CAUSES OF FATTY METAMORPHOSIS 339 



Lecithin and Other Intracellular Lipoids. It has often been sug- 

 gested that the lecithin of the cell might act as a source of the fat in 

 fatty degeneration, but it has been quite conclusively shown that this is 

 not the case, numerous investigators having found that the amount of 

 lecithin remains nearly normal in cells even during the most extreme 

 fatty degeneration. 1 The lecithin may be, and undoubtedly is, one of 

 the fatty substances that become visible during cell autolysis, and pre- 

 sumably other lipoids also appear. 



Kaiserling and Orgler 2 have described under the non-committal name 

 of "myelin'' certain intracellular droplets that may be found in the 

 cortical cells of the normal adrenal, in amyloid kidneys, pneumonic exu- 

 dates, tumor cells, retrogressive thymus tissue, corpus luteum, and bron- 

 chial secretions ; and which differ from fat in being doubly refractile 

 and in staining but faintly gray with osmic acid, although taking up fat 

 stains well. Their average size is 4-6 microns, and they dissolve in ether 

 and chloroform readily, but poorly in alcohol. Probably this myelin is 

 one of the cell lipoids, possibly " protagon " made visible by cell degen- 

 eration, for except in the adrenal the cells containing it are in a necro- 

 biotic state. This is supported by Albrecht's observation that post- 

 mortem myelin formation is checked by heating the cells to 58 -62, a 

 temperature which destroys the autolytic enzymes. 3 



Summary. We must conclude, therefore, that fatty de- 

 generation of an organ means, in the case of the liver, myocar- 

 dium, and pancreas an infiltration of fat from outside into cells 

 which have been degenerated by the action of poisons or other 

 injurious influences. In the kidney, spleen, and muscles an 

 increase of fat seldom occurs from these causes, but the cells 

 may show a marked fatty metamorphosis through the setting 

 free of the invisible intracellular fat by autolytic changes. 



CAUSES OF FATTY METAMORPHOSIS 



Nevertheless, the old anatomical distinction of infiltration 

 and degeneration still remains, provided we do not hold to the 

 original idea that the term degeneration implies that the cell 

 proteid has been converted into fat ; for we must recognize that 

 under some conditions the cells may take up great quantities of 

 fat without suffering any appreciable degenerative changes, 

 whereas in other instances the appearance of fat is associated 



l Lusena, Lo Sperim., 1903 (57), 29; Kubow, Dissert., Kopenhagen, 1903; 

 Rubow, Arch. f. exp. Pathol., 1905 (52), 173. Waldvogel, however, maintains 

 that in fatty degeneration and in autolysis there occurs a decrease in the lecithin, 

 associated with an increase in " jecorin," " protagon," fatty acids, neutral fats, 

 and cholesterin. There is so much doubt concerning the chemical status of 

 "jecorin" and "protagon" that these statements are in need of much con- 

 firmation. (See Waldvogel and Mette, Munch, med. Woch., 1906 (53), 402, 

 for review of Waldvogel's work.) 



2 Virchow's Arch., 1902 (167), 296. 



3 Cent. f. Path., 1904 (15), 982. See also Orgler, Virchow's Arch., 1904 

 (176), 413; and Albrecht, Verh. Deut. Path. Gesellsch., 1903 (6), 95. 



