from PART II - INFERTILITY EVALUATION AND TREATMENT
Published online by Cambridge University Press: 04 August 2010
INTRODUCTION
Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of ovulation induction, which may cause serious impact on the patient's health, with 0.1–2 percent of the patients developing severe forms of the syndrome (1). This low incidence is increasing worldwide through the expansion of assisted reproductive techniques (ART) (2). Generally speaking, OHSS is a consequence of exogenous gonadotropin/clomiphene citrate administration for ovulation induction – restoring ovulation in anovulatory patients through pharmacological induction of two or three follicles – and more frequently for aggressive controlled ovarian hyperstimulation (COH) used in ART, trying to increase the cohort of follicles achieving maturation in normal ovulatory women. This potentially life-threatening disorder causes massive extracellular exudate accumulation combined with profound intravascular volume depletion and hemoconcentration, accompanied by ovarian enlargement with exaggerated esteroidogenesis and multiple system failure as end point (3).
There are many hormonal variables that are closely related to the pathophysiology of OHSS syndrome, perhaps the most important of which is whether being exogenous or endogenous (e.g., pregnancy derived) (4,5). Elimination of hCG will prevent the full-blown picture of OHSS. In fact, when hCG was replaced for progesterone as luteal support in ovulation induction (OI) or COH, the incidence of OHSS was reduced, maintaining excellent pregnancy rates (6). If hCG is used for luteal phase support, the risk of OHSS is enhanced.
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