Preoperative systemic inflammatory response index as a prognostic marker for distal cholangiocarcinoma after pancreatoduodenectomy.

BACKGROUND: The relationship between preoperative inflammation status and tumorigenesis as well as tumor progression is widely acknowledged. AIM: To assess the prognostic significance of preoperative inflammatory biomarkers in patients with distal cholangiocarcinoma (dCCA) who underwent pancreatoduodenectomy (PD). METHODS: This single-center study included 216 patients with dCCA after PD between January 1, 2011, and December 31, 2022. The individuals were categorized into two sets based on their systemic inflammatory response index (SIRI) levels: A low SIRI group (SIRI < 1.5, n = 123) and a high SIRI group (SIRI ≥ 1.5, n = 93). Inflammatory biomarkers were evaluated for predictive accuracy using receiver operating characteristic curves. Both univariate and multivariate Cox proportional hazards analyses were performed to estimate SIRI for overall survival (OS) and recurrence-free survival (RFS). RESULTS: The study included a total of 216 patients, with 58.3% being male and a mean age of 65.6 ± 9.6 years. 123 patients were in the low SIRI group and 93 were in the high SIRI group after PD for dCCA. SIRI had an area under the curve value of 0.674 for diagnosing dCCA, showing better performance than other inflammatory biomarkers. Multivariate analysis indicated that having a SIRI greater than 1.5 independently increased the risk of dCCA following PD, leading to lower OS [hazard ratios (HR) = 1.868, P = 0.006] and RFS (HR = 0.949, P < 0.001). Additionally, survival analysis indicated a significantly better prognosis for patients in the low SIRI group (P < 0.001). CONCLUSION: It is determined that a high SIRI before surgery is a significant risk factor for dCCA after PD.

Atypical Infective Endocarditis Presenting With Euthermia and Right Lower Quadrant Abdominal Pain.

Infectious endocarditis (IE) is an infection of the heart's endothelial lining, often stemming from an underlying bacteremia. High-risk populations include intravenous substance users, individuals with structural heart disease, those with intravascular devices, and those with prosthetic heart valves. In the emergency department, IE is often suspected in patients with a fever, known risk factors, and unexplained systemic symptoms due to systemic thromboemboli. We present a case of atypical IE occurring in an afebrile 38-year-old woman with a remote history of intravenous drug use. The patient's clinical presentation was characterized by systemic inflammatory response syndrome, stabbing-like right lower quadrant abdominal pain radiating to the right lower back and the rest of the abdomen, malaise, fatigue, and an absence of a fever. A CT scan revealed a right renal embolism and an infarcted right kidney, prompting a bedside point-of-care echocardiogram that showed a large vegetation on the mitral valve, suggestive of IE with systemic thromboembolic disease. The patient received broad-spectrum antibiotics and antipyretics and ultimately underwent mitral valve replacement, with good recovery upon discharge. Patients with IE are at high risk for life-threatening complications due to tissue damage from systemic microemboli and sepsis. It is important to identify IE's atypical presentation and risk factors for early recognition, prompt point-of-care echocardiogram, and initiation of treatment. This is particularly important in the era of increased opioid use among our patient population which could potentially conceal an underlying fever.

Extracted Plasma Cell-Free DNA Concentrations Are Elevated in Colic Patients with Systemic Inflammation.

Colic is a common and potentially life-threatening condition in horses; in many cases, it remains challenging for clinicians to determine the cause, appropriate treatment, and prognosis. One approach that could improve patient care and outcomes is identification of novel diagnostic and prognostic biomarkers. Plasma cell-free DNA (cfDNA) is a biomarker that shows promise for characterizing disease severity and predicting survival in humans with acute abdominal pain or requiring emergency abdominal surgery. In horses, we recently determined that extracted plasma cfDNA concentrations are elevated in colic patients compared to healthy controls. For this current study, we hypothesized that extracted plasma cfDNA concentrations would be significantly higher in horses with strangulating or inflammatory colic lesions, in colic patients with systemic inflammatory response syndrome (SIRS), and in non-survivors. Cell-free DNA concentrations were measured in extracted plasma samples using a compact, portable Qubit fluorometer. Colic patients that met published criteria for equine SIRS had significantly higher median extracted plasma cfDNA compared to non-SIRS colic patients. There were no significant differences in extracted plasma cfDNA concentrations between other groups of interest. Our data offer early evidence that extracted plasma cfDNA concentration may provide information about systemic inflammation in colic patients, and additional research is warranted to expand on these findings.

MLKL-mediated endothelial necroptosis drives vascular damage and mortality in systemic inflammatory response syndrome.

The hypersecretion of cytokines triggers life-threatening systemic inflammatory response syndrome (SIRS), leading to multiple organ dysfunction syndrome (MODS) and mortality. Although both coagulopathy and necroptosis have been identified as important factors in the pathogenesis of SIRS, the specific cell types that undergo necroptosis and the interrelationships between coagulopathy and necroptosis remain unclear. In this study, we utilized visualization analysis via intravital microscopy to demonstrate that both anticoagulant heparin and nonanticoagulant heparin (NAH) pretreatment protect mice against TNF-α-induced mortality in SIRS. Moreover, the deletion of Mlkl or Ripk3 resulted in decreased coagulation and reduced mortality in TNF-α-induced SIRS. These findings suggest that necroptosis plays a key role upstream of coagulation in SIRS-related mortality. Furthermore, using a genetic lineage tracing mouse model (Tie2-Cre;Rosa26-tdT), we tracked endothelial cells (ECs) and verified that EC necroptosis is responsible for the vascular damage observed in TNF-α-treated mice. Importantly, Mlkl deletion in vascular ECs in mice had a similar protective effect against lethal SIRS by blocking EC necroptosis to protect the integrity of the endothelium. Collectively, our findings demonstrated that RIPK3-MLKL-dependent necroptosis disrupted vascular integrity, resulting in coagulopathy and multiorgan failure, eventually leading to mortality in SIRS patients. These results highlight the importance of targeting vascular EC necroptosis for the development of effective treatments for SIRS patients.

