WITHDRAWN O-422 Wednesday, October 16, 2013 05:15 PM LETROZOLEVERSUSCLOMIPHENECITRATEINANOVULATORY PCOSWOMEN:ACOST-EFFECTIVENESSANALYSIS. NIH/NICHD Reproductive Medicine NetworkNIH/NICHD Reproductive Medicine Network, Bethesda, MD. OBJECTIVE: To compare the cost effectiveness of Letrozole to Clomiphene for treatment of anovulatory infertility related to the Polycystic Ovary Syndrome. DESIGN: A randomized controlled trial was conducted as part of the Reproductive Medicine Network with randomization to either Letrozole or Clomiphene citrate. This cost-effectiveness analysis was based on the results of that study. MATERIALS AND METHODS: Differences in conception, pregnancy and live birth rates were calculated from the trial data. These were supplemented with hospital charge data from Healthcare Cost and Utilization ProjS128 ASRM Abstracts ect, which were converted to costs using national Medicare charge to cost ratios. Results were corrected for differences in cesarean rates and pregnancy complications. Medication and monitoring costs constituted the costs per treatment cycle. The outcome was cost per live birth. The study adopted the societal perspective. RESULTS: The rates of conception, pregnancy and live birth were statistically significantly higher among patients treated with Letrozole versus Clomiphene. 25.2% of treated women in the Letrozole arm had a live birth versus 16.8% for Clomiphene (p1⁄40.036). Rates of pregnancy complications were insignificantly different (p1⁄4 .81) as were the cesarean rates. The cost per event was higher for the Clomiphene arm, driven both by the comparable medication and monitoring treatment costs and lower rates of birth. The cost per live birth was equal to a weighted average of $6660.55. Given that inputs were comparable in all other areas, the higher pregnancy rate for Letrozole dominated Clomiphene citrate. CONCLUSION: Comparable treatment costs for Letrozole and Clomiphene citrate are largely offset by its higher effectiveness, yielding lower cost per live birth. Given the lack of downstream cost increases due to similar rates of cesarean section and pregnancy complications, Letrozole is the more cost effective alternative. Supported by: The content is solely the responsibility of the authors and does not represent the official views of the NICHD or NIH. O-423 Wednesday, October 16, 2013 05:30 PM IMPAIRED FLUX VIA THE PENTOSE PHOSPHATE PATHWAY CORRELATES WITH ABNORMAL ENDOMETRIAL RECEPTIVITY IN PCOS PATIENTS. M. M. B. Schulte, J.-H. Tsai, K. Moley. Obstetrics & Gynecology, Washington University in St. Louis, St. Louis, MO. OBJECTIVE: Markers of uterine receptivity are decreased in PCOS patients. Recent work from our laboratory suggests that elevated DHEA levels in vitro inhibit the pentose phosphate pathway resulting in inhibition of endometrial decidualization. Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme in this pathway. As DHEA levels are elevated in 50% of PCOS patients, alterations in the pentose phosphate pathway may contribute to impaired endometrial function and thus subfertility. DESIGN: Basic Science. MATERIALS AND METHODS: Controls are normo-ovulatory women with proven fertility while cases have primary infertility and PCOS (Rotterdam). All patients underwent an endometrial biopsy, blood draw for DHEA and Testosterone and completed a survey. ESC decidualization was induced and the mRNA expression levels of prolactin, IGFBP1, and interleukin-15, and G6PD expression were measured by quantitative RT-PCR. The fold change in gene expression between non-decidualized and decidualized samples was calculated. Enzymatic assays investigating G6PD activity in each tissue sample are currently underway. RESULTS: The fold changes in gene expression of decidual markers exhibit a decrease in PCOS patients. Additionally, they have a decrease in G6PD expression suggesting that the pentose phosphate pathway is inhibited by elevated DHEA levels thus inhibiting proper decidualization and leading to subfertility. Further correlation with DHEA laboratory values and endometrial receptivity markers are pending. Fold Change in Gene Expression PCOS vs Control Fold change PRL IGFBP1 IL-15 G6PDH Vol. 100 , No. 3, Suppleme nt, Septem PCOS (N1⁄420) 615.0 620.6 57587.4 97426.3 7.9 3.2 2.2 0.5 Control (N1⁄420) 3740.8 11217.3 190860.9 341586.0 10.2 4.1 2.3 0.8 Values are a mean SEM. CONCLUSION: By controlling the in vitro hormonal environment, measuring markers of endometrial decidualization and G6PD expression we found that women with PCOS have ESCs that demonstrate decreased pentose phosphate enzyme expression and reduced ability to undergo normal decidualization. Supported by: ACOG/Merck.