Uterine fibroid is the most frequently seen benign gynecological tumor of the female genital tract. Although it has a relatively high prevalence rate of around 40% in women aged 40 years and older, the majority of the patients with uterine fibroids are asymptomatic. Many different treatment modalities have been used for symptomatic patients, ranging from medical to surgical interventions. Surgical management may be performed through laparotomy or minimally invasive surgery, among others.
The advent of power morcellators has made it easy for large leiomyomas to be removed laparoscopically with less blood loss, shorter hospital stay, and faster recovery time. There are many methods for tissue retrieval, such as through a mini-laparotomy incision or through a colpotomy, and they are becoming less popular. But we need to keep in mind that the fragmentation of the fibroids using the morcellator may also lead to peritoneal seeding, which, if not detected early at the time of the operation, may grow to form parasitic leiomyomas (Figs 1 and 2).
Uterine fibroid growth is dependent on the sex steroid hormones, estrogen, and progesterone. Studies from in vitro and animal models over decades suggest that estradiol (E2) plays a central role in myoma growth via its receptor, estrogen receptor α (ERα). Most medical treatments such as the gonadotrophin-releasing hormone agonist (GnRHa), aromatase inhibitors (AIs), selective estrogen receptor modulators (SERMs), progestins, and selective progesterone receptor modulators (SPRMs) reduce menstrual bleeding in patients with myoma. It is theorized that exposure to estrogen and progesterone could be a risk factor for the development of parasitic myomas as only GnRHa, AI, and SPRMs treatment options can reduce both myoma volume and menstrual bleeding.