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NOTE a Case of Graves' Disease with Anti-Triiodothyronine Antibodies The Endocrinol. Japon. 1985, 32 (1), 181-188 NOTE A Case of Graves' Disease with Anti-triiodothyronine Antibodies SHIGEKI SAKATA, TAKASHI KOMAKI, SHIGENORI NAKAMURA, KEITA KAMIKUBO, KAORU TAKAKUWA*, MASAAKI KAMETANI*, NAOKI TOKIMITSU*, AND KIYOSHI MIURA The Third Department of Internal Medicine, Gifu University School of Medicine, Gifu 500 *Department of Internal Medicine, Takayama Red Cross Hospital, Takayama 504 Abstract A case of Graves' disease with high serum thyroxine (T4) and low triiodo- thyronine (T3) levels which was therefore initially diagnosed as a T4-thyrotoxi- cosis is reported. Examination of the serum from the patient showed the presence of unusual protein which bound T3. It was later confirmed as IgG class anti-T3 anti- bodies. In addition to treatment with methylmercaptoimidazole (MMI), the patient was treated with prednisolone for 30 days (total amount 500mg). Titers of and-T3 antibodies in the sera were unchanged before and after prednisolone treatment. Our present case indicates that it is clinically important to bear the presence of autoantibodies in mind to account for a possible error in measuring T3 and T4 by radioimmunoassay (RIA). In the case that RIA determination gives an unexpectedly high or low T3 and/or T4 value, the presence of autoantibodies to them should be considered and a test for them is recommended. Circulating autoantibodies to thyroid mone in Hashimoto's thyroiditis. The ac- hormone have been reported in various cumulation of reports up to the present sug- thyroidal (Robbins et al., 1956; Ikekubo et gest that the spontaneous occurrence of al., 1978; Ginsberg et al., 1878; Jcbrgensen antibodies to T4 and/or T3 in man may not et al., 1979; Inada et al., 1980; Pearce et be a rare phenomenon, especially in patients al., 19 81) and nonthyroidal illnesses (Tri- with Hashimoto's thyroiditis. In Graves' marchi et al., 1982; Ordonez-Llanos et al., disease, however, only several cases with 1984). This was originally reported by autoantibodies to thyroid hormone have Robbins et al. (1956) in a patient with been so far reported (Staeheli et al., 1975; papillary carcinoma of the thyroid treated JOrgensen et al., 1979; Inada et al., 1980). with 131I. Later Premachandra et al. (1967) We wish to report here a patient with demonstrated autoantibodies to thyroid hor- Graves' disease associated with circulating anti-T3 IgG class antibodies. Received July 27, 1984 Enclocrinol. Japon. 182 SAKATA et al. February 1985 Table 1 Materials and Methods (A) Serum T4, T3, 3, 3', 5'-triiodothyronine (rT3), thyroid stimulating hormone (TSH) and thyro- xine binding globulin (TBG) in this patient were measured with commercially available RIA kits by single antibody (T4, T3, rT3: Dainabot RIA kit, TBG: RIA-gnost TBG, Hoechst) and by the double antibody method (T4, T3: Eiken RIA kit, TSH: Daiichi TSH kit). The normal range of T4, T3, rT3 and TBG are 4.5-13.0ƒÊg/dl, 90-210ng/dl, 177-368pg/ml and 17.0-23.0ƒÊg/ml, respectively. The normal range of TSH is below 8.0ƒÊU/ml. Anti-thyroglobulin antibodies were detected either with a commercially available hemagglutination kit (Thyroid test, Fuji Zoki) or by solid phase RIA using 125I-protein A developed and evaluated (B) in our laboratory (Sakata et al., 1983a). Anti- microsomal antibodies were examined with a commercially available kit (Microsome test, Fuji Zoki). In order to examine the presence of anti- thyroid hormone antibodies, 20ƒÊl of the patient's serum obtained 31 months after the beginning of the MMI treatment and a control serum were incubated with 380ƒÊl of 0.06 M barbital buffer, pH 8.6 with or without 120ƒÊg of 8-anilino-1- naphthalene sulfonic acid (ANS) and 100ƒÊl of 125I-T3(20pg)or 125I-T4(100pg)fbr 24 hours at 40℃, followed by precipitation with 12.5% polyethylene glycol(PEG, MW 7,500). Radio- activities of the precipitates were counted. Immunoglobulin fraction from the sera of the Table 1. Bir ding of 125I-T3 (A) and 125I-T4 (B) to the ƒÁ-globulin fraction of the presented patient. patient and healthy subjects was obtained by 125I-T3 (100pg precipitating 4 times weth 50% ammonium sul- , 31,000cpm) and 125I-T4 (500pg, fate, followed by extensive dialysis against phos- 45,000cpm) were added and co-precipitated 125I- T3 and 125I-T4 with 12.5%PEG were expressed phate-buffered saline (PBS, pH 7.4). The volume of the dialyzed fraction was diluted twice as the by both cpm bound and by percentage of bound original volume with PBS and kept frozen at radioactivities. Ni, N2, N3 represent three nor- mal controles. -20℃ until use . Ten microliters of immuno. globulin fraction thus obtained had approximately 0.04mg of ƒÁ-globulin as measured by paper electrophoresis. Twenty microliters of immuno- globulin fraction