A Case of Graves' Disease in which Hypothyroidism First Developed, Followed by Hyperthyroidism, and Finally Hypothyroidism Recurred: A Four-year Follow up

Abstract

A 63-year-old female with a diffuse goiter was referred for evaluation of her thyroid function. When she visited the hospital in January 1991, her serum levels of free T3 (FT 3), free T4 (FT 4), and TSH were 3.1 pmol/l, 12 pmol/l, and less than 0.10 mU/l, respectively. Her thyroid function was thought to have changed from thyrotoxic to euthyroid or hypothyroid since she had been diagnosed as subclinically hyperthyroid at another clinic in November 1990. Her TSH level later increased to 83.2 mU/l. Treatment with T3 was started in March 1991. The T3 administration was terminated in January 1992, when her FT 4 level had increased to 8 pmol/l. Histological examination revealed the presence of chronic thyroiditis in January 1992. She developed mild hyperthyroidism in February 1992, followed by recurrent hypothyroidism in May 1993. The 24-hour thyroidal radioactive iodine uptake (RAIU) was 32.1% in March 1992. Treatment with T3 was restarted in June 1993. T3 therapy was replaced with T4 therapy in August 1994 since her FT 4 level remained low up to July 1994. Ultrasonography of the thyroid revealed diffuse low echogenicity in the hypothyroid state (January 1991 and March 1994). On the other hand, an ultrasonogram obtained during the mild hyperthyroid state (January 1993) showed echo levels increased in the anterior half of the thyroid. C-reactive protein (CRP) was positive at the first visit, in May 1993 when hypothyroidism recurred and in February and March 1994 when her thyroid function deteriorated. However, she did not complain of neck pain during the course of her illness. The results of TSH-binding inhibitor immunoglobulins (TBII) and thyroid-stimulating antibodies (TSAb) were strongly positive at her first visit. Their activities remained high through the end of 1991 and then gradually decreased, indicating that she had Graves' disease. Thyroid-stimulation-blocking antibodies (TSBAb) were not detected throughout the investigation period. The present findings indicate that her thyroid function changed depending on the balance between TSAb activities and the destructive changes in the thyroid. Inflammation might have played a role in the destruction of the thyroid.