased more (OR up to 4.05) for endometrial cancer and for ovarian cancer (OR up to 2.52), but stable for breast cancer [26].
