Physiologic-Inflammatory-Nutrition (TRIAD-TB) Score at 72 Hours Predicts 30-Day Mortality and Length of Stay in Pulmonary Tuberculosis: A Prospective Cohort Study.

The systemic immune-inflammation index (SII) showed an extensive link between immunological dysfunction and the activation of systemic inflammation. Several studies have confirmed the application of SII to orthopedic diseases. However, the significance of SII in critically ill elderly individuals with hip fracture who require intensive care unit (ICU) admission is not yet known. This study centered on exploring the relationship between SII and clinical outcomes among critically ill elderly hip fracture individuals. The study centered around elderly patients experiencing severe illness following hip fractures and requiring admission to the ICU. These patients from the MIMIC-IV database formed the basis of this study's cohort. We stratified them into quartiles according to their SII levels. The results involved the mortality at 30 days and 1 year post-admission. Then we employ Cox proportional hazards regression analysis as well as restricted cubic splines to explore the association between the SII and clinical results in critically ill elderly patients with hip fracture. The study encompassed 991 participants, among whom 63.98% identified as females. Notably, the mortality rates attributed to any cause within 30 days and 1 year after hospitalization stood at 19.68 and 33.40%, respectively. The multivariate Cox proportional hazards model disclosed a significant correlation between an elevated SII and all-cause mortality. Following adjustments for confounding variables, individuals with a high SII showed a notable correlation with 30-day mortality [adjusted hazard ratio (HR), 1.065; 95% confidence interval (CI), 1.044-1.087; p < 0.001] and 1-year mortality (adjusted HR, 1.051; 95% CI, 1.029-1.074; p < 0.001). Furthermore, the analysis of restricted cubic splines demonstrated a progressive increase in the risk of all-cause death as the SII value rose. Among critically ill elderly patients with hip fracture, the SII exhibits a non-linear association that positively correlates with both 30-day and 1-year all-cause mortality rates. The revelation indicates that the SII may play a vital role in identifying patients with hip fractures who face an escalated risk of mortality due to any cause.

Purpose Acute ischemic stroke (AIS) is a devastating disease and remains the leading cause of death and disability. This retrospective study aims to investigate associations between systemic immune-inflammation index (SII) and all-cause mortality in patients with AIS. Patients and Methods. We used the data from Medical Information Mart for Intensive Care IV. A total of 1,181 patients with acute ischemic stroke (AIS) were included. Systemic immune-inflammation index (SII) was calculated as platelet count (/L) × neutrophil count (/L)/lymphocyte count (/L). The main outcomes were 30-day all-cause mortality. The association between SII with mortality was evaluated using the Cox proportional hazards regression model. Results After adjusting for potential covariates, the highest quartiles of SII versus the lowest quartiles of SII, the HR was 2.74 (CI 1.79–4.19, P < 0.001). Log-transformed SII was significantly associated with 30-day all-cause mortality (HR 2.44; CI 1.72–3.46, P < 0.001). Furthermore, we found that there is a nearly linear relationship (P=0.265) between logarithmic transformed SII with all-cause mortality. Conclusion Elevated SII of patients with acute ischemic stroke increased the risk of 30-day all-cause mortality. SII may serve as a useful marker to elucidate the role of thrombocytosis, inflammation, and immunity interaction in the development of AIS.

