Exchanges of sodium and potassium in familial periodic paralysis.

The constant association of a fall in concentration of serum potassium with attacks of muscular weakness, plus the relief of the weakness by the administration of potassium salts, have clearly indicated that familial periodic paralysis involves a defect in potassium metabolism. The nature of this is not completely understood. Following the observation that the concentration of potassium in serum was lowered at the time of paralysis (1, 2), a number of other investigators studied potassium exchanges in this condition to ascertain the route of removal of potassium from serum and extracellular fluid. It has been found that the urinary excretion of potassium prior to and during attacks of paralysis, with but 1 exception, was minimal, and hence the lowered concentration of this cation must result from a shift into cells (3 to 7). Only during a water diuresis preceding an attack did Gammon and co-workers (6) find an increased excretion of potassium in the urine. It has been suggested that an abnormal demand for potassium in muscle cells is present in this condition (7). The production of lowered concentrations of serum potassium and of paralysis by the administration of carbohydrate, insulin, or epinephrine has also led to the hypothesis that potassium may be moved from extracellular fluid into cells of the liver or other tissues of the body during glycogenesis or carbohydrate combustion. Ferrebee, Gerity, Atchley, and Loeb (8) have reported the results of an extensive metabolic study of a patient with this disease. They confirmed the finding that potassium excretion diminished coincidently with the fall in serum concentration during an attack, and found erratic fluctuations in excretion of potassium and sodium between attacks. They did not, however, quantitate the exchanges of potassium and sodium between