Uterine Myomas

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Description

  • Uterine fibroids are benign monoclonal, pseudoencapsulated, hormone-dependent neoplasms of the myometrium, representing the most common tumors in women worldwide.
  • Depending on the location of tumor, four variants of uterine fibroids are identified:
    • Submucous uterine leiomyoma—~5% of all cases; internal, evoking abnormal uterine bleeding and infection; occasionally protruding from cervix
    • Intramural leiomyoma—common; within myometrium; may cause marked uterine enlargement
    • Subserous leiomyoma—common; external; may become pedunculated
    • Unspecified leiomyoma (code used for primary gynecological examination)
    • Rare locations: cervix, broad, round, and uterosacral ligaments
  • System affected: reproductive
  • Synonym(s): fibroids; myoma; fibromyoma; myofibroma; leiomyoma

Epidemiology

Uterine fibroids are extremely prevalent, particularly among women of reproductive age. The cumulative incidence by age 50 years approaches 70–80%, depending on racial and ethnic background (1).

Incidence

Ranged widely (217 to 3,745 cases per 100,000 women-years); highest among non-Hispanic Black women and women aged ≥40 years (1).

Prevalence

Ranging from 4.5% to 68.6% (1)

  • African American women: 60% by age 35 years; up to 80% by age 50 years.
  • White women: 40% by age 35 years; up to 70% by age 50 years.
  • Fibroids are rarely seen before puberty and tend to regress after menopause unless influenced by exogenous hormone therapy.

Etiology and Pathophysiology

  • Fibroids arise through a multistep, multifactorial process involving genetic, hormonal, and environmental influences. They represent monoclonal tumors, meaning each arises from a single transformed smooth muscle cell.
  • Hormonal influences:
    • Estrogen and progesterone both play significant roles in fibroid growth (2).
    • Myomas express more estrogen and progesterone receptors than adjacent normal myometrium.
    • Estrogen promotes cellular proliferation and matrix production.
    • Progesterone promotes fibroid growth through upregulation of growth factors and inhibition of apoptosis.
  • Growth factors:
    • Transforming growth factor beta (TGF-β), basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and insulin-like growth factor (IGF) contribute to proliferation and extracellular matrix accumulation (2).
    • Vascular endothelial growth factor (VEGF) promotes angiogenesis.

Genetics

  • Somatic chromosomal rearrangements are seen in 40% of fibroids.
  • MED12 gene mutations are present in ~70% of fibroids, particularly in women of African descent (2).
  • Higher levels of aromatase in fibroid tissue contribute to increased local estrogen production.

Risk Factors

  • Race: African American women are 3 times more likely to develop fibroids than Caucasian women; fibroids are more numerous, larger, and symptomatic (2).
  • Early menarche (<10 years of age)
  • Nulliparity: inverse relationship with fibroid risk
  • Oral contraceptive use before 16 years old, protective if used past adolescence
  • Obesity: risk increases by 21% for every 10 kg of excess weight
  • Hypertension: associated with earlier onset and increased risk
  • Family history: 2.5-fold increased risk with affected first-degree relatives
  • Vitamin D deficiency
  • Alcohol consumption

General Prevention

Protective factors

  • Use of progesterone-only contraception
  • Parity
  • Diets rich in citrus fruits, green vegetables, fish, and low-fat dairy; limited intake of red meat

Commonly Associated Conditions

  • Endometrial cancer: due to unopposed estrogen stimulation
  • Breast cancer: similar hormonal milieu may contribute

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