Hashimoto's thyroiditis

<h2 id="signs-and-symptoms">Signs and symptoms</h2>

<h3>Signs</h3>
In the early stages of autoimmune thyroiditis, patients may have normal thyroid hormone levels and no <a href="/facts/Goitre/0kNGMcb6">goiter</a> or a small one.<a class="footnote-ref" id="fnref:27" href="#fn:27">27</a> Enlargement of the thyroid is due to <a href="/facts/Lymphocyte/pS2pv2Ma">lymphocytic</a> infiltration and <a href="/facts/Fibrosis/VVSmVgr3">fibrosis</a>.<a class="footnote-ref" id="fnref:28" href="#fn:28">28</a> Early on, thyroid autoantibodies in the blood may be the only indication of Hashimoto’s disease.<a class="footnote-ref" id="fnref:29" href="#fn:29">29</a> They are thought to be the secondary products of the <a href="/facts/T_cell/5z6PQ9UN">T cell</a>-mediated destruction of the gland.<a class="footnote-ref" id="fnref:30" href="#fn:30">30</a>
As lymphocytic infiltration progresses, patients may exhibit signs of <a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a> in multiple bodily systems, including, but not limited to, a larger goiter, weight gain, <a href="/facts/Cold_intolerance/RG70F2Wg">cold intolerance</a>, fatigue, <a href="/facts/Myxedema/ElkkECa8">myxedema</a>, constipation, menstrual disturbances, pale or dry skin, and dry, brittle hair, depression, and <a href="/facts/Ataxia/suENWGS6">ataxia</a>.<a class="footnote-ref" id="fnref:31" href="#fn:31">31</a><a class="footnote-ref" id="fnref:32" href="#fn:32">32</a> Extended thyroid hormone deficiency may lead to muscle fibre changes, resulting in muscle weakness, muscle pain, stiffness, and rarely, <a href="/facts/Pseudohypertrophy/nwH51jtG">pseudohypertrophy</a>.<a class="footnote-ref" id="fnref:33" href="#fn:33">33</a> Patients with goiters who have had autoimmune thyroiditis for many years might see their goiter shrink in the later stages of the disease due to destruction of the thyroid.<a class="footnote-ref" id="fnref:34" href="#fn:34">34</a> <a href="/facts/Graves%2527_disease/6CjnWNdE">Graves disease</a> may occur before or after the development of autoimmune thyroiditis.<a class="footnote-ref" id="fnref:35" href="#fn:35">35</a>
While rare, more serious complications of the hypothyroidism resulting from autoimmune thyroiditis are <a href="/facts/Pericardial_effusion/JHybCM7I">pericardial effusion</a>, <a href="/facts/Pleural_effusion/34Y7pyFv">pleural effusion</a>, both of which require further medical attention, and <a href="/facts/Myxedema_coma/9jGRIUby">myxedema coma</a>, which is an <a href="/facts/Endocrine_system/PDvN5cpj">endocrine</a> emergency.<a class="footnote-ref" id="fnref:36" href="#fn:36">36</a>

<h3>Symptoms</h3>
Many symptoms are attributed to the development of Hashimoto's thyroiditis. Symptoms can include: <a href="/facts/Fatigue_(medicine)/C2oo4Hvg">fatigue</a>, weight gain, pale or puffy face, feeling cold, <a href="/facts/Arthralgia/jEHMRWX7">joint</a> and <a href="/facts/Myalgia/AbVybHB8">muscle pain</a>, <a href="/facts/Constipation/l4DHHM6L">constipation</a>, dry and thinning hair, <a href="/facts/Menorrhagia/cQUgAGNk">heavy menstrual flow</a> or <a href="/facts/Metrorrhagia/pgysn5pd">irregular periods</a>, <a href="/facts/Depression_(mood)/GDNFWm1L">depression</a>, a <a href="/facts/Bradycardia/70msP5HD">slowed heart rate</a>, <a href="/facts/Infertility/emky9q8L">problems getting pregnant</a>, <a href="/facts/Miscarriages/sFq0vdnU">miscarriages</a>,<a class="footnote-ref" id="fnref:37" href="#fn:37">37</a> and <a href="/facts/Myopathy/eklaDeY6">myopathy</a>.<a class="footnote-ref" id="fnref:38" href="#fn:38">38</a> Some patients in the early stage of the disease may experience symptoms of <a href="/facts/Hyperthyroidism/H9Eqmbgk">hyperthyroidism</a> due to the release of thyroid hormones from intermittent thyroid destruction<a class="footnote-ref" id="fnref:39" href="#fn:39">39</a><a class="footnote-ref" id="fnref:40" href="#fn:40">40</a> (also called "destructive thyrotoxicosis").<a class="footnote-ref" id="fnref:41" href="#fn:41">41</a> In non-medical settings, the term "flare" is used to refer to a sudden exacerbation of symptoms, whether hyper or hypo.<a class="footnote-ref" id="fnref:42" href="#fn:42">42</a>
While most symptoms are attributed to hypothyroidism, similar symptoms are observed in Hashimoto's patients with normal thyroid hormone levels.<a class="footnote-ref" id="fnref:43" href="#fn:43">43</a><a class="footnote-ref" id="fnref:44" href="#fn:44">44</a><a class="footnote-ref" id="fnref:45" href="#fn:45">45</a> According to one study, these symptoms may include lower quality of life, and issues of the "digestive system (<a href="/facts/Abdominal_distension/EV3Rv672">abdominal distension</a>, constipation and diarrhea), endocrine system (chilliness, gain weight and facial <a href="/facts/Edema/Q6MI3KdH">edema</a>), <a href="/facts/Neuropsychiatry/YrbzeLoc">neuropsychiatric</a> system (forgetfulness, anxiety, depressed, fatigue, insomnia, irritability, and indifferent [sic]) and <a href="/facts/Mucocutaneous_disease/Vkr5XpeG">mucocutaneous</a> system (dry skin, <a href="/facts/Pruritus/MBWq6SPc">pruritus</a>, and hair loss)."<a class="footnote-ref" id="fnref:46" href="#fn:46">46</a>

<h2 id="causes">Causes</h2>
The causes of Hashimoto's thyroiditis are complex. Around 80% of the risk of developing an autoimmune thyroid disorder is due to <a href="/facts/Genetics/bu8wne0A">genetic factors</a>, while the remaining 20% is related to <a href="/facts/Environmental_factor/T6FvWue8">environmental factors</a> (such as iodine, drugs, infection, stress, radiation).<a class="footnote-ref" id="fnref:47" href="#fn:47">47</a>

<h3>Genetics</h3>
Thyroid autoimmunity can be <a href="/facts/Heredity/t0aMmRWx">familial</a>.<a class="footnote-ref" id="fnref:48" href="#fn:48">48</a> Many patients report a family history of autoimmune thyroiditis or <a href="/facts/Graves%2527_disease/6CjnWNdE">Graves' disease</a>.<a class="footnote-ref" id="fnref:49" href="#fn:49">49</a> The strong genetic component is borne out in studies on <a href="/facts/Monozygotic_twins/9QSssff4">monozygotic twins</a>,<a class="footnote-ref" id="fnref:50" href="#fn:50">50</a> with a <a href="/facts/Concordance_(genetics)/yg11FFB8">concordance</a> of 38–55%, with an even higher concordance of circulating thyroid antibodies not in relation to <a href="/facts/Clinical_presentation/qzI0BK5P">clinical presentation</a> (up to 80% in monozygotic twins). Neither result was seen to a similar degree in <a href="/facts/Dizygotic_twins/9QSssff4">dizygotic twins</a>, offering strong favour for high genetic <a href="/facts/Etiology/Bz8MAeSq">etiology</a>.<a class="footnote-ref" id="fnref:51" href="#fn:51">51</a>
The genes implicated vary in different ethnic groups,<a class="footnote-ref" id="fnref:52" href="#fn:52">52</a> and the impact of these genes on the disease differs significantly among people from different ethnic groups. A gene that has a large effect in one ethnic group's risk of developing Hashimoto's thyroiditis might have a much smaller effect in another ethnic group.<a class="footnote-ref" id="fnref:53" href="#fn:53">53</a> 
The incidence of autoimmune thyroid disorders is increased in people with <a href="/facts/Chromosomal_disorders/6hL7p0cP">chromosomal disorders</a>, including <a href="/facts/Turner_syndrome/xQzCSDGI">Turner</a>, <a href="/facts/Down_syndrome/Y4XEQSMS">Down</a>, and <a href="/facts/Klinefelter_syndrome/lT7Gw3qp">Klinefelter syndromes</a>.<a class="footnote-ref" id="fnref:54" href="#fn:54">54</a>

<h4>HLA genes</h4>
The first gene <a href="/facts/Locus_(genetics)/JcIT8wLm">locus</a> associated with autoimmune thyroid disease was the <a href="/facts/Major_histocompatibility_complex/UEPsjx3u">major histocompatibility complex</a> (MHC) region on <a href="/facts/Chromosome/FRGf11FC">chromosome</a> 6p21. It encodes <a href="/facts/Human_leukocyte_antigen/6QRXe5QI">human leukocyte antigens</a> (HLAs). Specific HLA <a href="/facts/Allele/8FxCS9KA">alleles</a> have a higher affinity to auto-antigenic thyroidal <a href="/facts/Peptide/C4ltc7UG">peptides</a> and can contribute to autoimmune thyroid disease development. Specifically, in Hashimoto's disease, aberrant expression of HLA II on <a href="/facts/Thyroid_follicular_cell/fFWvPdCt">thyrocytes</a> has been demonstrated. They can present thyroid autoantigens and initiate autoimmune thyroid disease.<a class="footnote-ref" id="fnref:55" href="#fn:55">55</a> Susceptibility alleles are not consistent in Hashimoto's disease. In Caucasians, various alleles are reported to be associated with the disease, including <a href="/facts/Death_receptor_3/Q04dzvYD">DR3</a>, <a href="/facts/Death_receptor_5/9coXQeyD">DR5</a>, and <a href="/facts/HLA-DQ7/01JSAfTz">DQ7</a>.<a class="footnote-ref" id="fnref:56" href="#fn:56">56</a><a class="footnote-ref" id="fnref:57" href="#fn:57">57</a>

<h4>CTLA-4 genes</h4>
<a href="/facts/CTLA-4/7nhf4Nq6">CTLA-4</a> is the second major immune-<a href="/facts/Regulator_gene/oH86M9nI">regulatory</a> gene related to autoimmune thyroid disease. CTLA-4 gene polymorphisms may contribute to the reduced inhibition of T-cell <a href="/facts/Cell_proliferation/Jp3hWo2t">proliferation</a> and increase susceptibility to autoimmune response.<a class="footnote-ref" id="fnref:58" href="#fn:58">58</a> CTLA-4 is a major thyroid autoantibody susceptibility gene. A linkage of the CTLA-4 region to the presence of thyroid autoantibodies was demonstrated by a whole-genome <a href="/facts/Linkage_analysis/FxPcL2aQ">linkage analysis</a>.<a class="footnote-ref" id="fnref:59" href="#fn:59">59</a> CTLA-4 was confirmed as the main locus for thyroid autoantibodies.<a class="footnote-ref" id="fnref:60" href="#fn:60">60</a>

