Background Lower extremity arteriosclerotic obliteration (ASO) is a chronic disease characterized by the formation of atherosclerotic plaques in the lower extremity arteries, leading to arterial stenosis, occlusion, and subsequently chronic ischemia of the limbs, manifesting as pain, claudication, and even ischemic necrosis of the limbs. Inflammation and lipid infiltration play pivotal roles in the development of lower extremity atherosclerosis. However, there is currently a lack of relevant indices for its diagnosis and analysis.
Objective To explore the correlation between multiple inflammatory and oxidative stress indices and ASO, and to evaluate their diagnostic value by collecting case data from ASO patients.
Methods A retrospective study was conducted involving 600 ASO patients who visited the Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine from October 2014 to January 2024. Patients were divided into mild (n=200), moderate (n=200), and severe (n=200) groups based on the Rutherford classification. Additionally, 200 healthy individuals who underwent physical examinations at the outpatient clinic of the same hospital were randomly selected as controls. Baseline data were collected, and inflammatory and oxidative stress indices were calculated, including the pan-immune inflammation value (PIV), systemic immune-inflammation index (SIRI), systemic immune-inflammatory index (SII), monocyte-to-hdl cholesterol ratio (MHR), neutrophil-to-lymphocyte ratio (NLR), SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C. Spearman's rank correlation analysis was used to explore the correlation between these indices and ASO severity. Multivariate Logistic regression analysis was conducted to investigate the influencing factors of ASO. Receiver operating characteristic (ROC) curves were plotted to assess the diagnostic efficacy of the indices for ASO, and the area under the ROC curve (AUC) was calculated.
Results ASO patients had higher levels of monocyte count (MONO), platelet count (PLT), neutrophil count (NEUT), LDL-C, PIV, SIRI, SII, MHR, NLR, SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C, as well as lower HDL-C levels compared to healthy controls (P<0.05). Comparison of ASO patients across different Rutherford stages showed that the severe group had a higher proportion of males, hypertension, smoking rates, MONO, NEUT, PIV, SIRI, SII, MHR, NLR, SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C than the mild and moderate groups (P<0.05). The severe group also had lower lymphocyte count (LYMP) and HDL-C levels (P<0.05), higher age than the moderate group (P<0.05), and lower LDL-C than the mild group (P<0.05). The moderate group had a higher proportion of hypertension, MONO, NEUT, PIV, SIRI, SII, MHR, NLR, SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C than the mild group (P<0.05), as well as lower HDL-C levels (P<0.05). The mild group had a lower proportion of alcohol consumption than the moderate and severe groups (P<0.05), and lower PLT than the moderate and severe groups (P<0.05). Correlation analysis results indicated that PIV, SIRI, SII, MHR, NLR, SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C were positively correlated with ASO severity (P<0.05). Multivariate Logistic regression analysis revealed that SIRI was a protective factor for ASO (OR=0.009, 95%CI=0.000-0.181, P=0.009), while SIRI×LDL-C (OR=1.665, 95%CI=1.260-2.201, P=0.001) and PIV/HDL-C (OR=1.014, 95%CI=1.003-1.024, P=0.005) were risk factors for ASO. The AUC for predicting ASO using SIRI×LDL-C was 0.710, with a sensitivity of 0.442 and a specificity of 0.890. The AUC for predicting ASO using PIV/HDL-C was 0.761, with a sensitivity of 0.505 and a specificity of 0.975.
Conclusion The comprehensive indices included in this study, namely PIV, SIRI, SII, MHR, NLR, SIRI/HDL-C, SIRI×LDL-C, PIV/HDL-C, and PIV×LDL-C, are correlated with ASO severity. SIRI is a protective factor for ASO, while SIRI×LDL-C and PIV/HDL-C are independent risk factors for ASO and have predictive value for its occurrence.
