LYSOLECITHIN AS A FACTOR INFLUENCING ERYTHROCYTE SEDIMENTATION RATE

Abstract. In an experimental study increasing amounts of lysolecithin have been added to aliquots of plasma from 18 patients with a high erythrocyte sedimentation rate (ESR) and the final concentration of lysolecithin in the samples has been determined by means of thin layer chromatography and subsequent phosphorus determination as well as determination of the ESR. It was found that the ESR remained high in the different plasma samples until a critical level of lysolecithin was reached, whereafter the ESR abruptly dropped to lower values. This change took place within a very narrow concentration range, usually between 4.5 and 5.5 μg lysolecithin P/ml, and at a concentration of 7–8 μg/ml the ESR was consistently very low. In additional experiments, using decreasing amounts of red cells to the various plasma samples, the ESR had a normal tendency to increase inversely to the hematocrit, but in this case no threshold level could be observed. These findings clearly demonstrate that the lysolecithin concentration is of considerable importance for the ESR value. A low lysolecithin content of the plasma means a higher ESR value than expected from the amount of protein components, and a high lysolecithin concentration means a low ESR in spite of an unchanged protein pattern. Normally a decrease of the ESR takes place on incubation of a plasma sample due to the enzymatic formation of lysolecithin from lecithin. This phenomenon is explained by an increase of the lysolecithin amount above the demonstrated critical level. In a number of pathological conditions this “heat-stabilization” process does not occur, and in these cases the lysolecithin concentration is characteristically low and does not rise above the critical level even after incubation. A number of possible explanations of this drastical decrease of the ESR at a certain lysolecithin level are discussed in this presentation, but the most likely is that lysolecithin is bound to plasma proteins, e.g. albumin. In this form it is unable to exert its physiological effect on the red cell surface membranes until the saturation limit of the carrier protein is reached and “free” lysolecithin appears.