Available therapies include expectant, hormonal, surgical, and combination medical-and-surgical treatment. The choice of treatment depends on the patient’s individual circumstances, which include (1) the presenting symptoms and their severity, (2) the location and severity of endo-metriosis, and (3) the desire for future childbearing.
No treatment provides a permanent cure. Total abdominal hys-terectomy with bilateral salpingo-oophorectomy is associ-ated with a 10% risk of recurrent symptoms and a 4% risk of additional endometriosis. Reasonable goals for manage-ment of endometriosis include reduction in pelvic pain, minimizing surgical intervention, and preserving fertility.
Patients can be treated expectantly (i.e., without either medical or surgical therapy) in some selected cases, includ-ing patients with limited disease whose symptoms are minimal or nonexistent or patients who are attempting to conceive. Because endometriosis responds to estrogen and progesterone, older patients with mild symptoms may opt to wait until the natural decrease in levels of these hor-mones that occurs with menopause.
Because the glands and stroma of endometriosis respond to both exogenous and endogenous hormones, suppression of endometriosis is based on a medication’s potential abil-ity to induce atrophy of the endometrial tissue. This treat-ment approach is optimal for patients who are currently symptomatic, have documented endometriosis beyond minimal disease, or who desire pregnancy in the future. The patient should be aware that recurrence after the com-pletion of medical therapy is common and that medical therapy does not affect adhesions and fibrosis caused by the endometriosis. Medical therapy may often be instituted empirically without a definitive surgical diagnosis of endo-metriosis, if the patient’s symptoms are consistent with the disease and appropriate, thorough physical examination and workup have been performed to rule out other causes of pain, including gynecological, gastrointestinal, and uro-logic causes.
Because of their ease of administration and relatively low level of side effects, combined oral contraceptives used in conjunction with NSAIDs are often the first line of treatment for pain associated with endometriosis. Oral con-traceptive therapy induces a decidual reaction in the functioning endometriotic tissue. Continuous therapy, in which the oralcontraceptive regimen is taken continuously without the 7 days of inactive pills that induce withdrawal bleeding, can also be prescribed to prevent secondary dysmenorrhea.
Progesterone therapy, in the form of injectable depome-droxyprogesterone acetate (DMPA) or implants, suppresses gonadotropin release and, in turn, ovarian steroidogenesis; it also directly affects the uterine endometrium and endometrial implants. DMPA has been associated with an increased riskof bone mineral loss and its use should be weighed againsta woman’s existing risk factors for osteoporosis.
Danazol is a medication that suppresses both luteiniz-ing hormone (LH) and follicle-stimulating hormone (FSH) midcycle surges. In the absence of LH and FSH stimula-tion, the ovary no longer produces estrogen, which induces amenorrhea and endometrial atrophy. Side effects of dana-zol, which occur in a minority of patients, are related to its hypoestrogenic and androgenic properties and include acne, spotting and bleeding, hot flushes, oily skin, growth of facial hair, decreased libido, and atrophic vaginitis, and deepening of the voice. Some of these side effects do not resolve with the discontinuation of therapy. Lipoprotein metabolism is also altered; serum high-density lipoprotein (HDL) levels increase significantly while low-density lipo-protein (LDL) levels decrease.
Comparable symptom relief can be achieved with fewer effects using gonadotropin-releasing hormone (GnRH) agonists. GnRH agonists down-regulate the pituitary gland andcause marked suppression of LH and FSH. However, the sideeffects are less severe than those of danazol, because andro-genic side effects are eliminated. However, the hypoestro-genic effect produced by GnRH agonists may cause hot flushes and night sweats and a slight increase in the risk of bone density loss. If a patient develops side effects while tak-ing a GnRH agonist, if the therapy is required for longer than 6 months, or if repeated treatments are required, add-back therapy consisting of low-dose combination oralcontraceptives or medroxyprogesterone should be consid-ered. Add-back therapy is often started with GnRH agonist therapy, because it does not affect the drug’s control of pelvic pain and mitigates the vasomotor and bone density side effects.
The surgical management of endometriosis can be classified as either conservative or extirpative. Conservative surgeryincludes excision, cauterization, or ablation (by laser or electrocoagulation) of visible endometriotic lesions and preservation of the uterus and other reproductive organs to allow for a possible future pregnancy. Conservative surgery is often undertaken at the time of the initial laparoscopy performed for pain or infertility. If extensive disease is found, conservative surgery involves lysis of adhesions, removal of active endometriotic lesions, and possibly reconstruction of reproductive organs. Success rates of conservative surgery appear to correlate with the severity of the disease at the time of surgery as well as with the skill of the surgeon. Medical therapy can be instituted before surgery to reduce the amount of endometriosis, and after surgery to facilitate healing and prevent recur-rence. Pregnancy rates following electrical energy or argon laser range from 34% to 75%. Pregnancy rates after car-bon dioxide laser vaporization range from 25% to 100% for stage 2 disease, from 19% to 66% for stage 3 disease, and from 25% to 50% for stage 4 disease.
Extirpative surgery for endometriosis is reserved only for cases in which the disease is so extensive that conservative med-ical or surgical therapy is not feasible, or when the patient has completed her family and wishes definitive therapy. Definitivesurgery includes total abdominal hysterectomy, bilateral salpingo-oophorectomy, lysis of adhesions, and removal of endometriotic implants. One or both ovaries may be spared if they are uninvolved and the endometriosis can be resected completely. Approximately one-third of women treated conservatively will have recurrent endometriosis and require additional surgery within 5 years. Ovarian con-servation at the time of hysterectomy carries an increased risk of recurrent endometriosis requiring additional sur-gery. After bilateral oophorectomy, estrogen therapy may be initiated immediately, with little risk of reactivating residual disease.
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