<h4>PTPN22 gene</h4>
<a href="/facts/PTPN22/uD0HrE1j">PTPN22</a> is the most recently identified immune-regulatory gene associated with autoimmune thyroid disease. It is located on chromosome 1p13 and expressed in lymphocytes. It acts as a negative regulator of T-cell activation. <a href="/facts/Mutation/Ee4NnWbY">Mutation</a> in this gene is a risk factor for many autoimmune diseases. Weaker T-cell signaling may lead to impaired <a href="/facts/Negative_selection_(immunology)/2dUAKATR">thymic deletion</a> of autoreactive T cells, and increased PTPN22 function may result in inhibition of regulatory T cells, which protect against autoimmunity.<a class="footnote-ref" id="fnref:61" href="#fn:61">61</a>

<h4>Immune-related genes</h4>
<a href="/facts/IFN-%25CE%25B3/r51CXVph">IFN-γ</a> promotes cell-mediated <a href="/facts/Cytotoxicity/SQuTTLoL">cytotoxicity</a> against thyroid mutations causing increased production of IFN-γ were associated with the severity of hypothyroidism.<a class="footnote-ref" id="fnref:62" href="#fn:62">62</a> Severe hypothyroidism is associated with mutations leading to lower production of <a href="/facts/Interleukin_4/FacDJ3TY">IL-4</a> (Th2 cytokine suppressing cell-mediated autoimmunity),<a class="footnote-ref" id="fnref:63" href="#fn:63">63</a> lower secretion of <a href="/facts/TGF-%25CE%25B2/6bD65SWQ">TGF-β</a> (inhibitor of <a href="/facts/Cytokine/SdWpWABH">cytokine</a> production),<a class="footnote-ref" id="fnref:64" href="#fn:64">64</a> and mutations of <a href="/facts/FOXP3/JdLlsy1o">FOXP3</a>, an essential regulatory factor for the <a href="/facts/Regulatory_T_cells/1ECRAGMg">regulatory T cells</a> (Tregs) development.<a class="footnote-ref" id="fnref:65" href="#fn:65">65</a> Development of Hashimoto's disease was associated with mutation of the gene for <a href="/facts/TNF-%25CE%25B1/7NWNIaCb">TNF-α</a> (stimulator of the IFN-γ production), causing its higher concentration.<a class="footnote-ref" id="fnref:66" href="#fn:66">66</a>

<h3>Existential (endogenous environmental)</h3>
<h4>Sex</h4>
A study of healthy Danish twins divided into three groups (monozygotic and dizygotic same sex, and opposite sex twin pairs) estimated that genetic contribution to thyroid peroxidase antibodies susceptibility was 61% in males and 72% in females, and contribution to thyroglobulin antibodies susceptibility was 39% in males and 75% in females.<a class="footnote-ref" id="fnref:67" href="#fn:67">67</a>
The high female predominance in thyroid autoimmunity may be associated with the X chromosome. It contains sex and immune-related genes responsible for <a href="/facts/Immune_tolerance/hvDqPHTP">immune tolerance</a>.<a class="footnote-ref" id="fnref:68" href="#fn:68">68</a>
A higher incidence of thyroid autoimmunity was reported in patients with a higher rate of X-chromosome <a href="/facts/Monosomy/ovs7muhy">monosomy</a> in peripheral white blood cells.<a class="footnote-ref" id="fnref:69" href="#fn:69">69</a> Another potential mechanism might be skewed <a href="/facts/X-chromosome_inactivation/wMWHzvcw">X-chromosome inactivation</a>.<a class="footnote-ref" id="fnref:70" href="#fn:70">70</a> 

<h4>Pregnancy</h4>
In one population study, two or more births were a risk factor for developing autoimmune hypothyroidism in pre-menopausal women.<a class="footnote-ref" id="fnref:71" href="#fn:71">71</a>

<h3>Environmental</h3>
<h4>Medications</h4>
Certain medications or drugs have been associated with altering and interfering with thyroid function. There are two main mechanisms of interference:<a class="footnote-ref" id="fnref:72" href="#fn:72">72</a>

<ul><li>Altering thyroid hormone serum transfer proteins.<a class="footnote-ref" id="fnref:73" href="#fn:73">73</a> <a href="/facts/Estrogen/dPEewnDV">Estrogen</a>, <a href="/facts/Tamoxifen/oHU8n7ch">tamoxifen</a>, <a href="/facts/Heroin/rYwrKHPk">heroin</a>, <a href="/facts/Methadone/Gz6231sT">methadone</a>, <a href="/facts/Clofibrate/5tyjpuQY">clofibrate</a>, <a href="/facts/Fluorouracil/6xH4uUaf">5-fluorouracil</a>, <a href="/facts/Mitotane/8GBw1lz8">mitotane</a>, and <a href="/facts/Perphenazine/rf2wAucn">perphenazine</a> all increase <a href="/facts/Thyroid_binding_globulin/doovCmnL">thyroid binding globulin</a> (TBG) concentration.<a class="footnote-ref" id="fnref:74" href="#fn:74">74</a> <a href="/facts/Androgen/Rxey0HxX">Androgens</a>, <a href="/facts/Anabolic_steroid/f9KAXfTF">anabolic steroids</a> such as <a href="/facts/Danazol/unXJy9LL">danazol</a>, glucocorticoids, and slow release <a href="/facts/Nicotinic_acid/UAAqPpk6">nicotinic acid</a> all decrease TBG concentrations. <a href="/facts/Furosemide/tq9Lx0u4">Furosemide</a>, fenoflenac, <a href="/facts/Mefenamic_acid/75dEWxuW">mefenamic acid</a>, <a href="/facts/Salicylates/qz7RRQCR">salicylates</a>, <a href="/facts/Phenytoin/uFvxbwf2">phenytoin</a>, <a href="/facts/Diazepam/h7lIGqkM">diazepam</a>, <a href="/facts/Sulphonylureas/TJd2qFH3">sulphonylureas</a>, <a href="/facts/Free_fatty_acids/JGg3erIu">free fatty acids</a>, and <a href="/facts/Heparin/4lxSm2pB">heparin</a> all interfere with thyroid hormone binding to TBG and/or <a href="/facts/Transthyretin/7hxXqxja">transthyretin</a>.<a class="footnote-ref" id="fnref:75" href="#fn:75">75</a></li>
<li>Altering the extra-thyroidal metabolism of thyroid hormone. <a href="/facts/Propylthiouracil/zRId5hqt">Propylthiouracil</a>, <a href="/facts/Glucocorticoid/2P91Aj3S">glucocorticoids</a>, <a href="/facts/Propranolol/QvH2XYt1">propranolol</a>, iodinated <a href="/facts/Contrast_agent/uVoPWL7Q">contrast agents</a>, <a href="/facts/Amiodarone_induced_thyrotoxicosis/K94ArawC">amiodarone</a>, and <a href="/facts/Clomipramine/wnhL4NfS">clomipramine</a> all inhibit conversion of T4 and T3.<a class="footnote-ref" id="fnref:76" href="#fn:76">76</a> <a href="/facts/Phenobarbital/G236GSuW">Phenobarbital</a>, <a href="/facts/Rifampicin/9naa8C5l">rifampin</a>, <a href="/facts/Phenytoin/uFvxbwf2">phenytoin</a> and <a href="/facts/Carbamazepine/Hd1By1Mj">carbamazepine</a> all increase <a href="/facts/Hepatic/Rtp4Fk2b">hepatic</a> metabolism.<a class="footnote-ref" id="fnref:77" href="#fn:77">77</a> Finally, <a href="/facts/Colestyramine/BtL6h9hv">cholestryamine</a>, <a href="/facts/Colestipol/b7bvRUmr">colestipol</a>, <a href="/facts/Aluminium_hydroxide/e0pXvDGr">aluminium hydroxide</a>, <a href="/facts/Ferrous_sulphate/zyc7Fukb">ferrous sulphate</a>, and <a href="/facts/Sucralfate/jJ4BLDJ6">sucralfate</a> are all drugs that decrease T4 absorption or enhance excretion.<a class="footnote-ref" id="fnref:78" href="#fn:78">78</a></li></ul>
<h4>Iodine</h4>
Both excessive and insufficient <a href="/facts/Iodine/JlfMecMf">iodine intake</a> has been implicated in developing antithyroid antibodies.<a class="footnote-ref" id="fnref:79" href="#fn:79">79</a><a class="footnote-ref" id="fnref:80" href="#fn:80">80</a> Thyroid autoantibodies are found to be more prevalent in geographical areas after increasing iodine levels.<a class="footnote-ref" id="fnref:81" href="#fn:81">81</a> Several mechanisms by which excessive iodine may promote thyroid autoimmunity have been proposed:<a class="footnote-ref" id="fnref:82" href="#fn:82">82</a>

<ul><li>Via thyroglobulin iodination: Iodine exposure leads to higher iodination of thyroglobulin, increasing its <a href="/facts/Immunogenicity/QVxzK4tD">immunogenicity</a><a class="footnote-ref" id="fnref:83" href="#fn:83">83</a> by creating new iodine-containing <a href="/facts/Epitope/PL0oBuGh">epitopes</a> or exposing <a href="/facts/Cryptic_epitopes/EBXQjCPG">cryptic epitopes</a>.<a class="footnote-ref" id="fnref:84" href="#fn:84">84</a></li>
<li>Via <a href="/facts/Thyroid_follicular_cell/fFWvPdCt">thyrocyte</a> damage: Iodine exposure has been shown to increase the level of <a href="/facts/Reactive_oxygen_species/GpwSRugH">reactive oxygen species</a>. They enhance the expression of the <a href="/facts/Intracellular_adhesion_molecule/84EkpbAb">intracellular adhesion molecule</a>-1 on the thyrocytes, which could attract the immunocompetent cells into the thyroid gland.<a class="footnote-ref" id="fnref:85" href="#fn:85">85</a> Iodine also promotes thyrocyte <a href="/facts/Apoptosis/8dVzSm4y">apoptosis</a>.<a class="footnote-ref" id="fnref:86" href="#fn:86">86</a></li>
<li>Via immune cell behaviour: Iodine influences immune cells.<a class="footnote-ref" id="fnref:87" href="#fn:87">87</a></li></ul>
<h4>Comorbidities</h4>
<a href="/facts/Comorbidity/tX5TvuKJ">Comorbid</a> autoimmune diseases are a risk factor for developing Hashimoto's thyroiditis, and the opposite is also true.<a class="footnote-ref" id="fnref:88" href="#fn:88">88</a> Another thyroid disease closely associated with Hashimoto's thyroiditis is Graves' disease.<a class="footnote-ref" id="fnref:89" href="#fn:89">89</a> Autoimmune diseases affecting other organs most commonly associated with Hashimoto's thyroiditis include <a href="/facts/Celiac_disease/AKd5PkTc">celiac disease</a>, <a href="/facts/Diabetes_mellitus_type_1/IkuQadGx">type 1 diabetes</a>, <a href="/facts/Vitiligo/d8xPRXQB">vitiligo</a>, <a href="/facts/Alopecia/uEPKUafl">alopecia</a>,<a class="footnote-ref" id="fnref:90" href="#fn:90">90</a> <a href="/facts/Addison%2527s_disease/Lp8AqjEX">Addison disease</a>, <a href="/facts/Sj%25C3%25B6gren_syndrome/U1p9IbFU">Sjogren's syndrome</a>, and <a href="/facts/Rheumatoid_arthritis/qFK4Xwv7">rheumatoid arthritis</a><a class="footnote-ref" id="fnref:91" href="#fn:91">91</a><a class="footnote-ref" id="fnref:92" href="#fn:92">92</a> Autoimmune thyroiditis has also been seen in patients with <a href="/facts/Autoimmune_polyendocrine_syndrome/hNmcov4p">autoimmune polyendocrine syndromes</a> type 1 and 2.<a class="footnote-ref" id="fnref:93" href="#fn:93">93</a>

