The cerebrospinal fluid thromboxane A(2) and prostaglandin I-2 levels in patients with severe head injury

Uzan M. , TANRIVERDİ T. , Aydin S. , Gumustas K., TÜRECİ E. , KUDAY C.

NEUROSURGERY QUARTERLY, vol.13, no.2, pp.59-63, 2003 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 13 Issue: 2
  • Publication Date: 2003
  • Doi Number: 10.1097/00013414-200306000-00001
  • Page Numbers: pp.59-63


The aim of this study was to evaluate the levels of thromboxane A, (TXA(2)) and prostacyclin (also called prostaglandin I-2 or PGI(2)) production in the ventricular cerebrospinal fluid (CSF) in patients with severe head injury (SHI). CSF samples in the trauma group, which included 15 patients, were obtained via insertion of an intraventricular catheter, and in the control group, which included 5 patients, they were obtained while the patients' shunt procedures were being performed. Levels were measured using the corresponding kits for TXB2 and 6-keto PGF(1a) metabolites of TXA(2) and PGI(2) respectively, during the following four periods after trauma: 6 to 10 hours, 20 to 28 hours, 40 to 56 hours, and 64 to 74 hours. CSF concentrations of TXB2 significantly increased in patients with SHI at all times after trauma (P < 0.0001). There was a variation in the levels of 6-keto-PGF(1a), however. Between 6 and 10 hours after trauma, a significant decline was noted (P < 0.05). By the first day, levels were markedly increased, on average, three times those found in the controls, but there was a tendency for levels to decline again later. The TXA(2)/PGI(2) ratio was studied, and it remained high, particularly at 6 to 10 hours and 64 to 74 hours after trauma. The ratio revealed the close relation between the severity of injury and a poor Glasgow Outcome Scale score, with the latter being higher in more severe injury. These results suggest that an increased TXA(2)/PGI(2) ratio was closely related to the severity of the brain injury and therefore appears to be an important indicator of secondary brain damage.