补碘对缺碘机体甲状腺自身免疫的影响

目的 探讨补碘对缺碘机体甲状腺自身免疫的影响。方法 动态观察缺碘地区居民口服碘油补碘前后、血清免疫球蛋白（IgA、IgG、IgM）、补体C3、甲状腺过氧化物酶抗体（TPOAb)、甲状腺球蛋白抗体（TGAb)、促甲状腺激素受体抗体（TRAb)和甲状腺刺激抗体（TSAb)水平变化及其异常值检出率。结果 补碘3个月后IgA、IgG、补体C3水平明显高于补碘前的水平，IgG和C3高于正常值上限的比例分别高达38．9％、62．0％，6个月时IgA和IgG水平则明显下降。补碘之后的TPOAb、TGAb水平及其阳性检率均明显高于补碘前，且以3个月和6个月时增高较为显著并分别在79和64例受试者中出现7例双抗体阳性病例；这些抗体阳性者全为成年女性，平均年龄27．6岁，均无明显临床症状。TRAb和TSAb水平也均明显高于补碘前，12个月时TRAb的阳性检出率高达24.4%。结论 补碘可诱发缺碘机体免疫反应使免疫功能增强，存在产生自身抗体的倾向，导致甲状腺自身抗体水平明显升高、抗体阳性检出率增加，而易于产生亚临床性自身免疫性甲状腺疾病。

Effects of supplying iodine on thyroid autoimmunity in iodine deficiency subjects

Objective To study the effects of supplying iodine on thyroid autoimmunity in iodine deficiency subjects. Methods The levels and abnormal rates of immunoglobulins (IgA, IgG, IgM), complement C 3, and thyroid autoantibodies such as thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb), thyrotropin receptor antibody (TRAb) and thyroid stimulating antibody(TSAb) were observed in inhabitants in iodine deficiency area before and after oral iodized oil capsules were administered. Results The levels of IgA, IgG and C 3 increased after iodine supplying for three months, the proportions of IgG and C 3 which exceeded upper limit of the normal range reached to 38..9% and 62.0% respectively. The levels of IgA and IgG began to decrease markedly six months after iodine supplying. The levels of TPOAb, TGAb and their positive rates after iodine supplying were all higher than those before administration, and reached the highest level between three to six months after iodine supplement. And 7 cases out of 79 or 64 subjects with 2 kinds of positive autoantibodies were observed 3 or 6 months after iodine supplying respectively. The cases were all adult women with the average age of 27.6 yr, and had no clinical symptoms. The levels of TRAb and TSAb after iodine supplying were much higher than that before iodine supplying. The rate of positive TRAb was increasedmarkedlyandreachedto24.4% twelve months later. Conclusion Iodine supplying for the subjects with iodine deficiency seems to induce immune reaction, increase the levels of autoantibodies, and might develop autoimmune thyroid diseases.