390 RETROGRESSIVE CHANGES 



necrosis. ^^ Fat necrosis itself is not dangerous to the affected organ- 

 ism, the associated pancreatitis (and peritonitis) catfsing all the 

 symptoms. ^^ There is no evidence that sufficient quantities of soaps 

 (which are toxic) are absorbed from the necrotic areas to cause appre- 

 ciable intoxication. The soaps that are formed in the necrotic areas, 

 indeed, are probably not much absorbed, but are precipitated as cal- 

 cium soaps; in such areas at least as high as 85 per cent, of the soaps 

 may be insoluble. ^^ Healing follows rapidly in case of recovery; the 

 foci may disappear as early as eleven days after their formation (in 

 experimental animals). 



In the urine of persons with pancreatitis is frequently found a 

 substance forming an osazone, which has been the subject of much 

 investigation because of its possible diagnostic value. Cammidge,^^ 

 who first described a reaction based on this observation, considers 

 that the substance is a pentose,'*" derived from the nucleoproteins of the 

 pancreas; it bears no relation to the fat necrosis, but is commonly 

 found with fat necrosis because of the associated pancreatitis. Pre- 

 sumably cell necrosis elsewhere than in the pancreas may at times 

 cause the same reaction to appear.^^ In pancreatitis with fat necrosis, 

 or whenever there is any injury to the pancreas, there may be found 

 an increase in the amount of diastase in the blood and urine, sufficient 

 to be of diagnostic value according to Y. Noguchi.^- The peritoneal 

 exudate in acute pancreatitis is not toxic, contains no free trypsin and 

 is no more lipolytic than normal serum, presumably because of neu- 

 tralization of the enzymes and poisons by the exuded plasma.*^ 



3« See Berner, Virchow's Arch., 1907 (187), 360. 



" Guleke (Arch. klin. Chir., 1908 (85), 615) considers the intoxication of acuie 

 pancreatitis as an intoxication with trypsin, which can be checked by antitrypsin. 

 Doberauer (Beitr. kUn. Chir., 1906 (48), 456), Egdahl (Jour. Exp. Med., 1907 (9), 

 385), Petersen, Jobling, and Eggstein {ibid., 1916 (23), 491), and Cooke and 

 Whipple {ihid., 1918 (28), 222), however, look upon the products of cellular dis- 

 integration as the source of the intoxication, v. Bergmann (Zeit. exp. Path. u. 

 Ther., 1906 (3), 401), states that the toxicity is not due to either the enzymes or 

 to albumoses; and that it is a true autointoxication which can be prevented by 

 previous immunization with either pancreas extracts or commercial trypsin. (See 

 also Fischler, Deut. Arch. klin. Med., 1911 (103), 156; and v. Bergmann and 

 Guleke, Miinch. med. Woch., 1910 (57), 1673.) The histones and protamines 

 liberated from the digested tissue, ttnd which are very toxic, have boon suggested 

 as a possible factor by Schittenhelm and Weichardt (Zeit. Immunitiit., 1913 (14), 

 609), while the beta-nucleo-proteins are included among the toxic elements by 

 Goodpasture, Jour. Exp. Med., 1917 (25), 277. 



^* See Frugoni and Stradiotti, Arch. Sci. Med., Torino, 1910; also Berl. klin. 

 Woch., 1910 (47), 386. 



39 Proc. Royal Soc. Med., 1910 (III, pt. 2), 163, bibliography; Lancet, 1914, 

 Sept. 26. 



" Weber believes that it is a hexose (Deut. med. Woch., 1912 (38), 166), and 

 it may be urinary dextrin (Pekelharing and Van Koogenhuyze, Zeit. physiol. 

 Chem., 1914 (91;," 151). 



*' See Whipple, cl al., Johns Hopkins IIosp. Bull., 1910 (21), 339; Karas, Zeit. 

 klin. Med., 1913 (77), 125. 



^2 Arch. klin. Chir., 1912 (98), 11. 2. 



" Wliipi)le and Goodpasture, Surg., Gyn. and Obst., 1913 (17), 541. 



