Hum. Reprod. Advance Access originally published online on January 29, 2004
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Human Reproduction, Vol. 19, No. 3, 486-489,
March 2004
© 2004 European Society of Human Reproduction and Embryology
New insights into the pathophysiology of ovarian hyperstimulation syndrome. What makes the difference between spontaneous and iatrogenic syndrome?
1 Clinique de Fertilité and 2 Service de Génétique médicale, Hôpital Erasme, Brussels, 3 Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire (IRIBHM), Faculté de Médecine, Université Libre de Bruxelles, Brussels, Belgium, 4 Department of Obstetrics, Gynecology and Reproductive Sciences and 5 Reproductive Biology Research Unit, College of Medicine, University of Saskatchewan, Saskatoon, Canada
6 To whom correspondence should be addressed at Clinique de Fertilité, Hôpital Erasme, 808 route de Lennik, 1070 Brussels, Belgium. e-mail: adelbaer{at}ulb.ac.be
The recent identification of mutations in the FSH receptor gene, which display an increased sensitivity to hCG and are responsible for the development of spontaneous ovarian hyperstimulation syndrome (OHSS), provides for the first time the molecular basis for the physiopathology of spontaneous OHSS. Based on these recent findings, this paper underlines the differences between spontaneous and iatrogenic OHSS and proposes a model to account for the different chronology between the two forms of the syndrome. In the iatrogenic form, the follicular recruitement and enlargement occur during ovarian stimulation with exogenous FSH, while in the spontaneous form, the follicular recruitment occurs later through the stimulation of the FSH receptor by pregnancy-derived hCG. In both forms, massive luteinization of enlarged stimulated ovaries ensues, inducing the release of vasoactive mediators, leading to the development of the symptoms of OHSS.
Key words: FSH receptor/OHSS/physiopathology
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