Hyperglycemia and antibody titres against heat shock protein 27 in traumatic brain injury patients on parenteral nutrition

Document Type: Original Article

Authors

1 Department of Nutrition, Endoscopic and Minimally Invasive Surgery, and Cancer Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

2 Department of Neurosurgery, Research Center of Orthopedic Surgery of Shahid Kamyab Hospital, Mashhad, Iran

3 Department of Life and Health Sciences, School of Sciences and Engineering, University of Nicosia, Nicosia, Cyprus

Abstract

Objective(s):Hyperglycemia worsens the neuronal death induced by cerebral ischemia. Previous studies demonstrated that diabetic hyperglycemia suppressed the expression of heat shock protein 70 and 60 (HSP70 and 60) in the liver. IgG antibody titres against heat shock protein 27 (anti HSP27) were measured to determine whether hyperglycemia exacerbates ischemic brain damage by suppressing the expression of heat shock protein 27 (HSP27) 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 50% of their estimated daily energy requirements parenterally. Serum anti HSP27 antibody concentration was assessed at baseline, day 7 and day 14.
Results: Twenty-six out of 29 patients (n=13 in each group) completed the study. At baseline, there were no differences between the two groups. On day 14, there was a significant reduction in anti HSP27 titre concentration in the IIT compared to the GCG group (0.47±0.27 mg/dl vs 0.60±0.15 mg/dl, P=0.03).
Conclusion: In this study, intensive control of traumatic brain injury patients on parenteral nutrition reduced anti HSP27 titre, possibly suggesting a reduction in stress.

Keywords


 1. Fredduzzi S, Mariucci G, Tantucci M, Ambrosini MV. Generalized induction of 72-kDa heat-shock protein after transient focal ischemia in rat brain, Exp. Brain Res 2001; 136:19–24.

2. Izaki K, Kinouchi H, Watanabe K, Owada Y, Okubo A, Itoh H,et al. Induction of mitochondrial heat shock protein 60 and 10 mRNAs following transient focal cerebral ischemia in the rat. Brain Res Mol Brain Res 2001; 88: 14– 25.

3. Li PA, Siesjo BK. Role of hyperglycaemia-related acidosis in ischaemic brain damage. Acta Physiol Scand 1997; 161: 567– 580.

4. Kagansky N, Levy S, Knobler H. The role of hyperglycemia in acute stroke. Arch Neurol 2001; 58:1209– 1212.

5. Schirmer-Mikalsen K, Vik A, Gisvold SE, Skandsen T, Hynne H, Klepstad P. Severe head injury: control of physiological variables, organ failure and complications in the intensive care unit. Acta Anaesthesiol Scand 2007; 51:1194-1201.

6. Jeremitsky E, Omert LA, Dunham CM, Wilberger J,Rodriguez A. The impact of hyperglycemia on patients with severe brain injury. J Trauma 2005; 58:47-50.

7. Singer P, Berger MM, van den Berghe G, Biolo G, Calder P, Forbes A,et al. ESPEN guidelines on Parenteral Nutrition: intensive care. Clin Nutr 2009; 28:387-400.

8. Abe K, Kawagoe J, Aoki M, Kogure K. Changes of mitochondrial DNA and heat shock protein gene expressions in gerbil hippocampus after transient forebrain ischemia. J Cereb Blood Flow Metab 1993; 13:773– 780.

9. Nowak TS, Jacewicz M. The heat shock/stress response in focal cerebral ischemia. Brain Pathol 1994; 4:67– 76.

10. Wagstaff MJ, Collaco-Moraes Y, Aspey BS, Coffin RS, Harrison MJ, Latchman DS,et al. Focal cerebral ischaemia increases the levels of several classes of heat shock proteins and their corresponding mRNAs. Brain Res Mol Brain Res 1996; 42:236– 244.