From our present state of knowledge about PCOS it was very difficult to make final consensus regarding defination, patho-physiology, clinical manifestations and treatment modalities. Since last few years various concepts have emerged which have received agreement.
Concensus now agreed as regards defination that it should better defined as syndrome rather than disease since actual cause or causes of disease is still not known.1
Till date there is no supporting evidence regarding the pathophysiology of PCOS although recently familial cluster of PCOS is reported–suggesting a major Component of its etiology. Study was done intensively (Steven Franks) to find the Zenes involved in androgen production and secretion and action of Insulin. The results of both linkage and association studies suggest the involvement of two key genes in the aetiology of PCOS, the steroid synthesis gene CYP11a and insulin gene–Variable number tandem repeats (VNTR).
Urbanck et al2 concluded from his study that follistatin gene, found to have the strongest linkage with PCOS from 37 genes, but failed to confirm this finding in large series.
Helen Mason has scientifically setout the possible reasons for the increased follicular number and attenuated apoptosis.
Robert Rosenfield proposes that of dysregulation of androgen secretion accounts for this abnormality, probably due to hyperactivity of on enzyme, cytochrome P450c 17. A single genetic defect enhancing. Serine phosphorylation, which would decreased the activity of the insulin receptor activity could account for both the hyperandrogenism and the insulin resistance of PCOS.2
As Regards Clinical Menifestation
The concept of wide spectrum of signs (Adam Balen), ranging from single finding of polycystic ovarian morphology (detected by USG), to obesity, menstrual irregularities, infertility, cardiovascular diseases–all are due to metabolic disturbances involving increased level of LH, insulin and androgen and dyslipidemia.
Clomiphene citrate (CC) is still the first line of treatment for anovulatory women with PCOS who desire pregnancy. Chronic low-dose step-up protocol using follicle stimulating hormone (FSH) is advocated either in CC resistance or failure to conceive with CC with reasonable time.
The use of GnRH analogues and laparoscopic ovarian puncture can also be used alternatively or if low-dose FSH failed to conceive pregnancy.
Last resort of treatment is IVFαET (if all other treatment failed,) for which excellent results have been reported.
In conclusion the research into the causes of PCOS should focus in the mechanism underlying the hyperfunction at capacity of PCO and the factor that tiggers this hyperactivity. Hope in future an experimental animal model may be required to assist such investigations.2
REFERENCES
- Roy Homburg. Polycystic ovary syndrome consensus and controversy, PCOS edited by Roy Homburg, 2001;1–9.
- Urbanek, Legro RS, Driscoll Da, et al. Thirty-seven candidate genes for polycystic ovary syndrome. Strongest evidence for a linkage is with Follistatin. Proc Natl Sci USA 1999;96:8573–78.