Clinical Decision Making Regarding Leiomyomata: What We Need in the Next Millenium
Author(s) -
A.F. Haney
Publication year - 2000
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.00108s5835
Subject(s) - medicine , uterine artery embolization , myoma , pelvic pain , hysterectomy , leiomyoma , asymptomatic , infertility , tamoxifen , uterus , gynecology , obstetrics , surgery , pregnancy , cancer , breast cancer , biology , genetics
Leiomyomata represent the most common gynecologic tumors and are responsible for over 200,000 hysterectomies per year. They are almost invariably benign and represent clonal expansion of individual myometrial cells. They can cause a variety of symptoms including menometrorrhagia, dysmenorrhea, pelvic pain, reproductive failure, and compression of adjacent pelvic viscera, or be totally asymptomatic. Leiomyomata are more common in African-American women and have a non-Mendelian inheritance pattern with up to a 50% recurrence rate after surgical removal. The therapeutic choices depend on the goals of therapy, with hysterectomy most often used for definitive treatment, and myomectomy when preservation of childbearing is desired. Intracavitary and submucous leiomyomata can be removed by hysteroscopic resection. Laparoscopic myomectomy is now technically possible but apparently with an increased risk of uterine rupture during pregnancy. Although gonadotropin-releasing hormone-agonist-induced hypogonadism can reduce the volume of leiomyomata, the severe side effects and prompt recurrences make them useful only for short-term goals such as reversing anemia or shrinking an intracavitary tumor prior to hysteroscopic resection. Nonextirpative approaches such as myolysis and uterine artery embolization are being evaluated, and may provide more options if they prove to be safe and efficacious in long-term follow-up. Ultimately, if the genetic basis for fibroid development and/or the molecular mechanism(s) of myometrial proliferation are understood, additional nonsurgical therapeutic interventions may be forthcoming. Current clinical needs are to a) determine an effective prevention strategy in genetically predisposed individuals; b) slow the growth of leiomyomata; c) identify the mechanisms of infertility; d) improve early detection; e) develop better surgical techniques; f) reduce recurrences after myomectomy; g) develop nonextirpative options; and h) evaluate their long-term results.
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