The available literature concerning the association between gonadotrophin-releasing hormone agonist and ovarian hyperstimulation syndrome has been reviewed and the different patterns by which this agent may contribute to the development of such iatrogenic complication has been elicited, and guidelines have been presented for prevention of this malady. Gonadotrophin-releasing hormone agonist acts directly on human granulosa cells, probably in its own dose-dependent manner. The extent of this action is probably subjected to follicular maturation stage and to the degree of gonadotrophin pre-treatment. Various agonist effects in assisted reproduction may be implicated in the development of ovarian hyperstimulation syndrome: a higher amount of menotrophin; premature luteinization prevention; 'flare-up' effect; and a higher pregnancy rate. Different methods for prevention of ovarian hyperstimulation syndrome may be attempted: (i) all embryo cryopreservation with luteal phase reinitiation of agonist; (ii) avoidance of ovulatory human chorionic gonadotrophin (HCG) and continuation of agonist; (iii) cancellation of ovulatory HCG, prolongation of agonist and later recommencement of menotrophin; (iv) pre-ovulatory LH surge triggering by agonist instead of the conventional HCG. Gonadotrophin-releasing hormone agonist may affect the steroidogenic ovarian stroma directly and such interaction may aggravate the development of ovarian hyperstimulation syndrome.
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http://dx.doi.org/10.1093/oxfordjournals.humrep.a137973 | DOI Listing |
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