Excessive menstrual
bleeding reflects aberrant angiogenesis, generally due to submucosal
myomas and endometrial
polyps, although it is also frequently observed with long-term
progestin-only
contraception, impaired haemostasis and hormonal disorders. Surgery (
hysterectomy,
endometrial ablation) is used too frequently. Uterine artery embolisation is also an option for
myomas. Medical treatments include combined oral
contraception,
progestins and
levonorgestrel-releasing Intrauterine System.
Gonadotropin-releasing hormone agonists provide significant improvements in
bleeding for
myomas, but also decrease
estrogen secretion (e.g. hot flushes, decreased bone mass).
Progestins, although used widely, remain poorly effective as they promote
myoma cell growth. Recently, Selective
Progesterone Receptor Modulators (SPRMs) have been shown to induce
amenorrhea whilst maintaining endogenous
estrogen secretion. Phase II studies have also demonstrated decreased
fibroid size in SPRM-treated women. Although the mechanism of
amenorrhea observed after SPRM treatment is still poorly understood, they may control
uterine bleeding via a direct effect on endometrial blood vessels. Suppression of
bleeding in women with
uterine fibroids receiving SPRMs is associated with moderate reductions in uterine artery blood flow, without major changes in angiogenic factors and extracellular matrix composition; a clear difference to modifications observed with
progestins. These data suggest major progress in the treatment of excessive menstrual
bleeding.