ABSTRACT
Leiomyomata, or fibroids, are abnormal nonmalignant growths of smooth muscle cells (SMC) of the uterine myometrium. The clinical description of leiomyomata is well docu mented.1,2 Over 25% of women in most popula tions report clinical symptoms caused by leiomyomata.2 The incidence of symptomatic leiomyomata is higher in African-American women.1 Patients with symptomatic leiomy omata commonly experience infertility, abnor mal uterine bleeding, and pelvic pain during their reproductive years.2 Typical treatments of leiomyoma symptoms include myomectomy, hysterectomy, uterine artery embolization, and pharmacologic treatments that reduce symp toms. The only permanent cure for symptomatic leiomyomata is hysterectomy. Many of the phar macologic treatments have major side effects, such as severe bone loss with gonadotropin releasing hormone (GnRH) agonist therapy. Medical treatments typically produce only a temporary decrease in leiomyoma volume, which increases again after cessation of treat ment. For this reason, pharmacologic treatments are often used only to reduce leiomyoma size prior to surgical intervention. Many women with symptomatic leiomyomata, particularly
those that are planning pregnancy, prefer to retain their uterus rather than undergo hys terectomy. Thus, pharmacologic agents that decrease leiomyoma size for long periods without major side effects are needed. Achiev ing this goal requires a much more detailed understanding of the cellular and molecular mechanisms controlling the pathogenesis of leiomyoma initiation and growth.
