Abnormal Pathways in Endometriosis in Relation to Progesterone Resistance: A Review

Lise Lode, Magnhild Often Sveen, Martin Rudnicki
In: Journal of Endometriosis and Pelvic Pain Disorders · 2017 · vol. 9(4) , pp. 245–251 · doi:10.5301/jeppd.5000302 · W2759051901
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This review identifies biomarkers associated with a downregulated progesterone response in eutopic endometrial biopsies, supporting the theory of progesterone resistance in endometriosis.

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Abstract

Introduction Endometriosis is an estrogen-dependent disorder, and recent studies suggest that progesterone resistance may contribute to the development and pathophysiology of the disorder. Based on this, identification of genetic and molecular perturbations in the endometrium of women with endometriosis is an important step towards understanding the pathogenesis of the disease, and the development of novel treatment and diagnostic strategies. Methods A systematic literature search in PubMed and Embase was performed, and 118 articles were identified for further screening. Two reviewers performed article screening independently using Covidence, and 16 studies fulfilled the inclusion criteria. The Newcastle-Ottawa Scale was used to assess the quality of these studies. Results This review presents data from eutopic endometrial biopsies from women with and without endometriosis. Several biomarkers related to a downregulated progesterone response were identified and discussed in detail. Conclusions Our review demonstrates significant results concerning the biomarkers investigated, which may substantiate the theory of progesterone resistance in women with endometriosis. However, further research is necessary to determine their specific role and relevance.

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Condition tags

endometriosis

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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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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