<h4>Other</h4>
Other environmental factors include <a href="/facts/Selenium_deficiency/rwlSpwjw">selenium deficiency</a>,<a class="footnote-ref" id="fnref:94" href="#fn:94">94</a> infectious diseases such as <a href="/facts/Hepatitis_C/kwb7IIht">hepatitis C</a>, <a href="/facts/Rubella/GaCHuPtc">rubella</a>, and possibly <a href="/facts/Covid-19/YsUgvsaX">Covid-19</a>,<a class="footnote-ref" id="fnref:95" href="#fn:95">95</a><a class="footnote-ref" id="fnref:96" href="#fn:96">96</a><a class="footnote-ref" id="fnref:97" href="#fn:97">97</a> toxins,<a class="footnote-ref" id="fnref:98" href="#fn:98">98</a> dietary factors,<a class="footnote-ref" id="fnref:99" href="#fn:99">99</a> radiation exposure,<a class="footnote-ref" id="fnref:100" href="#fn:100">100</a> and <a href="/facts/Dysbiosis/nq80zc9d">gut dysbiosis</a>.<a class="footnote-ref" id="fnref:101" href="#fn:101">101</a>

<h2 id="mechanism">Mechanism</h2>
The <a href="/facts/Pathophysiology/Tp3Dny0c">pathophysiology</a> of autoimmune thyroiditis is not well understood.<a class="footnote-ref" id="fnref:102" href="#fn:102">102</a> However, once the disease is established, its core processes have been observed:
Hashimoto's thyroiditis is a <a href="/facts/T-lymphocyte/5z6PQ9UN">T-lymphocyte</a> mediated <a href="/facts/Autoimmunity/5cASmcfI">attack</a> on the thyroid gland.<a class="footnote-ref" id="fnref:103" href="#fn:103">103</a> <a href="/facts/T_helper_cell/nhwAYkDj">T helper 1 cells</a> trigger <a href="/facts/Macrophage/z7hkQu3o">macrophages</a> and <a href="/facts/Cytotoxic_t-lymphocytes/e5eRg3XJ">cytotoxic lymphocytes</a> to destroy <a href="/facts/Thyroid_follicular_cell/fFWvPdCt">thyroid follicular cells</a>, while T helper 2 cells stimulate the excessive production of <a href="/facts/B_cell/6Y1tgwwp">B cells</a> and <a href="/facts/Plasma_cell/1fY4bFHR">plasma cells</a> which generate <a href="/facts/Antibody/MX8pdTdP">antibodies</a> against the thyroid <a href="/facts/Antigen/9JlAernG">antigens</a>, leading to thyroiditis.<a class="footnote-ref" id="fnref:104" href="#fn:104">104</a> The three major antibodies are: <a href="/facts/Thyroid_peroxidase/Ga1ExEn4">Thyroid peroxidase</a> Antibodies (TPOAb), <a href="/facts/Thyroglobulin/whhQ9Dyb">Thyroglobulin</a> Antibodies (TgAb), and <a href="/facts/Thyroid_stimulating_hormone_receptor/t6tjeKe3">Thyroid stimulating hormone receptor</a> Antibodies (TRAb),<a class="footnote-ref" id="fnref:105" href="#fn:105">105</a> with TPOAb and TgAb being most commonly implicated in Hashimotos.<a class="footnote-ref" id="fnref:106" href="#fn:106">106</a> They are hypothesized to develop as a result of thyroid damage, where T-lymphocytes are sensitized to residual thyroid peroxidase and thyroglobulin, rather than as the initial cause of thyroid damage.<a class="footnote-ref" id="fnref:107" href="#fn:107">107</a> However, they may exacerbate further thyroid destruction by binding the <a href="/facts/Complement_system/vRSrQDUv">complement system</a> and triggering <a href="/facts/Apoptosis/8dVzSm4y">apoptosis</a> of thyroid cells.<a class="footnote-ref" id="fnref:108" href="#fn:108">108</a> TPO antibody levels may correlate with the degree of <a href="/facts/Lymphocyte/pS2pv2Ma">lymphocyte</a> infiltration of the thyroid.<a class="footnote-ref" id="fnref:109" href="#fn:109">109</a><a class="footnote-ref" id="fnref:110" href="#fn:110">110</a>
Gross morphological changes within the thyroid are seen in the general enlargement, which is far more locally nodular and irregular than more diffuse patterns (such as that of <a href="/facts/Hyperthyroidism/H9Eqmbgk">hyperthyroidism</a>). While the capsule is intact and the gland itself is still distinct from surrounding tissue, microscopic examination can provide a more revealing indication of the level of damage.<a class="footnote-ref" id="fnref:111" href="#fn:111">111</a> Hypothyroidism is caused by replacement of follicular cells with <a href="/facts/Parenchyma/NlGkFWlQ">parenchymatous tissue</a>.<a class="footnote-ref" id="fnref:112" href="#fn:112">112</a>
Partial regeneration of the thyroid tissue can occur, but this has not been observed to normalise hormonal levels.<a class="footnote-ref" id="fnref:113" href="#fn:113">113</a><a class="footnote-ref" id="fnref:114" href="#fn:114">114</a> 

<h3>Pathology</h3>

Gross pathology of a thyroid with autoimmune thyroiditis may show a symmetrically enlarged thyroid.<a class="footnote-ref" id="fnref:115" href="#fn:115">115</a> It is often paler in color, in comparison to normal thyroid tissue, which is reddish-brown.<a class="footnote-ref" id="fnref:116" href="#fn:116">116</a> 
Microscopic examination (<a href="/facts/Histology/yrI90zlU">histology</a>) will show lymphocytes (including <a href="/facts/Plasma_cell/1fY4bFHR">plasma B-cells</a>) diffusely infiltrating the <a href="/facts/Parenchyma/NlGkFWlQ">parenchyma</a>.<a class="footnote-ref" id="fnref:117" href="#fn:117">117</a> The lymphocytes are predominately T-lymphocytes with a representation of both <a href="/facts/CD4%252B_cells/nhwAYkDj">CD4+</a> and <a href="/facts/CD8%252B/e5eRg3XJ">CD8+</a> cells.<a class="footnote-ref" id="fnref:118" href="#fn:118">118</a> The plasma cells are <a href="/facts/Polyclonal_B_cell_response/00QJzQyy">polyclonal</a>, with present <a href="/facts/Germinal_center/hdCfNIQc">germinal centers</a> resembling the structure of a <a href="/facts/Lymph_node/vkwfcQjH">lymph node</a><a class="footnote-ref" id="fnref:119" href="#fn:119">119</a> (also called secondary lymphoid follicles, not to be confused with the normally present <a href="/facts/Colloid/9EVucqND">colloid</a>-filled <a href="/facts/Thyroid_follicle/fFWvPdCt">follicles</a> that constitute the thyroid).<a class="footnote-ref" id="fnref:120" href="#fn:120">120</a> 
In late stages of the disease, the thyroid may be <a href="/facts/Atrophy/QNxSoxDV">atrophic</a>.<a class="footnote-ref" id="fnref:121" href="#fn:121">121</a> Colloid-filled follicles shrink, and the cuboidal cells that usually line the follicles become <a href="/facts/H%25C3%25BCrthle_cell/90yGzSGj">Hürthle cells</a>.<a class="footnote-ref" id="fnref:122" href="#fn:122">122</a> Fibrous tissue may be found throughout the affected thyroid as well.<a class="footnote-ref" id="fnref:123" href="#fn:123">123</a> Severe thyroid atrophy presents often with denser fibrotic bands of <a href="/facts/Collagen/KsyAb72K">collagen</a> that remain within the confines of the thyroid capsule.<a class="footnote-ref" id="fnref:124" href="#fn:124">124</a> 
Generally, pathological findings of the thyroid are related to the amount of remaining thyroid function — the more infiltration and fibrosis, the less likely a patient will have normal thyroid function.<a class="footnote-ref" id="fnref:125" href="#fn:125">125</a> A rare but serious complication is <a href="/facts/Thyroid_lymphoma/QUkDqEAn">thyroid lymphoma</a>, generally the B-cell type, <a href="/facts/Non-Hodgkin_lymphoma/KIFxt74F">non-Hodgkin lymphoma</a>.<a class="footnote-ref" id="fnref:126" href="#fn:126">126</a>

<h2 id="diagnosis">Diagnosis</h2>

<h3>Tests</h3>
<h4>Physical exam</h4>
Physicians will often start by assessing reported symptoms and performing a thorough physical exam, including a neck exam.<a class="footnote-ref" id="fnref:127" href="#fn:127">127</a> Patients may have a "firm, bumpy, symmetric, painless goiter", however, up to 10% of patients may have an <a href="/facts/Atrophy/QNxSoxDV">atrophied</a> thyroid.<a class="footnote-ref" id="fnref:128" href="#fn:128">128</a>

<h4>Antithyroid antibodies tests</h4>
Tests for <a href="/facts/Antibodies/MX8pdTdP">antibodies</a> against <a href="/facts/Thyroid_peroxidase/Ga1ExEn4">thyroid peroxidase</a>, <a href="/facts/Thyroglobulin/whhQ9Dyb">thyroglobulin</a>, and <a href="/facts/Thyrotropin_receptor/t6tjeKe3">thyrotropin receptors</a> can detect autoimmune processes against the thyroid. 90% of Hashimoto's patients have elevated levels of thyroid peroxidase antibodies.<a class="footnote-ref" id="fnref:129" href="#fn:129">129</a> However, seronegative (without circulating autoantibodies) thyroiditis is also possible.<a class="footnote-ref" id="fnref:130" href="#fn:130">130</a> There may be circulating antibodies before the onset of any symptoms.<a class="footnote-ref" id="fnref:131" href="#fn:131">131</a>

