**Author details**

Fulfilling two of three diagnostic criteria implies that PCOS can be diagnosed in the absence of androgen excess or menstrual irregularity—the very factors that were once considered absolute requisite for the syndrome [7]. Task force appointed by the Androgen Excess and PCOS society in 2006 considered the menstrual disorder and the ultrasonography finding of polycystic ovaries to be the presentation of similar pathophysiology and considered them to be one. At present, there is no definitive diagnostic criteria for polycystic ovarian disease rather it is a diagnosis of exclusion [7]. For evaluation of hyperandrogenemia, there is no consensus about which testosterone to be measured, when to be measured, what range should be taken, and what method of measurement is to be used. For features of hyperandrogenism assessment of hirsutism, acne and alopecia are more of subjective feature. Assessment of menstrual irregularities and serum progesterone for anovulation is also not confirmatory. Ultrasonographic findings of polycystic ovary are also subjective. None of the above criteria states for diagnosis of polycystic disease in adolescents where these features could be present

There has been extensive work on finding the etiology and pathophysiology behind this disease. None could find exact etiology behind this. There is halt in the dynamic endocrinal milieu of the ovary [1]. There is increase in both LH pulse frequency and production of more bioactive LH, and there is increased LH:FSH ratio leading to neuroendocrinologic origin hypothesis. The feedback signal from periphery may be inappropriate or there may be intrinsic hypothalamic dysfunction [1]. Hyperandrogenemia came into scene while searching for a cause of both aberrant peripheral feedback and dysfunctional hypothalamus. The rises in androgen were both from ovary and adrenal glands, shifting the focus on ovarian pathology [11–14]. Some attribute the chronic anovulation to be the cause of hyperandrogenemia, and some authors say the other way. Insulin resistance causes hyperandrogenemia. Insulin causes selective stimulation of receptor that causes hyperandrogenemia. About 35% of patients have impaired glucose tolerance and 7–10% have diabetes mellitus [1]. It is a more common finding in obese polycystic disease patient than in lean PCOS patient. Nearly 25–50% of women with PCOS have no demonstrable insulin resistance. Approximately 60% of women with PCOS are obese. The prevalence of PCOS is comparable in women with BMI <18.5, normal weight women, and BMI 25–30 and BMI ≥30 [1]. Modern lifestyle and obesity can also be the cause. Recent researchers are giving significance to the genetic cause. There are genetic and nongenetic theories for etiopathogenesis of polycystic ovarian disease. Recently, two-hit hypothesis has been given. Patient presenting with PCOS are thought be genetically predisposed, and after environmental insult, they become symptomatic. Genetic predisposition can be because of mutations affecting ovarian function, female virilization, or intrauterine nutritional status of fetus. Environmental insult can be hyperinsulinemia, obesity, and others. There has been evolutionary theory behind PCOS; to compensate for hyperandrogenemia in male, there was evolutionary decrease in female fertility and also that in the process of evolution a more androgenic environment helped nutritionally deprived population to reproduce which in

due to pubertal changes [8–10].

4 Debatable Topics in PCOS Patients

today's scenario is not beneficial [11].

**3. The challenges for pathophysiological basis**

Abha Kiran1 , Uma Pandey1 \* and Neeraj Kumar Agarwal2

\*Address all correspondence to: uma.pandey2006@yahoo.com

1 Department of Obstetrics and Gynaecology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

2 Department of Endocrinology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
