IT IS estimated that $70 million of potent oral diuretics are sold yearly in the United States. This makes this group of drugs second only to antibiotics in volume of prescription drug sales. More significant than the sheer volume of diuretics dispensed is the recognition that large numbers of patients with congestive heart failure and hypertension are being maintained for months or years on thiazide drugs. It is frequently important to determine the status of thyroid function in this group of patients, especially those in heart failure. In this regard, it has been our experience that patients with congestive heart failure suspected of hyperthyroidism have had unusually low serum protein-bound iodine (PBI) levels, and we have suspected that this might be due to prior thiazide administration.
Chlorothiazide has been shown to inhibit thyroidal carbonic anhydrase activity in vitro.1 This causes a suppression of the thyroidal uptake of radioiodine and