[Skip to Content]
[Skip to Content Landing]
September 1975

Triiodothyronine-Induced Thyrotoxicosis in Ophthalmic Graves Disease

Author Affiliations

From the Thyroid Unit and Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston.

Arch Intern Med. 1975;135(9):1242-1244. doi:10.1001/archinte.1975.00330090114012

The origin of Graves disease remains elusive despite considerable experimental and speculative effort. Throughout the years, a series of ill-defined "stressful" situations have been implicated in its pathogenesis. The increased incidence of thyrotoxicosis during the German occupation of Denmark during World War II,1 as well as a host of noncontrolled clinical observations, suggest that psychological factors may be important determinants.2,3 In addition, the "metabolic stress" of rapid weight loss has been reported to precipitate thyrotoxicosis.4 Endogenous thyrotoxicosis, developing during or in the wake of thyroid hormone therapy, has been linked causally with this medication.5 Exacerbations of active thyrotoxicosis have been reported during triiodothyronine (T3) suppression testing.6,7

We report a case of endogenous thyrotoxicosis developing coincident with a T3 suppression test in a patient with ophthalmic Graves disease who was euthyroid at the onset of testing.

MATERIALS AND METHODS  Determinations of serum total thyroxine