Hyperthyroidism is most commonly seen in Grave's disease, Hashimoto's thyroiditis, or following inflammation of the thyroid. We have identified a patient in whom transient hyperthyroidism presented during the acute phase of an Hydralazine-induced lupus erythematous (LE) syndrome. This association has not been previously described. A 15 year old female with pyelonephritis and hypertension on Hydralazine, Propranolol and diuretics presented with a one month history of 20 lbs weight loss, amenorrhea and polyarthralgia. On physical examination: HR 110/min, non-tender, symmetric goitre (3X N), and synovitis of wrists and knees. On investigation: ESR 103, LE Prep positive, DNA binding positive, ANF >1:1280, and complement levels normal. Serum T4 was 17 μgm/dl (N 4-12), total T3 160 ng/dl (N 90-220), T3 resin uptake 37% (N 25-35), TSH <1 μU/m1 (N <10). I131 uptake was depressed: 2 hrs, 2.1% (N 3-9); 24 hrs, 4.9% (N 5-25). The patient's serum was negative for thyroid stimulating immunoglobulin (TSI), anti-thyroglobulin and anti-microsomal antibodies. Off Hydralazine, the synovitis rapidly resolved and three months later without anti-thyroid therapy, she appeared completely normal with regain in her weight and reappearance of menses. Her T4 was 5.8 μgm/dl, TSH 4.2 μU/ml. The parallel courses of the LE syndrome and the hyperthyroidism imply a common etiology. Depression of I131 uptake and absence of TSI suggest an inflammatory process, while absence of specific thyroid antibodies make Hashimoto's disease unlikely. We conclude that hyperthyroidism may be a feature of the LE syndrome caused by Hydralazine.