Ten cases of Ménétrier's disease (`giant hypertrophic gastritis') have been studied with radioiodine-labelled albumin (all 10 cases), IgG (eight cases), transferrin (two cases), and IgM (six cases). Abnormal gastric loss of plasma protein was present in all cases as demonstrated by 59Fe-iron dextran (eight cases), 51Cr-albumin (one case), and 131I-polyvinylpyrrolidone (one case).
None of the patients had more distal gastrointestinal lesions. The synthetic rate of the proteins studied was normal or slightly elevated.
The fractional catabolic rate of the proteins was increased. The increase above the normal mean was similar for albumin, transferrin, and IgG. Since the molecular weight of IgG is more than twice that of albumin and transferrin, it is concluded that the protein loss in Ménétrier's disease is nonselective in the sense that it affects a similar fraction of the intravascular masses of all plasma proteins. IgM catabolism was strongly accelerated. Simultaneous studies with 50Fe-iron dextran, radioiodine-labelled albumin or IgG showed that IgM hypercatabolism could only partly be due to abnormal gastric protein loss, since IgM catabolism was significantly more raised than that of albumin and IgG. Faecal radioiodine excretion was normal in most patients after the injection of radioiodine-labelled proteins. It confirms a previous observation that increased gastrointestinal 59Fe clearance after injection of 59Fe-iron dextran associated with normal faecal radioiodine excretion after the injection of radioiodine-labelled proteins permits of a diagnosis of protein loss in the stomach.
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