Leiomyoma-related bleeding: A classic hypothesis updated for the molecular era

Elizabeth A. Stewart, Romana A. Nowak

Research output: Contribution to journalReview articlepeer-review

165 Scopus citations


Leiomyomas are an important cause of menorrhagia and other forms of abnormal uterine bleeding. The pathogenesis of this process is largely unknown, however. A classic theory, first suggested by Sampson's work in 1912, states that local dysregulation of the vascular structures in the uterus is responsible for this abnormal bleeding. Recent work demonstrates dysregulation of a number of growth factors in the myomatous uterus. As many of these factors regulate the process of angiogenesis or have other effects on vascular structures, we hypothesize that this dysregulation of growth factors or their receptors provides the molecular mechanism underlying these vascular abnormalities. In turn, these abnormal vessels lead women with leiomyomas to experience menorrhagia. Factors that may prove to be important in this process include basic fibroblast growth factor, vascular endothelial growth factor, heparin-binding epidermal growth factor, platelet-derived growth factor, transforming growth factor-β, parathyroid hormone-related protein and prolactin. Current treatment regimens for women with leiomyoma-related bleeding depend on manipulation of the steroid hormone environment. By better understanding the pathogenesis of this disease process, therapies directed against growth factor abnormalities may result in better treatment with less harmful side-effects.

Original languageEnglish (US)
Pages (from-to)295-306
Number of pages12
JournalHuman Reproduction Update
Issue number4
StatePublished - 1996


  • Angiogenesis
  • Basic fibroblast growth factor
  • Leiomyoma
  • Menorrhagia
  • Uterus

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology


Dive into the research topics of 'Leiomyoma-related bleeding: A classic hypothesis updated for the molecular era'. Together they form a unique fingerprint.

Cite this