Studies on Plasma Lipid and Phospholipid Composition in Pernicious Anemia before and after Specific Treatment

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Abstract
Patients with pernicious anemia (PA) were compared with a reference group concerning the concentration of lipids in plasma before (34 cases) and after (15 cases) treatment with vitamin B12. The lipid parameters in plasma and in postheparin plasma were measured before and after 6 h incubation at 37.degree. C before and after specific treatment. In a limited number of cases the lecithin:cholesterol acyl transfer (LCAT) rate was determined. In relapse, the PA cases showed increased free fatty acid (FFA) and triglyceride (TG) concentrations but decreased concentrations of total cholesterol (TC), unesterified cholesterol (UC) and all examined phospholipid fractions. After treatment, FFA remained unchanged and TG decreased, while TC and possibly also UC and the phospholipid fractions were in line with reference levels. After incubations, UC and phosphatidylcholine (PC) decreased and lysolecithin (LL) increased. FFA increased and TG decreased. Incubation of postheparin plasma resulted in an augmented decrease in TG and PC and increase in FFA and LL. In relapse, the changes on incubation were less pronounced than after treatment. The LCAT rate was low but within the normal range before treatment in the 6 cases examined. After treatment, LCAT rates increased but were still normal in relation to the plasma lipid concentrations. The study showed a decreased net esterification of cholesterol and LL formation on incubation of plasma in PA cases in relapse. This finding might be explained by the low concentration of plasma substrates for the LCAT reaction and phospholipases. After treatment the concentration of lipid substrates was restored to normal, with subsequent normal LL formation and cholesterol esterification. The observations could also explain the frequent lack of stabilization of erythrocytes suspended in plasma of PA after incubation, resulting in virtually the same ESR after as before this procedure. Due to low LL formation following the insufficient substrate availability for LCAT and phospholipase, the previously reported critical level of the LL concentration is not reached and cannot achieve its normal reduction of the ESR.