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抗独特型甲状旁腺激素抗体作为特发性甲状旁腺功能减退症中免疫反应性甲状旁腺激素升高的原因:第二例病例——自身免疫性内分泌疾病的另一种表现?

Antiidiotypic PTH antibodies as a cause of elevated immunoreactive parathyroid hormone in idiopathic hypoparathyroidism, a second case: another manifestation of autoimmune endocrine disease?

作者信息

McElduff A, Lackmann M, Wilkinson M

机构信息

Department of Endocrinology, Royal North Shore Hospital, St. Leonards, NSW, Australia.

出版信息

Calcif Tissue Int. 1992 Aug;51(2):121-6. doi: 10.1007/BF00298499.

Abstract

A 69-year-old man became hypocalcemic under medical observation. The hypocalcemia occurred in the presence of circulating immunoreactive parathyroid hormone (PTH). Common causes of secondary hyperparathyroidism were excluded, as was PTH resistance using PTH infusions. The immunoreactive PTH was examined in detail. PTH immunoreactivity (1) was not retained on a C18 SPE-column, suggesting unusual molecular or physicochemical properties, unlike bona fide PTH; (2) was precipitated with 15% PEG, indicating a molecular size far in excess of native PTH; (3) had an apparent molecular size similar to immunoglobulins on size exclusion chromatography; (4) was retained on affinity chromatography with both Protein A and anti-hIgG antibodies. These data lead us to conclude that the immunoreactive PTH was due to antiidiotypic PTH autoantibodies. No significant quantities of true PTH were found in the patient's serum suggesting that his hypoparathyroidism was a result of PTH deficiency. Autoimmunity might explain the occurrence of both processes if an arrested antiidiotypic antibody cascade is assumed.

摘要

一名69岁男性在医学观察期间出现低钙血症。低钙血症发生时循环中的免疫反应性甲状旁腺激素(PTH)存在。继发性甲状旁腺功能亢进的常见原因被排除,使用PTH输注也排除了PTH抵抗。对免疫反应性PTH进行了详细检查。PTH免疫反应性:(1)在C18固相萃取柱上不保留,提示其分子或物理化学性质异常,与真正的PTH不同;(2)用15%聚乙二醇沉淀,表明其分子大小远超过天然PTH;(3)在尺寸排阻色谱上的表观分子大小与免疫球蛋白相似;(4)在蛋白A和抗人IgG抗体的亲和色谱上保留。这些数据使我们得出结论,免疫反应性PTH是由于抗独特型PTH自身抗体所致。在患者血清中未发现大量真正的PTH,提示其甲状旁腺功能减退是PTH缺乏的结果。如果假设抗独特型抗体级联反应受阻,自身免疫可能解释这两个过程的发生。

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