<h4>Ultrasound</h4>

An <a href="/facts/Ultrasound/31Pa5IH9">ultrasound</a> may be useful in detecting Hashimoto thyroiditis, especially in those with seronegative thyroiditis,<a class="footnote-ref" id="fnref:132" href="#fn:132">132</a> or when patients have normal laboratory values but symptoms of autoimmune thyroiditis.<a class="footnote-ref" id="fnref:133" href="#fn:133">133</a> Key features detected in the ultrasound of a person with Hashimoto's thyroiditis include "<a href="/facts/Echogenicity/LCNlf0od">echogenicity</a>, <a href="/facts/Homogeneity_and_heterogeneity/y84KQJxl">heterogeneity</a>, <a href="/facts/Hypervascularity/ymrELf0e">hypervascularity</a>, and presence of small <a href="/facts/Thyroid_nodule/EmYsNFpb">cysts</a>."<a class="footnote-ref" id="fnref:134" href="#fn:134">134</a> Images obtained with ultrasound can evaluate the size of the thyroid, reveal the presence of nodules, or provide clues to the diagnosis of other thyroid conditions.<a class="footnote-ref" id="fnref:135" href="#fn:135">135</a>

<h4>Nuclear medicine</h4>
<a href="/facts/Nuclear_imaging/L9Dzjd90">Nuclear imaging</a> showing thyroid uptake can also be helpful in diagnosing thyroid function, particularly differential diagnosis.<a class="footnote-ref" id="fnref:136" href="#fn:136">136</a>

<h4>TSH levels test</h4>
Elevated <a href="/facts/Thyroid-stimulating_hormone/w8ettSpY">Thyroid-stimulating hormone</a> (TSH) levels may indicate <a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a> (underperforming thyroid).<a class="footnote-ref" id="fnref:137" href="#fn:137">137</a> Hypothyroidism is a common symptom and potential indication of Hashimoto's disease.<a class="footnote-ref" id="fnref:138" href="#fn:138">138</a> As blood levels of thyroid hormones fall due to hypothyroidism, the anterior <a href="/facts/Pituitary_gland/gdrQyldF">pituitary</a> gland increases production of TSH, which stimulates increased production of thyroid hormones in the thyroid.<a class="footnote-ref" id="fnref:139" href="#fn:139">139</a> The elevation is usually a marked increase over the normal range.<a class="footnote-ref" id="fnref:140" href="#fn:140">140</a> TSH is the preferred initial test of thyroid function as it has a higher <a href="/facts/Sensitivity_and_specificity/pzc9qfdz">sensitivity</a> to changes in thyroid status than free T4.<a class="footnote-ref" id="fnref:141" href="#fn:141">141</a>
Biotin can cause this test to read "falsely low".<a class="footnote-ref" id="fnref:142" href="#fn:142">142</a> Time of day can affect the results of this test; TSH peaks early in the morning and slumps in the late afternoon to early evening,<a class="footnote-ref" id="fnref:143" href="#fn:143">143</a> with "a variation in TSH by a mean of between 0.95 m<a href="/facts/International_unit/1rSTv1TL">IU</a>/mL to 2.0 mIU/mL".<a class="footnote-ref" id="fnref:144" href="#fn:144">144</a> Hypothyroidism is diagnosed more often in samples taken soon after waking.<a class="footnote-ref" id="fnref:145" href="#fn:145">145</a> 

<h4>T3 or T4 levels test</h4>
These tests detect levels of two thyroid hormones: <a href="/facts/Thyroxine/9k4xJtCq">Thyroxine</a> (<a href="/facts/Thyroxine/9k4xJtCq">T4</a>) and <a href="/facts/Triiodothyronine/MPBz6ApV">Tri-iodothyronine</a> (<a href="/facts/Triiodothyronine/MPBz6ApV">T3</a>). Low levels of these hormones (hypothyroidism) may indicate autoimmune damage to the thyroid due to Hashimoto's, while elevated levels may indicate an attack of destructive thyrotoxicosis.<a class="footnote-ref" id="fnref:146" href="#fn:146">146</a> Hashimoto's with normal levels is possible, however.
Free or total levels can be measured. Typically, Free T4 is the preferred test for hypothyroidism,<a class="footnote-ref" id="fnref:147" href="#fn:147">147</a> as Free T3 <a href="/facts/Immunoassay/eHo2YM9S">immunoassay tests</a> are less reliable at detecting low levels of thyroid hormone,<a class="footnote-ref" id="fnref:148" href="#fn:148">148</a> and they are more susceptible to interference.<a class="footnote-ref" id="fnref:149" href="#fn:149">149</a> Both immunoassay tests of Free T4 and Free T3 may overestimate concentrations, particularly at low thyroid hormone levels, which is why results are typically read in conjunction with TSH, a more sensitive measure.<a class="footnote-ref" id="fnref:150" href="#fn:150">150</a> <a href="/facts/Liquid_chromatography%25E2%2580%2593mass_spectrometry/nGlDC6Hw">LC-MSMS</a> assays are rarer, but they are "highly specific, sensitive, precise, and can detect hormones found in low concentrations."<a class="footnote-ref" id="fnref:151" href="#fn:151">151</a>

<h4>Muscle Biopsy</h4>
Muscle <a href="/facts/Biopsy/A0TdRRlr">biopsy</a> is not necessary for diagnosis of <a href="/facts/Myopathy/eklaDeY6">myopathy</a> due to hypothyroid <a href="/facts/Skeletal_muscle/en1tVYFN">muscle fibre</a> changes, however it may reveal confirmatory features.<a class="footnote-ref" id="fnref:152" href="#fn:152">152</a>

<h2 id="treatment">Treatment</h2>
There is no cure for Hashimoto's Thyroiditis.<a class="footnote-ref" id="fnref:153" href="#fn:153">153</a><a class="footnote-ref" id="fnref:154" href="#fn:154">154</a> There is currently no known way to stop auto-immune <a href="/facts/Lymphocyte/pS2pv2Ma">lymphocytes</a> infiltrating the thyroid or to stimulate <a href="/facts/Regeneration_(biology)/DHkSrakp">regeneration</a> of thyroid tissue.<a class="footnote-ref" id="fnref:155" href="#fn:155">155</a> However, the condition can be managed.<a class="footnote-ref" id="fnref:156" href="#fn:156">156</a><a class="footnote-ref" id="fnref:157" href="#fn:157">157</a>

<h3>Managing hormone levels</h3>
Hormone Terminology<table><tbody><tr><th></th><th>Endogenous</th><th>Synthetic</th></tr><tr><th>T3</th><td>Tri-iodothyronine</td><td>Liothyronine</td></tr><tr><th>T4</th><td>Thyroxine</td><td>Levothyroxine</td></tr></tbody></table>
<a href="/facts/Hypothyroidism/oqtQDu2F">Hypothyroidism</a> caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents such as <a href="/facts/Levothyroxine/AarfgbeG">levothyroxine</a> (LT4),<a class="footnote-ref" id="fnref:158" href="#fn:158">158</a> <a href="/facts/Liothyronine/wU0LlRE6">liothyronine</a> (LT3),<a class="footnote-ref" id="fnref:159" href="#fn:159">159</a> or <a href="/facts/Desiccated_thyroid_extract/UWyqs3P2">desiccated thyroid extract</a> (T4+T3).<a class="footnote-ref" id="fnref:160" href="#fn:160">160</a> In most cases, the treatment needs to be taken for the rest of the person's life.<a class="footnote-ref" id="fnref:161" href="#fn:161">161</a>
The standard of care is <a href="/facts/Levothyroxine/AarfgbeG">levothyroxine</a> (LT4) therapy, which is an oral medication identical in molecular structure to <a href="/facts/Endogeny_(biology)/DFkSLkRI">endogenous</a> thyroxine (T4).<a class="footnote-ref" id="fnref:162" href="#fn:162">162</a> Levothyroxine sodium has a <a href="/facts/Sodium/eYuSPu2V">sodium</a> salt added to increase the <a href="/facts/Intestinal_epithelium/32hWmspE">gastrointestinal</a> absorption of levothyroxine.<a class="footnote-ref" id="fnref:163" href="#fn:163">163</a> Levothyroxine has the benefits of a long <a href="/facts/Half-life/kGVH8BAB">half-life</a><a class="footnote-ref" id="fnref:164" href="#fn:164">164</a> leading to stable thyroid hormone levels,<a class="footnote-ref" id="fnref:165" href="#fn:165">165</a> ease of <a href="/facts/Monitoring_(medicine)/cTc3d1j5">monitoring</a>,<a class="footnote-ref" id="fnref:166" href="#fn:166">166</a> excellent safety<a class="footnote-ref" id="fnref:167" href="#fn:167">167</a><a class="footnote-ref" id="fnref:168" href="#fn:168">168</a> and efficacy record,<a class="footnote-ref" id="fnref:169" href="#fn:169">169</a> and usefulness in pregnancy as it can cross the fetal <a href="/facts/Blood%25E2%2580%2593brain_barrier/xYzvVwdu">blood-brain barrier</a>.<a class="footnote-ref" id="fnref:170" href="#fn:170">170</a> 
Levothyroxine dosing to normalise TSH is based on the amount of residual <a href="/facts/Endogeny_(biology)/DFkSLkRI">endogenous</a> thyroid function and the patient’s weight, particularly <a href="/facts/Lean_body_mass/RxWgCrJq">lean body mass</a>.<a class="footnote-ref" id="fnref:171" href="#fn:171">171</a> The dose can be adjusted based upon each patient, for example, the dose may be lowered for elderly patients or patients with certain <a href="/facts/Heart/fF4KSGdk">cardiac</a> conditions, but is increased in pregnant patients.<a class="footnote-ref" id="fnref:172" href="#fn:172">172</a> It is administered on a consistent schedule.<a class="footnote-ref" id="fnref:173" href="#fn:173">173</a> Levothyroxine may be dosed daily or weekly, however weekly dosing may be associated with higher <a href="/facts/Thyroid-stimulating_hormone/w8ettSpY">TSH</a> levels, elevated thyroid hormone levels, and transient "<a href="/facts/Echocardiography/X0rQzVe3">echocardiographic</a> changes in some patients following 2-4 h of thyroxine intake".<a class="footnote-ref" id="fnref:174" href="#fn:174">174</a><a class="footnote-ref" id="fnref:175" href="#fn:175">175</a>
Some patients elect combination therapy with both levothyroxine and <a href="/facts/Liothyronine/wU0LlRE6">liothyronine</a> (which is identical in molecular structure to <a href="/facts/Triiodothyronine/MPBz6ApV">tri-iodothyronine</a>) however studies of combination therapy are limited,<a class="footnote-ref" id="fnref:176" href="#fn:176">176</a> and five <a href="/facts/Meta-analysis/IcfChd8z">meta-analyses</a>/reviews "suggested no clear advantage of the combination therapy."<a class="footnote-ref" id="fnref:177" href="#fn:177">177</a> However, <a href="/facts/Subgroup_analysis/9wfKYw3C">subgroup analysis</a> found that patients who remain the most symptomatic while taking levothyroxine may benefit from therapy containing liothyronine.<a class="footnote-ref" id="fnref:178" href="#fn:178">178</a>
There is a lack of evidence around the benefits, side effects, and long-term risks of desiccated thyroid extract. It is no longer recommended for the treatment of hypothyroidism.<a class="footnote-ref" id="fnref:179" href="#fn:179">179</a>

