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Original Article Change in Thyroid Autoantibodies According to the Clinical Course of Painless Thyroiditis Excluding Postpartum Thyroiditis.
Ihn Suk Lee, Young Suk Jo, Bon Jeong Ku, Minho Shong, Young Kun Kim, Heung kyu Ro
Endocrinology and Metabolism 2008;23(4):245-252
DOI: https://doi.org/10.3803/jkes.2008.23.4.245
Published online: August 1, 2008
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1Department of Internal Medicine, Chungnam National University, College of Medicine, Korea.
2Department of Internal Medicine, Eulji University, College of Medicine, Korea.

BACKGROUND
Painless thyroiditis is characterized by painless, destructive inflammation of the thyroid gland. Although thyroid autoantibodies are frequently detected in patients suffering from this condition, the clinical significance of these antibodies is not well understood. Therefore, this study was conducted to investigate the relationship between thyroid function and thyroid autoantibodies in painless thyroiditis according to clinical course. METHODS: Patients proven to have painless thyroiditis were retrospectively included in this study. We analyzed their clinical features, thyroid function and titers of thyroid autoantibodies according to clinical course, which was divided into three phases; thyrotoxic, hypothyroid and recovery. RESULTS: Of the 21 patients included in this study, 2 were male and 19 were female. During the thyrotoxic phase, the mean free T4 concentration was 4.03 (2~6.8) ng/mL and the mean concentration of thyroid stimulating hormone (TSH) was 0.02 (0.01~0.07) U/mL. In addition, the titer of antithyroglobulin antibody and antithyroid peroxidase antibody was 298 (4.8~995) U/mL and 3318 (0.1~25280) U/mL, respectively during this phase. During the hypothyroid phase, the mean TSH was 16.3 (4.3-49.5) U/mL and was found to be positively correlated with the level of free T4 observed during the thyrotoxic phase (r = 0.523, P = 0.031). During the recovery phase, the titer of antithyroglobulin antibody was significantly reduced to 180 (38~487) U/mL when compared with the titer taken during the thyrotoxic phase (P = 0.016). Additionally, during the hypothyroid phase, patients found to have antithyroid peroxidase antibody had a higher titer of TSH than those that did not (23.9 (6.5~49.5) vs. 11.2 (5.3~18.2) U/mL, P = 0.004). CONCLUSION: The titer of free T4 and the presence of antithyroid peroxidase observed during the thyrotoxic phase were related to the titer of TSH during hypothyroid phase. Additionally, the titer of antithyroglobulin antibody was significantly reduced during the recovery phase.

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