非创伤性蛛网膜下腔出血（SAH）主要由颅内动脉瘤破裂引起，是全球中风人口的重要组成部分。一种新型生物标志物，泛免疫炎症值 (PIV) 或称为全身炎症综合指数 (AISI)，与非小细胞肺癌的无进展生存期和总生存期以及 2019 年冠状病毒病 (COVID-19) 的死亡率相关-19) 患者，最近已浮出水面。然而，其在非创伤性蛛网膜下腔出血患者中的作用仍未得到充分研究。本研究旨在确定 PIV 与非创伤性 SAH 患者全因死亡率之间的关系。使用重症监护医疗信息市场 (MIMIC-IV) 数据库的数据进行回顾性分析，以检查 PIV 与所有原因之间的关系。 -导致非创伤性 SAH 危重患者死亡。 PIV 测量值是在重症监护病房 (ICU) 入院时收集的，并检查了一些死亡率指标。为了控制潜在的混杂效应，采用了 1:1 倾向评分匹配 (PSM) 方法。使用 X-tile 软件确定最佳 PIV 截止值为 1362.45，该软件常用于计算生存分析和医学或流行病学研究的连续数据中的最佳截止值。使用多变量 Cox 比例风险回归模型和 Kaplan-Meier (K-M) 生存曲线分析来分析 PIV 与短期和长期全因死亡率之间的关系。还进行了交互作用和亚组分析。该研究包括 774 名非创伤性 SAH 患者。 PSM 后，生成了 241 对评分匹配的患者。针对潜在混杂因素进行调整后的 Cox 比例风险模型发现，高 PIV (≥ 1362.45) 与 90 天全因死亡率独立相关（风险比 [HR]：1.67；95% 置信区间 (CI)：1.05） -2.65；P = 0.030）和 PSM 后（HR：1.58；95% CI：1.14-2.67；P = 0.042）。 K-M生存曲线显示，PIV≥1362.45的患者在PSM之前（31.1% vs. 16.1%%，P < 0.001）和PSM之后（68.9% vs. 80.9%，P < 0.001）90天生存率较低。同样，PIV 升高与 ICU 风险增加相关（PSM 前：HR：2.10；95% CI：1.12-3.95；P = 0.02；PSM 后：HR：2.33；95% CI：1.11-4.91；P = 0.016），住院（PSM 前：HR：1.91；95% CI：1.12-3.26；P = 0.018；PSM 后：2.06；95% CI：1.10-3.84；P = 0.034），30 天（ PSM 前：HR：1.69；95% CI：1.01-2.82；P = 0.045；PSM 后：1.66；95% CI：1.11-2.97；P = 0.047）和 1 年（PSM 前：HR： 1.58；95% CI：1.04-2.40；P = 0.032；PSM 后：1.56；95% CI：1.10-2.53；P = 0.044）全因死亡率。 K-M 生存曲线证实，在 ICU 的 PSM 前后，PIV 较高的患者生存率较低（PSM 前：18.3% vs. 8.4%，P < 0.001；PSM 后：81.7% vs. 91.3%，P < 0.001 ），院内（PSM 前：25.3% vs. 12.8%，P < 0.001；PSM 后：75.1 vs. 88.0%，P < 0.001），30 天（PSM 前：24.9% vs. 11.4%） ，P < 0.001；PSM 后：74.7 对比 86.3%，P < 0.001)，和 1 年（PSM 前：36.9% 对比 20.8%，P < 0.001；P = 0.02；PSM 后：63.1 对比. 75.1%, P < 0.001) 全因死亡率。分层分析表明，PIV 与全因死亡率之间的关系在不同亚组中存在差异。在患有非创伤性 SAH 的危重患者中，入院时 PIV 升高与各个阶段（包括 ICU、ICU、ICU、ICU）全因死亡率的上升相关。院内、30 天、90 天和 1 年死亡率，巩固了其作为独立死亡风险决定因素的地位。这项研究试图弥合当前的知识差距，并提供对基于炎症的生物标志物在非创伤性蛛网膜下腔出血中的作用的更细致的了解。然而，为了认可 PIV 对非创伤性 SAH 患者预后结果的预测价值，额外的前瞻性病例对照研究被认为是必要的。版权所有 © 2023 Huang、Zhang、Li 和 Yin。

Non-traumatic subarachnoid hemorrhage (SAH), primarily due to the rupture of intracranial aneurysms, contributes significantly to the global stroke population. A novel biomarker, pan-immune-inflammation value (PIV) or called the aggregate index of systemic inflammation (AISI), linked to progression-free survival and overall survival in non-small-cell lung cancer and mortality in Coronavirus Disease 2019 (COVID-19) patients, has surfaced recently. Its role in non-traumatic SAH patients, however, remains under-researched. This study aims to determine the relationship between PIV and all-cause mortality in non-traumatic SAH patients.A retrospective analysis was conducted using data from the Medical Information Mart for Intensive Care (MIMIC-IV) database to examine the association between PIV and all-cause mortality in critically ill patients with non-traumatic SAH. PIV measurements were collected at Intensive Care Unit (ICU) admission, and several mortality measures were examined. To control for potential confounding effects, a 1:1 propensity score matching (PSM) method was applied. The optimal PIV cutoff value was identified as 1362.45 using X-tile software that is often used to calculate the optimal cut-off values in survival analysis and continuous data of medical or epidemiological research. The relationship between PIV and short- and long-term all-cause mortality was analyzed using a multivariate Cox proportional hazard regression model and Kaplan-Meier (K-M) survival curve analysis. Interaction and subgroup analyses were also carried out.The study included 774 non-traumatic SAH patients. After PSM, 241 pairs of score-matched patients were generated. The Cox proportional hazard model, adjusted for potential confounders, found a high PIV (≥ 1362.45) independently associated with 90-day all-cause mortality both pre- (hazard ratio [HR]: 1.67; 95% confidence intervals (CI): 1.05-2.65; P = 0.030) and post-PSM (HR: 1.58; 95% CI: 1.14-2.67; P = 0.042). K-M survival curves revealed lower 90-day survival rates in patients with PIV ≥ 1362.45 before (31.1% vs. 16.1%%, P < 0.001) and after PSM (68.9% vs. 80.9%, P < 0.001). Similarly, elevated PIV were associated with increased risk of ICU (pre-PSM: HR: 2.10; 95% CI: 1.12-3.95; P = 0.02; post-PSM: HR: 2.33; 95% CI: 1.11-4.91; P = 0.016), in-hospital (pre-PSM: HR: 1.91; 95% CI: 1.12-3.26; P = 0.018; post-PSM: 2.06; 95% CI: 1.10-3.84; P = 0.034), 30-day (pre-PSM: HR: 1.69; 95% CI: 1.01-2.82; P = 0.045; post-PSM: 1.66; 95% CI: 1.11-2.97; P = 0.047), and 1-year (pre-PSM: HR: 1.58; 95% CI: 1.04-2.40; P = 0.032; post-PSM: 1.56; 95% CI: 1.10-2.53; P = 0.044) all-cause mortality. The K-M survival curves confirmed lower survival rates in patients with higher PIV both pre- and post PSM for ICU (pre-PSM: 18.3% vs. 8.4%, P < 0.001; post-PSM:81.7 vs. 91.3%, P < 0.001), in-hospital (pre-PSM: 25.3% vs. 12.8%, P < 0.001; post-PSM: 75.1 vs. 88.0%, P < 0.001), 30-day (pre-PSM: 24.9% vs. 11.4%, P < 0.001; post-PSM:74.7 vs. 86.3%, P < 0.001), and 1-year (pre-PSM: 36.9% vs. 20.8%, P < 0.001; P = 0.02; post-PSM: 63.1 vs. 75.1%, P < 0.001) all-cause mortality. Stratified analyses indicated that the relationship between PIV and all-cause mortality varied across different subgroups.In critically ill patients suffering from non-traumatic SAH, an elevated PIV upon admission correlated with a rise in all-cause mortality at various stages, including ICU, in-hospital, the 30-day, 90-day, and 1-year mortality, solidifying its position as an independent mortality risk determinant. This study represents an attempt to bridge the current knowledge gap and to provide a more nuanced understanding of the role of inflammation-based biomarkers in non-traumatic SAH. Nevertheless, to endorse the predictive value of PIV for prognosticating outcomes in non-traumatic SAH patients, additional prospective case-control studies are deemed necessary.Copyright © 2023 Huang, Zhang, Li and Yin.