A Study of the Role of Proteinorrhoea (protein-losing Gastro-enteropathy) in Bilharzial Hepatic Fibrosis.

Hypoproteinaemia is present in many patients suffering from schistosomal (bilharzial) hepatic fibrosis, especially when associated with ascites. In most patients with hypoproteinaemia undergoing treatment on a well-balanced diet the fall in serum proteins can be corrected except in a small group of cases. Hypoproteinaemia, mainly hypoalbuminaemia, cannot be ascribed to diminished protein synthesis, which remains within normal limits as does parenchymal liver function in patients with bilharzial hepatic fibrosis till the terminal stage (Salah, 1962). Loss of proteins into the gastro-intestinal tract has been shown to be a major factor in the hypoproteinaemia associated with regional enteritis (Steinfeld, Davidson, and Gordon, 1957), ulcerative colitis (Holman, Nickel, and Sleizenger, 1959), sprue (Parkins 1960), gastric neoplasm (Schwartz and Jarnum, 1959), giant hypertrophy of the gastric mucosa (Chokas, 1959), hypertrophic gastritis (Citrin, Stirling, and Halsted, 1957), congestive heart failure, constrictive pericarditis (Davidson, Waldmann, Goodman, and Gordon, 1961), and the syndrome of idiopathic hypercatabolic hypoproteinaemia (Gordon, 1959; Schwartz and Jarnum, 1959). Several methods have been employed to study this phenomenon. Paper electrophoresis and immunophoresis have been used to determine the presence of autogenous human albumins and globulins in intestinal juices (Schwartz and Jarnum, 1959; Gross, Embree, Bally, Shipp, and Thorn, 1960). But such methods are mainly qualitative. Gordon (1959) used radio-iodinated polyvinylpyrrolidone and Schwartz and Thomsen (1957) radioiodinated human serum albumin, but Waldmann (1961) used 51Cr-labelled albumin in attempts to study intestinal protein loss quantitatively. MATERIAL AND METHODS