In order to assess the influence of poor diabetes control on function of leukocytes, polymorphonuclear leukocytes (PMN's) from patients with poorly controlled but nonketotic disease were studied before and after therapy. Before treatment, phagocytosis was significantly reduced (p < .001) and, consequently, the rate of killing the test organism (type 25 pneumococcus) was decreased (p < .01). Following antidiabetes therapy phagocytosis improved significantly; while microbicidal rates also improved, they remained less than control values (p < .01).Serum from the untreated diabetics uniformly reduced phagocytosis and microbicidal rates of control granulocytes; serum from controls improved phagocytosis by the diabetic PMN's, but restored normal microbicidal rates in only half of the patients. This transferable inhibitory effect of hyperglycemic diabetic serum on control granulocytes was abolished by dilution, and was reproduced in normal serum by the isosmotic addition of glucose. These studies suggest that (1) PMN function may be impaired during periods cf poor diabetes control, as has been shown previously in ketoacidosis, and (2) hyperglycemia or a closely related factor may contribute to the defect. DIABETES 23:9-15, January, 1974. It has long been believed that an abnormality in host defense predisposes the diabetic patient to both bacterial and fungal infection. However, experimental approaches to the study of host defense in the diabetic have often yielded confusing and conflicting results and, in general, have failed to consistently demonstrate either a humoral or a cellular defect which might increase the susceptibility of diabetic patients to infection. 1
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