Abstract
Red cell sodium and potassium contents were investigated in 57 patients with histologically proven liver cirrhosis and were compared with 13 controls without clinical evidence of liver disease. Patients with normal serum electrolytes (and without digoxin treatment) had normal red cell sodium content indicating no influence of the cirrhosis per se on the sodium-potassium pump or membrane permeability for sodium. Red cell potassium content was elevated, possibly as a consequence of subclinical hemolysis and a relatively young cell population. Hypokalemia was correlated to increased red cell sodium. Hyponatremia was correlated to low red cell sodium indicating reduced influx due to a decreased concentration gradient. According to the concept of the “sick cell syndrome,” membrane failure and cellular gain of sodium and loss of potassium can lead to hyponatremia. Our findings of normal or low red cell sodium contents provide evidence against this mechanism as explanation for the often severe hyponatremia in terminal liver failure. The abnormalities found in the red cells could be attributed to secondary complications to the cirrhosis.
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