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The role of the levonorgestrel-releasing intrauterine device in the management of symptomatic endometriosis

Purpose of review The aim of this article is to evaluate the biological rationale for the use of an intrauterine device releasing 20 μg/day of levonorgestrel in women with endometriosis, and to assess its efficacy in relieving pelvic pain symptoms. Recent findings Levonorgestrel induces endometrial glandular atrophy and extensive decidual transformation of the stroma, downregulates endometrial cell proliferation, increases apoptotic activity, and has antiinflammatory and immunomodulatory effects. Up to 85% of patients wearing the device have anovulatory cycles during the first 3 months of use, but the proportion falls to below 35% by 12 months. After the first year of use, a 70–90% reduction in monthly blood loss is observed; few women report intermenstrual bleeding and about 20–30% amenorrhea. This is advantageous in patients experiencing dysmenorrhea. Although it is maintained that the hormonal activity of the levonorgestrel intrauterine device is local, a systemic effect secondary to uterine absorption of levonorgestrel is probable. The levonorgestrel intrauterine device has proven effective in relieving pelvic pain symptoms caused by peritoneal and rectovaginal endometriosis and in reducing the risk of recurrence of dysmenorrhea after conservative surgery. Summary Intrauterine administration of levonorgestrel with direct distribution to pelvic tissues would imply a local concentration greater than plasma levels. This could result in a superior effectiveness with limited adverse effects and increased patient compliance during long-term treatment. Further trials are needed, however, to verify whether the good results observed are maintained during an entire 5-year period, to confirm the efficacy on dyspareunia and dyschezia, and to compare the effects of the levonorgestrel intrauterine device with those of other treatment options.