LEUKEMIA 309 



action seems to be insufficient to prevent leucocytic autolysis, for 

 even in freshly drawn l)lood proteoses (or at least nou-coa<iulable pro- 

 teins) may be present.'" Aceordin<r to Erben, tliis is tr-ue only of 

 rayelog-enous leukemia, the fresh blood in lymphatic leukemia not only 

 being: free from non-eoag:ulable protein, but furthermore this product 

 of proteolysis does not soon develop when the blood is kept aseptically 

 at incubator temperature. This is, of course, what one would expect 

 in view of the well-known enzyme-richness of the polymorphonuclear 

 leucocytes and the scarcity of proteolytic enzymes in lymphocytes. 

 Erben states that the neutrophile cells seem to be the chief source of 

 proteoses, since their granules soon disappear in blood that is undergo- 

 ing: autolysis, whereas the eosinophiles preserve their granules well, and 

 true proteoses are not present in blood rich in mast cells (i. e., mye- 

 loma) . The marrow, spleen and lymph grlands are found strongly pro- 

 teolytic (according: to the plate method), in myelogenous leukemia, but 

 in lymphatic leukemia and pseudoleukemia, only the marrow shows a 

 slight activity.'^ Schnmm ''^ found in the blood in a case of myelogen- 

 ous leukemia several varieties of proteoses, most abundant being the 

 so-called deutero-albumose ; in another he also found peptone, leucine, 

 and tyrosine. In addition he demonstrated the autolytic nature of 

 the changes that occur in leukemic blood after death (see also "Auto- 

 lysis in Leukemia," Chap. iii). Most observers have failed to find 

 alhumose in the urine in leukemia. Because of the involvement of 

 the bone marrow, small amounts of Bence-Jones protein, as well as 

 Morner's body, may be found in the urine.®" Kolisch and Burian ^^ 

 not only found nucleoprotein constantly, and albumose frequently, 

 but in one case of lymphatic leukemia they found histon in the urine, 

 which undoubtedly came from nucleoprotein decomposition. 



The oxidase reaction is conspicuous in certain of the cells of mye- 

 loid leukemia, especially the large, non-granular cells of acute leu- 

 kemia,®^ but it is not known that these oxidases influence the chem- 

 istry of the disease. In spite of the richness of leucocytes in lipases 

 the serum shows no increased lipolytic activity. ^^-"^ 



Protein Metabolism. — Stejskal and Erben ®^ studied the metabolism 

 of a case of myelogenous and of a case of lymphatic leukemia, and 

 found the nitrogen loss much greater in the myelogenous form, al- 

 though food-absorption was better than in the lymphatic ; they con- 

 sider that protein-destroying forces are at work in myelogenous 

 leukemia, similar to those of cancer cachexia, so that nitrogenous equi- 

 librium cannot be attained. 



7TFor literature see Erben, Zeit. f. Keilk. (Int. Med. Abt.), in03 (24), 70. 



•8 Jochmann and Zioo^ler, Miineh. med. Woch., 1906 (.53), 200.1. 



-n Hofmeister's Beitr., 1003 (4), 442: Dout. med. Woeh., lOOo (31), 183. 



soBofrfrs and Oiithrie. Bull. .Tolins Hopkins llosp., 1013 (24), 308. 



S2 Zeit. klin. Med., 1806 (29). 374 (literature on albuminuria in leukemia). 



Ri Dimn, Quart. Jour. Med., 1013 (6). 203. 



siararo. Zeit. klin. Med., 1913 (78), 286. 



83 Zeit. f. klin. Med., 1900 (39), 151. 



