Uterine
leiomyomas are the most frequent gynecological benign
tumors. Their growth is regulated by ovarian
steroids, therefore a hypoestrogenic state, like menopause or pharmacologically induced pseudo-menopause by
GnRH-agonists or
GnRH-antagonists, is associated with the decrease of their volume. This volume reduction allows a less invasive
surgical procedure and may reduce the amount of blood loss during surgery. Therefore,
GnRH-agonists and antagonists are used in presurgical treatment of uterine
fibromatosis. This review analyses the effects of
GnRH-agonists and
GnRH-antagonists
therapies.
GnRH-agonists produce a down-regulation of
GnRH receptor, while
GnRH-antagonists compete with endogenous
GnRH for pituitary binding sites. Due to the lack of any intrinsic activity of
GnRH-antagonists, the characteristic initial flare-up observed with
GnRH-agonist treatment is absent. So,
GnRH-antagonists rapidly suppress
gonadotropin release within 4-8 h, while
GnRH-agonists show clinical effects after 2 or 3 weeks of treatment.
GnRH-antagonist activity is dose-dependent so it is possible to adjust the dose to obtain the proper levels of inhibition. The
GnRH-agonist presurgical treatment usually is a short-term
therapy (3-6 months), because it causes side-effects like menopause symptoms.
GnRH-antagonist clinical effects can be achieved with a short-time
therapy too. Their side-effects include flushes and head-ache. After stopping
therapy with both drugs,
leiomyomas rapidly achieve their original size while side-effects disappear. Further studies are necessary to establish the use of
GnRH-antagonists in
leiomyomas therapy, but in Italy this is not possible because their use is not approved.