308 DISTURBANCES OF CIRCULATION 



by the hemolytic poisons. In some instances cholesterol administra- 

 tion improves the anemia, which suggests that the poison attacks 

 the lipoids of the corpuscles,^' as so many hemolytic agents do. Both- 

 riocephalus anemia, which so closely resembles the "pernicious" form, 

 seems to be caused by a hemolytic lipoid, ^ presumably a cholesterol 

 ester of oleic acid, and there is a growing tendency to associate hemoly- 

 tic lipins with the etiology of pernicious anemia.^ However, although 

 in hemolytic anemias there is an increased amount of unsaturated 

 lipins in the blood^ Medak* did not find the isolated lipoids to be 

 particularly hemolytic.^ (See Hemolysis, Chapter ix.) The origin 

 and the nature of the specific hypothetical poisons have been sought 

 in vain. Some authors have referred them to infections of unknown 

 nature, occurring perhaps in the mouth and gastrointestinal tract 

 ( Hunter), ^^ or to hemolytic products of intestinal putrefaction,^ or to 

 faulty metabohsm. For example, Iwao^ has found that tyramine 

 (p-oxyphenyl-ethylamine) produces in guinea pigs a blood picture 

 resembling pernicious anemia, and this amine ma 5^ be produced either 

 in the intestines or during metabolism. Others, with perhaps the best 

 of grounds, would ascribe pernicious anemia to a multiplicity of causes, 

 which produce a protracted slight hemolysis that continues until the 

 hematogenetic organs give out, their exhaustion being perhaps hastened 

 by the influence of the toxic substances in the blood; hematogenesis 

 then becomes insufficient to replace the lost corpuscles, and the picture 

 of pernicious anemia is established.^ The relatively great proportion 

 of the iron that is stored in the liver supports the view that the 

 hemolysis takes place in portal territory, and many other facts point 

 to the same conclusion, but it is not generally accepted that the 

 spleen plays an essential role in causing pernicious anemia through 

 excessive phagocytosis or production of hemolytic poisons.' 



»^ See Reicher, Bed. klin. Woch., 1908 (45), 1838. 



1 Tallquist, Zeit. klin. Med., 1907 (61), 427; Arch. exp. Path. u. Pharm., 1907 

 (57), 367. 



^ SeeLiidke and Fejes, Deut. Arch. klin. Med., 1913 (109), 433. 



3 See King, Arch. Int. Med., 1914 (14), 145; Csonka, Jour. Biol. Cheni., 191S 

 (33), 401. 



■» Biochem. Zeit., 1914 (59), 419. 



« See McPhedran, Jour. Exp. Med., 1914 (18), 527. 



^ See Kiilbs (Arch. exp. Path. u. Pharm., 1906 (55), 73), who found the in- 

 testinal contents of patients with chronic intestinal disorders to contain hemo- 

 lytic substances of undetermined character. IfcMiiolytic lijioids in the intestinal 

 contents have been described by Bergor and Tsuchiga (Deut. Arcli. klin. Med., 

 1909 (96), 252) and Liidke and Fejes, loc. cit.; but this observation failed of con- 

 firmation by Ewald (Deut. med. Woch., 1913 (39), 1293). 



Herter (Jour. Biol. Chem., 190i) (2), 1) suggested a relation between intestinal 

 infection with B. acrocjencR capsulatiits, wliich produces hemolytic substances, and 

 pernicious anemia. 



^ Biochem. Zeit., 1914 (59), 436. 



'^ Sec also limiting, .Johns Hopkins llosp. Bull., 1905 (16), 222; Pai)penheim, 

 Folia Serologica, 1910 (10), 217. 



«See Hirschlield, Zeit. klin. Med., 1919 (87), 165. 



