968 ANAPHYLAXIS AND ANAPHYLACTOID REACTIONS 



sensitiveness of human beings. It is a remarkable fact that this sensitiveness, though 

 inherited most probably as a Mendelian dominant character, manifests itself in a 

 number of clinical forms. The recognized forms are hay fever (atopic rhinitis), 

 bronchial asthma, urticaria, eczema, angioneurotic edema and gastro-intestinal dis- 

 turbance (pains, vomiting, diarrhoea). Duke^ offers strong evidence that atopic sensi- 

 tiveness can manifest itself also in outspoken bladder symptoms, chiefly pain 



The possibility that other obscure conditions are expressions of hyper sensitiveness 

 should be kept in mind" (p. 72). Since it has become established that h^'persensitive- 

 ness may be produced by enteral absorption of protein the occurrence of atopy as a 

 natural state is now in doubt. In fact, Coca admits that the heritable factor may be 

 regarded as a state of susceptibility to sensitization. Although Cooke and Van der 

 Veer^ assumed the factor to be a single Mendelian dominant, and Spain and Cooke^ 

 suggested that it may be a multiple factor, neither satisfactorily excluded the assump- 

 tion of Adkinson-* that it is a Mendelian recessive. The fact that in the combined 

 studies of Cooke and Van der Veer and of Spain and Cooke 41.6 per cent of atopic 

 children show a negative antecedent history is of significance as indicating that at 

 least some of the cases are probably not hereditary. They may have become sensitive 

 in ways not yet clear or by absorption of the "atopen." The arguments are more fully 

 discussed in Coca's chapter in this volume (p. 1004). 



The hypersensitiveness of infection is referred to by Coca as that exhibited in the 

 tuberculin and mallein reactions. That such manifestations, at least the tuberculin 

 test, are truly those of hypersensitiveness is not to be regarded as finally established 

 (Zinsser,^ Long and Seyfarth*). The fact that a patient who has had pneumonia is 

 apparently more susceptible to a subsequent attack is presumably upon a humoral 

 basis, since the lung is anatomically restored to normal in the interim. The incidence 

 of acute endocarditis superimposed on a chronically diseased valve may well be due 

 to alteration of local tissue resistance. Swift and Boots' were unable to sensitize joints 

 to non-hemolytic streptococci. There appears to be no clear experimental evidence 

 as yet to support the conception, in the true sense, of hypersensitiveness to infection. 

 Nevertheless, there are phenomena in infectious disease that strongly suggest this 

 possibility. 



ANAPHYLACTOm PHENOMENA 



The parenteral introduction of certain agents, especially into the vascular system, 

 and also by intraperitoneal and subcutaneous routes, leads to certain symptoms and 

 signs which resemble closely anaphylactic shock. When all the features are evaluated, 

 particularly in the light of the criteria offered by Wells, these reactions are not to be 

 regarded as anaphylactic. The resemblance is signified by the term "anaphylactoid 



I Duke, W. W.: Allergy — Asthma, Hay Fever, Urticaria, etc. St. Louis: Mosby, 1925. 



^ Cooke, R. A., and Van der Veer, A.: /. Immunol., i, 201. 1916. 



3 Spain, W. C, and Cooke, R. A.: ibid., 9, 251. 1924. 



-t Adkinson, J.: Genetics, 5, 363. 1920. 



s Zinsser, H.: Injection and Resistance (2d ed.), p. 440. New York: Macmillan, 1918. 



^Long, E. R., and Seyfarth, Mac II.: Am. Rev. Tiiberc, 9, 254. 1924. 



^ Swift, II. F., and Boots, R. II.: /. Exper. Med., 38, 573. 1923. 



