Abstract

Recent studies have suggested that endogenous angiogenesis inhibitor endostatin/collagen XVIII might play an important role in the secondary brain injury following traumatic brain injury (TBI). In this study, we measured endostatin/collagen XVIII concentrations serially for 1 week after hospitalization by using the enzyme-linked immunosorbent assay method in the cerebrospinal fluid (CSF) of 30 patients with TBI and a Glasgow Coma Scale (GCS) score of 8 or less on admission. There was a significant trend toward increased CSF levels of endostatin after TBI versus control from 72 h after injury. In patients with GCS score of 3–5, CSF endostatin concentration was substantially higher at 72 h after injury than that in patients with GCS score of 6–8 (P < 0.05) and peaked rapidly at day 5 after injury, but decreased thereafter. The CSF endostatin concentration in 12 patients with an unfavorable outcome was significantly higher than that in 18 patients with a favorable outcome at day 5 (P = 0.043) and day 7 (P = 0.005) after trauma. Receiver operating characteristic curve analysis suggested a reliable operating point for the 7-day CSF endostatin concentration predicting poor prognosis to be 67.29 pg/mL. Our preliminary findings provide new evidence that endostatin/collagen XVIII concentration in the CSF increases substantially in patients with sTBI. Its dynamic change may have some clinical significance on the judgment of brain injury severity and the assessment of prognosis. This trial is registered with the ClinicalTrials.gov Identifier: NCT01846546.

Highlights

  • Angiogenesis following traumatic brain injury (TBI) is critical to the posttraumatic tissue reparative processes and restoration of function, but is associated with the development of secondary brain injury [1,2,3]

  • The increase of endostatin/collagen XVIII+ macrophages/microglial cells has been reported in patients with traumatic brain injury [12], nothing is known about changes in cerebrospinal fluid (CSF) endostatin/collagen XVIII concentrations

  • We describe the time-dependent increase of endostatin/ collagen XVIII levels in CSF of patients with severe TBI that elevated within the first week after injury

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Summary

Introduction

Angiogenesis following traumatic brain injury (TBI) is critical to the posttraumatic tissue reparative processes and restoration of function, but is associated with the development of secondary brain injury [1,2,3]. It is characterized by vessel sprouting and arborisation reaching maximum levels 3–5 days after TBI [4, 5] and is regulated by pro- and antiangiogenesis factors [6]. We examined the concentrations of endostatin/collagen XVIII in the CSF of noninjured controls and the changes in patients with severe TBI during early posttraumatic period, to determine whether differences exist, and assessed the relation

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