Parenchymal Siderosis in Patients with Cirrhosis after Portasystemic-Shunt Surgery

Abstract

THE syndrome of hemochromatosis, consisting of diffuse parenchymal siderosis, parenchymal-cell damage and fibrosis, and dysfunction of the organs so involved, has been observed in several clinical circumstances. In patients with "idiopathic" hemochromatosis the evolution of the disease complex has been attributed to unknown, perhaps genetically determined defects in iron metabolism. In others with so-called "secondary" hemochromatosis, the combination of chronic anemia, increased iron absorption and repeated blood transfusions has apparently led to excessive iron storage and tissue damage. Uncommonly, pyridoxine deficiency,1 folic acid deficiency,2 prolonged iron ingestion3 and pre-existent cirrhosis4 have been implicated in the pathogenesis of the hemochromatosis syndrome. . . .