ACUTE YELLOW ATROPHY OF THE LIVER 547 



insists, similar amounts may be found in other conditions associated 

 with convulsions and partial asphyxia, or in partial starvation, such 

 as results from the vomiting of pregnancy. The excretion of these 

 organic acids, as well as the large proportion of unoxidized sulphur 

 in the urine, indicates that incomplete oxidation is an important 

 feature of eclampsia, and under such conditions a large number of 

 imperfectly known toxic substances may accumulate in the blood 

 and tissues. The defective oxidation indicated by the urinary find- 

 ings arc probablj^ the result of the injury to the liver-cells, wliich 

 have such a prominent oxidizing function. The hypotheses which 

 ascribe the intoxication to products of specific proteolysis of the for- 

 eign proteins of the placenta which have entered the maternal organ- 

 ism, are suggestive, but as yet are not sufficiently developed to permit 

 of any definite conclusions as to the extent to which they apply. 



ACUTE YELLOW ATROPHY OF THE LIVER 



In this condition there is presented a striking picture of autolysis, 

 in that a large parenchymatous organ undergoes a rapid reduction 

 of size because of a solution of its structural elements, while at the 

 same time products of protein digestion (leucine, tyrosine, etc.) 

 appear free in the liver, the blood, and the urine. Because of these 

 prominent features and their relation to the questions of metabohsm 

 in general, and the function of the hver in particular, acute yellow 

 atrophy of the liver has been the object of much greater interest and 

 investigation than its clinical importance would warrant, for it is 

 not a common disease. ^^ 



The etiologj^ of the disease is quite unknown, but it is very probably 

 not a specific one for we find that numerous forms of intoxication 

 may lead to a condition closely resembling acute yellow atrophy, .^^ 

 particularly puerperal eclampsia, and some cases of septicemia (espe- 

 cially with the streptococcus),^^ and poisoning with phosphorus, 

 arsenic, nitrophenols and mushrooms.^ It seems probable that any 

 poison w^hich does not directly cause death, but which causes a severe 

 injury to the liver-cells without at the same time destroying the auto- 

 lytic enzymes, so that the cells die and undergo rapid autolysis, maj' 

 produce a condition identical with or similar to acute yellow atrophy 

 (Wells and Bassoe).- Inthetypicalcasesof the disease, of "idiopathic" 

 origin, the poisonous agent possibly comes from the alimentary canal, 

 as indicated by a prehminary period of gastro-intestinal disturbance 



'^ Up to 1903 there had been reported about 500 cases (Best, Thesis, University 

 of Chicago, 1903). 



'* It is to be borne in mind that the color is yellow only during the earlier 

 stages, "red atrophy" occurring later, but the name acute "yellow atrophy" has 

 come through usage to apply to the disease as a whole. 

 "" Babes, Ann. Inst. Path. Bucarest, vol. 6. 



1 Frev, Zeit. klin. Med., 1912 (75), 455; Prym, Virchow's Arch., 1919 (226), 229. 

 - Jour. Amer. Med. Assoc, 1904 (44), 685. 



