·         Tr of CC Resistant women : How best to trat anovulatory disorders?:--

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·         CC resistance:-She continued to said:-The case she is referring to is a case of  PI  aged 25 yrs and there were  4 attempts of CC (100 mg)  which haven’t worked though follicular monitoring was duly done. . She lamented that pt is aggrieved as clomiphene failed to ovuate after 4 cycles-then Sir, what is your advice? Her ovarian morphological features are suggestive of PCO but there is no oligomeno, nether there is raised BMI, or clinical features of androgen excess (Hirsute/ Acne./ Baldness)/.. Wahat next? ?

·         I remarked that it seems to be a case of CC Resistant in a case of primary infertility with the provisional diag of PCOD. Well,  if U have done monitoring and if she has consumed CC tab regularly as per your instruction then it seems to be a case of CC Resistant because she did not respond to 100 mg of clomiphene citrate/ later 150 mg even after due monitoring of the M cycles. She said there were no development   of follicles even at 150 mg dosage (the last of 4cycles). . Now the Q is before us what are the steps that we can be adopted in such CC reistanant cases? Should we go for gonadotrophins, if so what choice of gonadotrophins, Sir?

Etiology of CC resistance?? I said:- Before going for HMG  there are few steps as per global consensus .Threfore it seems to me that instead of jumping to gonadotrophins which may or may not work we have to find out why at all she had CC resistance(etiology)  that has to be sought of like!) High  BMI, 2) Insulin resistance, 3) > PRL, 4) > Day 3 LH, 5) > Free testosterone and 6) < suboptimal AFC (if facilities exists) .Therefore in short these are the steps which is usually , but by not all. Be that as it may   it is a more or less a routine practice as a  pre-induction protocol with gonadotrophin , we have to consider her age & duration of  marital life.(trying time). .

What further tests for CC resistance?/ So, I said her to proceed with, if affordable for such tets including AMH, AFC , baseline FSH, LH, She interrupted me by saying that in view of morphological appearance of PCO(as per sonologist)  from second  cycle of  CC à PCO she was prescribing  Metformin –SR 1Gm OD basis & Vit D empirically 60K per fortnightly with the idea  Vit D correction will accelerate/  sensitize her insulin receptors (the other insulin entering channels).

Role of Vit to improve peripheral insulin sensitivity  ?? She claimed that it is reported that  Vit D ,if receptors are all right than corrections of Vit D will decrees In resistance and improve me anovulation.

Does raided adrenal androgen cause anovulation?? However ,  I insisted on that   that if  DHEASO4  if high may supplement Decdac 0,25( if BMI  < 24 kg/2. But if BMI is high (say,  If BMI is > 24 then possibly 0.5 mg Decadron tab suppl along with CC or letrozole may help her . Decdan reduces adrenal component of androgen.

To exclude  hyperprolactinaemia :--Role of hyperprolactinaemia including transient hyper prolactinaemia may cause anovulation disregarding CC/Letrozole .She reminded me that her PRL from pooled sample of this pt (blood was drawn for 4 times on the same day and serum was mixedà pooled sample of PRL was normal.

U-HMG or u-HP FSH?? :--However I reminded her  for anovulatory disorders where LH is high in such cases you should opt for LH free gonadotrophins if U at all opt for gonadotrophins. HP-FSH (with very minimal LH activity, and minimal urinary proteins)  will be marginally better than cheaper u-HMG which contains 50% of LH: FSH and urinary proteins too. This urinary proteins separation is a costly procedure and many companies don’t invest such difficult machines.