548 ABNORMALITIES IN METABOLISM 



that usually precedes the onset of the disease, and secondly by the 

 fact that the liver seems to receive the chief effect of the poison. 

 Whether these h3^pothetical poisons are produced by abnormal fer- 

 mentation and putrefaction 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-instructive results. In the countries where phosphorus poisoning 

 is common (especially Austria) there has been found much difficulty 

 in distinguishing in many cases the results of phosphorus poisoning 

 from acute yellow atrophy of the fiver, and many have contended 

 that there is no real difference; i.e., that phosphorus, as well as un- 

 known poisons, may cause acute yellow atrophy. The present trend 

 of opinion, however, seems to favor the view that there is a primary 

 liver atrophy which is different from that caused by phosphorus or 

 other known poisons in several essential respects.^ 



Phosphorus Poisoning. — Between phosphorus poisoning and "primary" hepatic 

 atrophy the following chief differences may he discerned: Phosphorus produces a 

 general injurious effect upon all the organs of the body, the liver merely showing 

 the most marked anatomical changes, which at first consist of a fatty metamor- 

 phosis of the liver, due to migration of the body fat from the fat deposits into the 

 injured cells ,(Roseneld, Taylor); subsequently the liver cells disintegrate, 

 the cytoplasm being affected before the nucleus, and the liver may be- 

 come smaller than normal, although it is usually enlarged because of the fat 

 deposition. Typical acute yellow atrophy is characterized by an early necrosis 

 of a large proportion of the liver-cells, the nucleus becoming unstainable while the 

 cytoplasm is still little altered in appearance, and fatty changes play a subordi- 

 nate role or are absent. As Anschtitz says, the poison'seems to strike at the life 

 of the cell, its nucleus, while phosphorus attacks the cytoplasm. Furthermore, 

 the poison of yellow atrophy seems to be very specific, for it attacks the other 

 organs of the body almost not at all, and within the liver it affects only the hepatic 

 cells proper, while the bile-duct epithelium and the stroma cells are so little injured 

 that they are able to proliferate greatly, this proliferation being a prominent feature. 

 There are also clinical and chemical differences that will be discussed later, but 

 yet, on the whole, the resemblances of yellow atrophy and phosphorus poisoning 

 are so great that we have obtained much information concerning the former by 

 means of experimental studies of phoshorus poisoning. 



Delayed Chloroform Poisoning. — After chloroform narcosis, and rarely after 

 ether, there occasionally develops a severe intoxication, with clinical and anatomical 

 findings very similar to acute yellow atrophy and i)hosphorus poisoning;' in point 

 of the fatty changes the cases usually stand intermediate between acute yellow 

 atrophy and phosphorus poisoning. This action of chloroform would seem, from 

 the studies of Evarts Graham,^ to be produced l)y the liydrochloric acid formed 

 from it in the liver. Some cases of puerperal eclampsia also present such profound 



2 See Anschlitz, Arb. a. d. Path. Inst. Tubingen, 1902 (3), 280; Paltauf, Verh. 

 Deut. Path. Gesell., 1903 (5), 91; Riess, Berl. klin. Woch., 1905 (42), No. 4-la, 

 p. 54. 



••Complete review and literature by Bevan and Favill, Jour. Amer. Med. 

 Assoc, 1905 (45), 691; Muskens, Mitt. Grenz. Med. u. Cliir., 1911 (22), 56S. Full 

 discussion of chemistry of chloroform necrosis liy ^^'olls, Jour. Biol. Cliom., 190S 

 (5), 129. Exixniinental necrosis — see \\'lui)ple and Sporrv, Johns Hopkins 

 Hosp. Bull., 1909 (20), 278; Graham, Jour. Exper. Med., 1912 (15), 307; Simonds, 

 Arch. Int. Med., 1919 (23), 3()2; Davis and Whipple, ibid., p. 012. 



'■ Jour. Ex)). Med., 1915 (22), 48. Tliis hypothesis receives supi)ort from the 

 conclusion reached by many investigators that ilichl()rethylsuli)hide ("mustard 

 gas") also injures tissues through intracellular dissociation liberating IICI. (See 

 Lillie ('/ ai, Jour. Pharm., 1919 (14), 75.) 



