Hypothyroidism followed by hyperthyroidism in a patient with I131 treated Graves disease Parallel changes in the properties of TSH-receptor antibodies

The serum of a patient with Graves disease was found to contain TSH receptor antibodies with TSH antagonist activity 1 year after 1131 therapy and at this time the patient was subclinically hypothyroid. One year later the patient was once again hyperthyroid and this was associated with a change in the serum TSH receptor antibody activity from blocking to stimulating. It is now well established that hyperthyroidism in Graves disease is caused by autoantibodies which bind to the TSH receptor and mimic the actions of TSR. TSH receptor antibodies with thyroid stimulating [TSH agonist] activity are detected in more than 90% of hyperthyroid Graves patients [1]. Occasionally TSH receptor antibodies fail to stimulate the thyroid and in some cases these types of antibody appear to behave as TSR antagonists, such antibodies have been described in Hashimoto's disease and primary myxoedema and have been associated with transient neonatal hypothyroidism[2]. TSR receptor antibodies with TSH antagonist properties have also been reported in two patients who had received 1131 therapy for Graves' disease[3]. We report a case of Graves' disease in which induced hypothyroidism was associated with TSR receptor antibodies with TSH antagonist properties and was followed by recurrent hyperthyroidism associated with TSH receptor antibodies with thyroid stimulating properties