Inflammatory markers such as neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) have shown promise in predicting mortality in various types of cancer. The purpose of this study was to assess NLR, PLR, and SII in predicting 30-day mortality and overall survival (OS) among surgically treated patients with spinal metastasis. This was a retrospective study including 153 patients who underwent surgery for spinal metastasis between 2012 and 2022. Electronic medical records were manually reviewed, and NLR, PLR, and SII were calculated from preoperative neutrophil, platelet, and lymphocyte counts. Receiver operating characteristic curves with areas under the curve were generated to determine cutoff values. Logistic regression was used to determine the odds ratios (ORs) for 30-day mortality. The Kaplan-Meier method and Cox regression were used to determine the hazard ratio (HR) for OS limited to 5 years postoperatively. Preoperative cutoff values were as follows: NLR > 10.2, PLR > 260, and SII > 2900. Overall, 35.9% (55/153) of patients had elevated NLR, 45.7% (70/153) had elevated PLR, and 30.7% (47/153) had elevated SII. The overall 30-day mortality was 8.5% (13/153). After controlling for confounders such as performance status and primary tumor type, high NLR (OR 5.20, 95% CI 1.21-22.28; p = 0.026) and SII (OR 4.92, 95% CI 1.17-20.63; p = 0.029) were associated with increased odds of 30-day postoperative mortality. The median OS time in the study population was 26 months (95% CI 12-40 months). After controlling for confounders such as Eastern Cooperative Oncology Group status, primary tumor, and hypoalbuminemia, high NLR was associated with shorter OS (HR 2.23, 95% CI 1.48-3.97; p = 0.003). High preoperative NLR and SII were independently associated with 30-day postoperative mortality in this study. Elevated NLR was also found to be associated with shorter OS. The prognostic role of these metrics warrants further investigation.

Introduction: Inflammation plays a important role in determining the prognosis of heart failure. Recent studies have demonstrated that both established and novel inflammatory biomarkers—such as the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), Systemic Immune-Inflammation Index (SII), and, in particular, the Systemic Inflammation Response Index (SIRI)—serve as important predictors of mortality in heart failure patients. Nonetheless, data from developing countries like Vietnam remain limited. Hypothesis: Inflammatory markers are associated with 30-day all-cause mortality in patients hospitalized with acute heart failure (AHF). Methods: We performed a prospective cohort study at Can Tho Central General Hospital—a tertiary care center in Vietnam—from May 2024 through April 2025. Consecutive adults (≥18 years) admitted with acute heart failure (NT-proBNP &gt;300 pg/mL) who provided informed consent were enrolled, while those with active infection, immunosuppressant use within the prior three months, chronic liver disease, or active malignancy were excluded. Survivors were followed for 30 days after discharge, with all-cause mortality as the primary endpoint. Relative risks were derived from a modified Poisson log-linear regression using a robust (sandwich) variance estimator, adjusting for baseline demographics and comorbidities. Results: Among 411 AHF patients (mean age 69.6 ± 12.6 years; 47.4 % men), 262 (63.7 %) completed 30-day follow-up, during which 56 deaths occurred (all-cause mortality 21.4 %). Non-survivors were older, carried a greater comorbidity burden, and exhibited higher median levels of NLR, MLR, PLR, SII, and SIRI than survivors. In multivariable Poisson models adjusted for age, sex, coronary artery disease, prior heart failure, hypertension, and diabetes, individuals in the highest biomarker quartile had markedly increased 30-day mortality risk compared with those in the lowest quartile: NLR (RR 3.6; 95 % CI 1.6–8.3), MLR (RR 6.1; 95 % CI 2.2–16.5), PLR (RR 2.3; 95 % CI 1.2–4.4), SII (RR 2.4; 95 % CI 1.2–4.8), and SIRI (RR 4.3; 95 % CI 1.8–10.4). Conclusion: Inflammatory markers independently predict 30-day mortality in Vietnamese AHF patients; adding them to risk models may enhance short-term prognosis, while its longer-term predictive value warrants further investigation.

