X. EFFECTS OF DEFICIENCY 113 



trabeciilae (Fig. 11), and for these the pathologist may have to search as- 

 siduously. If such a search is successful, the clinical pathologist is well 

 rewarded in cases of cirrhosis in which the pathogenesis may he shrouded 

 in obscurity,''^^ for fatty cysts at any stage imply, by their very existence, 

 that at one time li\'er cells had l:)een distended to the bursting point by fat 

 and this finding may provide an important clue to the etiology (Fig. 12). 



The foregoing should serve to establish that the presence of large amounts 

 of stainable fat in cirrhotic li\'ers is not a criterion for determining whether 

 or not the lesions were initiated by an excess accumulation of fat. Although 

 stainable fat is usually demonstrated with ease in experimental cirrhosis 

 of dietary origin, such animals are most freciuently sacrificed before they 

 become moribund and while their food intake is still within normal limits. 

 Consecjuently the investigator commonly observes this type of cirrhosis at 

 the height of active progression of lesions when fat is abundant. This is in 

 sharp contrast to the clinical situation. Patients have usually been treated 

 by withdrawal of their alcohol, and terminal complications may have pro- 

 duced significant degrees of weight loss, ])oth of which are potent factors 

 in clearing hepatic cells of stainable fat. These considerations may well 

 explain the frequent absence of stainable fat in livers of alcoholics at death. 



2. Ceroid 



In the trabeculae of cirrhotic, choline-deficient rats, abundant amounts 

 of an orange-brown pigment may l^e demonstrated. This material, which 

 was named ceroid by Lillie et al.,^-^ is sudanophilic, acid-fast, and insoluble 

 in alcohol, xylol, and other common fat solvents. It is most easily and cer- 

 tainly identified by staining paraffin sections (from which all soluble lipids 

 have been removed by the dehydrating agents) with any of the dyes which 

 demonstrate fat (Sudan, Oil Red 0, etc.). Ceroid in cases of cirrhosis in man 

 is absent or scanty ;^-®'^'^ at most, only small amounts can be demonstrated 

 in alcoholics. 



Deposition of ceroid in cirrhotic rats can be greatly reduced by either 

 supplementing their diet with large amounts of a-tocopherol, or replacing 

 unsaturated fats in the diet with hydrogenated vegetable oils such as Crisco 

 or Primex.^^-*' 438-440 goth in vitro and in vivo experiments^^^ have now demon- 

 strated the possibility that ceroid is the product of the oxidation of unsatu- 

 rated fatty acids into an insoluble polymer, which, however, retains the 

 characteristic of sudanophilia. Tocopherol may act to inhibit this reaction 

 l^y \irtue of its role as an antioxidant. Small hemorrhages freciuently occur 



"' W. S. Hartroft, Federation Proe. 11, 417 (1952). 



^'8 J. Victor and A. M. Pappenhoimer, ./. E.c/,ll. Me,l. 82, .375-383 (1945). 



"9 p. Gyorgy and H. Goldhlatt, ./. Exptl. Med. 89, 24.5^2GS (1949). 



"0 P. Gyorgy and H. Goldblatt, ./. Exptl. Med. 90, 73-84 (1949). 



<" W. S. Hartroft, Science 113, 673-674 (1951). 



