In vitro fertilization versus conversion to intrauterine insemination in Bologna-criteria poor responders: how to decide which option?

OBJECTIVE: To compare the continuation of in vitro fertilization (IVF) with the conversion to intrauterine insemination (IUI) in cases of suboptimal ovarian response in Bologna-criteria poor responders. DESIGN: Retrospective and multicenter comparative study. SETTING: Three academic fertility centers and a fertility private clinic. PATIENT(S): Analysis of 7,176 initiated IVF cycles from January 2010 to January 2013. The 461 cycles with poor ovarian response (fewer than three follicles ≥16 mm at hCG trigger) in patients with poor response according to the Bologna criteria were included. INTERVENTION(S): Decision to pursue IVF (n = 184), convert to IUI (n = 141), or cancel cycle (n = 136) when only one or two follicles were recruited. MAIN OUTCOME MEASURE(S): Live birth, ultrasound pregnancy, and early pregnancy rates were compared depending on whether they resulted from IVF or IUI and were stratified according to patient age and the number of mature follicles at trigger. RESULT(S): Live birth rates were significantly higher for IVF patients compared with IUI conversion when two follicles were present (11.6% IVF vs. 1.6% IUI), especially for patients <40 years of age (13.1% IVF vs. 2% in IUI). In case of a monofollicular recruitment, the pregnancy outcomes were similar. CONCLUSION(S): A therapeutic strategy could therefore be to pursue IVF for women demonstrating two follicles and to convert to IUI for cycles with only one follicle if the sperm and tubal parameters are favorable.

The permissive role of prolactin as a regulator of luteinizing hormone action in the female mouse ovary and extragonadal tumorigenesis.

Transgenic female mice overexpressing the hCGß subunit (hCGß(+)) and producing elevated levels of luteinizing hormone (LH)/hCG bioactivity present as young adults with enhanced ovarian steroidogenesis, precocious puberty, and infertility. They subsequently develop pituitary prolactinomas, high circulating prolactin (PRL) levels, and marked mammary gland lobuloalveolar development followed by adenocarcinomas. None of these phenotypes appear in gonadectomized mice, indicating that the hCG-induced aberrations of ovarian function are responsible for the extragonadal phenotypes. PRL receptor-deficient (PRLR(-/-)) female mice are sterile, despite ovulating, due to a failure of embryo implantation, as a consequence of decreased ovarian LH receptor (Lhcgr) expression and inadequate corpus luteum formation and progesterone production. To study further the presumed permissive role of PRL in the maintenance of gonadal responsiveness to LH/hCG stimulation, we crossed the hCGß(+) and PRLR(-/-) mice. The double-mutant hCGß(+)/PRLR(-/-) females remained sterile with an ovarian phenotype similar to PRLR(-/-) mice, indicating that LH action, Lhcgr expression, and consequent luteinization are not possible without simultaneous PRL signaling. The high frequency of pituitary prolactinomas in PRLR(-/-) mice was not affected by transgenic hCGß expression. In contrast, none of the hCGß(+)/PRLR(-/-) females showed either mammary gland lobuloalveolar development or tumors, and the increased mammary gland Wnt-5b expression, possibly responsible for the tumorigenesis in hCGß(+) mice, was absent in double-mutant mice. Hence, high LH/hCG stimulation is unable to compensate for missing PRL signaling in the maintenance of luteal function. PRL thus appears to be a major permissive regulator of LH action in the ovary and of its secondary extragonadal effects.