Uterine Leiomyomas

Uterine Leiomyomas

Uterine leiomyomata (also called fibroids and myomas) U represent localized proliferation of smooth muscle cellssurrounded by a pseudocapsule of compressed muscle fibers. The highest prevalence occurs during the fifth decade of a woman’s life, when they may be present in 1 in 4 white women and 1 in 2 black women. Uterineleiomyomata are clinically apparent in 25% to 50% of women, although studies in which careful pathologic examination of the uterus is carried out suggest that the prevalence may be as high as 80%. Uterine fibroids vary in size, from microscopic tolarge multinodular tumors that literally fill the patient’s abdomen. Leiomyomata are the most common indication for hysterectomy, accounting for approximately 30% of all such cases. Additionally, they account for a large number of more conservative operations, including myomectomy, uterine curettage, operative hysteroscopy, and uterine artery embolization (UAE).

Leiomyomata are classified into subgroups based on their anatomic relationship to the layers of the uterus. Thethree most common types are intramural (centered in the mus-cular wall of the uterus), subserosal( just beneath the uterine serosa), and submucosal ( just beneath the endometrium). Asubset of the subserosal category is the pedunculatedleiomyoma, which appears on stump-like structures. Mostleiomyomata initially develop from within the myometrium as intramural leiomyomata. Roughly 5% of uterine myomas originate from the cervix. Rarely, leiomyomata may occur without evidence of a uterine origin in places such as the broad ligament and peritoneal cavity. Leiomyomata are considered hormonally responsive, benign tumors, because estrogen may induce their rapid growth in high-estrogen states, such as pregnancy. In contrast, menopause gener-ally causes cessation of tumor growth and even some atro-phy. Estrogen may work by stimulating the production of progesterone receptors in the myometrium. In turn, pro-gesterone binding to these sites stimulates the production of several growth factors, causing the growth of myomas. Although exact mechanisms are unknown, chromosomal translocations/deletions, peptide growth factor, and epi-dermal growth factor are implicated as potential pathogenic factors of leiomyomata. Sensitive DNA studies suggest that each myoma arises from a single smooth muscle cell and that, in many cases, the smooth muscle cell is vascular in origin.

The uterine smooth muscle may also develop a rare cancer, such as leiomyosarcoma. These are not thought to represent “degeneration” of a fibroid, but, rather, a new neoplasm. Uterine malignancy is more typical in postmenopausalpatients who present with rapidly enlarging uterine masses, postmenopausal bleeding, unusual vaginal discharge, and pelvic pain. An enlarging uterine mass in a postmenopausal patientshould be evaluated with considerably more concern for malignancy than one found in a younger woman. These heterologous, mixed tumors contain other sarcomatous tis-sue elements not necessarily found only in the uterus.