Sestre Milosrdnice University hospital and Institute of Clinical Medical Research
Abstract
Ovarian hyperstimulation syndrome is the most serious iatrogenic complication resulting from ovarian stimulation. Currently there is no clear evidence of absolute efficacy for most of standard preventive and curative methods. Recent studies indicate that human chorionic gonadotropin increases vascular endothelial growth factor, vascular endothelial cadherin and vascular permeability via endothelial adherence junctions. Vascular endothelial growth factor plays a pivotal role in the pathophysiology of the condition and therefore vascular endothelial factor antagonism has been suggested for the prevention of the syndrome. Since vascular endothelial growth factor is also a physiological regulator of folliculogenesis, progesterone secretion and endometrial angiogenesis, its complete inactivation by specific blockers could produce undesirable effects interfering with early pregnancy development and therefore they cannot be used clinically. Recently, low doses of dopamine agonists (cabergoline) have been shown to counteract vascular endothelial growth factor induced vascular hyperpermeability, reducing the incidence of the syndrome by prophylactic treatment without compromising pregnancy outcome. The absence of undesirable side effects could make cabergoline an effective and safe etiologic approach for the prevention and treatment of the syndrome. A novel approach has suggested that metformin may also be helpful in the syndrome prevention in women with or without polycystic ovary disease.Ovarijski hiperstimulacijski sindrom je najozbijnija jatrogena komplikacija koja nastaje nakon stimulacije jajnika. Zasad nema jasnih dokaza o apsolutnoj djelotvornosti većine standardnih i preventivnih i kurativnih metoda. Novije studije pokazuju da humani korionski gonadotropin povisuje vaskularni čimbenik rasta, vaskularni endotelni kaderin i vaskularnu propusnost na spojevima adherentnog endotela. Kako vaskularni endotelni čimbenik rasta igra ključnu ulogu u patofiziologiji sindroma, ukazuje se na onemogućavanje djelovanja vaskularnog čimbenika rasta u prevenciji bolesti. Budući da je vaskularni čimbenik rasta ujedno i fiziološki regulator folikulogeneze, stvaranja progesterona i krvnih žila endometrija, njegova bi potpuna inaktivacija specifičnim blokatorima dovela do neželjenih nuspojava koje bi ometale razvoj rane trudnoće, što onemogućuje njihovu kliničku primjenu. Odnedavno se pokazalo kako niske doze agonista dopamina (kabergolin) suzbijaju pojačanu vaskularnu propusnost izazvanu vaskularnim endotelnim čimbenikom rasta, smanjujući profilaktično pojavnost sindroma bez nepovoljnog djelovanja na ishod trudnoće. Zbog izostanka nepoželjnih nuspojava kabergolin bi mogao biti djelotvoran i siguran u etiološkom pristupu te u prevenciji i liječenju sindroma. Noviji pristup ukazuje na to da primjena metformina može isto koristiti u prevenciji sindroma kod žena s policističnim jajnicima ili bez njih
