An important new adaption of a specific drug?

摘要

We read with interest the case report of Knoepfelmacher (1) about cabergoline effectiveness in the treatment of ovarian hyperstimulation syndrome (OHSS) due to gonadotro-pin-producing adenomas. Similar results were previously reported by others (2) with bromocriptine. Gonadotropin secretion reduction was the mechanism suggested. However, the work of Basu et al. (3) clarified that dopamine, through its D2 receptor, is able to antagonize vascular endothelial growth factor vascular effects blocking vascular endothelial growth factor R2 receptor. It is well known that vascular endothelial growth factor production by the conceptus starts at the beginning of embryo development inducing, at the en-dometrial level, both the increase of vascular permeability and the neoangiogenesis that contribute to embryo implantation. In fact, a complete vascular endothelial growth factor antagonism by high doses of specific monoclonal antibody prevented embryo implantation (4) in the monkey. However the long-lasting clinical use of cabergoline to treat hyper-prolactinemia-related infertility, its use in the treatment of macroprolactinoma during pregnancy, and the lack of tera-togenic evidence for this drug, induced our group to propose (5) cabergoline administration, to the best of our knowledge for the first time, to reduce the vascular endothelial growth factor-mediated pathologic increase of vascular permeability observed in human OHSS. Our preliminary experience with cabergoline (0.5-1 mg every day from pickup) confirms that it promptly reduces hematocrit in patients with severe OHSS.