Elimination of OHSS

14 03 2012

To the Editor:

I read with interest the recently published discussion on the etiology and prevention of OHSS (1-2). While the reviews comprehensively covered their aims, there are some issues that should be highlighted.

Agonist and antagonist coast

Coasting, or the complete discontinuation of exogenous gonadotropin while continuing GnRH analogues administration, is a preventive measure that is completely related on serum E2 levels at gonadotropin discontinuation and on the drop in E2 levels on day of hCG administration (1). However, while “it is well established that high E2 levels are associated with a high incidence of OHSS” (1), OHSS may occur in patients who conceived spontaneously, and in those with low or high serum E2 levels on the day of hCG administration (details in ref. 3). These versatile observations actually suggest that the previously accepted risk factors to develop OHSS, especially high serum E2 levels, are unreliable for the prediction of severe OHSS (3).

Therefore, we were not surprised at the finding of the recently published Cochrane review (4), which reported no difference in the incidence of moderate or severe OHSS after coasting. Read the rest of this entry »

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Etiology of OHSS

14 03 2012

To the Editor:

I read with interest the recently published discussion on the etiology and prevention of OHSS (1). While the review comprehensively covered its aims, there are some issues that should be highlighted.

OHSS, being a major complication of controlled ovarian hyperstimulation (COH), is characterized by marked ovarian enlargement and acute third space fluid sequestration that almost always develops after hCG administration or in early pregnancy. OHSS is similar to vascular leak syndrome (VLS), which may be attributable to the massive increase in systemic inflammatory cytokines, including vascular endothelial growth factor (VEGF), observed also during the course of severe OHSS (2).

As was already mentioned (1), many factors and mediators have been proposed as the intermediate, released by gonadotropin-hyperstimulated ovaries at ovulation, which causes the increase in capillary permeability. However, no significant evidence exists to prove any absolute or ultimate role of these ovarian regulators in the pathophysiology of OHSS (2). Read the rest of this entry »