[Uterine fibromas and the hormonal pattern: the therapeutic considerations]

Uterine fibromyomatosis is a widely recognised and well studied pathology that is found in around 30% of over 35-year-old women. It has been extensively demonstrated that the etiology of fibromyomas is hormone dependent and to date the main pathogenetic role in the development of these benign tumours has largely been attributed to estrogens. Uterine fibromyomas have been found to contain a higher level of estrogen and progesterone receptors than in normal uterus. This suggests an etiopathogenetic role also for progesterone, which is confirmed by the higher mitotic index of myomatous tissue cells in luteal phase. Growth factors also seem to be involved in the origin of uterine fibromyomatosis: concentrations of epidermal growth factor (EGF), insulin like growth factor 1 (IGF-I) and platelet derived growth factor (PDGF AB) are present in myomatous tissues together with their receptors. Recent studies have shown that the administration of an anti-progestin compound, like RU 486, causes a reduction in fibromyoma size. The role of progesterone in promoting uterine growth opens new horizons in the treatment of uterine fibromyomatosis. Treatment with GnRH analogs has proved effective in reducing the size of fibromyomas, even if the problem of their regrowth once treatment has been suspended remains unsolved. The administration of 100 mg of danazol for 6 months after treatment using GnRH analogs reduce fibromyoma rebound growth by around 30%.