Hashimoto Thyroiditis

Abstract

Hashimoto thyroiditis is an autoimmune disease characterized by destruction of thyroid follicular cells via cell- and antibody-mediated mechanisms. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis. Hashimoto thyroiditis is the most common cause of hypothyroidism in developed countries. The pathophysiology of this disease involves the formation of antithyroid antibodies and T cell activation that target thyroid tissue, leading to progressive fibrosis. Together with Graves disease, this condition comes in the category of autoimmune thyroid disorders. This condition was initially described by the Japanese physician Haruto Hashimoto in 1912 as "struma lymphomatosa" after he observed enlarged thyroids with lymphocytic infiltration. Women are more commonly affected. The female-to-male ratio is at least 7:1 to 10:1. The incidence of Hashimoto thyroiditis increases with age, with most cases occurring between ages 45 and 55. The incidence tends to be higher in countries with lower iodine deficiency prevalence. Hashimoto thyroiditis can occur alone or as part of autoimmune polyglandular syndrome. Some individuals with Graves disease might transform into Hashimoto thyroiditis and vice versa. This could indicate a common pathogenesis for these disorders, but different clinical presentations. Background: Hashimoto thyroiditis (HT) is the most common cause of hypothyroidism in iodine-sufficient areas. Selenium is an essential trace element required for thyroid hormone synthesis and exerts antioxidant effects. Therefore, it may be of relevance in the management of HT. Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the effect of selenium supplementation on thyroid function (thyrotropin [TSH], free and total thyroxine [fT4, T4], free and total triiodothyronine [fT3, T3]), thyroid antibodies (thyroid peroxidase antibodies [TPOAb], thyroglobulin antibodies [TGAb], thyrotropin receptor antibody [TRAb]), ultrasound findings (echogenicity, thyroid volume), immune markers, patient-reported outcomes, and adverse events in HT. The study protocol was registered on PROSPERO (CRD42022308377). We systematically searched MEDLINE, Embase, CINHAL, Web of Science, Google Scholar, and the Cochrane CENTRAL Register of Trials from inception to January 2023 and searched citations of eligible studies. Two independent authors reviewed and coded the identified literature. The primary outcome was TSH in patients without thyroid hormone replacement therapy (THRT); the others were considered secondary outcomes. We synthesized the results as standardized mean differences (SMD) or odds ratio (OR), assessed risk of bias using the Cochrane RoB 2 tool, and rated the evidence using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Results: We screened 687 records and included 35 unique studies. Our meta-analysis found that selenium supplementation decreased TSH in patients without THRT (SMD -0.21 [confidence interval, CI -0.43 to -0.02]; 7 cohorts, 869 participants; I 2  = 0%). In addition, TPOAb (SMD -0.96 [CI -1.36 to -0.56]; 29 cohorts; 2358 participants; I 2  = 90%) and malondialdehyde (MDA; SMD -1.16 [CI -2.29 to -0.02]; 3 cohorts; 248 participants; I 2  = 85%) decreased in patients with and without THRT. Adverse effects were comparable between the intervention and control groups (OR 0.89 [CI 0.46 to 1.75]; 16 cohorts; 1339 participants; I 2  = 0%). No significant changes were observed in fT4, T4, fT3, T3, TGAb, thyroid volume, interleukin (IL)-2, and IL-10. Overall, certainty of evidence was moderate. Conclusions: In people with HT without THRT, selenium was effective and safe in lowering TSH, TPOAb, and MDA levels. Indications for lowering TPOAb were found independent of THRT.

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• Hashimoto thyroiditis