ObjectivePrognostic indicators in acute coronary syndrome (ACS) would aid in decision-making and identifying high-risk patients. The systemic immune-inflammation index (SII) has good prognostic value in many diseases; however, its use has not been reported for ACS. We aimed to determine the associations between the SII and outcomes in patients with ACS, with adjustment for confounders.MethodsIn this retrospective cohort study, we used the MIMIC-III (Multiparameter Intelligent Monitoring in Intensive Care) database and the eICU Collaborative Research Database. The primary outcome was 30-day mortality. Cox regression analysis was performed to determine the relationship between the SII and patient outcomes, and we conducted subgroup analysis and smooth curve fitting.ResultsWe identified 4699 patients with ACS: 1741 women and 2949 men, mean age 82.8±29.7 years, and mean SII 72.58±12.9. For 30-day all-cause mortality, the unadjusted hazard ratio (HR) (95% confidence interval [CI]) of SII <69.4 and SII >88.8 were 1.25 (1.04, 1.50) and 1.38 (1.15, 1.65), respectively. With SII >88.8, this association remained significant after adjustment for numerous potential confounders: HR 1.27 (1.06, 1.52). A similar relationship was observed for 90-day and 1-year all-cause mortality.ConclusionsSII is a promising prognostic indicator for unselected patients with ACS. This finding needs to be confirmed in prospective studies.

Systemic Immune-Inflammatory Marker of High Meld Patients Is Associated With Early Mortality After Liver Transplantation

Diabetic kidney disease (DKD) is linked to immunity and inflammation. We aimed to investigate if systemic inflammatory indicators can predict mortality in DKD patients in intensive care units (ICUs) and determine potential associations between them. This study included a cohort of 840 adults with DKD in the ICU. Three systemic inflammatory indicators were evaluated by peripheral blood tests: systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), neutrophil-to-lymphocyte ratio (NLR). Cox regression analysis, restricted cubic spline (RCS), and Kaplan-Meier curves were used to evaluate the associations between the inflammatory indicators and the mortality of the DKD population. Receiver operating characteristic (ROC) was employed to ascertain the predictive accuracy of varied systemic inflammatory indicators. After adjusting for all covariates, Cox regression analysis showed that inflammatory indicators were all significantly positively associated with 28-day mortality (SII: HR 1.39, 95% CI, 1.16-1.67, P<0.001; SIRI: HR 1.36, 95% CI, 1.14-1.62, P=0.001; NLR: HR 1.48, 95% CI, 1.20-1.84, P<0.001). Compared with the lowest tertile (tertile 1), participants in the highest tertile (tertile 3) had significantly increased risk of 28-day mortality (SII: HR 2.46, 95% CI, 1.51-4.02, P<0.001; SIRI: HR 3.31, 95% CI, 1.87-5.84, P<0.001; NLR: HR 3.42, 95% CI, 1.94-6.03, P<0.001). Furthermore, ROC curves showed that NLR and SIRI had higher predictive values than SII (NLRAUC vs. SIIAUC: 0.681 vs. 0.633, P=0.006; SIRIAUC vs. SIIAUC: 0.675 vs. 0.633, P=0.041) in predicting 28-day mortality. Our study demonstrated that systemic inflammatory indicators (SII, SIRI, and NLR) were positively associated with 28-day and 365-day mortality in critically ill patients with DKD. Inflammatory indicators may serve as predictors of mortality in critically ill DKD patients.

Recent evidence suggests a link between platelet-to-lymphocyte ratio (PLR) and coronary artery disease (CAD) outcomes. However, studies on asymptomatic CAD (ACAD) and short-term outcomes like 28-day mortality are limited. This research will explore the correlation between PLR and 28-day mortality in ACAD patients and assess a potential dose-response relationship. This retrospective cohort study leverages data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. We included patients diagnosed with ACAD and collected baseline characteristics, laboratory test results, and clinical data during hospitalization. The primary endpoint was 28-day all-cause mortality. Analytical approaches included multivariable Cox proportional hazards regression models, stratified analysis, restricted cubic splines (RCS), and threshold effect analyses to evaluate the association between PLR and 28-day all-cause mortality. Given the skewed distribution of PLR values, natural logarithm (ln) transformation was applied for statistical analyses. Our study encompassed 4,563 ACAD patients, of whom 71.7% were male, with a mean age of 71.8years. Overall, 12.8% of patients experienced 28-day mortality. Analysis revealed a J-shaped curve relationship between PLR and 28-day all-cause mortality. Threshold analysis indicated that participants with lnPLR < 4.308 had a Hazard Ratio (HR) of 0.814 for 28-day all-cause mortality (95% CI 0.627-1.057; P = 0.122), whereas those with lnPLR > 4.308 had an HR of 1.441 (95% CI 1.245-1.668; P < 0.001). Below the threshold, increasing lnPLR did not significantly correlate with changes in 28-day mortality risk. Conversely, above this threshold, each unit increase in lnPLR was associated with a 44.1% increased risk of 28-day mortality. Among adult patients with ACAD in the United States, there exists a J-shaped relationship between PLR and 28-day all-cause mortality. Elevated PLR levels are associated with adverse outcomes in ACAD patients.

