Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations
Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations
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DOI：
10.1210/jc.87.4.1687
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发表时间：
2002-04-01
影响因子：
5.8
通讯作者：
Angstwurm, MWA
中科院分区：
文献类型：
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作者：
Gärtner, R;Gasnier, BCH;Angstwurm, MWA
在严重缺硒的地区，由于甲状腺细胞内依赖硒的谷胱甘肽过氧化物酶活性降低，甲状腺炎的发病率较高。依赖于硒的酶对免疫系统也有几种调节作用。因此，即使轻度缺硒也可能导致自身免疫性甲状腺疾病的发生和维持。我们对自身免疫性甲状腺炎和甲状腺过氧化物酶抗体(TPOAb)和/或甘油三酯抗体(TgAb)超过350IU/ml的女性患者(n=70，平均年龄47.5±0.7岁)进行了一项盲法、安慰剂对照的前瞻性研究。研究的主要终点是TPOAb浓度的变化。次要终点是TgAb、TSH和游离甲状腺激素水平的变化，以及甲状腺的超声模式和生活质量评估。患者被随机分成2个年龄和抗体(TPOAb)匹配的组；36例患者服用200杯(2.53摩尔)亚硒酸钠/d，连续3个月，34例患者接受安慰剂治疗。所有患者均用L-T-4替代，使TSH维持在正常范围。TPOAb、TgAb、TSH和游离甲状腺激素测定采用商业化方法。用高分辨率超声监测甲状腺的回声。平均TPOAb浓度在硒组显著降低至63.6%(P=0.013)，而在安慰剂组为88%(P=0.95)。对TPOAb高于1200IU/ml的患者进行的亚组分析显示，与安慰剂组TPOAb增加10%相比，硒治疗患者的TPOAb平均降低了40%。在研究开始时，安慰剂组的TgAb浓度较低，并进一步显著下降(P=0.018)，但在补硒组中没有变化。硒治疗组有9名患者的抗体浓度完全正常化，而安慰剂组有2名患者(经X(2)检验，P=0.01)。这些患者的甲状腺超声显示正常回声。两组患者的平均TSH、游离T-4和游离T-3水平均无明显变化，提示补硒可改善自身免疫性甲状腺炎患者的炎症活动，尤其是高活动度患者。这种效应是否只对自身免疫性甲状腺炎有效，或者对其他内分泌性自身免疫性疾病也有效，还有待研究。
In areas with severe selenium deficiency there is a higher incidence of thyroiditis due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells. Selenium-dependent enzymes also have several modifying effects on the immune system. Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases. We performed a blinded, placebo-controlled, prospective study in female patients (n = 70; mean age, 47.5 +/- 0.7 yr) with autoimmune thyroiditis and thyroid peroxidase antibodies (TPOAb) and/or Tg antibodies (TgAb) above 350 IU/ml. The primary end point of the study was the change in TPOAb concentrations. Secondary end points were changes in TgAb, TSH, and free thyroid hormone levels as well as ultrasound pattern of the thyroid and quality of life estimation. Patients were randomized into 2 age- and antibody (TPOAb)-matched groups; 36 patients received 200 mug (2.53 mumol) sodium selenite/d, orally, for 3months, and 34 patients received placebo. All patients were substituted with L-T-4 to maintain TSH within the normal range. TPOAb, TgAb, TSH, and free thyroid hormones were determined by commercial assays. The echogenicity of the thyroid was monitored with high resolution ultrasound. The mean TPOAb concentration decreased significantly to 63.6% (P = 0.013) in the selenium group vs. 88% (P = 0.95) in the placebo group. A subgroup analysis of those patients with TPOAb greater than 1200 IU/ml revealed a mean 40% reduction in the selenium-treated patients compared with a 10% increase in TPOAb in the placebo group. TgAb concentrations were lower in the placebo group at the beginning of the study and significantly further decreased (P = 0.018), but were unchanged in the selenium group. Nine patients in the selenium-treated group had completely normalized antibody concentrations, in contrast to two patients in the placebo group (by chi(2)test, P = 0.01). Ultrasound of the thyroid showed normalized echogenicity in these patients. The mean TSH, free T-4, and free T-3 levels were unchanged in both groups.We conclude that selenium substitution may improve the inflammatory activity in patients with autoimmune thyroiditis, especially in those with high activity. Whether this effect is specific for autoimmune thyroiditis or may also be effective in other endocrine autoimmune diseases has yet to be investigated.