<h4>Side Effects</h4>
Side effects of thyroid replacement therapy are associated with "inadequate or excessive doses."<a class="footnote-ref" id="fnref:180" href="#fn:180">180</a> Symptoms to watch for include, but are not limited to, <a href="/facts/Anxiety/Geekl883">anxiety</a>, <a href="/facts/Tremor/rD6ogM7X">tremor</a>, weight loss, <a href="/facts/Heat_intolerance/dHGL9y38">heat sensitivity</a>, diarrhea, and shortness of breath. More worrisome symptoms include <a href="/facts/Atrial_fibrillation/Rzkq1tmN">atrial fibrillation</a> and <a href="/facts/Bone_density/poUvLR69">bone density</a> loss.<a class="footnote-ref" id="fnref:181" href="#fn:181">181</a> Long term over-treatment is associated with increased mortality and <a href="/facts/Dementia/T0MRDE9I">dementia</a>.<a class="footnote-ref" id="fnref:182" href="#fn:182">182</a>

<h4>Monitoring</h4>
Thyroid Stimulating Hormone (TSH) is the laboratory value of choice for monitoring response to treatment with levothyroxine.<a class="footnote-ref" id="fnref:183" href="#fn:183">183</a> When treatment is first initiated, TSH levels may be monitored as often as a frequency of every 6–8 weeks.<a class="footnote-ref" id="fnref:184" href="#fn:184">184</a> Each time the dose is adjusted, TSH levels may be measured at that frequency until the correct dose is determined.<a class="footnote-ref" id="fnref:185" href="#fn:185">185</a> Once <a href="/facts/Drug_titration/z9CpgSqy">titrated</a> to a proper dose, TSH levels will be monitored yearly.<a class="footnote-ref" id="fnref:186" href="#fn:186">186</a> The target level for TSH is the subject of debate, with factors like age, sex, individual needs and special circumstances such as pregnancy being considered.<a class="footnote-ref" id="fnref:187" href="#fn:187">187</a> Recent studies suggest that adjusting therapy based on thyroid hormone levels (T4 and/or T3) may be important.<a class="footnote-ref" id="fnref:188" href="#fn:188">188</a>
Monitoring liothyronine treatment or combination treatment can be challenging.<a class="footnote-ref" id="fnref:189" href="#fn:189">189</a><a class="footnote-ref" id="fnref:190" href="#fn:190">190</a><a class="footnote-ref" id="fnref:191" href="#fn:191">191</a> Liothyronine can suppress TSH to a greater extent than levothyroxine.<a class="footnote-ref" id="fnref:192" href="#fn:192">192</a> Short-acting Liothyronine's short half-life can result in large fluctuations of free T3<a class="footnote-ref" id="fnref:193" href="#fn:193">193</a> over the course of 24 hours.<a class="footnote-ref" id="fnref:194" href="#fn:194">194</a>
Patients may have to adjust their dosage several times over the course of the disease. Endogenous thyroid hormone levels may fluctuate, particularly early in the disease.<a class="footnote-ref" id="fnref:195" href="#fn:195">195</a> Patients may sometimes develop hyperthyroidism, even after long-term treatment.<a class="footnote-ref" id="fnref:196" href="#fn:196">196</a> This can be due to several factors, including acute attacks of destructive <a href="/facts/Thyrotoxicosis/H9Eqmbgk">thyrotoxicosis</a> (autoimmune attacks on the thyroid resulting in rises in thyroid hormone levels as thyroid hormones leak out of the damaged tissues).<a class="footnote-ref" id="fnref:197" href="#fn:197">197</a><a class="footnote-ref" id="fnref:198" href="#fn:198">198</a> This is usually followed by hypothyroidism.<a class="footnote-ref" id="fnref:199" href="#fn:199">199</a> 

<h4>Reverse T3</h4>
Measuring <a href="/facts/Reverse_triiodothyronine/q4hjnhoY">reverse tri-iodothyronine</a> (rT3) is often mentioned in the lay (non-medical) press as a possible marker to inform T4 or T3 therapy, "however, there is currently no evidence to support this application" as of 2023.<a class="footnote-ref" id="fnref:200" href="#fn:200">200</a> Although cited in the lay press as a possible competitor to T3, it is unlikely that rT3 causes hypothyroid symptoms by out-competing T3 for <a href="/facts/Thyroid_hormone_receptor/7fBRzmmo">thyroid hormone receptors</a>, as it has a binding affinity 200 times weaker.<a class="footnote-ref" id="fnref:201" href="#fn:201">201</a> It is also unlikely that rT3 causes poor T4 to T3 conversion; despite being demonstrated <a href="/facts/In_vivo/kWcWyl6f">in vivo</a> to have the potential to inhibit <a href="/facts/Iodothyronine_deiodinase/eqsE32xA">DIO</a>-mediated T4 to T3 conversion, this is considered improbable at normal body hormone concentrations.<a class="footnote-ref" id="fnref:202" href="#fn:202">202</a>

<h3>Persistent Symptoms</h3>
Multiple studies have demonstrated persistent symptoms in Hashimoto's patients with normal thyroid hormone levels (euthyroid)<a class="footnote-ref" id="fnref:203" href="#fn:203">203</a><a class="footnote-ref" id="fnref:204" href="#fn:204">204</a><a class="footnote-ref" id="fnref:205" href="#fn:205">205</a><a class="footnote-ref" id="fnref:206" href="#fn:206">206</a> and an estimated 10%-15% of patients treated with levothyroxine monotherapy are dissatisfied due to persistent symptoms of hypothyroidism.<a class="footnote-ref" id="fnref:207" href="#fn:207">207</a><a class="footnote-ref" id="fnref:208" href="#fn:208">208</a> Several different <a href="/facts/Hypothesis/gMABEJul">hypothesised</a> causes are discussed in the <a href="/facts/Medical_literature/C01NYutX">medical literature</a>:<a class="footnote-ref" id="fnref:209" href="#fn:209">209</a><a class="footnote-ref" id="fnref:210" href="#fn:210">210</a><a class="footnote-ref" id="fnref:211" href="#fn:211">211</a>

<h4>Low tissue tri-iodothyronine (T3) hypothesis</h4>
Peripheral tissue T4 to T3 conversion may be inadequate: Some patients on LT4 monotherapy may have blood T3 levels low or below the normal range,<a class="footnote-ref" id="fnref:212" href="#fn:212">212</a><a class="footnote-ref" id="fnref:213" href="#fn:213">213</a> and/or may have local T3 deficiency in some tissues.<a class="footnote-ref" id="fnref:214" href="#fn:214">214</a> Although both <a href="/facts/Molecule/N9ljSfFq">molecules</a> can have biological effects, thyroxine (T4) is considered the "storage form" of thyroid hormone with much less effect, while tri-iodothyronine (T3) is considered the active form used by <a href="/facts/Tissue_(biology)/H7CpML7A">body tissues</a>.<a class="footnote-ref" id="fnref:215" href="#fn:215">215</a><a class="footnote-ref" id="fnref:216" href="#fn:216">216</a> Thus, the body must convert thyroxine into triiodothyronine.<a class="footnote-ref" id="fnref:217" href="#fn:217">217</a> Tri-iodothyronine is produced primarily by conversion in the <a href="/facts/Liver/Rtp4Fk2b">liver</a>, <a href="/facts/Kidney/HBspPrv9">kidney</a>, <a href="/facts/Skeletal_muscle/en1tVYFN">skeletal muscle</a> and <a href="/facts/Pituitary_gland/gdrQyldF">pituitary gland</a>.<a class="footnote-ref" id="fnref:218" href="#fn:218">218</a> 
Adequate conversion requires sufficient levels of the micronutrients <a href="/facts/Zinc/80b1qgk3">zinc</a>,<a class="footnote-ref" id="fnref:219" href="#fn:219">219</a> <a href="/facts/Selenium/k975NApC">selenium</a>,<a class="footnote-ref" id="fnref:220" href="#fn:220">220</a> <a href="/facts/Iron/DkICCKIC">iron</a>,<a class="footnote-ref" id="fnref:221" href="#fn:221">221</a> and possibly <a href="/facts/Vitamin_A/5ewDf9LF">vitamin A</a>.<a class="footnote-ref" id="fnref:222" href="#fn:222">222</a> Conversion rates may decline with age.<a class="footnote-ref" id="fnref:223" href="#fn:223">223</a> Since <a href="/facts/DIO2/DKWS8AI9">deiodinase type 2</a> is necessary for T4 to T3 conversion in some peripheral tissues, "patients with DIO2 gene polymorphisms may have variable peripheral T3 availability", leading to localised <a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a> in some tissues.<a class="footnote-ref" id="fnref:224" href="#fn:224">224</a><a class="footnote-ref" id="fnref:225" href="#fn:225">225</a><a class="footnote-ref" id="fnref:226" href="#fn:226">226</a> The Thr92Ala DIO2 polymorphism is present in 12–36% of the population.<a class="footnote-ref" id="fnref:227" href="#fn:227">227</a>
For the latter patients, levothyroxine monotherapy may not be sufficient<a class="footnote-ref" id="fnref:228" href="#fn:228">228</a> and patients may have improvement on combination therapy of T4 and T3.<a class="footnote-ref" id="fnref:229" href="#fn:229">229</a><a class="footnote-ref" id="fnref:230" href="#fn:230">230</a><a class="footnote-ref" id="fnref:231" href="#fn:231">231</a> As standard immunoassay tests can overestimate blood T4 and T3 levels, Ultrafiltration LC-MSMS T4 and T3 tests may help to identify patients who would benefit from additional T3.<a class="footnote-ref" id="fnref:232" href="#fn:232">232</a> 

<h4>Inadequate markers hypothesis</h4>
There is ongoing debate about how to define euthyroidism and whether TSH is its best indicator.<a class="footnote-ref" id="fnref:233" href="#fn:233">233</a> TSH may be useful to detect poor thyroid output and may reflect the state of thyroid hormones in the <a href="/facts/Hypothalamic%25E2%2580%2593pituitary%25E2%2580%2593thyroid_axis/vl2UQ4YN">hypothalamic-pituitary-thyroid axis</a>, but not the presence of hormones in other body tissues.<a class="footnote-ref" id="fnref:234" href="#fn:234">234</a><a class="footnote-ref" id="fnref:235" href="#fn:235">235</a><a class="footnote-ref" id="fnref:236" href="#fn:236">236</a> As a result, LT4 monotherapy may not result in a "truly biochemically euthyroid state."<a class="footnote-ref" id="fnref:237" href="#fn:237">237</a> Patients may express a preference for "low normal or below normal TSH values"<a class="footnote-ref" id="fnref:238" href="#fn:238">238</a> and/or T4 and T3 monitoring. The monitoring of other <a href="/facts/Biomarker_(medicine)/uVSh5z78">biomarkers</a> that reflect the action of thyroid hormone on tissues has also been proposed.<a class="footnote-ref" id="fnref:239" href="#fn:239">239</a><a class="footnote-ref" id="fnref:240" href="#fn:240">240</a><a class="footnote-ref" id="fnref:241" href="#fn:241">241</a>
As <a href="/facts/Immunoassay/eHo2YM9S">immunoassay</a> Free T3 and Free T4 tests can overestimate levels, particularly at low thyroid hormone levels, hypothyroidism may be undertreated.<a class="footnote-ref" id="fnref:242" href="#fn:242">242</a> <a href="/facts/Liquid_chromatography%25E2%2580%2593mass_spectrometry/nGlDC6Hw">LC-MSMS</a> tests may provide more reliable measures.<a class="footnote-ref" id="fnref:243" href="#fn:243">243</a>

