3,5,3'-Triiodothyroacetic Acid (
Triac) is reputed to suppress pituitary secretion of TSH with minimal metabolic effects.
Triac has been used successfully to treat eight patients with
thyroid hormone resistance. We gave
Triac to a woman with selective pituitary resistance for treatment of
hyperthyroidism (patient 1) and to a man with generalized resistance and chronic
schizophrenia to determine whether it would improve his
schizophrenia (patient 2). Patient 1 was given 0.35-3.5 mg
Triac/day; patient 2 was given 0.7-4.2 mg/day. Dosages were increased by 0.7 mg/day every 2 weeks. Serum T3, T4, free T4, TSH, TSH response to TRH, systolic time intervals (
STI),
angiotensin-converting enzyme (ACE), and
lipids were monitored bimonthly. In both patients, there was no change in symptoms, weight,
lipids, or
STI. In patient 1, basal TSH suppressed from 16.3 to 1.5 mU/L; in patient 2, from 2.0 to 0.5 mU/L. The peak TSH response to TRH stimulation decreased from 144 to 12.5 mU/L in patient 1 and from 14.2 to 2.8 mU/L in patient 2. Serum T4 decreased from 160 to 109 nmol/L in patient 1 and from 270 to 192 nmol/L in patient 2. ACE levels were persistently elevated in both patients. Resting energy expenditure, measured by oxygen consumption, was increased by
Triac in both patients (12% in patient 1 and 9% in patient 2). Although
Triac suppressed TSH and T4 secretion in both patients, it did not reduce peripheral action of
thyroid hormone as expressed in
STI, resting energy expenditure, and ACE. We conclude that in these two patients with resistance to
thyroid hormone, at the doses used to suppress TSH and T4 secretion, the intrinsic peripheral action of
Triac offset whatever decrease in
thyroid hormone secretion it produced.