Search

To the Editor.— In their article on the pharmacokinetics of digoxin after a single dose of quinidine sulfate, Chen and Friedman (1980;244:669) found that quinidine given 24 hours after the last dose of digoxin causes no change in serum digoxin levels. The authors interpreted the lack of effect of quinidine on serum digoxin levels 24 hours after the last dose of digoxin as an indication that the observed elevations of serum digoxin after simultaneous administration of quinidine is probably not caused by displacement of digoxin-binding sites by quinidine. The authors refer to an abstract published by our laboratory reporting "that quinidine displaces ouabain from beef heart membrane sodiumpotassium adenosine triphosphatase." We did, indeed, report that quinidine alters ouabain binding in the beef heart sodium potassium adenosine triphosphatase preparations but not by displacing already bound ouabain. Quinidine eliminates binding sites that are unoccupied by ouabain; it does not change the equilibrium

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus. ( Arch Intern Med 139:86-88, 1979)