Lecithin:cholesterol acyltransferase deficiency associated with hepatic schistosomiasis mansoni.

Plasma and erythrocyte lipid abnormalities occur in chronic human schistosomiasis mansoni and appear to be related to mild lecithin:cholesterol acyltransferase (LCAT) deficiency. Plasma LCAT activity is about 50% lower than normal in decompensated hepatosplenic schistosomiasis, whilst the plasma concentrations of cholesteryl ester and lysolecithin and decreased and that of lecithin increased in the earlier hepatointestinal and compensated hepatosplenic forms of the disease as well as in the later decompensated stage. Plasma lipoproteins are also altered in schistosomiasis. Agarose gel electrophoresis showed reduced alpha and pre-beta lipoproteins, whilst other studies consistently showed that lipoproteins from patient plasma are better substrates for LCAT than those of normal plasma. Erythrocyte cholesterol is increased in all forms of the disease, and the cells show increased resistance to lysis either in hypotonic media or in 0.3 M glycerol. The severity of these lipid changes clearly shows a gradation through the successive stages of the disease. In the experimentally infected mouse LCAT deficiency does not seem to be a feature of the disease, but several significant changes in plasma and erythrocyte lipids occur which contrast with those seen in human schistosomiasis.