PCO-What we know??

PCO  :---What is the prevalence?? Polycystic ovary syndrome (PCOS) is responsible for more than eighty percent of anovulatory infertility and 5-10% of infertile women at all

 What other syndromes may confuse us??  Hyper-androgenic disorders like 1)  late onset congenital adrenal hyperplasia, 2) hyperprolactinemia, 3) thyroid diseases, and 4)  Cushing’s syndrome and 5) androgen-secreting tumors.

How do we diagnose this condition??  PCOS is usually diagnosed according to the following criteria

: A) Oligomenorrhea and/or amenorrhea; B) clinical and/or biochemical signs of hyperandrogenism; and C)  transvaginal sonographic appearance of polycystic ovaries (12 follicles or more and 2-9 mm in their diameter or an ovarian vol­ume >10 cm ').

Q. 4: What is the etiology?? Pathogenesis is not clearly known though insulin resistance leading to hyperinsulinemia is considered as one of the most important factor in both obese and lean women. Insulin resistance and hyperinsulinemia leads to hyperandrogenaemia.

Q. 5: What Laboratory tests?? Patients may for research work at least can be  evaluated for FSH, LH,  17 β Estradiol,  sex Hormone Binding Globulin androstenedione , free testosterone and dehydroepiandrosterone sulphate levels. Insulin resistance may be measured by means of Homeostasis Model

How to treat ?? Lifestyle mod­ifications and physical exercises are essential to weight loss in the obese PCOS patients. For menstrual disorders we have to offer OCP or only cyclical progesterone. For abnormal hair growth there is a great demand of OCP with aldactone or some other antiandrogens (Finasteride) ,

So far as subfertility treatment is concerned letrozole or Clomiphene citrate are  con­sidered the first line of infertility treatment, the second line includes gonadotropins or laparoscopic ovarian drilling (LOD), and the third is assisted reproductive techniques

The pregnancy rate following LOD is more than 50% in CC-resistant PCOS; hence, it can be concluded that LOD reduces the need for ART by 50% in CC-resistant PCOS and is a safe option, especially for women who cannot afford the

Metformin & PCO:- Ans:-Metformin causes 1) increases   peripheral  insulin sensitivity by   activating  glucose   transporters   which  allows      passage of glucose into hepatic  and muscle cells 2)  inhibition of hepatic   glucose production 3)

reduction of circulating free fatty    acid concentration  which  helps    in reducing    gluconeogenesis . What else are the actions of metformin in cellular dynamics?? Ans :- 1) decreased  glucose   production at liver 2) inhibits  hepatic   gluconeogenesis  .  Metformin  activates  the adenosine monophosphate  activated protein kinase pathway    phosphorylaction of threonine in AMPK   is necessary   for  metformin  action resulting   in decreased  glucose   production  and increased  fatty  acid oxidation in hepatocytes  skeletal muscle   cells   and mouse   ovarian tissue.

Furthermore metformin  inhibits  hepatic   gluconeogenesis  through  an AMP   activated protein    kinase   dependent regulation  of the orphan  nuclear    receptor   small heterodimer partner. Metformin affects ovarian   function    in a dual way 1) alleviation of systemic  insulin   excess acting  upon the ovary   particularly   on steroidogenesis  and follicular    growth 2) direct  ovarian   effect. 3) Modulates LHaction:-   metformin acts at the hypothalamic levels  on AMPK   pathway the latter  is essential in the modulation of LH  secretion 4) Effects on androstenedione:-studies   demonstrated  that metformin  inhibits  androstenedione    and testosterone    production form theca  cells through inhibition  of  the steroidogenic    acute regulatory    protein   and 17 a hydroxylase  expression. 5) Metformin reduces  FSH      without     altering   cAMP  levels

What about Myoinositol?? Finding from different  recent studies  points to the fact a  combined therapy with MI plus DCI in their physiological plasma ratio can positively influence the outcome of patients with PCOS,.  Women who received MI plus DCI as a combination therapy ratio of 40:1  as a soft gel capsule containing  550 mg of MI 13 .8 mg of DCI and 200 mg of folic acid  at BD dosage fair better so far pregancy outcome. They act as insulin second messengers and help in increasing insulin sensitivity     of different tissues leading on to improvement in metabolic and ovulatory functions. In particular MI exerts it beneficial effects mainly at the ovary level where it is highly concentrated.

What about Vitamin D??   Role of vitamin D in reproductive functions of mammals has been known sine long. There are numerous evidences through studies in animals about role of vitamin D in female infertility though evidences in humans

To measure levels of serum Folate, RBC Folate, total plasma homocysteine vitamin B12 vitamin.

In reproductive age group polycystic ovary syndrome can involve a growing number of women. The diagnosis is usually based upon different factors mainly oligo or anovulation, clinical / biochemical hyperandrogenism and polycystic ovary with the presence on ultrasound of >12 follicles in each ovary measuring 2+ 9 mm in diameter and /or increased ovarian volume. cost of ART