Endometriosis and infertility: the debate continues

A causal relationship between minor endometriosis and infertility or subfertility has not yet been demonstrated, although a significant association is shown by prevalence studies. This article critically reviews the evidence for pituitary-ovarian dysfunction as a cause for subfertility in women with minor endometriosis. The lack of fertile controls with endometriosis presents a methodological problem. Group comparison in studies using tubal infertility cases as controls has demonstrated impaired follicular growth, reduced circulating oestradiol concentrations during the preovulatory phase and oestradiol and progesterone during the early luteal phase, and disturbed luteinizing hormone (LH) surge patterns. LH concentration in preovulatory follicular fluid is also reduced, and granulosa cells collected at the same time have impaired steroidogenic capacity in vitro. However, these findings are not consistent in published studies. Significantly lower oocyte fertilization rates (49%) are found compared with controls (69%), even after maximum stimulation with exogenous follicle-stimulating hormone and human chorionic gonadotrophin (52% versus 69%). The implantation rate is also lower (11% versus 13%). An inherent disorder of follicular function seems likely, and LH surge impairment is probably a secondary effect. Impairment of oocyte fertilization would thus contribute substantially to the natural subfertility associated with endometriosis, but in vitro fertilization is still successful as excess numbers of oocytes are available.