Discussion
The diagnosis of endometriosis was confirmed by histology of the surgical specimen and was consistent with the patient’s clinical history of premenstrual pain exacerbation. The histologic sections showed irregular endometrial glands and stroma interspersed within muscular and other soft tissue (Figure 1). The glands were lined by columnar epithelium surrounded by endometrial stromal tissue. Evidence of hemorrhage and hemosiderin-laden macrophages were observed, consistent with menstrual cycle changes (Figure 2).
Figure 1.
Figure 2.
The presence of cholesterol clefts and giant cells also suggested past hemorrhage. The glandular tissue was estrogen-receptor positive, further supporting a uterine endometrial origin. The diagnosis of endometriosis was made on the basis of the typical histologic appearance.
First described in 1860, endometriosis continues to be a benign but debilitating disease that burdens millions of women each year. It is a chronic gynecologic disorder whose principal manifestations are chronic pain and infertility. Pelvic endometriosis is the presence of endometrial glands and stromal tissue outside of the uterine cavity but confined to the pelvis. Extrapelvic endometriosis refers to endometrial tissue found anywhere in the body outside of the pelvic cavity.[1,2] Although the pathophysiology of endometriosis is poorly understood, several theories have been proposed.
The first and best supported is the implantation theory, which suggests that endometrial tissue passes through the fallopian tubes in a retrograde fashion to attach and proliferate at ectopic sites in the peritoneal cavity. This theory has been observed in menstruating females during laparoscopic surgery, as well as in animal models mimicking retrograde flow. These studies have not only demonstrated retrograde flow, but they support the idea that sloughed endometrial cells can reimplant and survive outside the pelvic cavity.[3]
A second proposed theory is the direct extension theory, which states that endometriosis results from direct invasion of ectopic endometrium through the uterine musculature. However, studies have thus far failed to show a connection between direct invasion and ectopic endometrial implants.[3] A third theory, the lymphatic/vascular metastases theory, suggests that endometrial cells can metastasize through lymphatic and hematogenous routes. This theory has been supported by a few studies demonstrating endometrial tissue in pelvic lymph nodes and findings of endometrial tissue in uterine blood vessels.[3] Other theories have also been proposed, including coelomic metaplasia, but the most evidence seems to support the implantation theory.
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