Background and Objectives: Blood-borne inflammatory ratios have been proposed as inexpensive prognostic tools across a range of diseases, but their role in pulmonary tuberculosis (TB) remains uncertain. In this retrospective case–control analysis, we explored whether composite indices derived from routine haematology—namely the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), the systemic immune–inflammation index (SII) and a novel CRP–Fibrinogen Index (CFI)—could enhance risk stratification beyond established cytokine measurements among Romanian adults with culture-confirmed pulmonary T. Materials and Methods: Data were drawn from 80 consecutive TB in-patients and 50 community controls. Full blood counts, C-reactive protein, fibrinogen, and four multiplex cytokines were extracted from electronic records, and composite indices were calculated according to standard formulas. The primary outcomes were in-hospital mortality within 90 days and length of stay (LOS). Results: Among TB patients, the median NLR was 3.70 (IQR 2.54–6.14), PLR was 200 (140–277) and SII was 1.36 × 106 µL−1 (0.74–2.34 × 106), compared with 1.8 (1.4–2.3), 117 (95–140) and 0.46 × 106 µL−1 (0.30–0.60 × 106) in controls. Those with SII above the cohort median exhibited more pronounced acute-phase responses (median CRP 96 vs. 12 mg L−1; fibrinogen 578 vs. 458 mg dL−1), yet median LOS remained virtually identical (29 vs. 28 days) and early mortality was low in both groups (8% vs. 2%). The CFI showed no clear gradient in hospital stay across its quartiles, and composite ratios—while tightly inter-correlated—demonstrated only minimal association with cytokine levels and LOS. Conclusions: Composite cell-count indices were markedly elevated but did not predict early death or prolonged admission. In low-event European cohorts, their chief value may lie in serving as cost-free gatekeepers, flagging those who should proceed to more advanced cytokine or genomic testing. Although routine reporting of NLR and SII may support low-cost surveillance, validation in larger, multicentre cohorts with serial sampling is needed before these indices can be integrated into clinical decision-making.

Background and Objectives: The role of adenosine deaminase (ADA) in pulmonary tuberculosis (PTB) remains insufficiently defined in advanced forms of disease. Likewise, the systemic immune inflammatory index (SII) has not been validated in severe PTB. This 6-year prospective observational study aims to evaluate biomarker signatures of serum ADA and SII. Materials and Methods: According to the PTB case definition, 232 adult patients were divided into group 1, with a positive bacteriologic exam (n = 168), and group 2, without bacteriological confirmation (n = 64). ADA serum levels were compared by age, gender, nutritional status, morphologic and bacteriological pattern of PTB lesions, survival status, along with serum levels of other inflammatory biomarkers. All patients with comorbidities, interfering with the level of ADA, were excluded to avoid bias. Results: A total cohort of 208 PTB adults, aged 54.37 ± 14.365 years, included 156 males. The overall mortality was 11.53%. Death occurred after a mean interval of 1.63 ± 3.228 months after PTB diagnosis. ADA serum mean levels were 32.94 ± 9.146 IU/L, significantly higher in G1 (p = 0.002), in patients with delayed diagnosis of PTB (p = 0.000), with lung cavitation (p = 0.003), and death as a poor outcome (p ˂ 0.02). SII had a mean value of 1752.226 ± 2704.150, significantly increased in bacteriologically confirmed PTB cases (p = 0.018), delayed diagnosis (p = 0.002), cavitary advanced pulmonary tuberculosis (APT) (p = 0.002), and deceased (p = 0.003). Both an ADA cut-off elevated risk value of over 30 IU/L and SII of over 902 were fulfilled by 73 patients, with 2.10 higher risk of advanced PTB (p = 0.006) and 4.49 higher risk of mortality (p = 0.000). Conclusions: Serum ADA and SII are recommended as predictors of advanced and severe pulmonary TB. These findings indicate that ADA and SII, when elevated together, delineate a high-risk PTB phenotype with greater disease severity and early mortality. The combination offers a pragmatic, biomarker-based approach to risk stratification in PTB.

