Hospital Mortality of Patients with Severe Traumatic Brain Injury is Associated with Serum PTX3 Levels

• Published in: Neurocritical care 2011-04, Vol.14 (2), p.194-199
• Main Authors: Gullo, Jackson da Silva, Bertotti, Melina Moré, Silva, Cláudia Carvalho Pestana, Schwarzbold, Marcelo, Diaz, Alexandre Paim, Soares, Flávia Mahatma Schneider, Freitas, Fernando Cini, Nunes, Jean, Pinheiro, José Tadeu, Morato, Edelton Flavio, Prediger, Rui Daniel, Linhares, Marcelo Neves, Walz, Roger
• Format: Article
• Language: English
• Subjects: Abdomen; Adolescent; Adult; Biomarkers - blood; Brain Injuries - diagnosis; Brain Injuries - immunology; Brain Injuries - mortality; Brain research; C-Reactive Protein - metabolism; Contusions; Critical Care Medicine; Enzymes; Female; Glasgow Coma Scale; Hematoma; Hospital Mortality; Hospitals; Humans; Inflammation; Intensive; Intensive care; Internal Medicine; Leukocyte Count; Logistic Models; Male; Medicine; Medicine & Public Health; Middle Aged; Mortality; Neurology; Original Article; Patients; Prognosis; Regression analysis; Serum Amyloid P-Component - metabolism; Statistical analysis; Trauma; Traumatic brain injury; Variables; Young Adult
• ISSN: 1541-6933; 1556-0961
• DOI: 10.1007/s12028-010-9462-y

Background Traumatic brain injury (TBI) is a worldwide cause of morbidity and mortality. Pentraxin 3 (PTX3) is a humoral component of the innate immune system which has been studied as a marker of inflammatory, infections or cardiovascular pathologies. To investigate the association between serum levels of PTX3 and the hospital mortality of patients with severe TBI. Methods The independent association between serum PTX3 levels after severe TBI (Glasgow Coma Scale, GCS ≤ 8) and hospital mortality was analyzed in a prospective study of 83 consecutive patients by a multiple logistic regression analysis. The leukocyte count in the same sample was analyzed as another marker of inflammatory response. Results The mean age of patients was 35 years and 85% were male. Serum PTX3 levels were determined 18.0 (SD ± 17.0) h after TBI. Patients who died showed a mean serum PTX3 level of 9.95 μg/ml (SD ± 6.42) in comparison to 5.46 μg/ml (SD ± 4.87) of the survivor group ( P  = 0.007). Elevated serum PTX3 levels remain significantly associated with mortality ( P  = 0.04) in the subset of patients with isolated TBI ( n  = 34). There were no differences in the leukocytes count measured in the same blood sample used for PTX3 determination in survivors and non-survivors ( P  = 0.56). The final multiple logistic regression model including age, pupillary examination, GCS, associated trauma, and PTX3 levels shows that serum levels of PTX3 which were higher than 10 μg/ml were independently associated with the patients mortality (adjusted OR 3.06, CI 95% 1.03–9.15, P  = 0.04). Conclusions Serum PTX3 levels after severe TBI are independently associated with higher hospital mortality and may be a useful marker of TBI and its prognosis.