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Serial studies of plasma lipids and lipoproteins were performed in 4 patients with acute alcoholic liver disease characterized by a massive fatty liver and laboratory evidence of intrahepatic cholestasis. There were striking alterations in the plasma lipoprotein electrophoretic patterns characterized by the absence of α- and pre-β-lipoprotein bands and the presence of a single band of abnormal mobility. These changes were associated with an extreme decrease in plasma lecithin-cholesterol acyltransferase activity, resulting in greatly reduced levels of plasma cholesteryl esters and increased levels of unesterified cholesterol. In 2 patients hypertriglyceridemia and hypercholesterolemia were present, the latter because of an increase in unesterified cholesterol. Lipoproteins were isolated from the plasma by sequential ultracentrifugation at the densities used for separation of normal very low density, low density, and high density lipoproteins; however, the patients' lipoproteins were different from normal in lipid composition and ultrastructure. All of the lipoprotein fractions were decreased in cholesteryl esters and the major lipoprotein was a triglyceride-rich low density lipoprotein. Electron microscopic studies of the low and high density lipoprotein fractions revealed the presence of bilamellar vesicles and stacked discs. All of the changes in lipoprotein composition and ultrastructure gradually returned to normal with clinical improvement. These observations indicate that alcoholic liver injury is associated with profound alterations in lipoprotein composition and metabolism which may be related in part to lecithin-cholesterol acyltransferase deficiency.

Summary The association of excessive iron deposition in the liver and other tissues of patients with portal cirrhosis has implied a pathogenetic relationship between iron storage and tissue damage. In the present report patients with portal cirrhosis without iron storage, as proved by liver biopsy examination, eventually developed extensive hepatic and other parenchymal cell siderosis. Histologic examination of autopsy material disclosed pathologic features similar to those described in idiopathic and exogenous hemochromatosis. Because there is as yet no experimental evidence to justify the assumption that iron overloading can cause hepatic damage, it seems reasonable to assume that some instances of so called idiopathic or transfusional hemochromatosis actually represent parenchymal siderosis in preexisting portal cirrhosis. These cases are not recognized because of the lack of biopsy material before the accumulation of iron in the previously cirrhotic liver.