INFILTRATIVE EOSINOPHILIA

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Abstract
Analysis of the data derived from the clinical study of 33 cases of infiltrative eosinophilia would indicate that we have dealt with a variant, gradient stage or modality of the hypersensitivity state. The condition is in many respects indistinguishable from polyarteritis nodosa with diffuse pulmonary eosinophilic infiltrations. The severity of clinical manifestations generally depends upon the extent of the field of sensitivity (organs or system affected) and severity of the inflammatory reaction. Evidence is presented to demonstrate that the exact etiologic agent is elusive, and that the role of parasitic causation should be doubted in the arsenic-sensitive group. It appears that the poor eosinopenic response to corticotropin in violent hypersensitivity states is best explained on the basis of the adrenal cortical depression that accompanies the underlying, unrelenting stress. The eosinopenic responses to arsenic, typhoid vaccine and cortisone are governed by different mechanisms. The radical and rapid eosinopenic response to intravenous typhoid vaccine is explained by other mechanisms than the stimulation of the already depressed adrenal cortex. The beneficial effects of arsenical therapy remain unexplained. Its eosinopenic effects do not appear to depend upon paralysis of the SH groups. Administration of arsenicals leads to a depression of eosinophil production by bone marrow. Parenteral typhoid vaccine, cortisone and corticotropin fail to alter the bone marrow picture. Because of failure to demonstrate the exact etiologic agents, and the elusiveness of the eosinophil function, infiltrative eosinophila must remain in the allergic circle. A better understanding may perhaps be achieved by avoiding categorization, and by grouping all conditions characterized by diffuse vascular disease with profuse infiltration with eosinophils, and a circulating hyper-eosinophilia, under a common, descriptive term.
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