Delbaere A, Smits G, Olatunbosun O, Pierson R, Vassart G, Costagliola S
Clinique de Fertilité, Hôpital Erasme, Brussels, Belgium.
Hum Reprod. 2004 Mar;19(3):486-9. doi: 10.1093/humrep/deh124. Epub 2004 Jan 29.
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 recruitment 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.
最近在促卵泡激素(FSH)受体基因中发现的突变,对人绒毛膜促性腺激素(hCG)表现出更高的敏感性,并导致自发性卵巢过度刺激综合征(OHSS)的发生,首次为自发性OHSS的病理生理学提供了分子基础。基于这些最新发现,本文强调了自发性和医源性OHSS之间的差异,并提出了一个模型来解释该综合征两种形式之间不同的发病时间顺序。在医源性形式中,卵泡募集和增大发生在外源性FSH刺激卵巢的过程中,而在自发性形式中,卵泡募集随后通过妊娠衍生的hCG刺激FSH受体而发生。在两种形式中,增大的受刺激卵巢都会发生大量黄素化,诱导血管活性介质的释放,导致OHSS症状的出现。