Immunodepression After Aneurysmal Subarachnoid Hemorrhage

Sarrafzadeh, Asita; Schlenk, Florian; Meisel, Andreas; Dreier, Jens P.; Vajkoczy, Peter; Meisel, Christian

doi:10.1161/strokeaha.110.594705

Cited by 126 publications

(111 citation statements)

References 29 publications

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“…As an anti-inflammatory cytokine, IL-10 has pleiotropic effects: it could not only limit excessive inflammatory response, but also impair T1 helper cells and monocyte functions and induce immunosuppresion (8). The patients with subsequent infections presented a marked loss of lymphocytes and especially CD4+ subsets in our study, and similar results were also revealed in another study (18). A reversed correlation between IL-6 level and CD3 T cells count was also demonstrated in this study.…”

Section: █ Conclusionsupporting

confidence: 89%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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ABSTRACTcytokines such as interleukin-6 (IL-6) and C-reactive protein (CRP) would increase early after SAH, inflammatory response would have been involved in the course of EBI. So far, most recent studies on inflammatory cytokines in SAH have focused on DCV while fewer studies have focused on EBI and its complications such as pneumonia, which influence the clinical course of aneurysmal SAH. Clinically, a serious initial clinical grade usually indicates a severe EBI after SAH (15), and infection is usually associated with immune dysfunction. █ INTRODUCTION D espite early surgical or endovascular treatment, aneurysmal subarachnoid hemorrhage (SAH) still has a high mortality and morbidity rate. Recently, early brain injury (EBI) was considered as an important determinant factor of outcome except delayed cerebral vasospasm (DCV) after aneurysmal SAH (6,19). The exact mechanism of EBI has still not been clearly demonstrated and the levels of inflammatory 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-1β, 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.

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Section: █ Conclusionsupporting

confidence: 89%

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Zhong

Zhang²,

Zhao³

et al. 2015

Turkish Neurosurgery

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“…It can also be hypothesized that clipped patients are at increased risk to develop immunodepression, which increases the risk of infections after SAH. 9 The higher incidence of seizures in clipped patients was also observed in the International Subarachnoid Aneurysm Trial (ISAT) and most likely results from brain damage secondary to craniotomy. 2 In our study, cardiac arrest occurred in 6.9% of patients and was strongly associated with poor outcome.…”

Section: Vergouwen Et Al Complications After Clipped and Coiled Aneurmentioning

confidence: 93%

“…Patients with SAH with immunodepression might be good candidates to receive prophylactic treatment with antibiotics. 9 Several potential limitations need to be addressed. The reported incidence of in-hospital complications can be limited by ascertainment and interobserver bias.…”

Section: Vergouwen Et Al Complications After Clipped and Coiled Aneurmentioning

confidence: 99%

Higher Incidence of In-Hospital Complications in Patients With Clipped Versus Coiled Ruptured Intracranial Aneurysms

Vergouwen

Fang²,

Casaubon³

et al. 2011

Stroke

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on behalf of the Investigators of the Registry of the Canadian Stroke NetworkBackground and Purpose-After aneurysmal subarachnoid hemorrhage (SAH), patients with clipped aneurysms have a higher incidence of neurocognitive deficits and seizures compared with patients with coiled aneurysms. It remains unknown if patients with clipped aneurysms also have a higher incidence of other in-hospital complications. Methods-We used data from the Registry of the Canadian Stroke Network on consecutive patients admitted to hospital with aneurysmal SAH. Patients who died within 2 days after admission were excluded. Baseline characteristics, incidence of various in-hospital complications within 30 days after admission, length of stay, poor functional outcome (modified Rankin Scale score at discharge of Ն3), and mortality were compared between patients with clipped versus coiled aneurysms. Results-Of the 931 patients, 548 (59%) were clipped and 383 (41%) coiled. Baseline characteristics were similar.Compared with patients with coiled aneurysms, patients with clipped aneurysms had a higher incidence of in-hospital complications (

