Serum inhibin A levels as markers of follicle maturity for fertilization (IVF)

Because inhibin A originates from the dominant follicle(s) during folliculogenesis and falls prior to the preovulatory LH surge, we hypothesized that the mass ratio of inhibin A:estradiol (E2) might fall during the late follicular phase and provide a more sensitive index of follicular maturation than either levels of inhibin A or E2 alone. Retrospective analysis of archived blood samples from patients undergoing controlled ovarian hyperstimulation (COH) for IVF and ICSI. Blood samples were drawn on cycle day 2–3 (baseline) and on each of the 3–4 days preceding oocyte retrieval from each of 29 patients undergoing COH following pituitary suppression with GnRH agonist. hCG was given (10,000 IU, im) when the leading follicle(s) reached 18–20 mm diameter and secondary follicles were >15 mm. Oocyte retrieval was performed 33–35 hrs later, after which the maturity of recovered oocytes was determined. Serum inhibin A levels were measured using an enzymatically amplified ELISA (DSL, Inc.; Webster, Texas). The inter-assay CVs were near 7%, and the primary antibody cross-reacted <0.01% with inhibin B, activin A, activin B or pro-Alpha C. Serum E2 levels were determined using an automated chemiluminescent procedure (Immulite, DPC, Los Angeles, CA). Correlations between measured parameters were analyzed by least squares linear regression. Differences between group means were analyzed by ANOVA. The average (±SE) number of oocytes recovered was 13 (±1.5), of which 10 (±1.8) were mature. The fertilization rates (ICSI) for mature oocytes were 74(±6)%. Average levels of inhibin A in sera rose steeply from baseline values near 3 to maxima near 650 pg/mL 24h before oocyte retrieval. Baseline E2 values were near 25 pg/mL, rising to maximum levels near 3,000 pg/mL. The mass ratio of inhibinA:E2 was near 0.25 throughout folliculogenesis and early luteinization. By least-squares linear regression, neither the number nor proportion (%) of retrieved oocytes which was mature (MII) were significantly correlated with total levels of inhibin A in sera drawn 36 hrs before hCG injection, 12 hrs preceding hCG or 12 hrs after hCG injection. Furthermore, oocyte maturity on the day of oocyte retrieval was not correlated with the mass ratio of inhibin A:E2 in sera drawn at any of these times (r<0.11). Overall (within patients-between days and between patients-within days), levels of inhibin A in serum were closely correlated with serum estradiol levels (P<0.001). Despite our hypothesis that changes in inhibin A production would precede those of estradiol by ovarian follicles, levels of inhibin A in serum paralleled E2 values so closely that they did not augment traditional projections of follicle maturity through tracking serum E2 and monitoring follicle expansion by ultrasound.