The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis

Abstract

AimsTo investigate the relationship between oxidative stress and serum levels of pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis. MethodsSeventy-three patients presenting to hospital with diabetic ketoacidosis or non-ketotic hyperglycemia were studied. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, total antioxidant capacity (TAC), 8-iso-prostaglandin F2α (8-iso-prostaglandinF2α, 8-iso-PGF2α), tumor necrosis factor receptor-I (TNF-RI), interleukin -1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were measured in all patients. The patients were then given an intravenous infusion of insulin 0.1U • kg-1 • h-1, as well as fluids, symptomatic therapy and parenteral and intravenous nutrition. Results1.Before treatment, SOD and TAC were significantly lower (P<0.05), whereas MDA and 8-iso-PGF2α were significantly higher (P<0.05) in patients with hyperglycemic crises compared to controls. After treatment, SOD and TAC significantly increased (P<0.05), while MDA and 8-iso-PGF2α significantly decreased (P<0.05).2.TNF-RI, IL-1β, TNF-α and IL-6 were significantly higher, both before and after treatment, in patients with hyperglycemic crises compared to controls (P<0.05).3.Before treatment, IL-6 and TNF-α were positively correlated with 8-iso-PGF2α (r=0.32, r=0.36, P<0.05) in patients with hyperglycemic crises. After treatment, IL-6 and SOD were negatively correlated within patients (r=−0.33, P<0.05). Multiple regression analysis indicated that 8-iso-PGF2α affects the level of serum IL-6. ConclusionPatients with hyperglycemic crises have significantly increased oxidative stress and dysregulated serum pro-inflammatory cytokines that can be effectively treated by intensive insulin therapy.