Human Reproduction Update, Vol.6, No.1 pp.56-66, 2000
© European Society of Human Reproduction and Embryology 2000; all rights reserved
Pituitary–ovarian dysfunction and endometriosis
Centre for Reproductive Medicine, University of Bristol Division of Obstetrics and Gynaecology, St Michael’s Hospital, Southwell Street, Bristol BS2 8EG, UK cjagcdfi After a short illness, Michael Hull, Professor of Reproductive Medicine and Surgery in the Division of Obstetrics and Gynaecology, University of Bristol, died on 22 November aged 60 years. He came to Bristol from London in 1976 as Consultant Senior Lecturer in Obstetrics and Gynaecology with a developing reputation in clinical reproductive endocrinology from his time in London and elsewhere. His contributions to knowledge and practice of reproductive medicine, particularly in all aspects of male and female infertility, brought international renown to his unit. He was appointed to a Personal Chair in 1989. He brought strong ethical priniciples to his research and clinical practice and campaigned locally and nationally for public understanding and funding of infertility services. With a firm hand, he encouraged his trainees to excellence and to that same eye for detail that marked all his work. This paper was written during his final illness.
Received on June 21, 1999; accepted on October 20, 1999
Abstract
Significant association between endometriosis, including minor endometriosis, and infertility (or strictly subfertility) is shown by prevalence studies, but a causal relationship has not been established. This review focuses on evidence for pituitary–ovarian dysfunction as a cause for the subfertility. A methodological problem is lack of fertile controls with endometriosis. Group comparison with tubal infertility cases as controls have demonstrated: impaired follicular growth, reduction in circulating oestradiol concentrations during the pre-ovulatory phase and of oestradiol and progesterone during the early luteal phase, and disturbed luteinizing hormone (LH) surge patterns. Reduction in LH concentrations in pre-ovulatory follicular fluid has also been found, and granulosa cells collected at the same time have demonstrated impaired steroidogenic capacity in vitro, but these were not consistently proven findings. Pooled data from published studies show significantly reduced oocyte fertilization rates (49%) compared with controls (69%), even after maximal stimulation with exogenous follicle stimulating hromone (FSH) and human chorionic gonadotrophin (HCG) (54 versus 69%). The implantation rate is also slightly (though significantly) reduced (11 versus 13%). The findings suggest an inherent disorder of follicular function, with LH surge impairment probably being a secondary phenomenon. The resulting reduction in the chance of fertilization of the oocyte would contribute substantially to the subfertility associated with endometriosis. It seems that the benefit of in-vitro fertilization is gained through the excessive number of oocytes obtained by stimulation.
Key words: causal association/ / endometriosis/ / infertility/ / pituitary– / ovarian dysfunction/ / subfertility
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