Sub fertility with PCO how to investigate & TR in Indian context??

Subfertility :Routine evaluation: I assume that subfertile couple under your treatment   has normal seminal parameters with normal sexual relation.   For each type of subfertile women you quoted it will be better to plan the treatment according to her age & months of trying. I also presume you have assessed medical fitness for pregancy, in the sense of Viral screening, STI screening, Hepatitis serology and above all complete haemogram & ruled out Haemoglobinopathies. a Pap smear is appropriate. , though for financial reason such screening procedure is uncommon in most of the rural centers as is uncommon is CBE(Clinical Breast Examination on annual basis after the age of 40yrs). History immunization and  past medl or surgical history should be elicited , Drug abuse, life style , dietary habits and above all stress can be evaluated with some patience without hurting the couple. Regular intake of drug has to be enquired,. Any past history of miscarriage have to be enquired and cycle regularity and recent weight gain should be enquired. Family h/o Diabetes carries a risk factor for hyperinsulinaemia in fair number of cases. In such women life style modification and 3 yarely lipid profile estimation, LFT profile should be recorded and preserved in her diary.

Endocrine markers:--Coming to subfertility problems the relevant biomarkers which are important and relevant are AMH, Day 3 LH, DHEAO4, PRL & TSH . For prolactin disorders cabergolin , and for raised DHEASO4 Decdac (decadron) 0.25 mg(If BMI is < 28 ) and 0.5 mg at late night (before retiring ) if BMI is > 28   from cycle day 1 to cycle day 14 will curtail ACTH and hopefully normalize excess DHEASO4 and help follicles to grow in a synchronized way. Ovarian volumes and echotexture have to be assed although AFC measurement is not so essential at this stage .

Clinical classification of all subfertile women: Basically all kind of subfertile women can be classified on two types A) No palpable pelvic mass or pathology or fixity B) with palpable mass or pathology (say tenderness, fixity).

 In type B cases HSG or SIS(saline Infusion sonography)/ HSG  should better be avoided. A low threshold for pelvic antibiotics, exclusion of Kochs & STI and Tr of Chlamydial infection seems rational and worthy.

Group A:  In absence of any palpable pathology, or visible Cx lesion uterotubal evaluation should be done in addition to routine day 3 USG. But when the couple comes to you Basal scan : I presume basal scan has already been done and one can securitize that report. Now it will be your duty to insist on HSG Vs SIS if she is aged 26 yrs and TT(trying time is > 3 yrs) .By and large he working rule is to insist on HSG(or say SIS) after couple of months of ovarian stimulation. SIS, in my opinion, should be  done by an expert and this procedure has an edge over HSG because  polyps, small myoma, adhesions (Ashermans ) are better diagnosed by SIS . This is   my personal opinion, I may be wrong as well. I also have a feeling that these three uterine conditions (synechiae, small polyp/s or small submucous myoma) collectively account for about 7-10% of all cases of F subfertility. All these minor conditions are difficult to palpate clinically and often missed in traditional HSG. Such conditions which chiefly result in implantation failure or result early embryonic demise due to unreceptive endometrium.

Induction of Ovulation: Coming to ovulation induction letrozole has an edge over Clomiphene citrate as Letrozole do not yield to thin ET and PR(preg rate per initiated cyce is better) , CC quite often leads to polyfollicular growth which is uncommon in CC. But be it CC or Letrozole cycle monitoring by TVS is a justifiable procedure though with limited resources and long distance from clinic LH urinary lit is the next option. Serum progesterone assay 5 days after presumed ovulation is not a common procedure in Letrozole cycles.

PCOD : Now coming to your case No 1: pt diagnosed with pcod, primary infertility yet to start treat . In fact the terminology of PCOD is fainting in favour of hyperandrogenic hyperechogenic small or large volume ovaries with oligomenorrhoea. My suggestion will be to A) adjust BMI, and drug selection according to LH, serum testosterone and PPBS . B) Pretreatment OCP or only progesterone in preceding cycle : In such cases quite often there is modern trend to prescribe one cycle of OCP (sometimes 3 cycles of OCP) to suppress LH & testosterone and synchronize the follicles but opinion differs. Not all doctors prescribe Preinduction OCP/Progesterone prior to initiation of Letrozole treatment. Incidentally to my knowledge there is no Post pill amenorrhoea   after ingesting of short course of OCP intake to down regulate the hormones as. C) Metformin if serum creatinine is normal as metformin is largely excreted via kidneys  . There should be low threshold of prescribing Metformin in SE Asia . The dose gradually increased up to 1000 mg OD if yearly serum creatinine is normal to correct hyperinsulinaemia and to normalize hepatic cellular function and prevent miscarriage if preg ensues meanwhile. But many of us don’t believe empirical metformin therapy in PCO and or Vit D therapy more so in the western world. D) : Vit D therapy: its rationality?? AS we know  life style modification, avoiding oils and fried foods and street foods , Yoga and Metformin , LM Folate suppl, Vit D suppl (if Vid D estimation is unaffordable even then one can empirically prescribe 60,000 cap/ sachet with milk  as Vit D toxicity will appear only when serum Vit D is 100 times of normal highest value., Vit D is one of the avenue of glucose entry inside the cells independent of insulin and such mechanism is also true for Myoinositol &DCI . In Indian skin the receptors of Vit D are quantitavely and qualitatively poor. That is why most of the cultivators in our country who work in bright sun for long hours even have poor vit D serum level (see AIIMS study) and DM is common in rural hard working  Indian cultivators  due to genetic cause .