446 METABOLIC ABNORMALITIES, AUTOINTOXICATION 



affects other organs but little, the necrosis and autolysis continue 

 until there is so much loss of liver function that systemic poison- 

 ing results from the hepatic insufficiency and from the resulting 

 accumulation of poisonous products of incomplete metabolism. 

 The patient dies from this poisoning, 1 and the liver is found at 

 autopsy to have decreased by from one-third to one-half or more 

 in its volume. This great change would not be possible if the 

 poisons affected the heart, kidneys, or brain as much as they do 

 the liver structure, which is probably the reason that phosphorus, 

 bacterial poisons, snake poisons, and other poisons that destroy 

 liver-cells do not ordinarily produce the typical picture of liver 

 atrophy. When these poisons affect the liver more and the 

 other tissues less, we approach the condition of acute yellow 

 atrophy ; e. g., if the dose of phosphorus is not so great as to 

 kill the patient through injury of other more vital organs, after 

 a few days the necrosed liver-cells undergo autolysis, and if 

 enough liver-cells have been destroyed, hepatic insufficiency may 

 cause death, with the finding of an anatomical condition in the 

 liver that can be properly designated as acute atrophy. Hence 

 it is possible for many poisons to cause this condition under 

 certain circumstances, and there seem to be certain unknown 

 poisons (probably of intestinal origin 2 ) that are of such a nature 

 that they cause specifically acute hepatic atrophy. The above 

 hypothesis seems to explain all the known facts concerning this 

 disease. That phosphorus, chloroform, and some other poisons 

 lead particularly to fatty changes may, perhaps, be due to their 

 acting especially upon the oxidizing enzymes, leaving the auto- 

 lytic enzymes and the lipase free to digest the cell and to form 

 fat. 3 That it is particularly the oxidizing enzymes that are 

 attacked is well shown by the chemical findings, and also by 

 Loewy's 4 observation that in poisoning with CNH, which 

 acts by impairing oxidation, the alterations in proteid metabo- 

 lism are very similar to those of phosphorus poisoning. 5 



1 The mortality of cases sufficiently typical to be diagnosed antemortem is 

 estimated by Kondaky (Koussky Vratch; Oct. 28, 1900) at 97 to 98 per cent. 

 Concerning the regenerative changes in the cases which recover, see Yamasaki 

 (Zeit. f. Heilk., Path. Abt, 1903 (24), 248). 



2 See Carbone, Kiforma Med., 1902 (1), 687 and 698. 



3 Wells, Jour. Amer. Med. Assoc., 1906 (46), 341. 



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



5 The hypothesis suggested by Quincke (NothnagePs Handbook, 1899, vol. 

 18, p. 307) that possibly regurgitation of pancreatic juice up the bile-ducts 

 might be responsible for the degenerative changes in the liver, is contradicted 

 by the fact that the bile pressure is greater than the pancreatic juice pressure, 

 and that the bile-ducts and peripheral portions of the lobules are least affected. 

 Nor could Best prove that trypsin injected into the liver by way of the bile- 

 ducts is able to cause such changes. (See Wells and Bassoe, loc. cit.) 



