subjects have frequent associated infections despite adequate humoral antibody production.1 Cellular defense mechanisms have been given little attention in diabetes, though their role in body response to tissue injury by leukocyte emigration is vital. This study of inflammatory response in 35 diabetic children was done to determine if defective leukocyte emigration was present.
MethodsThirty-five juvenile diabetic patients were studied by Rebuck and Crowley's skin window technique.2 The patients were not acidotic or obviously infected. All had normal peripheral white blood cell counts (WBC) at 5,000 to 10,000/ cu mm. Thirteen normal control children, aged 3 to 20 years, with negative family history for diabetes were also studied. Rebuck and Crowley's skin window technique was used and the inflammatory exudate from a 4-mm sterile abrasion on the volar aspect of the forearm was studied at 2, 5, 8, and 12 hours. The cells responding to the abrasion adhered to the undersurface of a cover slip. The preparation was removed and dried quickly, stained with Giemsa's stain, and mounted on glass slides. The time of appearance of cellular inflammatory exúdate was recorded and the amount of exú¬ date quantitated 0 to 4+ in an unclumped area of the preparation. Differential counts of neutrophils and mononuclear cells (macrophaees) were done on 200 to 300 cells per slide. The criteria used for quantitation of cellular response were as follows:1. 0-cellular response not present or a few scattered cells seen per high powered field. 2. 4-|-comparable to the maximum response seen in a healthy control.