<h4>Extra-thyroidal effects of autoimmunity hypothesis</h4>
It is hypothesised that autoimmunity may play some role in euthyroid symptoms.<a class="footnote-ref" id="fnref:244" href="#fn:244">244</a><a class="footnote-ref" id="fnref:245" href="#fn:245">245</a><a class="footnote-ref" id="fnref:246" href="#fn:246">246</a> Hypothesised mechanisms include the proposal that TPO-antibody-producing <a href="/facts/Lymphocyte/pS2pv2Ma">lymphocytes</a> may travel out of the thyroid to other tissue, creating symptoms and inflammation due to <a href="/facts/Cross-reactivity/m2rBF6fw">cross-reaction</a>,<a class="footnote-ref" id="fnref:247" href="#fn:247">247</a><a class="footnote-ref" id="fnref:248" href="#fn:248">248</a> or "the inflammatory nature of [...] persistently increased circulating cytokine levels."<a class="footnote-ref" id="fnref:249" href="#fn:249">249</a> Multiple studies find that antibodies coincide with symptoms even in euthyroid patients,<a class="footnote-ref" id="fnref:250" href="#fn:250">250</a><a class="footnote-ref" id="fnref:251" href="#fn:251">251</a> and higher levels are associated with increased symptoms,<a class="footnote-ref" id="fnref:252" href="#fn:252">252</a> however "the found <a href="/facts/Association_(statistics)/egkluAEm">association</a> does not prove a <a href="/facts/Causality/Swh496X7">causality</a>".<a class="footnote-ref" id="fnref:253" href="#fn:253">253</a> No treatment currently exists for Hashimoto's autoimmunity, although observed well-being improvements after surgical thyroid removal are hypothesised to be due to removing the autoimmune stimulus.<a class="footnote-ref" id="fnref:254" href="#fn:254">254</a><a class="footnote-ref" id="fnref:255" href="#fn:255">255</a>

<h4>Physical and psychosocial co-morbidities hypothesis</h4>
It is hypothesised that euthyroid symptoms may not be due to Hashimoto's or hypothyroidism, but some other "physical and psychosocial <a href="/facts/Comorbidity/tX5TvuKJ">co-morbidities</a>".<a class="footnote-ref" id="fnref:256" href="#fn:256">256</a><a class="footnote-ref" id="fnref:257" href="#fn:257">257</a>

<h3>Improving well-being</h3>
Some patients may perceive improved well-being while in <a href="/facts/Thyrotoxicosis/H9Eqmbgk">thyrotoxicosis</a>, however overtreatment has risks (known risks for <a href="/facts/Levothyroxine/AarfgbeG">levothyroxine</a> and unknown risks for <a href="/facts/Liothyronine/wU0LlRE6">liothyronine</a>).<a class="footnote-ref" id="fnref:258" href="#fn:258">258</a> One study demonstrated <a href="/facts/Thyroidectomy/EkIQKkDw">surgical thyroid removal</a> may substantially improve fatigue and well-being,<a class="footnote-ref" id="fnref:259" href="#fn:259">259</a><a class="footnote-ref" id="fnref:260" href="#fn:260">260</a> see Surgery considerations, below.

<h3>Reducing antibodies</h3>
It is not established that reducing <a href="/facts/Antithyroid_autoantibodies/6j71eQUv">antithyroid antibodies</a> in Hashimoto's has benefits.<a class="footnote-ref" id="fnref:261" href="#fn:261">261</a><a class="footnote-ref" id="fnref:262" href="#fn:262">262</a><a class="footnote-ref" id="fnref:263" href="#fn:263">263</a> A systematic review and meta-analysis of selenium trials found that while selenium reduces TPO antibodies, there was a lack of evidence of effects on "disease <a href="/facts/Remission_(medicine)/8HuMct73">remission</a>, progression, lowered levothyroxine dose or improved <a href="/facts/Quality_of_life/37ljmgAH">quality of life</a>".<a class="footnote-ref" id="fnref:264" href="#fn:264">264</a>
Selenium,<a class="footnote-ref" id="fnref:265" href="#fn:265">265</a><a class="footnote-ref" id="fnref:266" href="#fn:266">266</a> <a href="/facts/Vitamin_D/No0zQB2W">vitamin D</a>,<a class="footnote-ref" id="fnref:267" href="#fn:267">267</a> and <a href="/facts/Metformin/ScXHFaPT">metformin</a><a class="footnote-ref" id="fnref:268" href="#fn:268">268</a> can reduce thyroid peroxidase antibodies. There is preliminary evidence that levothyroxine,<a class="footnote-ref" id="fnref:269" href="#fn:269">269</a><a class="footnote-ref" id="fnref:270" href="#fn:270">270</a> [needs update]<a href="/facts/Aloe_vera/d91m7N4a">aloe vera</a> juice<a class="footnote-ref" id="fnref:271" href="#fn:271">271</a> and <a href="/facts/Black_cumin/Q9EfPcjA">black cumin seed</a><a class="footnote-ref" id="fnref:272" href="#fn:272">272</a> may reduce thyroid peroxidase antibodies. Metformin can reduce thyroglobulin antibodies.<a class="footnote-ref" id="fnref:273" href="#fn:273">273</a> It is not established that a <a href="/facts/Gluten-free_diet/GXRvRR4K">gluten-free diet</a> can reduce antibodies when there is no comorbid <a href="/facts/Coeliac_disease/AKd5PkTc">coeliac disease</a>.<a class="footnote-ref" id="fnref:274" href="#fn:274">274</a><a class="footnote-ref" id="fnref:275" href="#fn:275">275</a> Gluten-free diets have been shown in several studies to reduce antibodies, and in other studies to have no effect, however there were significant confounding issues in these studies, including not ruling out <a href="/facts/Comorbidity/tX5TvuKJ">comorbid</a> coeliac disease.<a class="footnote-ref" id="fnref:276" href="#fn:276">276</a> One study found <a href="/facts/Thyroidectomy/EkIQKkDw">surgical thyroid removal</a> can substantially reduce anti-thyroid antibody levels,<a class="footnote-ref" id="fnref:277" href="#fn:277">277</a><a class="footnote-ref" id="fnref:278" href="#fn:278">278</a> see Surgery considerations, below.

<h3>Surgery considerations</h3>
Surgery is not the initial treatment of choice for autoimmune disease, and uncomplicated Hashimoto's thyroiditis is not an <a href="/facts/Indication_(medicine)/DLdGwxDY">indication</a> for <a href="/facts/Thyroidectomy/EkIQKkDw">thyroidectomy</a>.<a class="footnote-ref" id="fnref:279" href="#fn:279">279</a> Patients generally may discuss surgery with their doctor if they are experiencing significant pressure symptoms, or cosmetic concerns, or have <a href="/facts/Thyroid_nodule/EmYsNFpb">nodules</a> present on ultrasound.<a class="footnote-ref" id="fnref:280" href="#fn:280">280</a> One well-conducted study of patients with troublesome general symptoms and with anti-thyroperoxidase (anti-TPO) levels greater than 1000 IU/ml (normal <100 IU/ml) showed that total thyroidectomy caused the symptoms to resolve and median anti-thyroid peroxidase levels to reduce from 2232 to 152 IU/mL,<a class="footnote-ref" id="fnref:281" href="#fn:281">281</a><a class="footnote-ref" id="fnref:282" href="#fn:282">282</a> but post-operative complications were higher than expected:<a class="footnote-ref" id="fnref:283" href="#fn:283">283</a> <a href="/facts/Infection/182XrncP">infection</a> (4.1%), permanent <a href="/facts/Hypoparathyroidism/Dd79cfqo">hypoparathyroidism</a> (4.1%) and <a href="/facts/Recurrent_laryngeal_nerve/vMcn31Mw">recurrent laryngeal nerve</a> injury (5.5%).<a class="footnote-ref" id="fnref:284" href="#fn:284">284</a>

<h3>Other</h3>
<a href="/facts/Zinc/80b1qgk3">Zinc</a> may increase free T3 levels.<a class="footnote-ref" id="fnref:285" href="#fn:285">285</a> A small pilot study found <a href="/facts/Ashwagandha/SmYwczu1">Ashwagandha Root</a> may increase T3 and T4 levels, however, there's a lack of strong evidence of this benefit and Ashwagandha has a potential to cause <a href="/facts/Adrenal_insufficiency/7oxdJtF4">adrenal insufficiency</a>.<a class="footnote-ref" id="fnref:286" href="#fn:286">286</a>
As of 2022, there has been only one study of low-dose <a href="/facts/Naltrexone/SVduEm3W">naltrexone</a> in Hashimoto's, which did not demonstrate efficacy; therefore, nothing supports its use. Removing dairy products in those without <a href="/facts/Lactose_intolerance/sD6q8shx">lactose intolerance</a> is not supported.<a class="footnote-ref" id="fnref:287" href="#fn:287">287</a> While soy <a href="/facts/Isoflavone/Yfz7RTEo">isoflavones</a> have the potential to theoretically affect T3 and T4 production, studies in those with sufficient <a href="/facts/Iodine/JlfMecMf">iodine</a> find no effect.<a class="footnote-ref" id="fnref:288" href="#fn:288">288</a>

<h2 id="prognosis">Prognosis</h2>
Overt, symptomatic thyroid dysfunction is the most common <a href="/facts/Complication_(medicine)/uJHvzqUt">complication</a>, with about 5% of people with <a href="/facts/Subclinical_hypothyroidism/oqtQDu2F">subclinical hypothyroidism</a> and chronic autoimmune thyroiditis progressing to thyroid failure every year. Transient periods of <a href="/facts/Thyrotoxicosis/H9Eqmbgk">thyrotoxicosis</a> (over-activity of the thyroid) sometimes occur, and rarely the illness may progress to full hyperthyroid <a href="/facts/Graves%2527_disease/6CjnWNdE">Graves' disease</a> with active <a href="/facts/Graves%2527_ophthalmopathy/de2jpRVM">orbitopathy</a> (bulging, inflamed eyes).<a class="footnote-ref" id="fnref:289" href="#fn:289">289</a>
Rare cases of fibrous autoimmune thyroiditis present with severe <a href="/facts/Dyspnea/1jBfFzxU">shortness of breath</a> and <a href="/facts/Dysphagia/vgfd6FpV">difficulty swallowing</a>, resembling aggressive thyroid tumors, but such symptoms always improve with surgery or <a href="/facts/Corticosteroid/jeL2QeIL">corticosteroid</a> therapy. Although primary thyroid <a href="/facts/B-cell_lymphoma/q1m7JHdD">B-cell lymphoma</a> affects fewer than one in 1000 persons, it is more likely to affect those with long-standing autoimmune thyroiditis,<a class="footnote-ref" id="fnref:290" href="#fn:290">290</a> as there is a 67- to 80-fold increased risk of developing primary thyroid lymphoma in patients with Hashimoto's thyroiditis.<a class="footnote-ref" id="fnref:291" href="#fn:291">291</a>
<a href="/facts/Myopathy/eklaDeY6">Myopathy</a> as a result of muscle fibre changes due to thyroid hormone deficiency may take months or years of thyroid hormone treatment to resolve.<a class="footnote-ref" id="fnref:292" href="#fn:292">292</a><a class="footnote-ref" id="fnref:293" href="#fn:293">293</a>

