LEUKEMIA 'A 1 1 



but also fouiul that the relation be. ween the number of leii(;ocytc.s and 

 the utif acid is extreincly variaI)Io. Soiuctiincs the iiitroKen loss is very 

 great — even as much as 20 ^m. per day — and, corresponding with the destruction 

 of nucleoj)roteins and the resulting uric-acid formation, phosphoric-acid excretion 

 is often greatly increased — even up to 15 gm. ])er day. On the other hand, the 

 results obtained by many other writers have been in every respect extremely varia- 

 ble; some have found no increase in uric acid, some even report a decrease; likewise 

 the P2O;, has been found even less than normal. For example, in a carefully studied 

 case of lymphatic leukemia, Henderson and Edwards'-"-' found during six months 

 no excessive excretion of uric acid or phosphoric acid. Zalesky and Erben found 

 likewise no coasidcrable increase in the uric acid in lymphatic leukemia, but in 

 myelogenous leukemia the uric acid was much increased; on the other hand, the 

 amount of elimination of purine bases was reversed in the two forms, and creatin 

 was decreased in both. Lipstein'° found no excessive elimination of amino-acids 

 even in myelogenous leukemia. An increase in calcium is quite constantly ob- 

 served, and attributed to the bone destruction-^ occurring in this disease. 



Undoubtedly these variations in results depend upon the known fluctuations in 

 the course of the pathological processes of leukemia; the number of leucocytes, the 

 size of the lymphatic organs, and the general condition of the patient all vary 

 greatly from time to time, often with remarkable rapidity, and the excretion of 

 products of metabolic activity must vary likewise. It can hardly be questioned 

 that the enormous increase in the amount of lymphoid tissue in the body and 

 blood must give rise to a greatly increased nuclein catabolism, with consequent 

 appearance of its products (uric acid, purine bases, and phosphoric acid) in the 

 urine. This seems to be well demonstrated by the increased elimination of uric 

 acid and purine bases, together with a general increase in the nitrogen output that 

 has been frequently observed following the therapeutic use of a:-rays in leukemia, 

 which is attributed to the increased autolysis that x-rays are known to produce. 

 Radium has a similar effect, increasing enormously the urinary total nitrogen, urea, 

 ammonia, less markedly the uric acid, but especially the phosphates.^' 



According to Rosenstern^'- the x-rays affect chiefly the leucogenic tissues rather 

 than the adult leucocytes. Lipstein also found an excessive elimination of 

 amino-acids, in the urine of leukemic patients treated by .c-rays.^^ According to 

 Curschmann and Gaupp,^* the blood of leukemic patients who have been exposed 

 to x-rays contains a specific leucocytotoxin, which may be produced by a process of 

 autoimmunization against the leucocytic substance set free by the disintegrated 

 leucocytes. Capps and Smith^^ have obtained similar results. A'-rays seem not 

 to alter the total metabolism appreciably.''^ 



Charcot's crystals (also called Charcot-Ley den and Charcot-Neumann crystals) 

 represent a peculiar and striking product of nuclear destruction that has fre- 

 quently^ been found associated with leukemia. These crystals were first observed 

 by Robin3 7(1853) in leukemic tissues, but have been named after Charcot, who, 

 with Robin, described their properties. They were described by Charcot as color- 

 less, refractile, elongated octahedra; insoluble in alcohol, ether, and glycerol; 

 soluble in hot water, acids, and alkalies; size variable, from 0.016 by 0.005 mm. up. 

 These crystals have been found not only in the tissues and blood of cadavers, but 



23 Amer. Jour, of Physiol., 190.3 (9), 417. 



30 Hofmeister's Beitr., 1905 (7), 527. 



31 Knudsonand Erdos, Boston Med. Surg. Jour., 1917 (176), 503. 



32 Miinch. med. Woch., 1906 (53), 1063. 



" Literature on effects of x-rays in leukemia, see Arneth, Berl. klin. Woch., 



1905 (42), 1204; Musser and Edsall, Univ. of Penn. Med. Bull., 1905 (18), 174; 

 Rosenberger, Miinch. med. Woch., 1906 (53), 209; Williams, Biochem. Jour., 



1906 (1), 249; Lessen and Moraw^tz, Deut. Arch. klin. Med., 1905 (83), 288; 

 Koniger, Deut. Arch. klin. Med., 1906 (87), 31. 



34 Miinch. med. Woch., 1905 (52), 2409. 



36 Jour. Exp. Med., 1907 (9), 51; see also Klieneberger u. Zoeppritz, Miinch. 

 med. Woch., 1906 (53), No. 18; Milchner u. Wolff, Berl. klin. Woch., 1906 (43), 

 No. 23. 



36 Arch. Int. Med., 1917 (19), 890. 



3'^ Literature given by v. Leyden, Festschrift fiir Salkowski, Berlin, 1904, p. 1. 



