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Article: Role of thyroid dysimmunity and thyroid hormones in endometriosis

TitleRole of thyroid dysimmunity and thyroid hormones in endometriosis
Authors
KeywordsAutoimmunity
Endometriosis
Oxidative stress
Thyroid
Thyroid hormones
Issue Date2019
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings of the National Academy of Sciences, 2019, v. 116 n. 24, p. 11894-11899 How to Cite?
AbstractEndometriosis is characterized by the presence of ectopic endometrial cells outside the uterine cavity. Thyroid autoimmunity has been associated with endometriosis. This work investigated the potential pathophysiological link between endometriosis and thyroid disorders. Transcripts and proteins involved in thyroid metabolism are dysregulated in eutopic and ectopic endometrium of endometriotic patients, leading to resistance of ectopic endometrium to triiodothyronine (T3) action and local accumulation of thyroxine (T4). Thyroid-stimulating hormone (TSH) acts as a proliferative and prooxidative hormone on all endometria of endometriosis patients and controls, whereas T3 and T4 act to specifically increase ectopic endometrial cell proliferation and reactive oxygen species (ROS) production. Mouse studies confirmed the data gained in vitro since endometriotic implants were found to be bigger when thyroid hormones increased. A retrospective analysis of endometriosis patients with or without a thyroid disorder revealed an increased chronic pelvic pain and disease score in endometriotic patients with a thyroid disorder. © 2019 National Academy of Sciences. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/276137
ISSN
2023 Impact Factor: 9.4
2020 SCImago Journal Rankings: 5.011
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKavian-Tessler, NC-
dc.date.accessioned2019-09-10T02:56:43Z-
dc.date.available2019-09-10T02:56:43Z-
dc.date.issued2019-
dc.identifier.citationProceedings of the National Academy of Sciences, 2019, v. 116 n. 24, p. 11894-11899-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/276137-
dc.description.abstractEndometriosis is characterized by the presence of ectopic endometrial cells outside the uterine cavity. Thyroid autoimmunity has been associated with endometriosis. This work investigated the potential pathophysiological link between endometriosis and thyroid disorders. Transcripts and proteins involved in thyroid metabolism are dysregulated in eutopic and ectopic endometrium of endometriotic patients, leading to resistance of ectopic endometrium to triiodothyronine (T3) action and local accumulation of thyroxine (T4). Thyroid-stimulating hormone (TSH) acts as a proliferative and prooxidative hormone on all endometria of endometriosis patients and controls, whereas T3 and T4 act to specifically increase ectopic endometrial cell proliferation and reactive oxygen species (ROS) production. Mouse studies confirmed the data gained in vitro since endometriotic implants were found to be bigger when thyroid hormones increased. A retrospective analysis of endometriosis patients with or without a thyroid disorder revealed an increased chronic pelvic pain and disease score in endometriotic patients with a thyroid disorder. © 2019 National Academy of Sciences. All rights reserved.-
dc.languageeng-
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org-
dc.relation.ispartofProceedings of the National Academy of Sciences-
dc.rightsProceedings of the National Academy of Sciences. Copyright © National Academy of Sciences.-
dc.subjectAutoimmunity-
dc.subjectEndometriosis-
dc.subjectOxidative stress-
dc.subjectThyroid-
dc.subjectThyroid hormones-
dc.titleRole of thyroid dysimmunity and thyroid hormones in endometriosis-
dc.typeArticle-
dc.identifier.emailKavian-Tessler, NC: niloufar@hku.hk-
dc.identifier.doi10.1073/pnas.1820469116-
dc.identifier.pmid31142643-
dc.identifier.scopuseid_2-s2.0-85067100374-
dc.identifier.hkuros302860-
dc.identifier.volume116-
dc.identifier.issue24-
dc.identifier.spage11894-
dc.identifier.epage11899-
dc.identifier.isiWOS:000471039700054-
dc.publisher.placeUnited States-
dc.identifier.f1000735855184-
dc.identifier.issnl0027-8424-

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