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“…33 The results presented in our study corroborate these findings and suggest that these mechanisms also could be relevant in clinical aSAH. While IFNG has previously been reported in aSAH-induced immune depression, 34 the role of IL-12p70 in aSAH is unclear. The high correlation between IFNG and IL-12p70 in our participant population suggests the presence of a mechanism involving IL-12p70 stimulation of natural killer cells, which in turn express IFNG.…”

mentioning

confidence: 97%

Systematic model of peripheral inflammation after subarachnoid hemorrhage

Savarraj¹,

Parsha²,

Hergenroeder³

et al. 2017

Neurology

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Objective: To investigate inflammatory processes after aneurysmal subarachnoid hemorrhage (aSAH) with network models.Methods: This is a retrospective observational study of serum samples from 45 participants with aSAH analyzed at multiple predetermined time points: ,24 hours, 24 to 48 hours, 3 to 5 days, and 6 to 8 days after aSAH. Concentrations of cytokines were measured with a 41-plex human immunoassay kit, and the Pearson correlation coefficients between all possible cytokine pairs were computed. Systematic network models were constructed on the basis of correlations between cytokine pairs for all participants and across injury severity. Trends of individual cytokines and correlations between them were examined simultaneously.Results: Network models revealed that systematic inflammatory activity peaks at 24 to 48 hours after the bleed. Individual cytokine levels changed significantly over time, exhibiting increasing, decreasing, and peaking trends. Platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB, soluble CD40 ligand, and tumor necrosis factor-a (TNF-a) increased over time. Colony-stimulating factor (CSF) 3, interleukin (IL)-13, and FMS-like tyrosine kinase 3 ligand decreased over time. IL-6, IL-5, and IL-15 peaked and decreased. Some cytokines with insignificant trends show high correlations with other cytokines and vice versa. Many correlated cytokine clusters, including a plateletderived factor cluster and an endothelial growth factor cluster, were observed at all times. Participants with higher clinical severity at admission had elevated levels of several proinflammatory and anti-inflammatory cytokines, including IL-6, CCL2, CCL11, CSF3, IL-8, IL-10, CX3CL1, and TNF-a, compared to those with lower clinical severity. Conclusions:Combining reductionist and systematic techniques may lead to a better understanding of the underlying complexities of the inflammatory reaction after aSAH. Neurology ® 2017;88:1535-1545 GLOSSARY aSAH 5 aneurysmal subarachnoid hemorrhage; CSF 5 colony-stimulating factor; DCI 5 delayed cerebral ischemia; EGF 5 epidermal growth factor; FGF-2 5 fibroblast growth factor-2; FLT3L 5 FMS-like tyrosine kinase 3 ligand; HH 5 Hunt-Hess; IFN-a2 5 interferon-a2; IFNG 5 type-II interferon family; IL 5 interleukin; MIP 5 macrophage inflammatory protein; Pcc 5 Pearson correlation coefficient; PDGF 5 platelet-derived growth factor; sCD40L 5 soluble CD40 ligand; SI 5 similarity index; TNF 5 tumor necrosis factor; VEGF 5 vascular endothelial growth factor.Aneurysmal subarachnoid hemorrhage (aSAH) affects z30,000 people annually and accounts for 10% to 15% of all strokes.1 Despite improvements in clinical management, morbidity after aSAH remains high. Studies have shown that early elevation of central and peripheral inflammatory cytokines is associated with delayed neurologic deteriorations.2 However, such studies typically use methods to examine differences in concentrations of individual cytokines across disease severity or clinical outcomes. They fail to account for the complexities an...

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Immunodepression After Aneurysmal Subarachnoid Hemorrhage

Cited by 126 publications

References 29 publications

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

The impact of initial systemic inflammatory response after aneurysmal subarachnoid hemorrhage

Higher Incidence of In-Hospital Complications in Patients With Clipped Versus Coiled Ruptured Intracranial Aneurysms

Systematic model of peripheral inflammation after subarachnoid hemorrhage

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