Does endothelial dysfunction correlate with endocrinal abnormalities in patients with polycystic ovary syndrome?

Abstract

To study and critically analyze the published evidence on correlation of hormonal abnormalities and endothelial dysfunction (ED) in polycystic ovary syndrome (PCOS) through a systematic review. The databases including MEDLINE, PubMed, Up-To-Date, and Science Direct were searched using Medical subject handling terms and free text term keywords such as endocrine abnormalities in PCOS, ED assessment in PCOS, ED in combination with insulin resistance (IR), hyperandrogenism (HA), increased free testosterone, free androgen index (FAI), gonadotrophin levels, luteinizing hormone (LH), prolactin, estrogen, adipocytokines to search trials, and observational studies published from January 1987 to September 2015. Authors of original studies were contacted for additional data when necessary. PCOS increases the risk of cardiovascular disease in women. ED, which is a reliable indicator of cardiovascular risk in general population, is seen in most (but not all) women with PCOS. IR, seen in 70% patients with PCOS, is associated with ED in these women, but patients can have normal endothelial function even in the presence of IR. Free testosterone and FAI are consistently associated with ED, but endothelial function can be normal despite HA. Estradiol (not estrone) appears to be protective against ED though estrone is the predominant estrogen produced in PCOS. Increased levels of adipocytokines (visfatin) are promising in predicting ED and cardiovascular risk. However, more studies are required focusing on direct correlation of levels of prolactin, LH, estrone, and visfatin with ED in PCOS.

Polycystic ovary syndrome associated with increased adiposity interferes with serum levels of TNF-alpha and IL-6 differently from leptin and adiponectin

“…However, eutrophic individuals, may also exhibit these conditions, mainly due to visceral fat accumulation and metabolic and endocrine differences (13)(14)(15). The increased insulin resistance might be playing a central role in the development of endothelial dysfunction (early event in atherosclerosis process), increasing oxidative stress and secretion of hormones and adipokines by the adipose tissue (16)(17)(18). Endothelial dysfunction is also characterized by lower production of nitric oxide and its production not only modulates the tone of vascular smooth muscle, but also inhibits several atherogenic processes (16)(17)(18)(19).…”

“…The increased insulin resistance might be playing a central role in the development of endothelial dysfunction (early event in atherosclerosis process), increasing oxidative stress and secretion of hormones and adipokines by the adipose tissue (16)(17)(18). Endothelial dysfunction is also characterized by lower production of nitric oxide and its production not only modulates the tone of vascular smooth muscle, but also inhibits several atherogenic processes (16)(17)(18)(19). These processes are the adhesion of platelets and monocytes, LDL oxidation, synthesis of inflammatory cytokines and proliferation of vascular smooth muscle cells (16)(17)(18)(19).…”

“…Endothelial dysfunction is also characterized by lower production of nitric oxide and its production not only modulates the tone of vascular smooth muscle, but also inhibits several atherogenic processes (16)(17)(18)(19). These processes are the adhesion of platelets and monocytes, LDL oxidation, synthesis of inflammatory cytokines and proliferation of vascular smooth muscle cells (16)(17)(18)(19). In addition, these results can influence hormonal regulation, since increased insulin resistance may interfere with the steroidogenesis by increasing the androgens synthesis (20).…”

Вплив інфекції Нelicobacter рylori на гормонально-метаболічні показники й маркери хронічного запалення у жінок, хворих на синдром полікістозних яєчників

“…Останніми роками з'явилися докази, що одним із факторів, який призводить до ЕД, може бути підвищена концентрація сироваткового рівня ГЦ, амінокислоти, яка містить сірку та утворюється в результаті метаболізму метіоніну [43]. Під впливом гіпергомоцистеїнемії (ГГЦ) відбувається підвищення експресії прозапальних цитокінів, зміна біодоступності NO, індукція оксидативного стресу, активація апоптозу і дефектного метилювання, що інгібує ооцитарну та фолікулярну матурацію, а також стероїдогенез в яєчниках та ускладнює настання вагітності [44]. Проведений кореляційний аналіз виявив наявність прямої статистично значущої залежності між ГЦ та Тзаг.…”

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“…These factors are independent risk factors for CVD. Moreover, insufficient and inconsistent data of ED in PCOS demands further research 79 .…”