ACUTE YELLOW ATROl'IIY OF THE LI V Eli 539 



liver-cells, which have such a i)n)iiiiueut oxidizing function. The 

 hypotheses Avhich ascribe the intoxication to products of specific pro- 

 teolj^sis of the foreign proteins of the placenta which have entered 

 the maternal organism, 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 parenchjTuatous 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 metabolism 

 in general, and the function of the liver 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 a 

 rare disease, there probably being but about 500 cases reported in the 

 literature to 1903, according to Best's figures."'' 



The etiology of the disease is quite unknown, but it is very prob- 

 ably not a specific one, for we find that numerous forms of intoxi- 

 cation may lead to a condition closely resembling acute yellow atro- 

 phy, '^^ particularly phosphorus poisoning, chloroform poisoning, 

 puerperal eclampsia, and some cases of septicemia (especially with 

 the streptococcus).'- arsenic poisoning and mushroom poisoning."^ 

 It seems probable that any poison which does not directly cause 

 death, but which causes a severe injury to the liver-cells without at 

 the same time destroying the autolytie enzymes, so that the cells 

 die and undergo rapid autolysis, may produce a condition identical 

 with or similar to acute yellow atrophy (Wells and Bassoe).'"* In 

 the typical cases of the disease, of "idiopathic" origin, the poison- 

 ous agent possibly comes from the alimentary canal, as indicated by 

 a preliminary period of gastro-intestinal disturbance that usually pre- 

 cedes the onset of the disease, and secondly by the fact that the liver 

 seems to receive the chief effect of the poison. Whether these hypo- 

 thetical poisons are produced by abnormal fermentation and putre- 

 faction in the alimentary tract, or by a specific organism elaborating 

 its poison in this location, is quite unknown. Bacteriological studies 

 of the disease have so far given inconstant and non-instnictive re- 



"0 Thesis, University of Cliieaso, 1903. 



"1 It is to be borne in mind tliat tlie color is yellow only during the earlier 

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

 come through usage to ap]>ly to tlie disease as a whole. 



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



'3 Frey, Zeit. klin. Med.. 1012 (75). 4.'}.5. 



'* Jour. Amer. Med. Assoc, 1904 (44), 685. 



