日髙 尚子^{1, 2}, 南方 瑞穂^{1, 3}, 重田 真幸¹, 貴田岡 正史⁴

Naoko HIDAKA^{1, 2}, Mizuho MINAKATA^{1, 3}, Masayuki SHIGETA¹, Masafumi KITAOKA⁴

¹公立昭和病院糖尿病・内分泌内科, ²災害医療センター糖尿病・内分泌内科, ³自衛隊中央病院代謝内科, ⁴イムス三芳総合病院内分泌・代謝センター

¹Department of Diabetes and Endocrinology, Showa General Hospital, ²Department of Diabetes and Endocrinology, National Hospital Organization Disaster Medical Center, ³Department of Endocrinology and Metabolism, Self-Defense Forces Central Hospital, ⁴Endocrinology and Metabolism Center, IMS Miyoshi General Hospital

キーワード : painless thyroiditis, Graves’ disease, anti-TSH receptor antibody, thyroid blood flow

66歳，女性．約17年前にバセドウ病が寛解し，その後抗サイログロブリン抗体が陽性になり慢性甲状腺炎への移行を疑った．機能異常はなく経過観察していたが，今回偶発的に出現した甲状腺のびまん性腫大，エコーレベルの低下から無痛性甲状腺炎が疑われた．その後長期的な甲状腺機能低下症へ移行してホルモン補充を要した．無痛性甲状腺炎としては例外的に，抗TSH受容体抗体（TRAb）が経過を通して強陽性であった．刺激抗体（TSAb）は経過中に低下し（3,930％→127％），刺激阻害型抗体（TSBAb）は最終観察時102.7％と高値であった．14ヵ月にわたる経過を超音波検査で追ったところ，非典型的な血流所見を認めた．一般に無痛性甲状腺炎では，主にTSHの作用により，炎症極期は甲状腺血流の低下，回復期は血流の亢進を認める．一方，本症例では炎症極期は血流が亢進，回復期は低下し，TSAbとTSBAbの変化が関与したと考えられた．甲状腺自己抗体が経時的に変化し病態を複雑化させることはこれまでも報告されてきたが，超音波検査で血流所見を含めて詳細に検討した報告は稀である．甲状腺自己免疫疾患の病態は多彩で，病態が錯綜している症例では血液検査に加えて超音波所見を考察することが病態把握のために重要と考えられた．

A 66-year-old female developed chronic thyroiditis with positive conversion of anti-thyroglobulin antibody 17 years after remission of Graves’ disease. She had been euthyroid and did not need hormonal replacement. At a follow-up visit, diffuse goiter and a broad low echoic region were incidentally identified on ultrasonography, and painless thyroiditis (PT) was suspected. She remained hypothyroid for 6 months, and levothyroxine administration was started. Contrary to the general course of PT, her anti-TSH receptor antibody (TRAb) level was exceptionally high. Thyroid-stimulating antibody (TSAb) level decreased during a follow-up period of 14 months (3,930%→127%), and TSH-stimulation blocking antibody (TSBAb) was extremely high (102.7%) at the last examination. Echography showed atypical findings of thyroid blood flow. In PT, the blood flow is generally decelerated during the acute phase and accelerated during the recovery phase, due to the action of thyrotropin. This case presented the opposite pattern; acceleration in the acute phase and deceleration in the recovery phase, probably caused by the change in TSAb and TSBAb levels. There have been some reports in which thyroid autoantibodies changed over time, complicating the disease state. However, there have been no reports of sonographic changes in blood flow. This case demonstrates the importance of echography in conjunction with serologic markers in proper assessment of autoimmune thyroid disease.