Polycystic ovary syndrome: etiology and pathogenesis

Abstract

To provide a review of the pathogenesis of polycystic ovary syndrome. Literature survey. Three major pathophysiologic hypotheses have been proposed to explain the clinical findings of polycystic ovary syndrome (PCOS) related to three major laboratory findings: the LH hypothesis, the insulin hypothesis and the ovarian hypothesis. Although the presence of many small follicles with a high androgen to estrogen ratio was first thought to represent a high rate of follicular atresia in polycystic ovaries, recent studies have demonstrated that the granulosa cells are viable and able to respond to FSH stimulation with normal increases in estradiol production. Thus, a new hypothesis has arisen that FSH activity is somehow blocked at the ovarian level. PCOS is a syndrome involving defects in primary cellular control mechanisms that result in the expression of chronic anovulation and hyperandrogenism. In this syndrome, the relation between the various parameters is of particular interest. These relations constitute the cornerstone of the pathogenesis of PCOS. The fact that the pathogenesis of PCOS has not yet been clarified, despite the plethora of relative information, may be the result of a general way of thinking in the interpretation of several scientific data, and especially those that refer to biochemical phenomena. The use of the various models of the theory of chaos, that permits a concrete approach for the interpretation of data, may constitute an optional procedure for the future understanding of the association of different parameters and their disturbances in the pathogenesis of the polycystic ovary syndrome.