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LEIOMYOMAS

Pathogenesis

Often simply called myomas, uterine leiomyomas are benign smooth-muscle neoplasms that typically originate from the myometrium. Their prevalence among women is generally cited as 10 to 20 percent, but is as high as 70 to 80 percent in sonographic studies (Baird, 2003; Marshall, 1997).

Grossly, a typical off-white, whorled leiomyoma is autonomous from its surrounding myometrium because of a thin, outer connective tissue layer (Fig. 9-1). This clinically important cleavage plane allows leiomyomas to be easily “shelled” from the uterus during surgery. The blood supply within these tumors is tenuous, and thus ischemia and necrosis develop frequently in myomas. Following necrosis, their smooth muscle is replaced with various degenerative substances. Forms include hyaline, calcific, cystic, myxoid, red, and fatty, and these gross changes should be recognized as normal variants.

FIGURE 9-1

A. Microscopically, leiomyomas are composed of bland, spindled smooth-muscle cells characterized by elongate, blunt-ended nuclei and tapered eosinophilic cytoplasm. The cells are arranged in interlacing fascicles that intersect at right angles. B. The interface (asterisk) between the leiomyoma (L) and adjacent myometrium (M) can be seen grossly and microscopically. These tumors are usually more cellular than the surrounding myometrium. (Reproduced with permission from Dr. Kelley Carrick.)

Each leiomyoma is derived from a single progenitor myocyte. Following their genesis, uterine leiomyomas are estrogen- and progesterone-sensitive tumors. And, these tumors carry higher densities of both progesterone and estrogen receptors compared with their surrounding myometrium. Progesterone is considered the critical mitogen for uterine leiomyoma growth and development. In turn, estrogen functions to upregulate and maintain progesterone receptors (Ishikawa, 2010).

To help maintain and promote growth, leiomyomas themselves create a local hyperestrogenic environment (Bulun, 1994; Englund, 1998). Also, some conditions provide sustained estrogen exposure that encourages leiomyoma growth. Examples include early menarche, obesity, and polycystic ovarian syndrome (Wise, 2005,2007). Despite this hormonal responsiveness, myoma formation is not induced by combination oral contraceptive (COC) pills (Qin, 2013). And, depot medroxyprogesterone acetate (DMPA) use in young African-American women is associated with lower myoma risk (Harmon, 2015).

For myoma development, race and age are notable factors. Myomas are rare in adolescence, but rates rise with age during the reproductive years. In one study, the cumulative incidence by age 50 years was nearly 70 percent in whites and more than 80 percent in African-American women (Baird, 2003). However, once in the menopause, accruing age lowers the incidence (Sommer, 2015). Leiomyomas are more common in African-American women compared with white, Asian, or Hispanic women (Marshall, 1997). Thus, as noted earlier, heredity and gene mutations play a seminal role in myoma development.

Classification

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