Hyperglycemia and antibody titres against heat shock protein ۲۷ in traumatic brain injury patients on parenteral nutrition

Objective(s):Hyperglycemia worsens the neuronal death induced by cerebral ischemia. Previous studies demonstrated that diabetic hyperglycemia suppressed the expression of heat shock protein ۷۰ and ۶۰ (HSP۷۰ and ۶۰) in the liver. IgG antibody titres against heat shock protein ۲۷ (anti HSP۲۷) were measured to determine whether hyperglycemia exacerbates ischemic brain damage by suppressing the expression of heat shock protein ۲۷ (HSP۲۷) in the brain. Materials and Methods: A randomized controlled study of traumatic brain injury ICU patients treated either by intensive insulin treatment (IIT) or by conventional glucose control (CGC) was conducted. Patients received at least ۵۰% of their estimated daily energy requirements parenterally. Serum anti HSP۲۷ antibody concentration was assessed at baseline, day ۷ and day ۱۴. Results: Twenty-six out of ۲۹ patients (n=۱۳ in each group) completed the study. At baseline, there were no differences between the two groups. On day ۱۴, there was a significant reduction in anti HSP۲۷ titre concentration in the IIT compared to the GCG group (۰.۴۷±۰.۲۷ mg/dl vs ۰.۶۰±۰.۱۵ mg/dl, P=۰.۰۳). Conclusion: In this study, intensive control of traumatic brain injury patients on parenteral nutrition reduced anti HSP۲۷ titre, possibly suggesting a reduction in stress.

کلیدواژه ها:

Glucose control ، Heat shock protein ۲۷ ، Parenteral Nutrition ، Traumatic brain injury