Estrogen therapy implants

Medroxyprogesterone acetate (Fig. 46.13), administered by injection (Depo-Provera), orally, or delivered via lUD, effectively suppresses the HPO axis, induces anovulation, and reduces serum estrogen levels (83). This prevents menstruation and endometrial implant growth. As a result, endometriosis-related pain is minimized in approximately 90% of the patients. Drug therapy selection should reflect the fact that pharmacological therapy is likely to be required on a chronic basis. The progestins are fairly well tolerated and relatively inexpensive, but they are not without adverse effects. 

Normal endometrial tissues are devoid of aromatase activity. In patients with endometriosis, evidence suggests that high levels of aromatase are present in endometrial implants. Aromatase is the enzyme that catalyzes the conversion of androstenedione and testosterone to estrone and estradiol, respectively (Fig. 46.3). If an aromatase inhibitor, such as anastrozole (Fig. 46.11), is administered, then estrogen production will be decreased in the endometrial implants. A local state of estrogen deficiency will prevent growth of these implants (84). Unfortunately, one outcome of prolonged aromatase therapy is the development of osteoporosis. As a result, an OC typically is coadministered to provide baseline estrogen concentrations and limit the risk of osteoporosis. 

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