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Association Between Systemic Immune-Inflammation Index and in-Hospital and Long-Term All-Cause Mortality in Patients
Yongze Shen1, Aili Gao2, Yingjie Shen1
1Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Objective:
Patients with type 2 diabetes mellitus (T2DM) and spontaneous intracerebral hemorrhage (sICH) face high mortality. Systemic inflammation may play a key role, but the prognostic value of the systemic immune-inflammation index (SII) in this population remains unclear. This study aimed to investigate the association between SII and all-cause mortality in T2DM with sICH.
Methods:
A retrospective cohort study was conducted on 891 patients with T2DM and sICH hospitalized at the First Affiliated Hospital of Harbin Medical University from January 2021 to December 2024. SII was calculated using the formula: platelet count × neutrophil count/lymphocyte count. Patients were categorized into high and low SII groups based on the median value (817.5). Kaplan-Meier survival analysis, multivariate logistic and Cox regression models were used to assess the association of SII with in-hospital and long-term mortality. Subgroup and sensitivity analyses were performed to test the robustness of findings. Receiver operating characteristic (ROC) curves further evaluated predictive performance.
Results:
In fully adjusted models, high SII was independently associated with a significantly increased risk of in-hospital mortality (OR = 3.122, 95% CI: 1.759-5.544, P < 0.001) and long-term all-cause mortality (median follow-up 20.6 months, HR = 2.755, 95% CI: 1.938-3.919, P < 0.001). Each 1-standard deviation increase in SII was linked to a 75.9% higher in-hospital death risk (OR = 1.759), and a 17.0% increase in long-term mortality risk (HR = 1.170). ROC analysis demonstrated moderate discriminative ability for SII (AUC = 0.722 for in-hospital mortality, AUC = 0.748 for long-term mortality). Kaplan-Meier analysis revealed significantly poorer survival in the high SII group over a 50-month follow-up (log-rank P = 0.015). These associations remained stable across subgroups and after adjusting for confounding comorbidities and clinical parameters.
Conclusion:
Elevated SII is an independent predictor of both in-hospital and long-term all-cause mortality in patients with T2DM and sICH. This may be because high SII reflects an imbalance of inflammation and immunity, leading to increased mortality risk.
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