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1.
Front Immunol ; 15: 1376544, 2024.
Article in English | MEDLINE | ID: mdl-38638440

ABSTRACT

Background: Sarcopenia, common in the elderly, often linked to chronic diseases, correlates with inflammation.The association between SII and mortality in sarcopenia patients is underexplored, this study investigates this relationship in a U.S. adult cohort. Methods: We analyzed 1999-2018 NHANES data, focusing on 2,974 adults with sarcopenia. Mortality outcomes were determined by linking to National Death Index (NDI) records up to December 31, 2019. Using a weighted sampling design, participants were grouped into three groups by the Systemic Immune-Inflammation Index (SII). We used Cox regression models, adjusting for demographic and clinical variables, to explore SII's association with all-cause and cause-specific mortality in sarcopenia, performing sensitivity analyses for robustness. Results: Over a median follow-up of 9.2 years, 829 deaths occurred. Kaplan-Meier analysis showed significant survival differences across SII groups. The highest SII group showed higher hazard ratios (HRs) for all-cause and cause-specific mortality in both crude and adjusted models. The highest SII group had a higher HR for all-cause(1.57, 1.25-1.98), cardiovascular(1.61, 1.00-2.58), cancer(2.13, 1.32-3.44), and respiratory disease mortality(3.21, 1.66-6.19) in fully adjusted models. Subgroup analyses revealed SII's association with all-cause mortality across various demographics, including age, gender, and presence of diabetes or cardiovascular disease. Sensitivity analyses, excluding participants with cardiovascular diseases, those who died within two years of follow-up, or those under 45 years of age, largely reflected these results, with the highest SII group consistently demonstrating higher HRs for all types of mortality in both unadjusted and adjusted models. Conclusion: Our study is the first to demonstrate a significant relationship between SII and increased mortality risks in a sarcopenia population.


Subject(s)
Cardiovascular Diseases , Sarcopenia , Adult , Aged , Humans , Cause of Death , Nutrition Surveys , Inflammation
2.
Lung ; 198(4): 645-652, 2020 08.
Article in English | MEDLINE | ID: mdl-32661658

ABSTRACT

BACKGROUND: Many studies have indicated that S100A8 and S100A9 may be involved in the development and progression of chronic obstructive pulmonary disease (COPD). However, there has been no clinical study analyzing the role of the serum S100A8/S100A9 heterodimer in COPD patients. The aim of this study was to analyze the correlation of the serum S100A8/S100A9 heterodimer with pulmonary function in COPD patients during acute exacerbation (AE-COPD) based on a cross-sectional study. METHODS: A total of 131 AE-COPD patients and matched healthy subjects were recruited. Pulmonary function, arterial blood gas values, and serum inflammatory cytokines were measured. RESULTS: Serum S100A8/S100A9 was increased in AE-COPD patients. AE-COPD patients were ranked into different grades based on FEV1%. Serum S100A8/S100A9 was higher in Grade 4 than in Grade 1-2 and Grade 3 patients with AE-COPD. Univariate regression analysis found that serum S100A8/S100A9 was negatively correlated with FEV1% in AE-COPD patients. Furthermore, serum S100A8/S100A9 was positively associated with MCP-1 in AE-COPD patients. Further stratified analysis revealed that serum S100A8/S100A9 was negatively associated with FEV1/FVC in Grade 3 (OR 0.629, P < 0.05) and in Grade 4 (OR 0.347, P < 0.05). In addition, there was a positive relationship between serum S100A8/S100A9 and PaCO2 in Grade 3 (OR 1.532, P < 0.05) and Grade 4 (OR 1.925, P < 0.01). CONCLUSION: S100A8/S100A9 was negatively associated with pulmonary function in AE-COPD patients, indicating that the serum S100A8/S100A9 heterodimer may be involved in the progression of AE-COPD, and may be a relevant serum biomarker in the diagnosis for AE-COPD.


Subject(s)
Leukocyte L1 Antigen Complex/blood , Pulmonary Disease, Chronic Obstructive/blood , Aged , Blood Gas Analysis , Calgranulin A , Calgranulin B , Chemokine CCL2/blood , Disease Progression , Female , Forced Expiratory Volume , Humans , Interleukin-1beta/blood , Interleukin-6/blood , Male , Protein Multimerization , Pulmonary Disease, Chronic Obstructive/physiopathology , Tumor Necrosis Factor-alpha/blood , Vital Capacity
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