Uterine fibroids are derived from smooth muscle within the uterine wall (Mitwally 2013). Fibroids may also be located in the cervix; the broad ligament, which connects the uterus to the pelvic wall; or can be attached to the interior or exterior of the uterus by a stalk, in which case they are called pedunculated leiomyomas. In some cases, fibroids may develop in other abdominal structures; these are called parasitic leiomyomas (Ferri 2014; Phupong 2003; Jebunnaher 2013). Women can have a single fibroid or multiple fibroids of different sizes and in different locations (Elsevier BV 2011).
The exact cause of uterine fibroids is not completely understood. However, the sex hormones estrogen and progesterone play an important role in fibroid growth (Mitwally 2013). Estrogen and progesterone control the growth of the uterine lining (endometrium) during a woman’s reproductive cycle and help prepare the uterus for pregnancy (Goldsmith 2009). The incidence of fibroids fluctuates throughout different hormonal phases of a woman’s life, with the majority occurring during reproductive years (Ciavattini 2013). Some, but not all, studies have found that high estrogen levels and increased blood flow during pregnancy can cause existing fibroids to enlarge (Ferri 2014; UMMC 2014). This effect may depend on the trimester of pregnancy and size of the fibroids, though one study found no change in fibroid size for most women during pregnancy. In that study, the fibroids that did enlarge grew less than 25% (Lev-Toaff 1987; Aharoni 1988). After menopause, when hormone levels decline, existing fibroids often decrease in size (Elsevier BV 2011).
Compared with surrounding normal tissue, fibroids contain higher levels of receptors for progesterone and estrogen and are more responsive to hormonal stimulation. Estradiol, a type of estrogen, promotes fibroid cell replication, while progesterone blocks fibroid cell death. These combined effects can result in growth of fibroid tissue (Elsevier BV 2011). Moreover, fibroid tissue has higher levels of the enzyme aromatase, which converts testosterone into estrogen, compared with healthy uterine tissue. This may lead to higher levels of estrogen in the fibroid tissue, which may further stimulate fibroid growth (Ishikawa 2006; Bulun 2013; Ishikawa 2009).