Proust-Lemoine Emmanuelle, d'Herbomez Michèle, Marchandise Xavier, Wémeau Jean-Louis
CHRU de Lille, hôpital Huriez, pôle d'endocrinologie, 59037 Lille cedex, France.
Presse Med. 2011 Jan;40(1 Pt 1):e1-8. doi: 10.1016/j.lpm.2010.06.018. Epub 2010 Oct 29.
Hypothyroidism can occur after radioiodine treatment for Graves' disease. It may happen precociously and transiently in the first year after treatment. The purpose of this study was to understand the mechanisms responsible for precocious hypothyroidism.
36 patients treated for Graves disease by radiodiodine were prospectively studied; The following variables were included in the analysis: age, gender, attendance for Graves' orbitopathy (GO), delay before radioiodine treatment, number of recurrences, previous treatments, corticosteroid therapy, thyroid mass, and (131)I dose. The titres of free T4 (FT4), thyroid-stimulating hormone (TSH), anti-TSH receptor antibodies (TRAb), anti-thyroid peroxydase antibodies (TPOAb) and anti-thyroglobulin antibodies (TGAb) were monitored. Thyroid stimulating (TSAb) and blocking (TBAb) antibodies were determined and (123)I uptake was measured when hypothyroidism occurred.
23 patients became precociously hypothyroid (group A) while 13 patients did not (group B). The initial TGAb titre was higher in group A (p=0.0024), and corticosteroid therapy was used more frequently to avoid aggravating GO in group B (p=0.0276). TPOAb and TGAb titres increased significantly only in group A (p=0.0112 and p=0.0202, respectively). When hypothyroidism occurred, TBAb was present in 13 patients. Transient hypothyroidism due to TBAb was observed in 1 patient. No iodide organification impairment was disclosed by the perchlorate test.
Radioinduced thyroiditis appears to be the main mechanism involved in the pathogenesis of precocious hypothyroidism. A higher TGAb titre before treatment is associated with precocious hypothyroidism, suggesting the prognostic value of TGAb. Transient hypothyroidism directly due to TBAb remains rare.
放射性碘治疗格雷夫斯病后可能发生甲状腺功能减退。在治疗后的第一年可能过早且短暂地出现。本研究的目的是了解导致过早甲状腺功能减退的机制。
对36例接受放射性碘治疗格雷夫斯病的患者进行前瞻性研究；分析中纳入以下变量：年龄、性别、格雷夫斯眼病（GO）就诊情况、放射性碘治疗前的延迟时间、复发次数、既往治疗、皮质类固醇治疗、甲状腺肿块和（131）I剂量。监测游离T4（FT4）、促甲状腺激素（TSH）、抗TSH受体抗体（TRAb）、抗甲状腺过氧化物酶抗体（TPOAb）和抗甲状腺球蛋白抗体（TGAb）的滴度。当发生甲状腺功能减退时，测定甲状腺刺激（TSAb）和阻断（TBAb）抗体，并测量（123）I摄取量。
23例患者过早出现甲状腺功能减退（A组），13例未出现（B组）。A组初始TGAb滴度较高（p = 0.0024），B组更频繁地使用皮质类固醇治疗以避免加重GO（p = 0.0276）。仅A组TPOAb和TGAb滴度显著升高（分别为p = 0.0112和p = 0.0202）。当发生甲状腺功能减退时，13例患者存在TBAb。1例患者观察到由TBAb引起的短暂性甲状腺功能减退。高氯酸盐试验未发现碘有机化障碍。
放射性甲状腺炎似乎是过早甲状腺功能减退发病机制中的主要机制。治疗前较高的TGAb滴度与过早甲状腺功能减退相关，提示TGAb的预后价值。直接由TBAb引起的短暂性甲状腺功能减退仍然罕见。
