Eosinopenia Produced by ACTH in Patients with Schizophrenia

The contention that adrenal cortical function is deranged in patients with schizophrenia, particularly those with long-standing disease, has been advanced for several years by Pincus, Hoagland, and their associates (1). Using changes in urinary excretion of sodium, potassium, uric acid, blood lymphocytes as indices, they have reported that as few as 20% of schizophrenic subjects respond in normal fashion to the injuection of 25 mg of pituitary adrenocorticotropic hormone. Despite the demonstration by other investigators of an apparently normal response to ACTH by patients with schizophrenia (2-4) the postulated hypoadrenocorticism in such patients has been used as a rationale for therapy of this disporder with ocrtisone (5). In addition. the schizophrenic subject's response to ACTH has been considred of prognostic significance in terms of the anticipated efficacy of electro convulsive therapy (6). Hence it seemed pertinent to present material on the eosinopenia produced by ACTH‡ in 30 patients with long-standing mental illness.

Subjects and method. These data have been accumulated during the course of a project now in progress at the Elgin State Hospital desigtned to investigate nicotinic acid-tryptophane relationships in human subjects. The groups being studied includes 30male patients, aged 30 to 63 years, who have been hospitalized because of schizophrenia for 2 to 19 (average: 11) years. Eosinophil counts were determined on venous blood before, and 4 hours following intramuscular injections of 25 mg of ACTH, according to the method of Thorn (7). The initial studies were carried out prior to the institution of the experimental regimen, and the procedure was repeated after the subjects had been on a moderately low-protein diet for one year.

Results. All but 5 patients showed on at least one occasion a 50% or greater fall in circulating eosinophils following the injection of ACTH (Table I).