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 of poor diabetes control, as has been shown previously in ketoacidosis, and (2) hyperglycemia or a closely related factor may contribute to the defect.