Abstract
BackgroundTraumatic brain injury (TBI) causes activation of several neurochemical and physiological cascades, leading to neurological impairment. We aimed to investigate the level of novel chemokine RANTES in plasma, cerebrospinal fluid (CSF) and contused brain tissue in traumatic brain injury patients and to correlate the expression of this chemokine with the severity of head injury and neurological outcome.MethodsThis longitudinal case control study was performed on 70 TBI patients over a period of 30 months. Glasgow coma scale (GCS) and Glasgow outcome score were used to assess the severity of head injury and clinical outcome. Level of RANTES was quantified in plasma (n = 60), CSF (N = 10) and contused brain tissue (n = 5). Alterations in the plasma levels on 1st and 5th day following TBI were assessed. Patients were categorized as severe (GCS < 8) (SHI), moderate and mild Head injury (GCS > 8–14). 15 healthy volunteers were taken as the control group.ResultsThe median plasma RANTES levels were 971.3 (88.40–1931.1); 999.2 (31.2–2054.9); 471.8 (370.9–631.9) for SHI, MHI and healthy control respectively and showed statistically significant variation (p = 0.005). There was no statistical difference in the mean 1st and 5th day RANTES levels for the SHI group. However, admission RANTES levels were significantly higher in patients who died than those who survived (p = 0.04). Also, RANTES levels were significantly higher in plasma as compared to contused brain tissue and CSF (p = 0.0001).ConclusionThis is the first study of its kind which shows that there is significant correlation of admission RANTES levels and early mortality. Another interesting finding was the significant upregulated in the expression of RANTES in plasma, compared to CSF and contused brain tissue following severe TBI.
Highlights
Traumatic brain injury (TBI) causes activation of several neurochemical and physiological cascades, leading to neurological impairment
Setting and design We conducted a prospective longitudinal case–control study (STROBEs criteria followed), in a level 1 trauma care center, for the duration of 30 months (December 2010–May 2013). 70 isolated traumatic brain injury patients, were included in the study and categorized into four groups (n = 15) i.e. (i) severe head injury (SHI) (GCS ≤ 8) who died within 5 days of injury, (ii) SHI who survived beyond 5 days of injury, (iii) moderate and mild head injury (MHI) (GCS > 8–14) who were discharged within 5 days of injury, (iv) MHI who were hospitalized for more than 5 days of injury, following the assessment for injury using tools like Glasgow coma scale, and computed tomography (CT) findings
On comparing the baseline parameters for the study groups
Summary
Traumatic brain injury (TBI) causes activation of several neurochemical and physiological cascades, leading to neurological impairment. Traumatic brain injury leads to a complex cascade of pathophysiological and neurochemical events. Regulated upon activation normal T cells expressed and secreted (RANTES) is a C–C β chemokine (68 a.a.) is a selective chemo attractant of human monocytes and lymphocytes and induces the migration of monocytes, eosinophils, T cells, NK cells, mast cells, and basophils to sites of inflammation and infection [1], are released from multiple sources, predominantly CD8+ T cells, platelets, macrophages, eosinophils, fibroblasts, monocytes [2,3,4]. In addition to inducing chemotaxis, RANTES can act as an antigen-independent activator of T cells in vitro [4, 5]
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