In 1907 Wolff-Eisner1 stated the belief that simple chemical compounds act as sensitizing agents by means of their conjugation with autochthonous body protein. Recent experimental work has refocused attention on the problem of hypersensitivity to simple chemicals, in its relation not only to the development of delayed cutaneous hypersensitivity of the cellular type but also to the induction of anaphylactic states. In the light of this work it seemed advisable to reexamine the data pertaining to sensitiveness to arsphenamine and to perform experiments to clarify further the fundamental concepts of the pathogenesis of cutaneous hypersensitivity to arsphenamine.
The original experimental work on the production of cutaneous sensitivity to arsphenamine in the guinea pig was done by Frei.2 The various factors that contribute to the development of the sensitivity have recently been summarized.3 The attempted linkage of the sensitivity (as it exists in animals) with the induction, by
CORMIA FE. CUTANEOUS SENSITIZATION TO ARSPHENAMINE: ATTEMPTS TO INDUCE AN ANAPHYLACTIC STATE WITH DIFFERENT ARSPHENAMINES; ITS PRODUCTION WITH A CONJUGATE ARSPHENAMINE ANTIGEN, AND THE INCIDENTAL RELATION BETWEEN ANAPHYLACTIC AND CUTANEOUS HYPERSENSITIVITY. Arch Derm Syphilol. 1941;43(1):103–110. doi:10.1001/archderm.1941.01490190106007
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