Open Access

ARTICLE

Hypolipoproteinemia and hyperinflammatory cytokines in serum of severe and moderate traumatic brain injury (TBI) patients

Kyriaki Venetsanou¹, Konstantinos Vlachos², Athanassios Moles¹, Gerassimos Fragakis², George Fildissis¹, George Baltopoulos¹

1 Athens University School of Nursing Intensive Care and Research Unit, KAT General Hospital, Athens 14561, Greece
2 Neurosurgical Clinic, KAT General Hospital, Athens 14561, Greece

* Corresponding Author: K. Venetsanou,

European Cytokine Network 2007, 18(4), 206-209. https://doi.org/10.1684/ecn.2007.0112

Accepted 05 November 2007;

Abstract

Traumatic brain injury (TBI) acts as an inducer of the inflammatory reaction expressed by the release of pro-inflammatory cytokines (interleukin-1b [IL-1b], interleukin-6 [IL-6] and interleukin-8 [IL-8]), and causes metabolic alterations in the early, post-traumatic state, either in the brain or/and the systemic circulation. The metabolic changes involve carbohydrates, proteins and lipids. We focused on the serum lipid profile, the impact of trauma on lipoproteins, and their subsequent effects, on inflammation. We investigated the role of cytokines and serum lipids, in patient outcome, reviewing 30-day mortality and the Glasgow Coma Scale (GCS). A total of 75 patients with severe or moderate TBI (GCS ≤ 13) were allocated to two groups (group 1 non-survivors and group 2 survivors). One blood sample was collected from each patient within 24h of admission. Cytokines were measured in serum by ELISA and serum lipids using an enzymatic method. We found significantly decreased serum lipid levels and increased cytokines levels for all patients compared with healthy volunteers. Comparing the two groups, IL-6 and IL-8 levels were higher (p < 0.0001) and LDL levels lower (p = 0.003) in non-survivors than in survivors. We observed a significant inverse correlation between IL-8 and LDL (p = 0.04) in patients with an unfavorable outcome. Our results suggest that LDL alone, or in combination with IL-6 and IL-8, could be a possible prognostic factor for outcome in patients with TBI, as regards 30- day mortality.

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