{"title":"硒缺乏和补充对桥本甲状腺炎的影响:临床评价。","authors":"Hasan Acik, Yusuf Aydin","doi":"10.2174/0118715303424962251204064911","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Hashimoto thyroiditis (HT) is an autoimmune disorder that leads to hypothyroidism. Selenium (Se) is essential for thyroid hormone metabolism and immune function, but its role in HT remains debated. This study investigates Se levels in HT patients and evaluates the impact of supplementation on thyroid autoimmunity and thyroid function.</p><p><strong>Methods: </strong>This retrospective study analyzed HT patients and healthy controls. Biochemical parameters, including Se, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibodies, were compared. Se-deficient HT patients (<80 µg/L) received selenium supplementation for six months. Paired t-tests and Spearman correlation analyses were used for statistical evaluation.</p><p><strong>Results: </strong>Among 270 HT patients and 350 controls, TSH levels were significantly elevated in HT (p<0.001), whereas Se levels showed no significant baseline difference (p=0.87). In Se-deficient patients (n=60), supplementation increased Se levels from 68.60±12.10 µg/L to 104.92±34.45 µg/L (p<0.001). However, anti-TPO and anti-Tg levels increased after treatment (p=0.01 and p=0.03, respectively). No significant changes were observed in TSH (p=0.27), FT3 (p=0.20), or FT4 (p=0.19). Se positively correlated with anti-TPO (r=0.36, p=0.0102) and negatively with FT3 (r=-0.39, p=0.0046).</p><p><strong>Discussion: </strong>Selenium supplementation restored serum Se levels but was unexpectedly associated with increased antibody titers. This finding contrasts with several randomized trials reporting antibody reduction, suggesting that baseline Se status, the form of supplementation, or differences in study design may account for the discrepancy. The observed correlations should be interpreted with caution.</p><p><strong>Conclusion: </strong>Selenium supplementation normalizes selenium status in HT patients, but its effects on thyroid autoimmunity and thyroid function remain uncertain. Long-term randomized controlled trials are needed to determine its therapeutic value.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Impact of Selenium Deficiency and Supplementation on Hashimoto's Thyroiditis: A Clinical Evaluation.\",\"authors\":\"Hasan Acik, Yusuf Aydin\",\"doi\":\"10.2174/0118715303424962251204064911\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Hashimoto thyroiditis (HT) is an autoimmune disorder that leads to hypothyroidism. Selenium (Se) is essential for thyroid hormone metabolism and immune function, but its role in HT remains debated. This study investigates Se levels in HT patients and evaluates the impact of supplementation on thyroid autoimmunity and thyroid function.</p><p><strong>Methods: </strong>This retrospective study analyzed HT patients and healthy controls. Biochemical parameters, including Se, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibodies, were compared. Se-deficient HT patients (<80 µg/L) received selenium supplementation for six months. Paired t-tests and Spearman correlation analyses were used for statistical evaluation.</p><p><strong>Results: </strong>Among 270 HT patients and 350 controls, TSH levels were significantly elevated in HT (p<0.001), whereas Se levels showed no significant baseline difference (p=0.87). In Se-deficient patients (n=60), supplementation increased Se levels from 68.60±12.10 µg/L to 104.92±34.45 µg/L (p<0.001). However, anti-TPO and anti-Tg levels increased after treatment (p=0.01 and p=0.03, respectively). No significant changes were observed in TSH (p=0.27), FT3 (p=0.20), or FT4 (p=0.19). Se positively correlated with anti-TPO (r=0.36, p=0.0102) and negatively with FT3 (r=-0.39, p=0.0046).</p><p><strong>Discussion: </strong>Selenium supplementation restored serum Se levels but was unexpectedly associated with increased antibody titers. This finding contrasts with several randomized trials reporting antibody reduction, suggesting that baseline Se status, the form of supplementation, or differences in study design may account for the discrepancy. The observed correlations should be interpreted with caution.</p><p><strong>Conclusion: </strong>Selenium supplementation normalizes selenium status in HT patients, but its effects on thyroid autoimmunity and thyroid function remain uncertain. Long-term randomized controlled trials are needed to determine its therapeutic value.</p>\",\"PeriodicalId\":94316,\"journal\":{\"name\":\"Endocrine, metabolic & immune disorders drug targets\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2026-04-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Endocrine, metabolic & immune disorders drug targets\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/0118715303424962251204064911\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrine, metabolic & immune disorders drug targets","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0118715303424962251204064911","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Impact of Selenium Deficiency and Supplementation on Hashimoto's Thyroiditis: A Clinical Evaluation.
Introduction: Hashimoto thyroiditis (HT) is an autoimmune disorder that leads to hypothyroidism. Selenium (Se) is essential for thyroid hormone metabolism and immune function, but its role in HT remains debated. This study investigates Se levels in HT patients and evaluates the impact of supplementation on thyroid autoimmunity and thyroid function.
Methods: This retrospective study analyzed HT patients and healthy controls. Biochemical parameters, including Se, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibodies, were compared. Se-deficient HT patients (<80 µg/L) received selenium supplementation for six months. Paired t-tests and Spearman correlation analyses were used for statistical evaluation.
Results: Among 270 HT patients and 350 controls, TSH levels were significantly elevated in HT (p<0.001), whereas Se levels showed no significant baseline difference (p=0.87). In Se-deficient patients (n=60), supplementation increased Se levels from 68.60±12.10 µg/L to 104.92±34.45 µg/L (p<0.001). However, anti-TPO and anti-Tg levels increased after treatment (p=0.01 and p=0.03, respectively). No significant changes were observed in TSH (p=0.27), FT3 (p=0.20), or FT4 (p=0.19). Se positively correlated with anti-TPO (r=0.36, p=0.0102) and negatively with FT3 (r=-0.39, p=0.0046).
Discussion: Selenium supplementation restored serum Se levels but was unexpectedly associated with increased antibody titers. This finding contrasts with several randomized trials reporting antibody reduction, suggesting that baseline Se status, the form of supplementation, or differences in study design may account for the discrepancy. The observed correlations should be interpreted with caution.
Conclusion: Selenium supplementation normalizes selenium status in HT patients, but its effects on thyroid autoimmunity and thyroid function remain uncertain. Long-term randomized controlled trials are needed to determine its therapeutic value.