卵巢过度刺激综合征的发病机制：一个持续的谜团。
The pathogenesis of ovarian hyperstimulation syndrome: a continuing enigma.
作者信息
Simon A, Revel A, Hurwitz A, Laufer N
机构信息
Department of Obstetrics and Gynecology, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel.
出版信息
J Assist Reprod Genet. 1998 Apr;15(4):202-9. doi: 10.1023/a:1023052419627.
PURPOSE
Our purpose was to review the available literature concerning the pathogenesis of ovarian hyperstimulation syndrome and, in light of the most recent information, to attempt to provide further insight on this iatrogenic complication associated with the induction of ovulation.
METHODS
Published studies related to this topic were identified through a computerized bibliographic search.
CONCLUSIONS
The exact mechanism for the development of ovarian hyperstimulation syndrome is still obscure. It is well established that the syndrome is associated with the process of ovulation induced by either luteinizing hormone or human chorionic gonadotropin. Following ovulation, one or more substances produced by the ovary are liberated in excess, increasing capillary permeability, resulting in the clinical features of the syndrome. It may well be that the syndrome is not triggered by a single mechanism but by the production and secretion of several substances acting in concert. These may include prostaglandins, cytokines, the ovarian reninangiotensin system, vascular endothelial growth factor, and nitric oxide.
目的
我们的目的是回顾有关卵巢过度刺激综合征发病机制的现有文献，并根据最新信息，试图对这种与促排卵相关的医源性并发症提供进一步的见解。
方法
通过计算机化文献检索确定与该主题相关的已发表研究。
结论
卵巢过度刺激综合征的确切发病机制仍不清楚。众所周知，该综合征与促黄体生成素或人绒毛膜促性腺激素诱导的排卵过程有关。排卵后，卵巢产生的一种或多种物质过量释放，增加毛细血管通透性，导致该综合征的临床特征。很可能该综合征不是由单一机制触发，而是由几种协同作用的物质的产生和分泌触发。这些物质可能包括前列腺素、细胞因子、卵巢肾素 - 血管紧张素系统、血管内皮生长因子和一氧化氮。
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