PMID- 10319947 OWN - NLM STAT- MEDLINE DCOM- 19990617 LR - 20081121 IS - 1050-7256 (Print) IS - 1050-7256 (Linking) VI - 9 IP - 4 DP - 1999 Apr TI - Two Graves' disease patients who spontaneously developed hypothyroidism after antithyroid drug treatment: characteristics of epitopes for thyrotropin receptor antibodies. PG - 393-9 AB - Few reports have identified blocking thyrotropin receptor antibodies (TSHRAbs) as a pathogenic mechanism explaining spontaneous hypothyroidism after antithyroid drug (ATD) treatment of Graves' disease. Here we report 2 Graves' patients who showed different courses of hypothyroidism after ATD treatment. The first patient had Graves' hyperthyroidism and was treated with ATD for 1 year. After a short period of euthyroidism, she developed permanent hypothyroidism with blocking TSHRAb. The second patient became euthyroid after 1 year of ATD treatment. After 3 years, however, she presented with hypothyroidism with blocking TSHRAb activity. Her hypothyroidism was transient, and restoration of euthyroidism was followed by disappearance of blocking TSHRAb. Blocking and stimulating TSHRAbs activities of these 2 patients were serially measured using Chinese hamster ovary (CHO) cells transfected with wild-type human TSHR (CHO-hTSHR) and 2 TSHR chimeras with residues 8-165 (Mc1+2) or 90-165 (Mc2) substituted by equivalent residues of the luteinizing hormone/chorionic gonadotropin receptor (LH/CGR). During their hypothyroid phases, blocking TSHRAbs activities were positive in all 3 kinds of assays and stimulating TSHRAbs activities were negative in CHO-hTSHR or in Mc 1+2 assay. Mc2 stimulating TSHRAb activity was detected in sera of hypothyroid phase of the second patient who had transient hypothyroidism but not in the first whose hypothyroidism was permanent. In these 2 cases, we demonstrate the causative role of blocking TSHRAb in the development of hypothyroidism after ATD treatment in Graves' patients. Interestingly, the difference in the course of blocking TSHRAb-induced hypothyroidism was associated with the difference in epitope reactivities of TRAb during hypothyroid phase that developed after ATD treatment of Graves' disease. FAU - Chung, H K AU - Chung HK AD - Department of Internal Medicine, Seoul National University College of Medicine, Korea. FAU - Kim, W B AU - Kim WB FAU - Park, D J AU - Park DJ FAU - Kohn, L D AU - Kohn LD FAU - Tahara, K AU - Tahara K FAU - Cho, B Y AU - Cho BY LA - eng PT - Case Reports PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Thyroid JT - Thyroid : official journal of the American Thyroid Association JID - 9104317 RN - 0 (Antibodies) RN - 0 (Antithyroid Agents) RN - 0 (Autoantibodies) RN - 0 (Epitopes) RN - 0 (Immunoglobulins, Thyroid-Stimulating) RN - 0 (Receptors, Thyrotropin) RN - 0 (thyrotropin-binding inhibitory immunoglobulin) SB - IM MH - Adult MH - Animals MH - Antibodies/analysis/immunology MH - Antithyroid Agents/*therapeutic use MH - Autoantibodies/blood MH - CHO Cells MH - Chimera MH - Cricetinae MH - Epitopes/immunology MH - Female MH - Graves Disease/*drug therapy MH - Humans MH - Hypothyroidism/*etiology/immunology MH - Immunoglobulins, Thyroid-Stimulating MH - Microsomes/immunology MH - Receptors, Thyrotropin/blood/genetics/immunology/metabolism EDAT- 1999/05/13 00:00 MHDA- 1999/05/13 00:01 CRDT- 1999/05/13 00:00 PHST- 1999/05/13 00:00 [pubmed] PHST- 1999/05/13 00:01 [medline] PHST- 1999/05/13 00:00 [entrez] AID - 10.1089/thy.1999.9.393 [doi] PST - ppublish SO - Thyroid. 1999 Apr;9(4):393-9. doi: 10.1089/thy.1999.9.393.