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33 - Medical Management of Endometriosis

from PART II - INFERTILITY EVALUATION AND TREATMENT

Published online by Cambridge University Press:  04 August 2010

Botros R. M. B. Rizk
Affiliation:
University of South Alabama
Juan A. Garcia-Velasco
Affiliation:
Rey Juan Carlos University School of Medicine,
Hassan N. Sallam
Affiliation:
University of Alexandria School of Medicine
Antonis Makrigiannakis
Affiliation:
University of Crete
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Summary

The successful treatment of endometriosis-associated symptoms typically requires surgical as well as medical intervention. Although medical therapies are not curative per se, the medical management of endometriosis remains to be the cornerstone of the treatment of endometriosis-associated pelvic pain (1). However, medical treatment has no place in the management of infertility associated with endometriosis, with the exception of downregulation prior to in vitro fertilization in advanced disease. Historically, the treatment for endometriosis has been high-dose androgens and progestins. These options have been discontinued because of their significant side effects. The modern era for hormonal therapy began with Danazol in 1971. This has been replaced by GnRH agonists two decades ago (2); more recently, the treatment of endometriosis shifted to decreasing the local estrogen production by aromatase inhibitors. Clinical trials are awaited with interest for selective progesterone modulators, angiostatic agents, and matrix metalloproteinase inhibitors (Table 33.1).

Successful treatment of endometriosis depends on the understanding of the effect of hormones and therapeutics on the in situ endometrium. However, there is a significant difference between the in situ endometrium and the ectopic endometrium “endometriosis.” Significant aberrant gene expression has been demonstrated in the endometriotic tissue (3). These changes explain excessive local production and decrease inactivation of estrogen in the endometriotic tissue. These include inactivation of 17β-hydroxysteroid dehydrogenase (4), progesterone receptor isoform B (5), and HOXA10 (6) to the upregulation of matrix metalloproteinases (7) and P450 aromatase (8) and to massive gene expression aberration uncovered by the microarray technology (9–12).

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Publisher: Cambridge University Press
Print publication year: 2008

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References

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