<h3>Anti-thyroid antibodies</h3>
<a href="/facts/Antithyroid_autoantibodies/6j71eQUv">Thyroid peroxidase antibodies</a> typically (but not always) decline in patients treated with levothyroxine,<a class="footnote-ref" id="fnref:294" href="#fn:294">294</a> with decreases varying between 10% and 90% after a follow-up of 6 to 24 months.<a class="footnote-ref" id="fnref:295" href="#fn:295">295</a> One study of patients treated with levothyroxine observed that 35 out of 38 patients (92%) had declines in thyroid peroxidase antibody levels over five years, lowering by 70% on average. 6 of the 38 patients (16%) had thyroid peroxidase antibody levels return to normal.<a class="footnote-ref" id="fnref:296" href="#fn:296">296</a>

<h3>Children</h3>
Many children diagnosed with Hashimoto's disease will experience the same progressive course of the disease that adults do.<a class="footnote-ref" id="fnref:297" href="#fn:297">297</a> However, of children who develop anti-thyroid antibodies and hypothyroidism, up to 50% are later observed to have normal antibodies and thyroid hormone levels.<a class="footnote-ref" id="fnref:298" href="#fn:298">298</a> One case of true <a href="/facts/Remission_(medicine)/8HuMct73">remission</a> has been observed in a 12-year-old girl. Her thyroid was observed via <a href="/facts/Ultrasound/31Pa5IH9">ultrasound</a> to progress from early <a href="/facts/Inflammation/Ura86MIy">inflammation</a> to severe end-stage Hashimoto's thyroiditis with hypothyroidism, and then return to "almost normal with only minimal features of inflammation" and euthyroidism.<a class="footnote-ref" id="fnref:299" href="#fn:299">299</a>

<h2 id="epidemiology">Epidemiology</h2>
Hashimoto's Disease is estimated to affect 2% of the world's population.<a class="footnote-ref" id="fnref:300" href="#fn:300">300</a><a class="footnote-ref" id="fnref:301" href="#fn:301">301</a> About 1.0 to 1.5 in 1000 people have this disease at any time.<a class="footnote-ref" id="fnref:302" href="#fn:302">302</a>

<h3>Sex</h3>
Anyone may develop this disease, but it occurs between 8<a class="footnote-ref" id="fnref:303" href="#fn:303">303</a> and 15 times more often in women than in men. Some research suggests a connection to the role of the <a href="/facts/Placenta/7XUoks1b">placenta</a> as an explanation for the sex difference.<a class="footnote-ref" id="fnref:304" href="#fn:304">304</a> Other research suggests the difference in <a href="/facts/Prevalence/6UTuTGTH">prevalence</a> amongst genders is due to the effects of <a href="/facts/Sex_hormone/mI6bkHII">sex hormones</a>.<a class="footnote-ref" id="fnref:305" href="#fn:305">305</a>

<h3>High iodine consumption</h3>
Autoimmune thyroiditis has a higher prevalence in societies that have a higher intake of <a href="/facts/Iodine/JlfMecMf">iodine</a> in their diet, such as the United States and Japan, and among people who are <a href="/facts/Genetic_predisposition/rQkzYCYv">genetically susceptible</a>.<a class="footnote-ref" id="fnref:306" href="#fn:306">306</a> It is the most common cause of hypothyroidism in areas of sufficient iodine.<a class="footnote-ref" id="fnref:307" href="#fn:307">307</a> Also, the rate of lymphocytic infiltration increased in areas where the iodine intake was once low, but increased due to iodine supplementation.<a class="footnote-ref" id="fnref:308" href="#fn:308">308</a><a class="footnote-ref" id="fnref:309" href="#fn:309">309</a>
<a href="/facts/Iodine_deficiency/NsTLf3E5">Iodine deficiency disorder</a> is combated using an increase in iodine in a person's diet. When a dramatic change occurs in a person's diet, they become more at risk of developing hypothyroidism and other thyroid disorders. Treating iodine deficiency disorder with high salt intakes should be done carefully and cautiously, as the risk for Hashimoto's may increase.<a class="footnote-ref" id="fnref:310" href="#fn:310">310</a>

<h3>Geographic influence of dietary trends</h3>
Geography plays a large role in which regions have access to diets with low or high iodine. Iodine levels in both water and salt should be heavily monitored to protect at-risk populations from developing hypothyroidism.<a class="footnote-ref" id="fnref:311" href="#fn:311">311</a> Geographic trends of hypothyroidism vary across the world as different places have different ways of defining the disease and reporting cases. Populations that are spread out or defined poorly may skew data in unexpected ways.<a class="footnote-ref" id="fnref:312" href="#fn:312">312</a>

<h3>North America</h3>
Hashimoto's thyroiditis may affect up to 5% of the United States' population.<a class="footnote-ref" id="fnref:313" href="#fn:313">313</a> Hashimoto's thyroiditis disorder is thought to be the most common cause of primary hypothyroidism in North America.<a class="footnote-ref" id="fnref:314" href="#fn:314">314</a>

<h3>Age</h3>
Hashimoto's thyroiditis can occur at any age, including children,<a class="footnote-ref" id="fnref:315" href="#fn:315">315</a> but more commonly appears in <a href="/facts/Middle_age/RqzEKB9v">middle age</a>, particularly for men.<a class="footnote-ref" id="fnref:316" href="#fn:316">316</a> <a href="/facts/Incidence_(epidemiology)/2BB3FlBK">Incidence</a> peaks in the fifth decade of life, but patients are usually diagnosed between age 30–50.<a class="footnote-ref" id="fnref:317" href="#fn:317">317</a><a class="footnote-ref" id="fnref:318" href="#fn:318">318</a> The highest prevalence from one study was found in the elderly members of the community.<a class="footnote-ref" id="fnref:319" href="#fn:319">319</a> It has been shown that the prevalence of positive tests for thyroid antibodies increases with age, "with a frequency as high as 33 percent in women 70 years old or older."<a class="footnote-ref" id="fnref:320" href="#fn:320">320</a>

<h3>Race</h3>
The prevalence of Hashimoto's varies geographically. The highest rate is in Africa, and the lowest in Asia.<a class="footnote-ref" id="fnref:321" href="#fn:321">321</a> In the US, the African-American population experiences it less commonly but has greater associated mortality.<a class="footnote-ref" id="fnref:322" href="#fn:322">322</a>

<h3>Autoimmune diseases</h3>
Those who already have an autoimmune disease are at greater risk of developing Hashimoto's, as the diseases generally coexist with each other.<a class="footnote-ref" id="fnref:323" href="#fn:323">323</a> See Causes > Comorbidities, above.

<h3>Secular trends</h3>
The <a href="/facts/Secular_trends/55wVcxuE">secular trends</a> of hypothyroidism reveal how the disease has changed over time, given changes in technology and treatment options. Even though ultrasound technology and treatment options have improved, the incidence of hypothyroidism has increased according to data focused on the US and Europe. Between 1993 and 2001, the disease was found to vary between 3.9 and 4.89 per 1000 women. Between 1994 and 2001, the disease increased from 0.65 to 1.01 per 1000 men.<a class="footnote-ref" id="fnref:324" href="#fn:324">324</a>

<h2 id="history">History</h2>
Also known as Hashimoto's disease, Hashimoto's thyroiditis is named after Japanese physician <a href="/facts/Hakaru_Hashimoto/VHsDRDen">Hakaru Hashimoto</a> (1881−1934) of the medical school at <a href="/facts/Kyushu_University/duWa5tYG">Kyushu University</a>,<a class="footnote-ref" id="fnref:325" href="#fn:325">325</a> who first described the symptoms of persons with struma lymphomatosa, an intense infiltration of lymphocytes within the thyroid, in 1912 in the German journal called <a href="/facts/Archiv_f%25C3%25BCr_Klinische_Chirurgie/0FsBNNpe">Archiv für Klinische Chirurgie</a>.<a class="footnote-ref" id="fnref:326" href="#fn:326">326</a><a class="footnote-ref" id="fnref:327" href="#fn:327">327</a> This <a href="/facts/Scientific_literature/nJh0Bx22">paper</a> was made up of 30 pages and 5 illustrations all describing the <a href="/facts/Histology/yrI90zlU">histological</a> changes in the thyroid tissue. Furthermore, all results in his first study were collected from four women. These results explained the <a href="/facts/Pathology/U9b18LJG">pathological</a> characteristics observed in these women especially the infiltration of <a href="/facts/Lymphocyte/pS2pv2Ma">lymphocyte</a> and <a href="/facts/Plasma_cell/1fY4bFHR">plasma cells</a> as well as the formation of lymphoid follicles with <a href="/facts/Germinal_center/hdCfNIQc">germinal centers</a>, fibrosis, degenerated thyroid <a href="/facts/Epithelial_cells/ecKHcHC3">epithelial cells</a> and <a href="/facts/Leukocytes/vsDunUK0">leukocytes</a> in the <a href="/facts/Lumen_(anatomy)/3thJT4Hf">lumen</a>.<a class="footnote-ref" id="fnref:328" href="#fn:328">328</a> He described these traits to be histologically similar to those of Mikulic's disease. As mentioned above, once he discovered these traits in this new disease, he named the disease struma lymphomatosa. This disease emphasized the lymphocyte infiltration and formation of the lymphoid follicles with germinal centers, neither of which had ever been previously reported.<a class="footnote-ref" id="fnref:329" href="#fn:329">329</a>
Despite Hashimoto's discovery and publication, the disease was not recognized as distinct from <a href="/facts/Riedel%2527s_thyroiditis/l3yoNseC">Riedel's thyroiditis</a>, which was a common disease at that time in Europe. Although many other articles were reported and published by other researchers, Hashimoto's struma lymphomatosa was only recognized as an early phase of Riedel's thyroiditis in the early 1900s. It was not until 1931 that the disease was recognized as a disease in its own right, when researchers Allen Graham et al. from Cleveland reported its symptoms and presentation in the same detailed manner as Hashimoto.<a class="footnote-ref" id="fnref:330" href="#fn:330">330</a>
In 1956, Drs. Rose and Witebsky were able to demonstrate how <a href="/facts/Immunization/f2NLoleW">immunization</a> of certain rodents with extracts of other rodents' thyroid resembled the disease that Hakaru and other researchers were trying to describe.<a class="footnote-ref" id="fnref:331" href="#fn:331">331</a> These doctors were also able to describe <a href="/facts/Antithyroid_autoantibodies/6j71eQUv">anti-thyroglobulin antibodies</a> in blood serum samples from these same animals.<a class="footnote-ref" id="fnref:332" href="#fn:332">332</a>
Later in the same year, researchers from the Middlesex Hospital in London conducted human experiments on patients who presented with similar symptoms. They purified anti-thyroglobulin antibody from their serum and were able to conclude that these sick patients had an <a href="/facts/Immune_response/dtLulqIy">immunological reaction</a> to human thyroglobulin.<a class="footnote-ref" id="fnref:333" href="#fn:333">333</a> From this data, it was proposed that Hashimoto's struma could be an autoimmune disease of the thyroid gland: "Following these discoveries, the concept of organ-specific autoimmune disease was established and HT recognized as one such disease."<a class="footnote-ref" id="fnref:334" href="#fn:334">334</a>
Following this recognition, the same researchers from Middlesex Hospital published an article in 1962 in <a href="/facts/The_Lancet/UYtU5P4P">The Lancet</a> that included a portrait of Hakaru Hashimoto.<a class="footnote-ref" id="fnref:335" href="#fn:335">335</a> The disease became more well-known from that moment, and Hashimoto's disease started to appear more frequently in textbooks.<a class="footnote-ref" id="fnref:336" href="#fn:336">336</a>

