Ovarian hyperstimulation syndrome: pathophysiology and prevention.
OBJECTIVE
To review and discuss the pathophysiology and prevention strategies for ovarian hyperstimulation syndrome (OHSS), which is a condition that may occur in up to 20% of the high risk women submitted to assisted reproductive technology cycles.


METHODS
The English language literature on these topics were reviewed through PubMed and discussed with emphasis on recent data.


RESULTS
The role of estradiol, luteinizing hormone, human chorionic gonadotropin (hCG), inflammatory mediators, the renin-angiotensin system and vascular endothelial growth factor is discussed in the pathophysiology of OHSS. In addition we consider the prevention strategies, including coasting, administration of albumin, renin-angiotensin system blockage, dopamine agonist administration, non-steroidal anti-inflammatory administration, GnRH antagonist protocols, reducing hCG dosage, replacement of hCG and in vitro maturation of oocytes (IVM).


CONCLUSIONS
Among the many prevention strategies that have been discussed, the current evidence points to the replacement of hCG by GnRH agonists in antagonist cycles and the performance of IVM procedures as the safest approaches.
Departamento de Ginecologia e Obstetrícia da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo (DGO-HC-FMRP-USP), Avenida dos Bandeirantes 3900, 8 masculine andar, Ribeirão Preto, São Paulo, Brazil, CEP 14049-900.
Carolina O
CO
Nastri
Rui A
RA
Ferriani
Isa A
IA
Rocha
Wellington P
WP
Martins
D000328:Adult; D000418:Albumins / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002478:Cells, Cultured / Q000166:cytology; D006063:Chorionic Gonadotropin / Q000008:administration & dosage / Q000009:adverse effects / Q000502:physiology; D018491:Dopamine Agonists / Q000494:pharmacology; D004958:Estradiol / Q000097:blood / Q000502:physiology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D007378:Interleukins / Q000502:physiology; D007986:Luteinizing Hormone / Q000502:physiology; D009865:Oocytes / Q000166:cytology; D016471:Ovarian Hyperstimulation Syndrome / Q000503:physiopathology* / Q000517:prevention & control*; D010062:Ovulation Induction / Q000009:adverse effects* / Q000379:methods; D012084:Renin-Angiotensin System / Q000502:physiology; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
D000418:Albumins; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000894:Anti-Inflammatory Agents, Non-Steroidal; D006063:Chorionic Gonadotropin; D018491:Dopamine Agonists; D018836:Inflammation Mediators; D007378:Interleukins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D007986:Luteinizing Hormone