ABSTRACT
Ovarian hyperstimulation syndrome (OHSS) normally manifests itself as a serious complica tion of ovulation induction treatments, although there have also been reports of spontaneous and familial OHSS, associated with pregnancy1,2. The pathogenesis of this syndrome has not been fully clarified, although the description of two spontaneous cases with familial association sug gests that a certain genetic predisposition may prove necessary to induce the disorder. Human chorionic gonadotropin (hCG) probably stimu lates the ovarian secretion of vasoactive factors that in turn increase vascular permeability and contribute to third-compartment fluid accumu lation, these being characteristic physiopathological features of OHSS. Many substances have been suggested as possible mediators of the syn drome, including serotonin, histamine, pro lactin, estrogens and prostaglandins, although the renin-angiotensin system (RAS) and certain cytokines (interleukin-2 and -8) produced by the ovaries have been proposed as the main factors implicated in OHSS physiopathology. Thus, the renin-angiotensin system (RAS) is one of the mechanisms presumed to participate in ovarian hyperstimulation syndrome.
