TNF-α and sICAM-1 in intracranial aneurismal rupture

INTRODUCTION: Subarachnoidal hemorrhage (SAH) occurring after aneurismal rupture produces an inflammatory response in the cerebral circulation. Tumor necrosis factor (TNF)-α is a major cytokine in this process. Adhesion molecules provide information on inflammatory reactions taking place in the walls of blood vessels. Clinical evidence suggests a role of soluble intercellular adhesion molecule (sICAM)-1 in early hemorrhagic events. This study aimed to evaluate the implementation of early TNF-α and sICAM-1 serum measurement for the prognosis of patient outcome after intracranial aneurismal rupture. MATERIALS AND METHODS: The study consisted of 27 patients with a diagnosis of intracranial aneurysm. SAH was evaluated on admission according to the Fisher scale, patients-consciousness with the Glasgow Coma Scale, clinical grading with the Hunt and Hess scale, and clinical outcome with the Glasgow Outcome Scale (GOS). Blood samples were drawn within 72 h after arrival at the emergency room. Serum concentrations of TNF-α and sICAM-1 were assayed with the ELISA method. RESULTS: The initial serum TNF-α concentration in the aneurismal patients was low and did not correlate with radiological and clinical scores. The serum sICAM-1 level positively correlated with the severity of bleeding assessed by the Fisher scale and negatively with the patient’s scoring in the GOS. CONCLUSIONS: This study demonstrated the absence of a systemic TNF-α-mediated inflammatory response at the onset of subarachnoid hemorrhage. Early measurement of serum sICAM-1 levels offers a potential prognostic value in the assessment of patients-outcome after brain aneurismal rupture.