OBJECTIVE: DHEA supplementation for poor responders has been shown to improve ovarian response and IVF treatment outcome. We endeavored to determine whether this improvement is due to a quantitative increase in recruitable follicles- as reflected by AMH (very early follicles), inhibin B (early follicles), antral follicle count (AFC) or enhanced quality of oocytes, or other alternative mechanism(s).DESIGN: Prospective, self-controlled study.MATERIALS AND METHODS: 43 poor responders (<4 oocytes retrieved) aged < 44, were treated with at least three months of DHEA supplementation (75mg/day po). Biochemical, ultrasound and treatment outcome parameters before and after treatment were compared, including:Serum – cycle day 3 FSH, AMH, Inhibin B, DHEA.Ultrasound – AFC, endometrial thickness.Outcome – peak E2 levels, number of >15mm follicles on the day of hCG administration, number of oocytes retrieved, MII oocytes, oocytes/total FSH dose, number and grade of embryos, pregnancy rate. Paired student's t-test and Wilcoxon Signed rank test were used for statistical analysis.RESULTS: 32 women were suitable for analysis. Following DHEA supplementation, there was a significant increase in AFC (p = 0.0003) No significant changes in baseline biochemical parameters were established. Enhanced response to IVF treatment was significant, with increased peak E2 (p = 0.0005), number of follicles >15mm on day of hCG administration (p = 0.004), number of oocyte retrieved (p = 0.00001), oocyte/total FSH rate (p = 0.0009), and increased number of MII oocytes (p = 0.0004), embryos (P = 0.0006) and high quality embryos (NS). There were 10 clinical pregnancies (31%) after DHEA treatment.CONCLUSION: DHEA improves IVF treatment outcome in women with poor response to IVF treatment. It seems that the mechanism does not include recruitment of more pre-antral or very small antral follicles (no change in AMH and inhibin B) but rather rescue from atresia of small antral follicles (increased AFC). OBJECTIVE: DHEA supplementation for poor responders has been shown to improve ovarian response and IVF treatment outcome. We endeavored to determine whether this improvement is due to a quantitative increase in recruitable follicles- as reflected by AMH (very early follicles), inhibin B (early follicles), antral follicle count (AFC) or enhanced quality of oocytes, or other alternative mechanism(s). DESIGN: Prospective, self-controlled study. MATERIALS AND METHODS: 43 poor responders (<4 oocytes retrieved) aged < 44, were treated with at least three months of DHEA supplementation (75mg/day po). Biochemical, ultrasound and treatment outcome parameters before and after treatment were compared, including: Serum – cycle day 3 FSH, AMH, Inhibin B, DHEA. Ultrasound – AFC, endometrial thickness. Outcome – peak E2 levels, number of >15mm follicles on the day of hCG administration, number of oocytes retrieved, MII oocytes, oocytes/total FSH dose, number and grade of embryos, pregnancy rate. Paired student's t-test and Wilcoxon Signed rank test were used for statistical analysis. RESULTS: 32 women were suitable for analysis. Following DHEA supplementation, there was a significant increase in AFC (p = 0.0003) No significant changes in baseline biochemical parameters were established. Enhanced response to IVF treatment was significant, with increased peak E2 (p = 0.0005), number of follicles >15mm on day of hCG administration (p = 0.004), number of oocyte retrieved (p = 0.00001), oocyte/total FSH rate (p = 0.0009), and increased number of MII oocytes (p = 0.0004), embryos (P = 0.0006) and high quality embryos (NS). There were 10 clinical pregnancies (31%) after DHEA treatment. CONCLUSION: DHEA improves IVF treatment outcome in women with poor response to IVF treatment. It seems that the mechanism does not include recruitment of more pre-antral or very small antral follicles (no change in AMH and inhibin B) but rather rescue from atresia of small antral follicles (increased AFC).