SIGMFICANCE OF AUTOI S TOMCAT 10 \ o'Jo 



a certain type of cases of defective development led Herter'- to the 

 conclusion that intestinal intoxication is responsible, and hence he 

 designated this condition "intestinal infanlilisni." 



Tetany associated with gastric dilatation ott'ers perhaps the strongest 

 case, numerous observers having reported finding a marked toxicity 

 of the stomach contents.'^ Pineles''' considers that all forms of tet- 

 any, whether of gastric origin or following thyroidectomy, are due 

 to one and the same "tetany poison," but recent studies indicate that 

 alkalosis is an important factor in tetany. There is also considerable 

 evidence that the tetany, when present, is associated with a deficiency 

 in calcium in the blood and nervous tissue, and that this is further 

 related to the functional activity of the parathyroids {q. v.). 



Although there are usually evidences of intoxication in acute dila- 

 tation of the stomach, yet there is no good evidence as to its nature. 

 It is suggested by Woodyatt and Graham^^ that the dilatation is pro- 

 duced by COo secreted into the stomach from its walls. 



The relation of intestinal intoxication to the various anemias, par- 

 ticularly chlorosis and pernicious anemia, has been repeatedly indi- 

 cated and discussed. Clinical evidence strongly indicates that such a 

 relation exists, and there is no doubt that hemolytic substances may 

 be formed in the alimentary tract, ^*^ but that chlorosis and pernicious 

 anemia do depend upon intestinal putrefaction or infection is far 

 from established (see "Anemia," Chap. xiii). 



As yet, however, we cannot say positively that any human disease is 

 caused by the products of intestinal putrefaction, and with growing 

 knowledge the importance ascribed to this source of disease is becom- 

 ing steadily less.^' The fact must not be overlooked that many 

 persons habitually eat putrefied proteins, from the "high" game of 

 the epicure to the carrion masses that dehght many primitive people, 

 without the shghtest evidence of intoxication therefrom. 



It seems highly probable that gastro-intestinal "autointoxication" 

 would be a much more serious matter were it not for the mechanisms 

 of defence possessed by the body, especially in the liver. '^ For exam- 

 ple, Richards and Rowland have indicated the increased toxicity of 

 indole when the oxidizing power of the liver is reduced, and Herter 

 and Wakeman have shown the power of the liver to combine indole 

 and thus remove it from circulation. This topic has been discussed 

 more fully elsewhere (Chap, x) . 



12 See McCrudden, Jour. Exper. Med., 1912 (15), 107. 



1' Bibliography by Halliburton and McKendrick, Brit. Med. Jour., 1901 (i), 

 1607. 



1* Deut. Arch. klin. Med., 1906 (85), 491. 



'5 Trans. Chicago Path. Soc, 1912 (8), 354. 



'« See Kiilbs, Arch, exper. Path., 1906 (55), 73; also Herter, Jour. Biol. Chem., 

 1906 (2), 1. 



1^ See Alvarez, Jour. Amer. Med. Assoc, 1919 (72), 8; E. O. Jordan, "Food 

 Poisoning," Univ. Chicago Press. 1917. 



18 For discussion and literature see Lust, Hofmeister's Beitr., 1905 (6), 132. 



