5. Inflammation and PCO

There are many published studies about proinflammatory or inflammatory situations in PCOs woman. Increased level of circulatory inflammatory markers like C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukins (IL-16 and -18), and plasminogen activator inhibitor in PCO patients accompany with abdominal obesity and more specific with visceral fat [46]. Low-grade inflammation situation by increased level of adiponectin, resistin, IL-6, and TNF-α in non-obese PCO women have been approved [47]. Also, it has been shown that inhibition of nutrient-induced inflammation decreases ovarian androgen secretion and induces ovulation in lean PCOs woman without clinical IR or abdominal adiposity. Therefore, inflammation directly encourages ovarian dysfunction in PCOs women distinctly from insulin resistance or excess adiposity [48]. There is evidence that non-steroidal anti-inflammatory agent administration in lean PCO women can reduce androgen secretion from ovary [49].

Dose inflammation have pathophysiologic role in this syndrome or may be its consequence remain still unclear. Inflammation as a chronic immune activation, prevents ovulation, increases androgen production by ovary and adrenal gland and disrupts hormonal receptors. Most of long-term complications of PCOs like cardiovascular disease (CVD) are consequences of inflammatory state [50].

In non-obese PCO patients, visceral fat distribution, waist to hip ratio (WHR), and abdominal obesity have relation with inflammatory situation. In one study, in lean PCOs, level of white blood cell (WBC) has a positive predictive value with insulin resistance, while the neutrophil to lymphocyte ratio has a negative predictive value [51]. Also, it has been demonstrated that in clomiphene citrate (CC)-resistant patients, regardless to BMI, inflammatory markers like TNFα are too high, and TNF-α serum level may be used as a clinical predictive indicator before CC useless administration [52].
