Interleukin 1β and interleukin 6 relationship with paediatric head trauma severity and outcome

• DOI: 10.1007/s00381-004-1032-1
• Publication Date: 2004-09-28T17:26:41Z
• Authors: Antonio Chiaretti; Orazio Genovese; Luigi Aloe; Alessia Antonelli; Marco Piastra; Giancarlo Polidori; Concezio Di Rocco
• Keywords: Male; Time Factors; Adolescent; Interleukin 1 beta; Glasgow Outcome Scale; Interleukin 6; Observation; Glasgow Outcome Score; Immunoenzyme Techniques; 03 medical and health sciences; Traumatic brain injury; 0302 clinical medicine; Humans; Glasgow Coma Scale; Prospective Studies; Child; Interleukin-6; Infant; 3. Good health; Brain Injuries; Child, Preschool; Female; Hydrocephalus; Interleukin-1

Based on the known inflammatory role of interleukins (IL), we evaluated IL-1beta and IL-6 expressions and their association with the severity of traumatic brain injury (TBI; Glasgow Coma Scale [GCS]) and the outcome (Glasgow Outcome Score [GOS]) recorded in a paediatric population.The design was a perspective observational clinical study carried out in the paediatric intensive care unit of the University Hospital.We measured the IL-1beta and IL-6 levels in 14 children with severe TBI (patients) and in 12 children with obstructive hydrocephalus (control group). Cerebrospinal fluid (CSF) and plasma samples were collected 2 h (T1) and 24 h (T2) after TBI. Interleukins were assayed using the immunoenzymatic method.The IL-1beta mean level was significantly lower than the IL-6 mean level both in the CSF and plasma of TBI children. In the CSF, the IL-1beta level increased from 55.71+/-72.79 pg/ml at T1 to 106.10+/-142.12 pg/ml at T2 and the IL-6 level increased from 405.43+/-280.28 pg/ml at T1 to 631.57+/-385.35 pg/ml at T2; a similar trend was observed in plasma. We found a statistically significant correlation between the increase in CSF and plasma interleukin levels between T1 and T2 and head injury severity (GCS<or=5) as well as poor outcome (GOS<or=3).The increases in IL-1beta and IL-6 expression were correlated with head injury severity and were indicative of poor clinical outcome, reflecting an endogenous neuroinflammatory response after TBI.