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Updated: Jan 13, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Comprehensive Analysis of the Correlation Between Immune-Inflammatory Biomarkers and Intestinal Necrosis in Patients
Yu Tian1, Feifan Wang1, Mingshuo Zhang1,2
1Department of Hand and Foot Surgery, First Hospital of Qinhuangdao, Qinhuangdao, 066000, China, qhdsdyyy.com.
Background:
The relationship between immune-inflammatory biomarkers, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) and intestinal necrosis in different types of acute intestinal ischemia remains unclear.
Methods:
A total of 138 patients with acute intestinal ischemia were divided into a nonnecrosis group (n = 65) and a necrosis group (n = 73). Least absolute shrinkage and selection operator (Lasso)-logistic regression model was used to identify independent risk factors for intestinal necrosis. Multivariate logistic regression was conducted to assess the associations between NLR and SII levels and intestinal necrosis. Sensitivity analyses were performed using smooth curve fitting, threshold effect analysis, subgroup analysis, and propensity score matching (PSM). .
Results:
The optimal thresholds of NLR and SII for differentiating intestinal necrosis were 8.85 and 1492.11, respectively, while PLR showed no significant association. In Lasso-logistic regression analysis, vascular intestinal ischemia, NLR ≥ 8.85, SII≥ 1492.11, C-reactive protein (CRP), and D-dimer > 0.5 mg/L were independent risk factors for intestinal necrosis. After adjusting for potential confounding variables, the multivariate logistic regression analysis showed a positive correlation between natural logarithm (Ln)-NLR (OR = 20.187, 95% CI = 3.788-107.578, p < 0.001) and Ln-SII (OR = 5.375, 95% CI = 1.141-25.313, p < 0.033) and intestinal necrosis. Subgroup analysis showed a significant interaction between NLR, intestinal necrosis, and coronary heart disease (p interaction = 0.016). Smooth curve fitting indicated the relationship between Ln-NLR and Ln-SII and intestinal necrosis was nonlinear, with inflection points at 1.78 (NLR = 5.93) and 7.32 (SII = 1510.20), respectively. When NLR > 5.93 or SII < 1510.20, the risk of intestinal necrosis significantly increased. The associations remained robust after PSM.
Conclusion:
This study demonstrates that elevated levels of NLR and SII are significantly associated with intestinal necrosis, suggesting that these biomarkers may help identify patients at higher risk of intestinal necrosis in acute intestinal ischemia. However, prospective studies are needed to validate their predictive value.
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