Pathogenesis and Clinical Presentation
Several theories have been proposed for the pathogenesis of endometriosis. It was first hypothesized by Sampson that women with prolonged menses have an increased risk because of the retrograde flow of sloughed endometrial cells into the pelvic cavity from the fallopian tubes. The tissue implants onto the peritoneum, resulting in the growth of lesions. Estrogen plays a role in this process by promoting cellular proliferation. Patients with endometriosis have higher concentrations of activated macrophages, interleukins, and tumor necrosis factor, as well as repressed natural killer cell formation, further promoting lesion growth in the area and preventing the elimination of endometrial debris.[7–9] The development of endometriosis is characterized by an increase in cyclooxygenase-2 (COX-2), which results in prostaglandin excess and inflammation and in enhanced aromatase activity that raises estrogen levels. Progesterone resistance also occurs. A genetic component should not be excluded because endometriosis has an estimated heritability of about 50%.
A patient with endometriosis experiences consistent premenstrual pelvic and lower back pain that may be alleviated following menstruation. Endometriosis-related infertility is thought to be caused by the aforementioned development of lesions accompanied by pelvic distortion or by the presence of an ovarian cyst known as an endometrioma, or "chocolate cyst." Endometriomas adhere to surrounding structures, such as the fallopian tubes, and are suggested to increase the risk of ovarian cancer.
US Pharmacist. 2017;42(9):12/16/2017 © 2017 Jobson Publishing