Parathyroid Hormone-Like Effects of Acetazolamide

Abstract

The effects of acetazolamide which, like the parathyroid hormone, can produce not only bicarbonaturia but also phosphaturia were studied in 4 patients with idiopathic hypoparathyroidism (Id.H.) as well as in a patient with pseudohypoparathyroidism (Ps.H.). All patients were given 250 mg of acetazolamide perorally 3 times a day over a period of 10 days.
Acetazolamide increased serum total calcium concentration (corrected for serum protein), (P<0.01), and decreased serum phosphate concentration (P<0.05) significantly, causing chronic metabolic acidosis in all patients. In addition, Chvostek's and Trousseau's signs became clearly negative.
In all patients, acetazolamide elicited as much excretion of urinary phosphate as that of sodium and potassium but had no significant effect on the urinary excretion of cyclic AMP from the first day of its administration.
In Id.H., in comparison with Ps.H., a slight but significant increase in the urinary excretion of cyclic AMP and calcium began to manifest itself at later periods during the administration of acetazolamide and tended to continue even after it was withdrawn.
In Ps.H., both the increase in serum calcium and the decrease in serum phosphate were greater than in Id.H., in addition to the greater tendency to develop metabolic acidosis. However, little or no increase was observed in the excretion of urinary calcium despite severe chronic metabolic acidosis and high serum calcium levels in Ps.H.
The results suggest that in contrast to the parathyroid hormone, the phosphaturic effect of acetazolamide is not mediated through the renal adenylate cyclase-cyclic AMP system. In Ps.H., acetazolamide could produce an abnormally potent inhibition on the process of bicarbonate reabsorption in proximal tubules, and the inhibition of calcium reabsorption seemed to be hindered by the presence of chronic metabolic acidosis.