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Albumin Turnover in Schistosomal Liver Cirrhosis

With the use of ¹³¹I-labeled albumin administered intravenously and oral Amberlite® resin IRA 400, albumin metabolism was studied in eight normal persons and 16 patients with schistosomal liver cirrhosis, five of whom had ascites. The plasma volume was found to be expanded, and the serum albumin concentration, the halflife of labeled albumin, and the total exchangeable albumin were found to be reduced in schistosomiasis cases.

The ratio of the extravascular to the intravascular pool of albumin was also diminished. The albumin in the extravascular pool was diminished to a great extent while that in the intravascular pool was unchanged. An increased loss of albumin through the gastrointestinal tract was encountered in schistosomal liver cirrhosis and it may be an important factor in reducing the total body albumin.

A positive correlation was found between portal hypertension and the loss of albumin through the gastrointestinal tract. Thus, portal hypertension is held responsible for this increased exogeous loss of albumin. The mechanism of this loss in schistosomal liver cirrhosis is thought to be a passive leakage of plasma proteins through the gastrointestinal mucous membrane as a result of an abnormal increase in intestinal lymph beyond the capacity of drainage by intestinal lymphatic vessels.