Lysolecithin and Hemolytic Anemia. the Significance of Lysolecithin Production in the Differentiation of Circulating and Stagnant Blood.

Considerations regarding the etiology of hemolytic jaundice are inextricably bound up with the presence of spherocytosis and the associated increase in hypotonic saline fragility, and the effect of splenectomy in the amelioration of this disorder. Although many different opinions are advanced regarding the etiology of the disease, the outstanding ones are those postulating a faulty bone marrow or an increase in hemolysin production. The theory of faulty bone marrow production, as introduced by Naegeli (1), claims that spherocytes are produced by the bone marrow and that splenectomy does not change the production of abnormal red cells. The dramatic effect of this operation is explained by removal of the inhibitory effect of the spleen on the bone marrow (1). Careful studies of the hemoglobin metabolism in this disorder, however, have revealed that, after splenectomy, increased blood destruction (as measured by the urobilinogen output) and also increased erythrocyte production (as evaluated by the reticulocyte counts) return to normal values despite the continued presence of spherocytes. Some observers (2) believe that the spleen is the most important organ in this disease but do not deny production of spherocytes by the bone marrow. The hemolysin theory, on the other hand, states that the shape of the red cells is altered outside the bone marrow through the action of hemolysins. Dameshek and Schwartz (3) produced spherocytosis in experimental animals by the injection of specific hemolytic sera and Haden (4) was able to induce the same abnormality in vitro by the addition of hypotonic saline solutions to normal erythrocytes. The former authors have