AIM: To assess the association between inflammatory response and early brain injury (EBI), and the association between inflammatory response and the following pneumonia after aneurysmal subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: Eighty-nine patients with spontaneous SAH and 12 patients with unruptured aneurysm were included in this prospective study. The systemic inflammatory biomarkers such as C-reactive protein (CRP), IL-1?, IL-2,IL-6,IL-8, IL10 and T leukocyte subsets were measured within 24 hours after admission. Their clinical features and laboratory findings were clearly reviewed and univariate analysis was used to find the main predictors. RESULTS: The levels of serum inflammatory cytokines especially IL-6 (p=0.004) and CRP (p=0.014) would significantly increase after aneurysm SAH. Higher Fisher grades on admission result in higher levels of IL-6 and IL-10 (pIL-6=0.003. pIL-10=0.002), and higher levels of IL-6, IL-10 and CRP were significantly associated with severe EBI, and increased the susceptibility to pneumonia (p < 0.05). The counts of CD3+ T Cells would decrease after aneurysm rupture (p=0.001), especially in patients with a poor initial clinical grade. A reversed correlation between IL-6 level and CD3 T cells count was revealed in this study (p=0.014,r=-0.249); a lower CD4 T-Cells counts might lead to subsequent pneumonia after SAH (p=0.041). The levels of serum inflammatory cytokines were not different between aneurysmal and non-aneurysmal SAH. CONCLUSION: Systemic inflammatory response would be activated after aneurysm rupture; a similar systemic inflammatory response would be noticed in non-aneurysmal SAH. The degree of inflammatory response could reflect the severity of EBI, and excessive inflammatory response could also aggravate EBI, induce immunodepression and increase the susceptibility to infections. Inflammatory cytokines such as IL-6, IL-10 and CRP are important predictors.
AIM: To assess the association between inflammatory response and early brain injury (EBI), and the association between inflammatory response and the following pneumonia after aneurysmal subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: Eighty-nine patients with spontaneous SAH and 12 patients with unruptured aneurysm were included in this prospective study. The systemic inflammatory biomarkers such as C-reactive protein (CRP), IL-1?, IL-2,IL-6,IL-8, IL10 and T leukocyte subsets were measured within 24 hours after admission. Their clinical features and laboratory findings were clearly reviewed and univariate analysis was used to find the main predictors. RESULTS: The levels of serum inflammatory cytokines especially IL-6 (p=0.004) and CRP (p=0.014) would significantly increase after aneurysm SAH. Higher Fisher grades on admission result in higher levels of IL-6 and IL-10 (pIL-6=0.003. pIL-10=0.002), and higher levels of IL-6, IL-10 and CRP were significantly associated with severe EBI, and increased the susceptibility to pneumonia (p < 0.05). The counts of CD3+ T Cells would decrease after aneurysm rupture (p=0.001), especially in patients with a poor initial clinical grade. A reversed correlation between IL-6 level and CD3 T cells count was revealed in this study (p=0.014,r=-0.249); a lower CD4 T-Cells counts might lead to subsequent pneumonia after SAH (p=0.041). The levels of serum inflammatory cytokines were not different between aneurysmal and non-aneurysmalSAH. CONCLUSION: Systemic inflammatory response would be activated after aneurysm rupture; a similar systemic inflammatory response would be noticed in non-aneurysmalSAH. The degree of inflammatory response could reflect the severity of EBI, and excessive inflammatory response could also aggravate EBI, induce immunodepression and increase the susceptibility to infections. Inflammatory cytokines such as IL-6, IL-10 and CRP are important predictors.