The Occurrence of Thyrotropin Binding-Inhibiting Immunoglobulins and Thyroid-Stimulating Antibodies in Patients with Silent Thyroiditis
Authors:
- Hajime TamaiHTHajime Tamai
- Akira OshimaAOAkira Oshima
- Toshio MukutaTMToshio Mukuta
- Shuji FukataSFShuji Fukata
- Kanji KumaKKKanji Kuma
- Lindy F. KumagaiLKLindy F. Kumagai
- Shigenobu NagatakiSNShigenobu Nagataki
- 1 October 1990
- journal article
- research article
- Published by The Endocrine Society in The Journal of Clinical Endocrinology & Metabolism
- Vol. 71 (4) , 1051-1055
Abstract
Silent (painless) thyroiditis has been recognized as a clinical entity for over a decade and is characterized by spontaneously resolving thyrotoxicosis. Its etiology is uncertain; however, a few reports have indicated the occurrence of TSH binding-inhibiting immunoglobulins (TBII) and thyroid-stimulating antibodies (TSAb) in some of the patients. The present study was undertaken to evaluate thyroid function and the occurrence of TBII and TSAb and thyroid autoantibodies (antithyroglobulin and antimicrosomal) in 53 patients with silent thyroiditis during the course of their disease. The patients were divided into 2 major groups: I) those who developed transient hypothyroidism and II) those who did not. All patients initially had significantly increased concentrations of serum T4, free T4, and free T3, suppressed TSH levels, and decreased thyroid radioiodine uptake. TBII and TSAb were initially positive in 8 (15.1%) and 10 patients (18.9%), respectively. Forty patients were available for follow-up. TBII was positive in 6 of 24 (25.0%), and TSAb was positive in 8 of 24 (33.3%) of the patients who developed transient hypothyroidism during the course of their disease. Among the patients who did not become hypothyroid at any time, TBII was positive in only 2 of 16 (12.5%), and none of the patients became TSAb positive. The findings indicate that increased TSAb and TBII activity may be detected in patients with silent thyroiditis and, when present, are associated with transient hypothyroidism during the course of the disease.Keywords
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