The Effect of Experimental Salt Depletion and Aldosterone Load on Sodium and Chloride Concentration in the Sweat of Patients with Cystic Fibrosis of the Pancreas and of Normal Children

Abstract

Sodium and chloride excretion in sweat is partially controlled by aldosterone. If this corticosteroid is lacking, as in Addison''s disease, there is excessive salt loss in sweat. On the other hand, abnormally high sweat sodium and chloride concentrations in children suffering from cystic fibrosis of the pancreas are not related to a deficient production of endogenous aldosterone. This can be demonstrated by experimental salt depletion during which a very high urinary aldosterone output is found, and by the determination of urinary aldosterone in children with cystic fibrosis of the pancreas. In this disease sodium and chloride excretion in sweat remains pathological (Na > 80 mEq/litre and Cl >60 mEq/litre) even during salt depletion or aldosterone load. In normal persons these electrolytes show a striking decrease in the same condition. This observation can be used for the diagnosis of cystic fibrosis.