Systemic immune-inflammation index (SII) has been identified as a prognostic biomarker for various diseases. Our study aimed to investigate the association between SII and mortality risk in critically ill patients with sepsis, thus exploring possible tools for rapid screening. This retrospective cohort study was conducted using clinical data extracted from the Medical Information Mart for Intensive Care Database. The study included only patients diagnosed with sepsis admitted to the intensive care unit for the first time. We used the restricted cubic splines to explore the relationship between SII and 28-day mortality. Kaplan–Meier curve and Cox regression models were performed to evaluate the association between SII and mortality. Subgroup analysis was performed to explore the stability of the primary results. A total of 16,007 patients with sepsis were eligible in the final analysis. We found a J-shaped relationship between SII and mortality risk. The SII level associated with the lowest mortality risk was 774.46*109/L. Compared with the reference group (second SII quartile), the 28-day mortality was increased in the highest quartile and third quartile groups of SII levels; fully adjusted HRs were 1.16 (1.02 to 1.32) and 1.40 (1.23 to 1.58), respectively. However, although the lower SII (Q1 group) also showed a trend toward a higher hazard of 28-day mortality, there was no statistical difference, with a fully adjusted HR of 1.05 (0.92 to 1.21). In the population of critically ill patients with sepsis, low and high SII levels were associated with an increased risk of short-term mortality. The 28-day mortality risk was lowest at SII levels of 774.46*109/L.Supplementary InformationThe online version contains supplementary material available at 10.1007/s10238-023-01029-w.

Introduction: The aim of the study was to investigate the relationship between systemic immune-inflammation index (SII) and early allograft dysfunction (EAD) and 90-day mortality after liver transplantation (LT) in acute-on-chronic liver failure (ACLF). Methods: Retrospective record analysis was done on 114 patients who had LT for ACLF. To identify the ideal SII, the receiver operating characteristic curve was used. The incidence of EAD and 90-day mortality following LT were calculated. The prognostic value of SII was assessed using the Kaplan-Meier technique and the Cox proportional hazards model. Results: The cut-off for SII was 201.5 (AUC = 0.728, p < 0.001). EAD occurred in 40 (35.1%) patients of the high SII group and 5 (4.4%) patients of the normal SII group, p < 0.001. 18 (15.8%) deaths occurred in the high SII group and 2 (1.8%) deaths occurred in the normal SII group, p = 0.008. The multivariate analysis demonstrated that SII ≥201.5, MELD ≥27 were independent prognostic factors for 90-day mortality after LT. Conclusion: SII predicts the occurrence of EAD and is an independent risk factor for 90-day mortality after LT.

Background No epidemiological study has investigated the effect of anion gap (AG) on the prognosis of critically ill patients with acute kidney injury (AKI). Therefore, we aimed to determine the association between serum AG and all-cause mortality in these patients. Methods From MIMIC III, we extracted demographics, vital signs, laboratory tests, comorbidities, and scoring systems from the first 24 h after patient ICU admission. A generalized additive model was used to identify a nonlinear association between anion gap and 30-day all-cause mortality. We also used the Cox proportional hazards models to measure the association between AG levels and 30-day, 90-day, and 365-day mortality in patients with AKI. Results A total of 11,573 eligible subjects were extracted from the MIMIC-III. The relationship between AG levels and 30-day all-cause mortality in patients with AKI was nonlinear, with a U-shaped curve. In multivariate analysis, after adjusting for potential confounders, higher AG was a significant predictor of 30-day, 90-day, and 365-day all-cause mortality compared with lower AG (HR, 95% CI: 1.54, 1.33–1.75; 1.55, 1.38–1.73; 1.46, 1.31–1.60). Conclusions The relationship between AG levels and 30-day all-cause mortality described a U-shaped curve. High-AG levels were associated with increased risk 30-day, 90-day, and 365-day all-cause mortality in critically ill patients with AKI.

