Author details

factor for assessment of cardiovascular events in a 15-year period, in PCOs women. There was an insignificant increase in overall stroke risk and in ischemic stroke risk associated with "very irregular" menstrual cycles [57]. In PCO women, higher prevalence of hypertension is related to insulin. Hyperinsulinemia have been connected with an increase in intracellular sodium and calcium, along with vascular smooth muscle hypertrophy due to insulin-like growth factor-1 (IGF-1) activity [58]. Simultaneously, androgen excess stimulates sympathetic nerve activity, as

PCOs is also associated with elevated levels of plasma endothelin-1 (ET-1), one of several circulating indicators of endothelial injury and dysfunction. One study found that impairment of endothelial function is more severe in lean than obese women with PCOs, and that ET receptor downregulation plays an essential role in this probably adverse cardiovascular out-

The increase in carotid intima-media wall thickness (CIMT) in PCOs women has been associated in different studies with higher levels of insulin, hyperandrogenism, LDL level, and

Meanwhile, impaired nitric oxide (NO) production as a consequence of elevated androgen

Elevated plasma viscosity as a result of increased plasma fibrinogen concentration in PCOs patients exacerbates vascular dysfunction because autoregulation of vasomotor tone may not be able to adjust with compromised physical properties of blood [63]. Some possible reasons for increased plasma fibrinogen are: increased inflammatory processes [64], decreased fibrinolysis [65], and as an acute phase reactant. Enhancement in fibrinogen level stimulates RBC aggregation and significantly increased resistance in blood flow [66]. Low SHBG and high insulin stimulate prothrombotic state in all of PCOs women by increased plasminogen activa-

Dyslipidemia including elevated low-density lipoprotein (LDL), triglyceride levels and decreased high-density lipoprotein (HDL) are often seen in PCO women as a result of hyperandrogenism

Owing to many evidence about vitamin D deficiency and metabolic syndrome; there are many studies about 25(OH) D levels and PCOs. There are some evidences which support this relationship and encourage vitamin D administration in all of deficient PCOs women [69],

From another site, insulin resistance, increased central adiposity, higher levels of testosterone, and dyslipidemia beside oxidative stress and low grade inflammation contribute to cause hepatic steatosis or fatty liver in PCOs women. Advanced stage of this disease characterized by necrosis and steatohepatitis which called non-alcoholic fatty liver disease (NAFLD) and has

After blow-by-blow discussion about all of aspects in lean PCOs women, we cannot consider this syndrome as just a part of infertility or menstrual abnormality assessment, but should be

another etiology of hypertension in this population [59].

abdominal obesity; which is an early marker of atherosclerosis [61].

levels in PCOs women contribute to endothelial dysfunction [62].

and insulin resistance in both lean and obese PCO patients [68].

whereas some studies do not support it [70].

prevalence about 40% in lean PCOs women [71].

accepted as an alarm sign for serious health problem.

tor inhibitor 1 (PAI-1) activity and fibrinogen in a BMI-independent way [67].

come [60].

28 Debatable Topics in PCOS Patients

Elham Pourmatroud

Address all correspondence to: e.pourmatroud@yahoo.com

Sarem Women Hospital, Tehran, Iran
