Abstract
Our observations on the pathogenesis of xanthoma were reported. Direct immunofluorescence using anti-human β-lipoprotein antibody indicated that human β-lipoprotein was incorporated into foam cells of human xanthomas and an experimental rabbit xanthoma which was induced by human β-lipoprotein immune complexes in the blood stream. Foam cells originate from scavenger cells, such as dermal histiocytes and not from fibroblasts. Histiocytes incorporate more readily denatured lipoproteins than lipoproteins of native form. Cholesterol metabolism was investigated in experimental xanthoma tissues which were induced by intradermal dextran sulfate injection. Cholesterol synthesis was suppressed and cholesterol esterification was increased in the cholesterol-rich xanthoma tissues. Cholesterol was esterified more selectively with oleic acid than with palmitic acid. Therefore, cholesterol oleate increases in the tissues concomitantly with the accumulation of cholesteryl esters. The more important role in the esterification was played by the fatty acids of serum origin rather than those synthesized in situ. These findings suggest that the cholesterol esterification was mediated by acyl-CoA: cholesterol acyltransferase and that lecithin: cholesterol acyltransferase had contributed little to the esterification.
