Gamstedt A, Karlsson A
Department of Internal Medicine, Orebro Medical Center Hospital, Sweden.
J Clin Endocrinol Metab. 1991 Jul;73(1):125-31. doi: 10.1210/jcem-73-1-125.
The effects of betamethasone on thyroid autoantibody responses and outcome of radioiodine therapy were determined over a period of 1 yr in a prospective randomized study of 40 patients with Graves' disease. Twenty patients were given placebo tablets, and 20 patients were treated with beta-methasone from 3 weeks before until 4 weeks after 131I therapy. At the time of inclusion in the study, the mean serum concentrations of TSH receptor antibodies, thyroid peroxidase antibodies, and thyroglobulin antibodies (TgAb) were increased in both groups. Three weeks of treatment with betamethasone reduced the thyroid peroxidase antibody and TgAb titers as well as the serum concentrations of thyroid hormones. A decrease in the TSH receptor antibody level was not statistically significant. After radioiodine therapy, transient increases in thyroid autoantibody levels were observed. The titers of the different antibodies generally changed in parallel. In some patients a detectable level of a given antibody was found only after the radioiodine treatment, and in two cases, TgAb did not appear at all, although the two other antibodies increased temporarily. Betamethasone delayed, but did not abolish, the 131I-induced antibody peaks. Betamethasone also caused a reduction in the total serum immunoglobulin G, a reduction which persisted throughout the study period. When the study ended, 17 patients given placebo and 9 patients given betamethasone (P less than 0.001) were receiving replacement therapy due to the development of hypothyroidism. These patients at this point in time had lower antibody levels than those not requiring T4. The results of this study demonstrate that betamethasone reduces and modifies the thyroid autoantibody responses as well as the outcome of radioiodine therapy in patients with Graves' disease. From a clinical point of view, these effects may be in opposite directions.
在一项对40例格雷夫斯病患者进行的为期1年的前瞻性随机研究中，确定了倍他米松对甲状腺自身抗体反应和放射性碘治疗结果的影响。20例患者服用安慰剂片，20例患者在131I治疗前3周直至治疗后4周接受倍他米松治疗。纳入研究时，两组患者促甲状腺激素受体抗体、甲状腺过氧化物酶抗体和甲状腺球蛋白抗体（TgAb）的平均血清浓度均升高。倍他米松治疗3周可降低甲状腺过氧化物酶抗体和TgAb滴度以及甲状腺激素的血清浓度。促甲状腺激素受体抗体水平的降低无统计学意义。放射性碘治疗后，观察到甲状腺自身抗体水平短暂升高。不同抗体的滴度通常平行变化。在一些患者中，仅在放射性碘治疗后才发现特定抗体的可检测水平，在两例患者中，TgAb根本未出现，尽管另外两种抗体暂时升高。倍他米松延迟但并未消除131I诱导的抗体峰值。倍他米松还导致血清总免疫球蛋白G降低，这种降低在整个研究期间持续存在。研究结束时，17例服用安慰剂和9例服用倍他米松的患者（P<0.001）因甲状腺功能减退的发生而接受替代治疗。此时，这些患者的抗体水平低于不需要T4的患者。本研究结果表明，倍他米松可降低并改变格雷夫斯病患者的甲状腺自身抗体反应以及放射性碘治疗的结果。从临床角度来看，这些影响可能是相反的。
