THYROTOXICOSIS DUE TO PITUITARY RESISTANCE TO THYROID-HORMONES - SUCCESSFUL CONTROL WITH D-THYROXINE - A STUDY IN 3 PATIENTS

Selective pituitary resistance to thyroid hormone (PRTH) is responsible for thyrotoxicosis due to inappropriate secretion of TSH. The TSH suppressive action of D‐thyroxine (DT4) has been previously documented in euthyroid and hypothyroid subjects. This prompted us to treat with DT4 three patients with PRTH uncontrolled by anti‐thyroid drugs (ATD) alone or supplemented with bromocriptine, and whose follow‐up had been complicated by atrial fibrillation in two patients. Because of 100% cross‐reactivity between the D and L isomers of T4 and T3 in our RIAs, thyroglobulin (Tg) was used as an index of thyroid secretion. Under ATD, TSH and Tg levels were respectively: 35 mIU/l and 670.5 pmol/1 (patient 1), 87 mIU/1 and 453 pmol/1 (patient 2) and 110 mIU/1 and 906 pmol/1 (patient 3). When DT4 was added (patient 1, 3 mg daily; patients 2 and 3, 2 mg daily) to the same dose of ATD, plasma TSH and Tg levels fell but were still over the upper limit of normal and thyrotoxicosis persisted as illustrated by a recurrence of atrial fibrillation in one patient. When ATD were withdrawn and DT4 given alone (2 mg daily) all symptoms subsided within 1 month while TSH and Tg levels fell within the normal range. TSH normalization was documented within 1 week in one patient. After 16‐27 months of follow‐up the patients remained clinically euthyroid and plasma TSH and Tg levels were normal (patient 1, 0.65 mIU/1 and 5.6 pmol/l; patient 2, 1.4 mIU/1 and 49.8 pmol/l; patient 3, 0.83 mIU/1 and 104.2 pmol/l, respectively) as were the peripheral indexes of thyroid hormones actions serum enzymes, SHBG, ferritin and echocardiographic parameters. We conclude that DT4 at a daily dose of 2 mg is able to control safely thyrotoxicosis due to PRTH. DT4 could be tried as the first treatment of PRTH. Copyright © 1990, Wiley Blackwell. All rights reserved