Premachandra B N, Walfish P G
Am J Clin Pathol. 1982 Jul;78(1):63-8. doi: 10.1093/ajcp/78.1.63.
The effects of exogenous L-thyroxine therapy (0.2-0.3 mg/day) on spontaneously occurring thyroid hormone autoantibodies (THAA) and on serum levels of thyroxine (T4), triiodothyronine (T3) and reverse triiodothyronine (rT3) are described in a boy with lymphocytic thyroiditis. Prior to T4 medication, THAA bound virtually all thyroid hormones as noted by serum gamma globulin binding of tracer hormones. During T4 therapy, however, gamma globulin binding of tracer thyroid hormones decreased markedly. T4 and T3 levels as determined by radioimmunoassay (RIA) were grossly distorted prior to thyroxine therapy and bore no relation to clinical status, the single antibody technics yielding falsely low values whereas the double antibody procedures spuriously exaggerating serum hormone concentration. That spontaneously occurring THAA interfered in RIA hormone measurements was clearly shown by the lack of inconsistencies in laboratory and clinical evaluation when hormone determinations were performed in protein free serum extracts (to remove circulating THAA), or when RIAs were carried out in sera during thyroxine therapy when THAA were saturated by exogenous hormones. The thyroid stimulating hormone (TSH) level prior to therapy was 300 microunits/ml which decreases to less than 3 microunits/ml during T4 medication (0.3 mg/day). There was a gross inverse correlation between TSH secretion and T4 antibody saturation. The marked inhibition of antibody binding of tracer thyroid hormones observed during therapy suggested possible masking of thyroid hormone antibody activity during T4 treatment; experiments involving addition of tracer thyroid hormones to hormone stripped serums from thyroxine treated patients confirmed the hypothesis in two cases of hypothyroidism--one of which was diagnosed in the boy with chronic thyroiditis and the other a woman with postradioactive iodine-induced hypothyroidism. The pathophysiologic significance of thyroid hormone autoantibodies in the transport of thyroid hormones is briefly discussed.
本文描述了外源性左旋甲状腺素治疗（0.2 - 0.3毫克/天）对一名淋巴细胞性甲状腺炎男孩自发性甲状腺激素自身抗体（THAA）以及血清甲状腺素（T4）、三碘甲状腺原氨酸（T3）和反三碘甲状腺原氨酸（rT3）水平的影响。在进行T4药物治疗前，如通过示踪激素的血清γ球蛋白结合所显示，THAA几乎结合了所有甲状腺激素。然而，在T4治疗期间，示踪甲状腺激素的γ球蛋白结合显著减少。在甲状腺素治疗前，通过放射免疫测定（RIA）测定的T4和T3水平严重失真，与临床状况无关，单抗体技术得出的值虚假地低，而双抗体程序则虚假地夸大血清激素浓度。当在无蛋白血清提取物中进行激素测定（以去除循环中的THAA）时，或者在甲状腺素治疗期间当THAA被外源性激素饱和时进行RIA时，实验室和临床评估结果一致，这清楚地表明自发性THAA干扰了RIA激素测量。治疗前促甲状腺激素（TSH）水平为300微单位/毫升，在T4治疗（0.3毫克/天）期间降至低于3微单位/毫升。TSH分泌与T4抗体饱和度之间存在显著的负相关。治疗期间观察到的示踪甲状腺激素抗体结合的显著抑制表明，在T4治疗期间甲状腺激素抗体活性可能被掩盖；在两例甲状腺功能减退患者中，将示踪甲状腺激素添加到经甲状腺素治疗患者的激素去除血清中的实验证实了这一假设——其中一例是患有慢性甲状腺炎的男孩，另一例是放射性碘诱发甲状腺功能减退的女性。本文简要讨论了甲状腺激素自身抗体在甲状腺激素转运中的病理生理意义。
