Editing Hashimoto's thyroiditis (section)

=== Environmental ===

==== Medications ====
Certain medications or drugs have been associated with altering and interfering with thyroid function. There are two main mechanisms of interference:<ref name="Surks-1995" />

* Altering thyroid hormone serum transfer proteins.<ref name="Surks-1995">{{cite journal | vauthors = Surks MI, Sievert R | title = Drugs and thyroid function | journal = The New England Journal of Medicine | volume = 333 | issue = 25 | pages = 1688–1694 | date = December 1995 | pmid = 7477223 | doi = 10.1056/NEJM199512213332507 | veditors = Wood AJ }}</ref> [[Estrogen]], [[tamoxifen]], [[heroin]], [[methadone]], [[clofibrate]], [[Fluorouracil|5-fluorouracil]], [[mitotane]], and [[perphenazine]] all increase [[thyroid binding globulin]] (TBG) concentration.<ref name="Surks-1995" /> [[Androgen]]s, [[anabolic steroid]]s such as [[danazol]], glucocorticoids, and slow release [[nicotinic acid]] all decrease TBG concentrations. [[Furosemide]], fenoflenac, [[mefenamic acid]], [[salicylates]], [[phenytoin]], [[diazepam]], [[sulphonylureas]], [[free fatty acids]], and [[heparin]] all interfere with thyroid hormone binding to TBG and/or [[transthyretin]].<ref name="Surks-1995" />
* Altering extra-thryoidal metabolism of thyroid hormone. [[Propylthiouracil]], [[Glucocorticoid|glucocorticoids]], [[propranolol]], iondinated [[Contrast agent|contrast agents]], [[Amiodarone induced thyrotoxicosis|amiodarone]], and [[clomipramine]] all inhibit conversion of T<sub>4</sub> and T<sub>3</sub>.<ref name="Surks-1995" /> [[Phenobarbital]], [[Rifampicin|rifampin]], [[phenytoin]] and [[carbamazepine]] all increase [[hepatic]] metabolism.<ref name="Surks-1995" /> Finally, [[Colestyramine|cholestryamine]], [[colestipol]], [[aluminium hydroxide]], [[ferrous sulphate]], and [[sucralfate]] are all drugs that decrease T<sub>4</sub> absorption or enhance excretion.<ref name="Surks-1995" />

==== Iodine ====
Both excessive and insufficient [[Iodine#Dietary intake|iodine intake]] has been implicated in developing antithyroid antibodies.<ref name=":9" /><ref name=":8">{{Cite book | vauthors =  Weetman AP, Kahaly GJ |title=DeGroot's Endocrinology |year=2023 |edition=8th |pages=1178-1193 |chapter=Graves Disease}}</ref> Thyroid autoantibodies are found to be more prevalent in geographical areas after increasing iodine levels.<ref name=":8" /> Several mechanisms by which excessive iodine may promote thyroid autoimmunity have been proposed:<ref name=":9" />

* Via thyroglobulin iodination: Iodine exposure leads to higher iodination of thyroglobulin, increasing its [[immunogenicity]]<ref name=":9">{{cite journal | vauthors = Rayman MP | title = Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease | journal = The Proceedings of the Nutrition Society | volume = 78 | issue = 1 | pages = 34–44 | date = February 2019 | pmid = 30208979 | doi = 10.1017/S0029665118001192 }}</ref> by creating new iodine-containing [[Epitope|epitopes]] or exposing [[cryptic epitopes]].<ref>{{cite journal | vauthors = Teti C, Panciroli M, Nazzari E, Pesce G, Mariotti S, Olivieri A, Bagnasco M | title = Iodoprophylaxis and thyroid autoimmunity: an update | journal = Immunologic Research | volume = 69 | issue = 2 | pages = 129–138 | date = April 2021 | pmid = 33914231 | pmc = 8106604 | doi = 10.1007/s12026-021-09192-6 }}</ref>
* Via [[Thyroid follicular cell|thyrocyte]] damage: Iodine exposure has been shown to increase the level of [[reactive oxygen species]]. They enhance the expression of the [[intracellular adhesion molecule]]-1 on the thyrocytes, which could attract the immuno-competent cells into the thyroid gland.<ref name=":9" /> Iodine also promotes thyrocyte [[apoptosis]].<ref name=":9" />
* Via immune cell behaviour: Iodine has an influence on immune cells.<ref name=":9" />

==== Comorbidities ====
[[Comorbidity|Comorbid]] autoimmune diseases are a risk factor for developing Hashimoto's thyroiditis, and the opposite is also true.<ref name=NIH2014/> Another thyroid disease closely associated with Hashimoto's thyroiditis is Graves' disease.<ref name="Weetman2021"/> Autoimmune diseases affecting other organs most commonly associated with Hashimoto's thyroiditis include [[celiac disease]], [[diabetes mellitus type 1|type 1 diabetes]], [[vitiligo]], [[alopecia]],<ref name="Radetti2014">{{cite book |doi=10.1159/000363162 |chapter=Clinical Aspects of Hashimoto's Thyroiditis |title=Paediatric Thyroidology |series=Endocrine Development |year=2014 | vauthors = Radetti G |volume=26 |pages=158–170 |pmid=25231451 |isbn=978-3-318-02720-4 }}</ref> [[Addison's disease|Addison disease]], [[Sjögren syndrome|Sjogren's syndrome]], and [[rheumatoid arthritis]]<ref name="Singh2020"/><ref name="Niddk2021">{{Cite web |title=Hashimoto's Disease |url=https://www.niddk.nih.gov/health-information/endocrine-diseases/hashimotos-disease |url-status=live |archive-url=https://web.archive.org/web/20211208141910/https://www.niddk.nih.gov/health-information/endocrine-diseases/hashimotos-disease |archive-date=8 December 2021 |access-date=2023-01-23 |website=National Institute of Diabetes and Digestive and Kidney Diseases |language=en-US}}</ref> Autoimmune thyroiditis has also been seen in patients with [[autoimmune polyendocrine syndrome]]s type 1 and 2.<ref name="Weetman2021"/>

==== Other ====
Other environmental factors include [[selenium deficiency]],<ref name="Winther-2020" /> infectious diseases such as [[hepatitis C]], [[rubella]], and possibly [[Covid-19]],<ref>{{cite journal | vauthors = Saranac L, Zivanovic S, Bjelakovic B, Stamenkovic H, Novak M, Kamenov B | title = Why is the thyroid so prone to autoimmune disease? | journal = Hormone Research in Paediatrics | volume = 75 | issue = 3 | pages = 157–165 | date = 2011 | pmid = 21346360 | doi = 10.1159/000324442 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Lambert N, Strebel P, Orenstein W, Icenogle J, Poland GA | title = Rubella | language = English | journal = Lancet | volume = 385 | issue = 9984 | pages = 2297–2307 | date = June 2015 | pmid = 25576992 | pmc = 4514442 | doi = 10.1016/S0140-6736(14)60539-0 }}</ref><ref>{{cite journal | vauthors = Lui DT, Lee CH, Woo YC, Hung IF, Lam KS | title = Thyroid dysfunction in COVID-19 | journal = Nature Reviews. Endocrinology | volume = 20 | issue = 6 | pages = 336–348 | date = June 2024 | pmid = 38347167 | doi = 10.1038/s41574-023-00946-w }}</ref> toxins,<ref name="Ramos-Levi2023" /> dietary factors,<ref name="Weetman2021"/> radiation exposure,<ref name="Ramos-Levi2023" /> and [[dysbiosis|gut dysbiosis]].<ref name="Ludgate-2024" />