Serial changes in thyroid-stimulating antibody and thyrotropin binding inhibitor immunoglobulin at the time of postpartum occurrence of thyrotoxicosis in Graves' disease.
Serial changes in thyroid-stimulating antibody and thyrotropin binding inhibitor immunoglobulin at the time of postpartum occurrence of thyrotoxicosis in Graves' disease.
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格雷夫斯病产后发生甲状腺毒症时促甲状腺抗体和促甲状腺素结合抑制剂免疫球蛋白的连续变化。
DOI：
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发表时间：
1987
影响因子：
5.8
通讯作者：
K. Miyai
中科院分区：
文献类型：
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作者：
H. Tamaki;N. Amino;M. Aozasa;M. Mori;O. Tanizawa;K. Miyai
本文对10例Graves病患者产后发病（n = 2）或复发（n = 8）时及5例缓解期无产后复发的Graves病患者进行了甲状腺刺激抗体（TSAb）和TSH结合抑制剂免疫球蛋白（TBII）的动态检测。TSAb通过使用FRTL-5细胞的灵敏的cAMP积累测定法测定，TBII通过放射受体测定法测定。在复发或新发产后甲亢患者中，血清游离T3指数（FT 3 I）均未在游离T4指数（FT 4 I）之前升高。在10例产后甲状腺毒症患者中，仅1例患者观察到血清FT 4 I和FT 3 I以及TSAb和TBII同时升高。6例患者TSAb和TBII在FT 4 I和FT 3 I之后升高。在1例患者中，TBII的增加与甲状腺毒症的发生有关，但1个月后TSAb增加。在其他2例患者中，TSAb增加后发生甲状腺毒症，但TBII随后增加。在这10例患者中，3例患者升高的血清FT 4 I和FT 3 I值自发下降，而TSAb和TBII水平持续升高。5例Graves病患者产后未复发，TSAb、TBII均无阳性或增高。这些数据表明，产后Graves'甲状腺毒症的开始并不总是与循环抗TSH受体抗体的增加有关，这些参数是甲状腺功能的不良指标。甲状腺内体液或细胞介导的免疫机制也可能参与介导Graves病的甲状腺毒症。
Thyroid-stimulating antibody (TSAb) and TSH binding inhibitor immunoglobulin (TBII) were measured serially in 10 patients with Graves' disease at the time of postpartum onset (n = 2) or relapse (n = 8) of Graves' thyrotoxicosis and in 5 patients with Graves' disease who were in remission and had no postpartum relapse of Graves' thyrotoxicosis. TSAb was measured by a sensitive cAMP accumulation assay using FRTL-5 cells, and TBII was determined by radioreceptor assay. In no patient with either recurrent or new onset postpartum hyperthyroidism did the serum free T3 index (FT3I) rise before the free T4 index (FT4I). Of the 10 patients who had postpartum thyrotoxicosis, concomitant increases in serum FT4I and FT3I, and TSAb and TBII were observed in only 1 patient. Increases in TSAb and TBII after those in FT4I and FT3I occurred in 6 patients. In 1 patient, an increase in TBII was associated with the occurrence of thyrotoxicosis, but TSAb increased 1 month later. In the other 2 patients, a TSAb increase was followed by the development of thyrotoxicosis, but TBII increased later. In 3 of these 10 patients, the increased serum FT4I and FT3I values decreased spontaneously, whereas the TSAb and TBII levels increased continuously. No positive test or increase in TSAb or TBII was found in the 5 patients with Graves' disease who did not have a postpartum relapse of thyrotoxicosis. These data indicate that postpartum initiation of Graves' thyrotoxicosis is not always associated with an increase in circulating anti-TSH receptor antibodies and that such parameters are poor indicators of thyroid function. Intrathyroidal humoral or cell-mediated immunological mechanisms may also be involved in mediating thyrotoxicosis in Graves' disease.