Ikekubo K, Hino M, Saiki Y, Kajikawa M, Hattori N, Ishihara T, Moridera K, Kurahachi H
Department of Nuclear Medicine, Kobe City General Hospital.
Nihon Naibunpi Gakkai Zasshi. 1995 Jul 20;71(5):695-708. doi: 10.1507/endocrine1927.71.5_695.
Development and fluctuation of thyroid hormone autoantibody (THAA) titers were observed during long-term treatment of thyroid diseases in three patients. The presence of THAA was noticed by spuriously high serum free thyroid hormone levels measured with an analog tracer RIA (Amerlex-M FT3, FT4) in all three patients. Amerlex-M FT3 or FT4 levels gradually decreased to appropriate values for the clinical status according to the decreasing titers of THAA. Free thyroid hormone levels with radiolabeled antibody radioassay (Amerlex-MAB FT3, FT4) were not affected by the THAA and always reflected actual thyroid function. Case 1 was a 46-year-old man with untreated primary hypothyroidism. Auti-T4 autoantibody was detected in his serum. The 125I-T4 analog binding to the autoantibody (125I-T4 analog binding ratio) gradually declined after L-T4 therapy and finally almost disappeared two years and four months later. Amerlex-MAB FT4 level rose to the normal range two months after T4 therapy, but TSH level remained slightly elevated (5.4-13 microU/ml) for five months during T4 therapy. The 125I-T4 analog binding ratio and anti-Tg autoantibody (TgAb) titer were inversely correlated. Case 2 was a 72-year-old woman had received desiccated thyroid for a long time. Sequential changes of 125I-T4 analog binding ratio were very similar to those of TgAb titer. Case 3 was a 74-year-old woman with Graves' disease. She had been treated with methimazole (MMI) and desiccated thyroid for three years and five months. Ten months after stopping both drugs, anti-T3 autoantibody was detected. The 125I-T3 analog binding ratio was transiently elevated and gradually declined to reference range for four years during L-T4 therapy. 125I-T3 analog binding ratio and TgAb titer changed in a similar way. These results suggest that desiccated thyroid hormone therapy and TgAb formation are related to the development of THAA and that L-T4 therapy reduces the THAA titer.
观察了3例甲状腺疾病患者长期治疗过程中甲状腺激素自身抗体(THAA)滴度的变化及波动情况。在这3例患者中,采用模拟示踪剂放射免疫分析法(Amerlex-M FT3、FT4)测定血清游离甲状腺激素水平时发现存在THAA。随着THAA滴度降低,Amerlex-M FT3或FT4水平根据临床状况逐渐降至适当值。放射性标记抗体放射免疫分析法(Amerlex-MAB FT3、FT4)检测的游离甲状腺激素水平不受THAA影响,始终反映实际甲状腺功能。病例1为一名46岁未接受治疗的原发性甲状腺功能减退男性。在其血清中检测到抗T4自身抗体。左旋甲状腺素(L-T4)治疗后,与自身抗体结合的125I-T4类似物(125I-T4类似物结合率)逐渐下降,最终在两年零四个月后几乎消失。T4治疗两个月后,Amerlex-MAB FT4水平升至正常范围,但在T4治疗期间,促甲状腺激素(TSH)水平在五个月内仍略有升高(5.4 - 13微单位/毫升)。125I-T4类似物结合率与抗甲状腺球蛋白自身抗体(TgAb)滴度呈负相关。病例2为一名72岁长期接受甲状腺干粉治疗的女性。125I-T4类似物结合率的连续变化与TgAb滴度的变化非常相似。病例3为一名74岁患有格雷夫斯病的女性。她接受甲巯咪唑(MMI)和甲状腺干粉治疗三年零五个月。停用两种药物十个月后,检测到抗T3自身抗体。在L-T4治疗期间,125I-T3类似物结合率短暂升高,随后四年逐渐降至参考范围。125I-T3类似物结合率和TgAb滴度变化方式相似。这些结果表明,甲状腺干粉激素治疗和TgAb形成与THAA的发生有关,且L-T4治疗可降低THAA滴度。