PDF(Pubmed)
Abstract：
Neutrophil-mediated inflammation in the acute phase of intracerebral hemorrhage (ICH) worsens outcome in preclinical studies. sICAM-1 (soluble intercellular adhesion molecule-1), an inducible ligand for integrins and cell-cell adhesion molecules, is critical for neutrophil extravasation. We aimed to determine whether serum levels of sICAM-1 are associated with worse outcomes after ICH.
We conducted a post hoc secondary analysis of an observational cohort using data from the FAST trial (Factor-VII for Acute Hemorrhagic Stroke Treatment). The study exposure was the admission serum level of sICAM-1. The coprimary outcomes were mortality and poor outcome (modified Rankin Scale score 4-6) at 90 days. Secondary radiological outcomes were hematoma expansion at 24 hours and perihematomal edema expansion at 72 hours. We used multiple linear and logistic regression analyses to test for associations between sICAM-1 and outcomes, after adjustment for demographics, ICH severity characteristics, change in the systolic blood pressure in the first 24 hours, treatment randomization arm, and the time from symptom onset to study drug administration.
Of 841 patients, we included 507 (60%) with complete data. Hematoma expansion occurred in 169 (33%), while 242 (48%) had a poor outcome. In multivariable analyses, sICAM-1 was associated with mortality (odds ratio, 1.53 per SD increase [95% CI, 1.15-2.03]) and poor outcome (odds ratio, 1.34 per SD increase [CI, 1.06-1.69]). In multivariable analyses of secondary outcomes, sICAM-1 was associated with hematoma expansion (odds ratio, 1.35 per SD increase [CI, 1.11-1.66]), but was not associated with log-transformed perihematomal edema expansion at 72 hours. In additional analyses stratified by treatment assignment, similar results were noted in the recombinant activated factor-VII arm, but not in the placebo arm.
Admission serum levels of sICAM-1 were associated with mortality, poor outcome, and hematoma expansion. Given the possibility of a biological interaction between recombinant activated factor-VII and sICAM-1, these findings highlight the need to further explore the role of sICAM-1 as a potential marker of poor ICH outcomes.
We conducted a post hoc secondary analysis of an observational cohort using data from the FAST trial (Factor-VII for Acute Hemorrhagic Stroke Treatment). The study exposure was the admission serum level of sICAM-1. The coprimary outcomes were mortality and poor outcome (modified Rankin Scale score 4-6) at 90 days. Secondary radiological outcomes were hematoma expansion at 24 hours and perihematomal edema expansion at 72 hours. We used multiple linear and logistic regression analyses to test for associations between sICAM-1 and outcomes, after adjustment for demographics, ICH severity characteristics, change in the systolic blood pressure in the first 24 hours, treatment randomization arm, and the time from symptom onset to study drug administration.
Of 841 patients, we included 507 (60%) with complete data. Hematoma expansion occurred in 169 (33%), while 242 (48%) had a poor outcome. In multivariable analyses, sICAM-1 was associated with mortality (odds ratio, 1.53 per SD increase [95% CI, 1.15-2.03]) and poor outcome (odds ratio, 1.34 per SD increase [CI, 1.06-1.69]). In multivariable analyses of secondary outcomes, sICAM-1 was associated with hematoma expansion (odds ratio, 1.35 per SD increase [CI, 1.11-1.66]), but was not associated with log-transformed perihematomal edema expansion at 72 hours. In additional analyses stratified by treatment assignment, similar results were noted in the recombinant activated factor-VII arm, but not in the placebo arm.
Admission serum levels of sICAM-1 were associated with mortality, poor outcome, and hematoma expansion. Given the possibility of a biological interaction between recombinant activated factor-VII and sICAM-1, these findings highlight the need to further explore the role of sICAM-1 as a potential marker of poor ICH outcomes.
摘要：
背景：脑出血（ICH）急性期中性粒细胞介导的炎症使临床前研究的预后恶化。sICAM-1(可溶性细胞间粘附分子-1),整合素和细胞-细胞粘附分子的可诱导配体，是中性粒细胞外渗的关键.我们的目的是确定血清sICAM-1水平是否与ICH后不良预后相关。
方法：我们使用来自FAST试验（急性出血性卒中治疗的因子VII）的数据，对观察性队列进行了事后二次分析。研究暴露为入院血清sICAM-1水平。共同主要结果是90天的死亡率和不良结果（改良的Rankin量表评分4-6）。次要放射学结果是24小时血肿扩张和72小时血肿周围水肿扩张。我们使用多元线性和逻辑回归分析来检验sICAM-1与结果之间的关联。人口统计调整后，ICH严重性特征，前24小时收缩压的变化，治疗随机化臂，以及从症状发作到研究药物给药的时间。
结果：在841名患者中，我们纳入了507(60%)个完整数据.169例（33%）发生血肿扩大，而242（48%）的结局较差。在多变量分析中，sICAM-1与死亡率相关(比值比，每SD增加1.53[95%CI，1.15-2.03])和不良结果(赔率比，每标准差增加1.34[CI，1.06-1.69]）。在次要结果的多变量分析中，sICAM-1与血肿扩大相关(比值比，每标准差增加1.35[CI，1.11-1.66])，但在72小时时与对数转化的血肿周围水肿扩张无关.在按治疗分配分层的其他分析中，在重组激活因子VII臂中观察到类似的结果，但不是在安慰剂组。
结论：入院血清sICAM-1水平与死亡率相关，结果不佳,血肿扩大.考虑到重组激活因子VII和sICAM-1之间的生物学相互作用的可能性，这些发现强调需要进一步探索sICAM-1作为ICH不良结局的潜在标志物的作用。
方法：我们使用来自FAST试验（急性出血性卒中治疗的因子VII）的数据，对观察性队列进行了事后二次分析。研究暴露为入院血清sICAM-1水平。共同主要结果是90天的死亡率和不良结果（改良的Rankin量表评分4-6）。次要放射学结果是24小时血肿扩张和72小时血肿周围水肿扩张。我们使用多元线性和逻辑回归分析来检验sICAM-1与结果之间的关联。人口统计调整后，ICH严重性特征，前24小时收缩压的变化，治疗随机化臂，以及从症状发作到研究药物给药的时间。
结果：在841名患者中，我们纳入了507(60%)个完整数据.169例（33%）发生血肿扩大，而242（48%）的结局较差。在多变量分析中，sICAM-1与死亡率相关(比值比，每SD增加1.53[95%CI，1.15-2.03])和不良结果(赔率比，每标准差增加1.34[CI，1.06-1.69]）。在次要结果的多变量分析中，sICAM-1与血肿扩大相关(比值比，每标准差增加1.35[CI，1.11-1.66])，但在72小时时与对数转化的血肿周围水肿扩张无关.在按治疗分配分层的其他分析中，在重组激活因子VII臂中观察到类似的结果，但不是在安慰剂组。
结论：入院血清sICAM-1水平与死亡率相关，结果不佳,血肿扩大.考虑到重组激活因子VII和sICAM-1之间的生物学相互作用的可能性，这些发现强调需要进一步探索sICAM-1作为ICH不良结局的潜在标志物的作用。
