THE SOLUTION of the problems of eczema depends on the correlation of many interrelated facts. One apparent connecting link is the process of autoeczematization, which develops in many types of eczematous dermatoses. Autoeczematization, as considered here, consists in the development of scattered eczematous lesions complicating an acute eczematous process ordinarily of limited extent.
Because of the paucity of experimental work on what is felt to be a fundamental and important problem, a study has been instituted of some of the mechanisms involved. This paper is a preliminary report of such studies.
SURVEY OF THE LITERATURE
The concept of autoeczematization stems from the observations of Whitfield,1 who postulated that a person might become sensitized to split products of autogenous tissue proteins. Whitfield described three types of reactions, one, and possibly two, of which fits into the present day concept of autoeczematization. The first consisted of widely distributed,
CORMIA FE, ESPLIN BM. AUTOECZEMATIZATION: Preliminary Report. Arch Derm Syphilol. 1950;61(6):931–945. doi:https://doi.org/10.1001/archderm.1950.01530130049012
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