Numerous and diverse hypotheses have been offered to explain the mechanism involved in the production of arsphenamine dermatitis. The more intensively one reviews the literature the more confused the problem becomes. It is impossible, therefore, to give a satisfactory short summary as an introduction to this paper. Excellent reviews of such theories have been given recently by Franklin,1 Bernstein,2 Stokes,3 Raiziss4 and many others. A few of the outstanding theories should be mentioned, however, because of the causal suggestions they offer in the field of therapy.
According to Moore and his co-workers,5 it is now generally believed that postarsphenamine dermatitis is the result of direct sensitization to arsphenamine, to the products of its metabolism or to a state of general allergic instability or to a hypersensitiveness not necessarily absolutely specific for arsphenamine. This theory has been materially strengthened by experimentation on animals and the clinical