Aizawa Y, Yoshida K, Kaise N, Fukazawa H, Kiso Y, Sayama N, Hori H, Abe K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Clin Endocrinol (Oxf). 1997 Jan;46(1):1-5. doi: 10.1046/j.1365-2265.1997.d01-1737.x.
Recovery of thyroid function in patients following hypothyroidism induced by 131I therapy for Graves' disease has been described, but only a few detailed clinical and biochemical studies of this phenomenon (transient hypothyroidism) have been published. The prevalence, mechanism, and final outcome of transient hypothyroidism in 260 patients with Graves' disease treated with 131I was studied.
A retrospective study.
Two hundred sixty patients with Graves' disease, treated with 131I between 1 and 15 years previously, were categorized into 4 groups according to their thyroid function during and 1 year after therapy (Group 1: permanent hypothyroidism, 28 patients; Group 2: transient hypothyroidism, 39 patients; Group 3: euthyroidism without transient hypothyroidism, 83 patients; Group 4: hyperthyroidism, 110 patients).
We compared total T4, total T3, TSH, anti-thyroglobulin (TGHA) and anti-microsomal (MCHA) antibodies, the TSH-binding inhibitory immunoglobulin (TBII) index, thyroid weight, dose of 131I, and 24-hour 131I uptake as pretreatment variables. The mean time for permanent hypothyroidism to develop was estimated by the Kaplan-Meier product limit method. The TBII index and thyroid stimulating antibody (TSAb) activity were measured in seven patients from Group 1 and in nine patients from Group 2 at the time that they became hypothyroid.
Hypothyroidism developing within 12 months of therapy was transient in 58% (39/67) of patients. No pretreatment variables were found to differ between patients with and without transient hypothyroidism. The mean estimated time between therapy and the development of permanent hypothyroidism was 96 months in Group 2; this time interval was significantly shorter than 126 months in Group 3 and 129 months in Group 4 (P < 0.05, P < 0.01, respectively). TSAb activity was > 500% In 78% (7/9) of patients from Group 2, which was significantly higher than that found (14%, 1/7) in Group 1.
These results indicate that (1) more than half the patients who developed hypothyroidism within 6 months after 131I treatment for Graves' disease recovered spontaneously, (2) TSAb activity might play some role in the recovery of transient hypothyroidism, and (3) the development of transient hypothyroidism may influence long-term thyroid function.
已有关于131I治疗格雷夫斯病所致甲状腺功能减退患者甲状腺功能恢复的描述，但关于这一现象（短暂性甲状腺功能减退）的详细临床和生化研究报道较少。本研究对260例接受131I治疗的格雷夫斯病患者短暂性甲状腺功能减退的患病率、机制及最终结局进行了研究。
一项回顾性研究。
260例曾在1至15年前接受131I治疗的格雷夫斯病患者，根据治疗期间及治疗后1年的甲状腺功能分为4组（第1组：永久性甲状腺功能减退，28例；第2组：短暂性甲状腺功能减退，39例；第3组：无短暂性甲状腺功能减退的甲状腺功能正常，83例；第4组：甲状腺功能亢进，110例）。
我们比较了总T4、总T3、促甲状腺激素（TSH）、抗甲状腺球蛋白（TGHA）和抗微粒体（MCHA）抗体、TSH结合抑制性免疫球蛋白（TBII）指数、甲状腺重量、131I剂量及24小时131I摄取率作为预处理变量。采用Kaplan-Meier乘积限界法估计永久性甲状腺功能减退发生的平均时间。在第1组的7例患者和第2组的9例患者出现甲状腺功能减退时，测量其TBII指数和甲状腺刺激抗体（TSAb）活性。
治疗后12个月内发生的甲状腺功能减退在58%（39/67）的患者中为短暂性。未发现有或无短暂性甲状腺功能减退患者之间的预处理变量存在差异。第2组治疗至永久性甲状腺功能减退发生的平均估计时间为96个月；该时间间隔显著短于第3组的126个月和第4组的129个月（分别为P<0.05，P<0.01）。第2组78%（7/9）的患者TSAb活性>500%，显著高于第1组（14%，1/7）。
这些结果表明，（1）131I治疗格雷夫斯病后6个月内发生甲状腺功能减退的患者中，半数以上可自发恢复；（2）TSAb活性可能在短暂性甲状腺功能减退的恢复中起一定作用；（3）短暂性甲状腺功能减退的发生可能影响长期甲状腺功能。