<h2 id="pregnancy">Pregnancy</h2>
<h3>Conception</h3>
It is recommended that <a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a> be treated with <a href="/facts/Levothyroxine/AarfgbeG"> levothyroxine</a> before conception, to prevent adverse effects on the course of the pregnancy and the development of the child.<a class="footnote-ref" id="fnref:337" href="#fn:337">337</a> In <a href="/facts/IVF/kQNMtaBu">IVF</a>, <a href="/facts/Embryo_transfer/2N05Lrxj">embryo transfer</a> is improved when hypothyroidism is treated.<a class="footnote-ref" id="fnref:338" href="#fn:338">338</a>

<h3>Pregnancy</h3>
The <a href="/facts/Endocrine_Society/elmT4dVx">Endocrine Society</a> recommends screening in pregnant women who are considered high-risk for thyroid autoimmune disease.<a class="footnote-ref" id="fnref:339" href="#fn:339">339</a> Universal screening for thyroid diseases during pregnancy is controversial, however, one study "supports the potential benefit of universal screening".<a class="footnote-ref" id="fnref:340" href="#fn:340">340</a> Pregnant women may have <a href="/facts/Antithyroid_autoantibodies/6j71eQUv">antithyroid antibodies</a> (5%–14% of pregnancies<a class="footnote-ref" id="fnref:341" href="#fn:341">341</a>), poor thyroid function resulting in hypothyroidism, or both. Each is associated with risks:<a class="footnote-ref" id="fnref:342" href="#fn:342">342</a>

<h4>Anti-thyroid antibodies in pregnancy</h4>
The presence of Thyroid peroxidase antibodies at the outset of pregnancy are associated with a greater risk to the mother of hypothyroidism and thyroid impairment in the first year after <a href="/facts/Childbirth/KaWFJ4kG">delivery</a>.<a class="footnote-ref" id="fnref:343" href="#fn:343">343</a> The presence of antibodies is also associated with "a 2 to 4-fold increase in the risk of recurrent <a href="/facts/Miscarriage/sFq0vdnU">miscarriages</a>, and 2 to 3-fold increased risk of <a href="/facts/Preterm_birth/szMos8tu">preterm birth</a>", however the reason why is unclear. Thyroid peroxidase antibodies are speculated to indicate other autoimmune processes against the placental-fetal unit.<a class="footnote-ref" id="fnref:344" href="#fn:344">344</a> Levothyroxine treatment in euthyroid women with thyroid autoimmunity does not significantly impact the relative risk of miscarriage and preterm delivery, or outcomes with live birth. "Therefore, no strong recommendations regarding the therapy in such scenarios could be made, but consideration on a case-by-case basis might be implemented."<a class="footnote-ref" id="fnref:345" href="#fn:345">345</a>

<h4>Hypothyroidism in pregnancy</h4>
Women who have low thyroid function that has not been stabilized are at greater risk of complications for both parent and child. Risks to the mother include <a href="/facts/Gestational_Hypertension/qm4Lo70j">gestational hypertension</a> including <a href="/facts/Pre-eclampsia/FG1BrbC8">preeclampsia</a> and <a href="/facts/Eclampsia/K5roBd1g">eclampsia</a>, <a href="/facts/Gestational_diabetes/1Nn5kF5G">gestational diabetes</a>, <a href="/facts/Placental_abruption/W3aL2xF8">placental abruption</a>, and <a href="/facts/Postpartum_bleeding/VFqNRNQF">postpartum hemorrhage</a>.<a class="footnote-ref" id="fnref:346" href="#fn:346">346</a> Risks to the infant include miscarriage, preterm delivery, <a href="/facts/Low_birth_weight/IxqAPaKn">low birth weight</a>, <a href="/facts/Infant_respiratory_distress_syndrome/eGBl4uow">neonatal respiratory distress</a>, <a href="/facts/Hydrocephalus/HF9jQqTq">hydrocephalus</a>, <a href="/facts/Hypospadias/rr82Ll75">hypospadias</a>, fetal death, infant intensive care unit admission, and <a href="/facts/Developmental_disability/gXH6UNwm">neurodevelopmental delays</a> (lower child IQ, language delay or <a href="/facts/Global_developmental_delay/lgs7CQPB">global developmental delay</a>).<a class="footnote-ref" id="fnref:347" href="#fn:347">347</a><a class="footnote-ref" id="fnref:348" href="#fn:348">348</a><a class="footnote-ref" id="fnref:349" href="#fn:349">349</a>
Successful pregnancy outcomes are improved when hypothyroidism is treated.<a class="footnote-ref" id="fnref:350" href="#fn:350">350</a> Levothyroxine treatment may be considered at lower TSH levels in pregnancy than in standard treatment.<a class="footnote-ref" id="fnref:351" href="#fn:351">351</a> Liothyronine does not cross the fetal blood-brain barrier, so liothyronine (T3) only or liothyronine + levothyroxine (T3 + T4) therapy is not indicated in pregnancy.<a class="footnote-ref" id="fnref:352" href="#fn:352">352</a>
Close cooperation between the <a href="/facts/Endocrinologist/4SqQu1NN">endocrinologist</a> and <a href="/facts/Obstetrician/JbYHxtCd">obstetrician</a> benefits the woman and the infant.<a class="footnote-ref" id="fnref:353" href="#fn:353">353</a><a class="footnote-ref" id="fnref:354" href="#fn:354">354</a><a class="footnote-ref" id="fnref:355" href="#fn:355">355</a>

<h4>Immune changes during pregnancy</h4>
Hormonal changes and <a href="/facts/Trophoblast/dzVMtog3">trophoblast</a> expression of key <a href="/facts/Immunomodulation/fWlbBnHc">immunomodulatory</a> molecules lead to <a href="/facts/Immunosuppression/22GHUHkr">immunosuppression</a> and fetal tolerance. The main players in the regulation of the immune response are <a href="/facts/Tregs/1ECRAGMg">Tregs</a>. Both <a href="/facts/Cell-mediated_immunity/vPX39rt1">cell-mediated</a> and <a href="/facts/Humoral_immunity/qG9I4pGf">humoral</a> immune responses are attenuated, resulting in <a href="/facts/Immune_tolerance_in_pregnancy/eIhCErwk">immune tolerance</a> and suppression of autoimmunity. It has been reported that during pregnancy, levels of thyroid peroxidase and thyroglobulin antibodies decrease.<a class="footnote-ref" id="fnref:356" href="#fn:356">356</a>

<h3>Postpartum</h3>
Thyroid peroxidase antibody testing is recommended for women who have ever been pregnant, regardless of pregnancy outcome. "[P]revious pregnancy plays a major role in the development of autoimmune overt hypothyroidism in <a href="/facts/Premenopausal/b3Fz6NHb">premenopausal</a> women, and the number of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a young woman [sic]."<a class="footnote-ref" id="fnref:357" href="#fn:357">357</a>
<a href="/facts/Postpartum_thyroiditis/udHIBGkD">Postpartum thyroiditis</a> can occur in women with Hashimoto's.<a class="footnote-ref" id="fnref:358" href="#fn:358">358</a> In healthy women, Postpartum thyroiditis can occur up to 1 year after <a href="/facts/Childbirth/KaWFJ4kG">delivery</a>. It should be differentiated from Hashimoto's thyroiditis as it is treated differently.<a class="footnote-ref" id="fnref:359" href="#fn:359">359</a>
After giving birth, <a href="/facts/Regulatory_T_cell/1ECRAGMg">Tregs</a> rapidly decrease, and immune responses are re-established. It may lead to the occurrence or aggravation of autoimmune thyroid disease.<a class="footnote-ref" id="fnref:360" href="#fn:360">360</a> In up to 50% of females with thyroid peroxidase antibodies in the early pregnancy, thyroid autoimmunity in the postpartum period exacerbates in the form of postpartum thyroiditis.<a class="footnote-ref" id="fnref:361" href="#fn:361">361</a> Higher secretion of <a href="/facts/Interferon_gamma/r51CXVph">IFN-γ</a> and <a href="/facts/Interleukin_4/FacDJ3TY">IL-4</a>, and lower plasma <a href="/facts/Cortisol/5IvRV0cm">cortisol</a> concentration during pregnancy has been reported in females with postpartum thyroiditis than in healthy females. It indicates that weaker immunosuppression during pregnancy could contribute to postpartum thyroid dysfunction.<a class="footnote-ref" id="fnref:362" href="#fn:362">362</a>

<h3>Fetal microchimerism</h3>
Several years after the delivery, the <a href="/facts/Chimera_(genetics)/xs4NDyLP">chimeric</a> male cells can be detected in the maternal peripheral blood, thyroid, lung, skin, or lymph nodes. The fetal immune cells in the maternal thyroid gland may become activated and act as a trigger that initiates or exacerbates the autoimmune thyroid disease. In Hashimoto's disease patients, fetal <a href="/facts/Microchimerism/GQtBHdXu">microchimeric</a> cells were detected in the thyroid in significantly higher numbers than in healthy females.<a class="footnote-ref" id="fnref:363" href="#fn:363">363</a>

<h2 id="other-animals">Other animals</h2>
Hashimoto's disease is known to occur in <a href="/facts/Chicken/RD2eTd83">chickens</a>, <a href="/facts/Rat/J2daVSTB">rats</a>, <a href="/facts/Mice/6m1X7m0g">mice</a>, <a href="/facts/Dog/DvQVRVzy">dogs</a>, and <a href="/facts/Marmoset/dR1wnBIq">marmosets</a>, but Graves' disease does not.<a class="footnote-ref" id="fnref:364" href="#fn:364">364</a><blockquote></blockquote>
<h2 id="see-also">See also</h2>
<ul><li><a href="/facts/Hashimoto%2527s_encephalopathy/5U8QlP8c">Hashimoto's encephalopathy</a></li>
<li><a href="/facts/Myxedematous_psychosis/u8seNA0D">Myxedematous psychosis</a></li>
<li><a href="/facts/Hashitoxicosis/1YAex1J6">Hashitoxicosis</a></li>
<li><a href="/facts/Hoffmann_syndrome/rBzq7qzU">Hoffmann Syndrome</a></li></ul>

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</ol>

Hashimoto's thyroiditis open-in-new

Hashimoto's thyroiditis