| Literature DB >> 31142643 |
Marine Peyneau1, Niloufar Kavian1,2,3,4, Sandrine Chouzenoux1, Carole Nicco1, Mohamed Jeljeli1,2,3, Laurie Toullec1, Jeanne Reboul-Marty2,5, Camille Chenevier-Gobeaux2,6, Fernando M Reis1, Pietro Santulli1,2,7, Ludivine Doridot1, Charles Chapron1,2,7, Frédéric Batteux8,2,3.
Abstract
Endometriosis 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.Entities:
Keywords: autoimmunity; endometriosis; oxidative stress; thyroid; thyroid hormones
Year: 2019 PMID： 31142643 PMCID： PMC6575600 DOI： 10.1073/pnas.1820469116
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205