Paschke R, Vogg M, Winter J, Wawschinek O, Eber O, Usadel K H
Service de Génétique Médicale, Faculté de Médicine, Université Libre de Bruxelles.
Autoimmunity. 1994;17(4):319-25. doi: 10.3109/08916939409010672.
Several lines of evidence support an etiological role of iodine for the initiation and perpetuation of autoimmune thyroid disease. However, varying relapse rates after increased iodine supplementation have been reported for Graves' disease. Furthermore the effects of iodine on the intensity of human autoimmune thyroiditis have previously only been investigated by indirect parameters and actions of iodine on thyroid function and a possible enhancement of the intrathyroidal autoimmune process in Graves' disease are difficult to separate in previous studies. Moreover lymphocytic thyroiditis in animal models has always been induced by considerably higher iodine doses as those used in in vivo studies. Therefore we investigated the effect of low and high iodine concentrations on the intensity of the intrathyroidal autoimmune process in Graves' disease. The intensity of intrathyroidal infiltration by lymphocytes, memory T cells, plasma cells and antigen presenting cells was determined by quantitative immunohistologic methods in 38 Graves' disease patients. 12 patients received additional preoperative iodine (group II) and 26 were treated with thiourelene antithyroid drugs only (group I). Urinary and intrathyroidal iodine concentrations were determined by a modified cer arsenite method in both groups. Application of high iodine doses in group II induced a significant increase of kappa and lambda positive plasma cells and interdigitating reticulum cells. This was not observed for activated T cells. There was no correlation between the extent of intrathyroidal infiltration by activated T cells, plasma cells and antigen presenting cells, and intrathyroidal or urinary iodine or intrathyroidal iodine concentrations in group I.(ABSTRACT TRUNCATED AT 250 WORDS)
多条证据支持碘在自身免疫性甲状腺疾病的起始和持续发展中具有病因学作用。然而,已有报道称,格雷夫斯病患者补充碘后复发率各异。此外,此前仅通过间接参数研究了碘对人类自身免疫性甲状腺炎强度的影响,且在以往研究中,碘对甲状腺功能的作用以及格雷夫斯病甲状腺内自身免疫过程可能的增强难以区分。此外,动物模型中的淋巴细胞性甲状腺炎一直是由比体内研究中使用的碘剂量高得多的剂量诱导的。因此,我们研究了低碘和高碘浓度对格雷夫斯病甲状腺内自身免疫过程强度的影响。通过定量免疫组织学方法,测定了38例格雷夫斯病患者甲状腺内淋巴细胞、记忆T细胞、浆细胞和抗原呈递细胞浸润的强度。12例患者术前额外补充碘(II组),26例仅接受硫脲类抗甲状腺药物治疗(I组)。两组均采用改良砷铈法测定尿碘和甲状腺内碘浓度。II组中高碘剂量的应用导致κ和λ阳性浆细胞以及交错突网状细胞显著增加。活化T细胞未出现这种情况。I组中活化T细胞、浆细胞和抗原呈递细胞的甲状腺内浸润程度与甲状腺内或尿碘或甲状腺内碘浓度之间无相关性。(摘要截断于250字)