title: [Three thyroid patients showing fluctuation of thyroid hormone autoantibody titers during long-term treatment].
abstract: Development and fluctuation of thyroid hormone autoantibody (THAA) titers were observed during long-term treatment of thyroid diseases in three patients. The presence of THAA was noticed by spuriously high serum free thyroid hormone levels measured with an analog tracer RIA (Amerlex-M FT3, FT4) in all three patients. Amerlex-M FT3 or FT4 levels gradually decreased to appropriate values for the clinical status according to the decreasing titers of THAA. Free thyroid hormone levels with radiolabeled antibody radioassay (Amerlex-MAB FT3, FT4) were not affected by the THAA and always reflected actual thyroid function. Case 1 was a 46-year-old man with untreated primary hypothyroidism. Auti-T4 autoantibody was detected in his serum. The 125I-T4 analog binding to the autoantibody (125I-T4 analog binding ratio) gradually declined after L-T4 therapy and finally almost disappeared two years and four months later. Amerlex-MAB FT4 level rose to the normal range two months after T4 therapy, but TSH level remained slightly elevated (5.4-13 microU/ml) for five months during T4 therapy. The 125I-T4 analog binding ratio and anti-Tg autoantibody (TgAb) titer were inversely correlated. Case 2 was a 72-year-old woman had received desiccated thyroid for a long time. Sequential changes of 125I-T4 analog binding ratio were very similar to those of TgAb titer. Case 3 was a 74-year-old woman with Graves' disease. She had been treated with methimazole (MMI) and desiccated thyroid for three years and five months. Ten months after stopping both drugs, anti-T3 autoantibody was detected. The 125I-T3 analog binding ratio was transiently elevated and gradually declined to reference range for four years during L-T4 therapy. 125I-T3 analog binding ratio and TgAb titer changed in a similar way. These results suggest that desiccated thyroid hormone therapy and TgAb formation are related to the development of THAA and that L-T4 therapy reduces the THAA titer.
authors.affiliation: Department of Nuclear Medicine, Kobe City General Hospital.
authors.forename: K
authors.initials: K
authors.lastname: Ikekubo
authors.forename: M
authors.initials: M
authors.lastname: Hino
authors.forename: Y
authors.initials: Y
authors.lastname: Saiki
authors.forename: M
authors.initials: M
authors.lastname: Kajikawa
authors.forename: N
authors.initials: N
authors.lastname: Hattori
authors.forename: T
authors.initials: T
authors.lastname: Ishihara
authors.forename: K
authors.initials: K
authors.lastname: Moridera
authors.forename: H
authors.initials: H
authors.lastname: Kurahachi
mesh_terms: D000368:Aged; D001323:Autoantibodies / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D013959:Thyroid Diseases / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D013961:Thyroid Gland / Q000503:physiopathology; D013963:Thyroid Hormones / Q000276:immunology* / Q000627:therapeutic use
chemical_list: D001323:Autoantibodies; D013963:Thyroid Hormones