硒缺乏和补充对桥本甲状腺炎的影响:临床评价。

IF 2
Hasan Acik, Yusuf Aydin
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引用次数: 0

摘要

桥本甲状腺炎(HT)是一种导致甲状腺功能减退的自身免疫性疾病。硒(Se)对甲状腺激素代谢和免疫功能至关重要,但其在HT中的作用仍有争议。本研究调查了HT患者的硒水平,并评估补充硒对甲状腺自身免疫和甲状腺功能的影响。方法:回顾性分析HT患者和健康对照者。比较血清硒、促甲状腺激素(TSH)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、抗甲状腺过氧化物酶(anti-TPO)、抗甲状腺球蛋白(anti-Tg)抗体等生化指标。结果:在270名HT患者和350名对照者中,HT患者的TSH水平显著升高。讨论:补充硒恢复了血清Se水平,但出乎意料地与抗体滴度增加相关。这一发现与几项报告抗体降低的随机试验形成对比,表明基线硒水平、补充形式或研究设计的差异可能是导致差异的原因。观察到的相关性应谨慎解释。结论:补充硒可使HT患者的硒状态恢复正常,但其对甲状腺自身免疫和甲状腺功能的影响仍不确定。需要长期随机对照试验来确定其治疗价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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