542 ABXOiniMJTIES l.\ METABOlAfiM 



intestinal origin -") that are of suck a iiature that they cause spe- 

 cifically acute hepatic atrophy. The above hypothesis seems to ex- 

 plain all the known facts concerning this disease. That phosphorus, 

 chloroform, and some other poisons lead particularly to fatty changes 

 may, perhaps, be due to tlieir acting especially upon the oxidizing en- 

 zymes,*^ leaving the autolytic enzymes and the lipase free to digest 

 the cell and to form fat.^- That it is particularly the oxidizing en- 

 zymes that are attacked is well shown by the chemical findings, and 

 also by Loewy's^^ observation that in poisoning with CNH, which 

 acts by impairing oxidation, the alterations in protein metabolism are 

 ver}' similar to those of phosphonis poisoning.^* To be sure, Lusk ^^ 

 found no deficiency in general oxidation in phosphonis poisoning, 

 but this does not signify that tlie local changes do not depend upon 

 local defective oxidative processes. 



Not only phosphorus but many metals, especially mercury, seem 

 able to cause the anatomical changes of acute yellow atrophy, for the 

 condition has been observed very frequently in persons receiving 

 mercurial and arsenical treatment for syphilis.^*' Here the syphilis 

 has been held responsible hj some, but the fact that in many of the 

 eases the syphilis was quiescent or chronic at the time, and that mer- 

 cury and arsenic are known to kill cells and stimulate autolj'sis, seems 

 to incriminate the metals,^' at least in some cases. 



CHEMICAL CHANGES OF ACUTE YELLOW ATROPHY 



The Urine. — Most striking, and long regarded as pathognomonic, 

 is the presence of leucine and tyrosine in the urine, first described 

 by Frerichs. While we now know that these and other amino-acids 

 may occur in the urine in any conditions in which there is a great 

 breaking down of tissue within the body, yet it is true that in no 

 other condition are they found so abundantly as in acute hepatic 

 atrophy (as high as 1.5 gm. of tyrosine per diem has been found). ®^ 



80 See Carbone, Riforma Med., 1902 (1), 687 and 608. 



81 See Verworn, Dout. med. Woch., 1009 (35), 1593; Joannovics and Pick, 

 Arch. fjes. Physiol., 1911 (140), 327. 



82 Wells, Jour. Amer. Mod. Assoc, 1006 (46), 341. 

 S3 Cent. f. Physiol., 1906 (19), 23. 



8-t The liypothosis siiofffcstod by Quincke (Xothnatrel's Handbook, 1899. vol. 18, 

 p. 307) that possibly rofjurfjitation of pancreatic juice up tlie bile ducts mipht 

 lie responsible for the dopenerative chanfjes in the liver, is contradicted by the 

 fact tliat the bile pressure is greater tlian tiie pancreatic juice pressure, and that 

 the bile-ducts and periplieral portions of tlie h>bules are least afTected. Nor 

 could Best "0 prove that trypsin injected int^ tlie liver by way of the bile-duets is 

 able to cause such c]ian<res. (Soo Wells and Passoe.'-J) 



85 Science of Nutrition. Philadelphia, 1909. 



SfiSeverin, Zcit. klin. Mod., 1912 (76), 138. Pendip. :Miinch. med. Wooli.. 191.-) 

 (62), 1144. 



STTileston (Boston :\Io(l. and Surrr. Jour.. 1908 (158). 510) lias described a 

 case of acut<» yellow atrojihy from Tuercurialism without syphilis. 



88 An interostinp exccjition has boon reported liy W. 0. Smith (Practitioner, 

 1903 (70), 155) who found proat quantities of leucine in the urine of a younp 

 woman who was apparently not at all ill. Rosenbloom has found tyrosine crys- 



