Adenomyosis: the pathophysiology of an oestrogen-dependent disease

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This paper reviews the pathophysiology of adenomyosis, a disease characterized by the invasion of the uterine endometrium into the myometrium and driven by estrogen.

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Abstract

Adenomyosis uteri is a common gynaecological disorder that is characterized by the presence of ectopic endometrial glands and stroma in the myometrium. Although adenomyosis and endometriosis are different diseases, both of them grow and regress in an oestrogen-dependent fashion. Polymorphisms in the oestrogen receptor alpha gene are associated with a risk of adenomyosis. Adenomyotic tissue contains steroid receptors as well as aromatase and sulphatase enzymes. Together with the circulating oestrogen, locally produced oestrogens stimulate the growth of tissue mediated by the oestrogen receptors. Oestrogen metabolism, including the expression pattern of aromatase and the regulation of 17beta-hydroxysteroid dehydrogenase type 2 is altered in the eutopic endometrium of women with endometriosis, adenomyosis, and/or leiomyomas compared to that in the eutopic endometrium of women without disease. In addition to the conventional hormonal treatment with gonadotropin-releasing hormone agonists and danazol, the use of steroid-releasing intrauterine devices may be applicable to clinics.

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Condition tags

endometriosisadenomyosis

MeSH descriptors

Endometriosis Estrogens Uterine Diseases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Danazol Danazol Danazol Endometriosis Endometriosis Endometriosis Endometriosis Estrogen Antagonists Estrogen Antagonists Estrogen Antagonists Estrogens Estrogens Female Female

Citation neighborhood

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.

References (73)

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License: CC0 · commercial use OK