TNF-α and sICAM-1 in intracranial aneurismal rupture

Subarachnoidal hemorrhage (SAH) occurring after aneurismal rupture produces an inflammatory response in the cerebral circulation. Tumor necrosis factor (TNF)-alpha 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-alpha and sICAM-1 serum measurement for the prognosis of patient outcome after intracranial aneurismal rupture. 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-alpha and sICAM-1 were assayed with the ELISA method. The initial serum TNF-alpha 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. This study demonstrated the absence of a systemic TNF-alpha-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.