New concepts in the understanding of the ovarian hyperstimulation syndrome

In this review we will evaluate the recent developments in the pathophysiology of the ovarian hyperstimulation syndrome, with special emphasis on mediators of human chorionic gonadotropin action.

From all the different molecules investigated, it seems that vascular endothelial growth factor is the key mediator of human chorionic gonadotropin action on the vascular tree. Recent data show that although absolute serum vascular endothelial growth factor values are useless in predicting the occurrence of ovarian hyperstimulation syndrome, individual variations in binding profiles may account for clinical differences. It has been shown that vascular endothelial growth factor is produced, expressed and secreted in the ovary and that it mediates vascular permeability in response to human chorionic gonadotropin in a time-dependent fashion. This effect may be blocked by a synthetic compound (SU5416) developed to inhibit its high-affinity receptor, kinase domain containing receptor signaling in different cancers by avoiding the initial phosphorylation of vascular endothelial growth factor receptor-2.

Vascular endothelial growth factor is a promising molecule in the understanding of ovarian hyperstimulation syndrome. Future treatments should be directed to modulate or inhibit its action on the vascular wall.