Pathophysiology of Infertility in Endometriosis

Bruce A. Lessey, Steven L. Young
In: Endometriosis · 2011 · pp. 240–254 · doi:10.1002/9781444398519.ch23 · W1540423184
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This review explores the pathophysiology of infertility in endometriosis, highlighting potential progesterone resistance and estrogen hypersensitivity in the endometrium, and suggesting impaired endometrial receptivity as a leading mechanism.

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Abstract

Endometriosis is a disease affecting up to 10% of reproductive-aged women, but contributing to the majority of cases of pelvic pain and infertility. The association between infertility and mild endometriosis remains controversial, despite multiple lines of evidence. Treatment of endometriosis appears to be associated with improvement in cycle fecundity. The pathophysiology of endometriosis and infertility is not well understood, but is likely linked to the origins, maintenance and recurrence of the disease. Recognition of the biochemical alterations in eutopic endometrium of women with endometriosis suggests an underlying resistance to the actions of progesterone and an exaggerated responsiveness to estrogen. While the theories regarding the mechanisms of infertility associated with endometriosis are protean, a defect in endometrial receptivity leading to delayed fertility or pregnancy loss is the one that is most accepted, supported by available evidence. Identification of the key factors in the serum, peritoneal fluid or endometrium that are linked to infertility may provide diagnostic biomarkers for future studies of this enigmatic disease.

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Condition tags

endometriosisinfertility

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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License: CC0 · commercial use OK