thus obtained from the patient examined in the following manner. Each 10 pl and two healthy subjects was incubated with 125I- of the serum from the patient was incubated with T3 and titrated with increasing amounts of rabbit 950 ƒÊl of 0.06 M barbital buffer, pH 8.6, which anti-human IgG which was raised in a rabbit contains 250 ƒÊg of ANS, 50ƒÊl of 125I-T3 and 50 (GI-1). After centrifugation, the precipitates were μl of cold T3 of various concentration.s. After washed twice with 0.15M NaCl and radioac- incubation for 24 hours at 25•Ž, equal amounts tivities were counted. of 25% PEG were added to each tube, followed The binding constants (Ka) and binding capa- by centrifugation. Then the radioactivities of cities of and-T3 antibodies in this patient were the precipitaes were counted and analyzed with Vol.32, No.1 GRAVES' DISEASE WITH ANTI-T3 ANTIBODIES 183 Scatchard's plots. 125I-T3 and 125I-T4 with speci- fic activities of 1160ƒÊCi/ƒÊg and 1250ƒÊCi/ƒÊg, res- pectively, were obtained from New Engl. Nucl. Protein A was purchased from Sigma Chemi- cals and radioiodinated with 125INa (Amersham, A UK) by the chloramine T method (Hunter and Greenwood., 1962). The specific activity of 125I protein A was 4-6ƒÊCi/ƒÊg. T4 and T3 were obtained from Sigma Chemicals and further purified with HPLC. The other chemicals em- ployed were all reagent grade. B Case A 45-year-old woman consulted the Takayama Red Cross Hospital in January 1979 complaining of swelling of the neck, finger tremor, palpitation, excessive sweating, weight loss and irregular menstrual cycles. She had been in good health until July 1978 when she began to notice symptoms. Her past history was non-contributory and the family history was negative for thyroidal C disorders. On physical examination, she was found to be 152cm tall and her weight was 55kg. Her pulse was 100/min and regular. Blood pressure was 138/70mmHg. Her skin was warm, moist and exophthalmos was present. Her eye changes were classified as class 2 according to the classification of the Ameri- can Thyroid Associations (Werner, 1969). Fig. 1. Thyroid function tests prior to (A), and The thyroid was symmetrically enlarged with after MMI treatment (C) and change in the a soft, smooth surface. Auscultation over concentration of T3, T4 and TSH (B) are the thyroid gland revealed a systolic mur- shown. mur. The 24-hour 131I-uptake of the thyroid in the patient was markedly increased nation technique (Thyroid test) was negative (96.2%). T4 and T3 measured by single while the solid phase RIA using 125I-protein antibody RIA were 24.1ƒÊg/d1 and 124ng/dl, A proved positive. respectively (Fig. 1). Her basal TSH was She was started on treatment with MMI 0.8ƒÊU/ml and did not respond for two 30mg daily and her T4 as well as T3 levels hours to the intravenous injection of 500ƒÊg dropped rapidly. The clinical course of the of TRH (TRH test). The concentration of patient is summarized in Fig. 1. After be- thyroxine binding globulin was in the normal ginning treatment with MMI, she occasional- range. The test for circulating anti-thyroglo ly showed T4 levels above the normal range bulin antibodies detected by the hemaggluti- and a constantly low T3 level. Serum TSH Endocrinol. Japon. 184 SAKATA et al. February 1985 levels were suppressed throughout the in- In Oct. 1981, because she was in slightly vestigation period. hyperthyroid, an needle biopsy of the thyroid Fig. 2. Histology of the thyroid g'and. of this patient obtained by neae biopsy. (H & E,•~100) Fig. 3. Binding of 125I-T3 (10,000cpm) and 125I- T4 (20,000cpm) to the serum from the patient presented and a normal control with_??_or without_??_addition of 120ƒÊg of ANS. Left panel indicates the bind- ing of 125I-T3 and right panel indicates the bind- ing of 125I-T4. Vol.32, No.1 GRAVES' DISEASE WITH ANTI-T3 ANTIBODIES 185 gland was done. Histologically, diffuse were slightly higher than those obtained hyperplasia of the follicular epithelial cells from a healthy subject. The addition of without lymphocytic infiltration was com- 120ƒÊg of ANS enhanced the coprecipitated patible with Graves' disease (Fig. 2). radioactivities of 125I-T3 and 125I-T4 to In Nov. 1981, since she still had high 28.8% and 8.9%, respectively. titers of anti-T3 antibodies, she was started Accordingly, 20ƒÊl of immunoglobulin on treatment with oral prednisolone, (30mg fraction from the patient and two healthy per day for 10 days, 15 mg for 10 days, subjects (N1, N2) were incubated with 125I- and 5mg for 10 days) and the titers of T3 and titrated with increasing amounts of anti-T3 antibodies before and after treatment rabbit anti-human IgG. Fig. 4 shows the were compared. titration data. The results clearly indicate that the patient had IgG class immuno- globulin with antibody activity predominant- Results ly to T3.
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