Shigemasa C, Mitani Y, Taniguchi S, Adachi T, Ueta Y, Urabe K, Miyazaki S, Tanaka T, Yoshida A, Mashiba H
First Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Arch Intern Med. 1990 May;150(5):1105-9.
Three patients with Graves' disease who spontaneously developed hypothyroidism after treatment with antithyroid drugs are described herein. Patient 1 developed a painful tender thyroid enlargement with a fever and accelerated erythrocyte sedimentation rate when she was receiving maintenance therapy with methimazole, and she progressed to persistent hypothyroidism with increased titers of antithyroglobulin and antimicrosomal antibodies and marked reduction of goiter size within the subsequent 2 months. Thyroid-stimulating hormone-binding inhibitory immunoglobulins (TBIIs) and thyroid stimulation-blocking antibody (TSBAb) were absent when she was hypothyroid. Hypothyroidism probably resulted from autoimmune thyroid destruction due to subacute aggravation of Hashimoto's thyroiditis. During the clinical course of patient 2, accelerated erythrocyte sedimentation rate and later transient increases of antimicrosomal and antithyroglobulin antibody titers were observed repeatedly (four times), and she finally fell into overt hypothyroidism. She also had negative results of tests for TBII and TSBAb. Her hypothyroidism appeared to result from repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis. Patient 3 fell into hypothyroidism when receiving a small dosage of methimazole. The TBII and TSBAb were strongly active when she developed hypothyroidism, which thus seemed to be due to blocking antibody. Patients with Graves' hyperthyroidism may eventually progress to hypothyroidism later by several different mechanisms. Severe and sudden or slowly repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis is one mechanism. Another may be the appearance of a blocking antibody to the TSH receptor.
本文描述了3例 Graves 病患者，他们在接受抗甲状腺药物治疗后自发发生了甲状腺功能减退。患者1在接受甲巯咪唑维持治疗时出现甲状腺肿大伴疼痛、压痛，发热，红细胞沉降率加快，随后2个月内进展为持续性甲状腺功能减退，抗甲状腺球蛋白和抗微粒体抗体滴度升高，甲状腺肿大小明显缩小。甲状腺功能减退时，促甲状腺激素结合抑制性免疫球蛋白（TBII）和甲状腺刺激阻断抗体（TSBAb）均为阴性。甲状腺功能减退可能是由于桥本甲状腺炎亚急性加重导致自身免疫性甲状腺破坏所致。在患者2的临床过程中，反复观察到红细胞沉降率加快，随后抗微粒体和抗甲状腺球蛋白抗体滴度短暂升高（4次），最终发展为明显的甲状腺功能减退。她的TBII和TSBAb检测结果也为阴性。她的甲状腺功能减退似乎是由于桥本甲状腺炎加重导致甲状腺反复破坏所致。患者3在接受小剂量甲巯咪唑治疗时出现甲状腺功能减退。发生甲状腺功能减退时，她的TBII和TSBAb活性很强，因此似乎是由于阻断抗体所致。Graves 病甲亢患者最终可能通过几种不同机制进展为甲状腺功能减退。桥本甲状腺炎加重导致严重且突然或缓慢反复的甲状腺破坏是一种机制。另一种可能是出现促甲状腺激素受体阻断抗体。
