Because colonization with Staphylococcus aureus probably predisposes to staphylococcal infections, we examined several factors that may be associated with staphylococcal carriage in outpatients with non-insulin-dependent diabetes mellitus and in nondiabetic controls. Nose and skin carrier rates for 59 diabetic patients were significantly greater (30.5%) than for 44 controls (11.4%) (P = .02), but rates did not differ significantly between diabetic patients who injected insulin (31.0%) and those who did not (30.0%). Among the diabetic patients, staphylococcal colonization was not significantly correlated (P greater than .05) with recent antibiotic treatment, age, race, or clinical duration of diabetes but was inversely correlated (P less than .03) with glycemic control, as measured by fasting plasma glucose and glycosylated hemoglobin levels. Hospitalization in the previous year was also associated with staphylococcal colonization, and it was significantly more common among the diabetic patients than the controls; however, this did not account for the increased colonization rates observed. Our results in a well-characterized population confirm an increased rate of staphylococcal colonization among diabetic as compared with nondiabetic outpatients but demonstrate that neither injections of insulin nor various pertinent demographic factors explain this finding.

It has recently been reported that glucose and its analogues inhibit in vitro ascorbic acid transport across the cell membrane of polymorphonuclear leukocytes and fibroblasts. We have studied the effect of in vivo hyperglycemia on the intracellular ascorbic acid level of mononuclear leukocytes in normal and diabetic human subjects. Administration of an intravenous glucose load resulted in a prompt decrease of mononuclear leukocyte ascorbic acid level in the normal subjects. The rate of its decline correlated closely with the rate of change of plasma glucose. Among the NIDDM subjects in the fasting state, the plasma glucose was high and the leukocyte ascorbic acid level was low when compared with that of the normal subjects. The decrease in the leukocyte ascorbic acid level during disposition of the i.v. glucose load was not statistically significant in the diabetics. The hyperglycemia-induced intracellular depletion of ascorbic acid could be clinically important and requires further evaluation.

Competition for membrane transport between glucose and ascorbic acid (AA) has been shown in vitro in human lymphocytes, granulocytes, and fibroblasts. Therefore, we examined the effects of acute administration of i.v. glucose on AA levels in mononuclear (MNL) and polymorphonuclear leukocytes (PMN) and on leukocyte chemotaxis. Plasma glucose and AA, MNL AA, PMN AA, and chemotaxis by MNL and PMN were measured before and after i.v. glucose in fasted normal male volunteers. A decline in AA occurred in PMN as well as MNL, but decreases in AA induced acutely by transient hyperglycemia were not associated with changes in chemotaxis. However, under conditions of prolonged hyperglycemia maintained by a glucose clamp technique, significant changes (p less than 0.01) in chemotaxis by both PMN and MNL were observed after 210 and 240 min, with changes in chemotaxis to several chemoattractants significantly correlated with decreases in intracellular AA after 240 min (p less than 0.05). These results are consistent with the hypothesis that chronic hyperglycemia may be associated with intracellular deficits of leukocyte AA, an impaired acute inflammatory response, and altered susceptibility to infection and faulty wound repair in patients with diabetes.

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