Limited research has explored the prognostic significance of the neutrophil-percentage-to-albumin ratio (NPAR), derived neutrophil-to-lymphocyte ratio (dNLR), and systemic immune-inflammation index (SII) in individuals with advanced chronic liver disease (ACLD). This study aimed to examine the association between these inflammatory markers and 90-day transplant-free mortality among patients with ACLD. We prospectively recruited hospitalized patients with ACLD from the tertiary teaching hospital. Cox regressions were used to determine the associations between NPAR, dNLR, SII, and mortality. A total of 412 patients with ACLD were included in this study. The 90-day transplant-free mortality increased with higher levels of NPAR, dNLR, and SII. In multivariate analysis, higher NPAR, dNLR, and SII were independently associated with an increased risk of mortality in patients with ACLD after adjustment for confounders. After the adjustment for covariables, the risk of 90-day transplant-free mortality in ACLD patients increased by 66% and 18% for every unit increase in NPAR (OR: 1.66, 95% CI 1.09-2.53) and dNLR (OR: 1.18, 95% CI 1.01-1.38), respectively (p<0.05). The patients with NPAR <3.5 (OR: 3.65, 95% CI 1.30-10.27) and dNLR <3.5 (OR: 2.40, 95% CI 1.19-4.86) had the highest risk. Subgroup analysis revealed that NPAR, dNLR, and SII demonstrated a strong correlation with 90-day transplant-free mortality in both acute decompensation and acute-on-chronic liver failure populations. Subsequent analysis showed a significant association between NPAR, dNLR, SII, and 90-day transplant-free mortality in patients presenting with ascites, infection, and gastrointestinal hemorrhage. Increased NPAR, dNLR, and SII were independently correlated with a higher risk of mortality in patients with ACLD.

BackgroundNo epidemiological study has determined the association between the anion gap (AG) and all-cause mortality in critically ill patients with cardiogenic shock (CS). This study was conducted to clarify the relationship between the AG and mortality in CS.MethodsWe extracted clinical data from the public database, MIMIC-III V1.4, by using a generalized additive model to identify the nonlinear relationship between the AG and the 30-day mortality in 1248 intensive care unit patients. Cox proportional hazard models were used to assess the association between the AG and the 30-day, 90-day, and 365-day mortality in CS.ResultsThe AG and 30-day all-cause mortality showed a nonlinear relationship, indicated by a J-shaped curve. In the multivariate analysis, after adjusting for potential confounders, a high AG was associated with an increased risk of 30-day, 90-day, and 365-day all-cause mortality in patients with CS compared with patients who had low AG (hazard ratio [95% confidence interval] 1.62 [1.14–2.30]; 1.35 [1.04–1.84]; and 1.38 [1.03–1.84], respectively). Similar results were shown in Model I (adjusted for age, sex and ethnicity) and in Model II (fully adjusting for age, ethnicity, sex, acute kidney injury stage, CHF, renal disease, stroke, malignancy, respiratory failure, pneumonia, sodium, potassium, chloride, BUN, PT, WBC, pH, creatinine, albumin, glucose, bicarbonate, vasopressor use, diastolic blood pressure, respiration rate, temperature, the Elixhauser Comorbidity Index, SOFA score and SAPSII score).ConclusionThe relationship between the AG and 30-day all-cause mortality followed a J-shaped curve. Higher AG was associated with an increased risk of 30-day, 90-day, and 365-day all-cause mortality in critically ill patients with CS.