The early prognostic value of the 1-4-day BCM/PA trend after admission in neurocritical patients.

The purpose of this study was to investigate early stage dynamic changes in relevant indicators in neurocritical patients to identify biomarkers that can predict a poor prognosis at an early stage (1-4 days after admission). This study retrospectively collected clinical data, inflammatory indicators, and nutritional indicators from 77 patients at the neurology intensive care unit. The 3-month modified Rankin scale score was used as the outcome indicator. A linear mixed model was used to analyze changes in inflammatory indicators and nutritional indicators in neurocritical patients over time from 1-4 days after admission. Logistic regression was used to determine the independent risk factors for a poor prognosis in neurocritical patients and to construct a predictive model. The predictive efficacy of the model was verified using leave-one-out cross-validation and decision curve analysis methods. The analysis results showed that 1-4 days after admission, the inflammatory indicators of white blood cell and absolute monocyte counts and the nutritional indicators of body cell mass(BCM), fat-free mass, body cell mass/phase angle (BCM/PA), intracellular water, extracellular water, and skeletal muscle index increased overall, while the nutritional indicators of albumin and visceral fat area decreased overall. The logistic multivariate regression model showed that the Charlson comorbidity index (CCI) (odds ratio (OR) = 2.526, 95% CI [1.202, 5.308]), hemoglobin (Hb)(on admission)-Hb(min) (OR = 1.049, 95% CI [1.015, 1.083), BCM(on admission) (OR = 0.794, 95% CI [0.662, 0.952]), and the change in BCM/PA 1-4 days after admission (OR = 1.157, 95% CI [1.070, 1.252]) were independent risk factors for a poor prognosis in neurocritical patients. The predictive analysis showed that the predictive power of Model 1 with BCM/PA (area under the curve (AUC) = 0.95, 95% CI (0.90, 0.99)) was 93%, 65%, 141%, and 133% higher than that of Model 2 without BCM/PA, the CCI, the APACHE II score, and the NRS2002 score (all P < 0.05), respectively. The CCI, Hb(on admission)-Hb(min), BCM(on admission), and an increase in BCM/PA 1-4 days after admission were independently associated with a poor prognosis in neurocritical patients. Of these variables, BCM/PA may be a valid indicator for early stage prediction of a poor prognosis in neurocritical patients.

Inflammatory indices-Systemic Immune-Inflammation Index (SII) and Systemic Inflammatory Response Index (SIRI)-during Pregnancy and Associations with Gestational Diabetes Mellitus.

Purpose: Gestational diabetes mellitus (GDM) is a prevalent complication during pregnancy. This study aimed to explore the associations between inflammatory indices during pregnancy and the development of GDM. Methods: Data from the Fujian Birth Cohort Study between March 2019 and December 2022 were used. Participants who delivered a live-born singleton were included and categorized into GDM and non-GDM groups. Two inflammatory indices, the systemic immune-inflammation index (SII) and systemic inflammatory response index (SIRI), were calculated for each trimester of pregnancy via hematological parameters from complete blood count tests. The distributions of inflammatory indicators across trimesters were compared between the GDM and non-GDM groups. Additionally, multivariable logistic regression models were employed to investigate the associations between inflammatory indices and the incidence of GDM. Results: A total of 17297 participants were included, 21.2% of whom were diagnosed with GDM. In the first trimester, the median SIIs for the GDM and non-GDM groups were 817.7×109/L and 756.9×109/L, respectively, whereas the median SIRIs were 1.6×109/L and 1.5×109/L, respectively. In both groups, the SII increased to its peak in the second trimester before declining, whereas the SIRI progressively increased throughout pregnancy. The SII and SIRI were greater in the GDM group than in the non-GDM group during the first two trimesters but lower in the third trimester. Nonlinear positive associations between first-trimester SII and SIRI levels and GDM were observed, with extreme quartile odds ratios of 1.32 (95% CI: 1.19, 1.48) and 1.39 (95% CI: 1.24, 1.55), respectively. Conclusion: The SII and SIRI increased and reached their peak values in the second and third trimesters of pregnancy, respectively. Elevated levels of the SII and SIRI in early pregnancy were linked to an increased risk of GDM, suggesting their potential utility as screening tools for GDM.

Plasma-derived extracellular vesicles (EVs) as biomarkers of sepsis in burn patients via label-free Raman spectroscopy.

Sepsis following burn trauma is a global complication with high mortality, with ∼60% of burn patient deaths resulting from infectious complications. Diagnosing sepsis is complicated by confounding clinical manifestations of the burn injury, and current biomarkers lack the sensitivity and specificity required for prompt treatment. There is a strong rationale to assess circulating extracellular vesicles (EVs) from patient liquid biopsy as sepsis biomarkers due to their release by pathogens from bacterial biofilms and roles in the subsequent immune response. This study applies Raman spectroscopy to patient plasma-derived EVs for rapid, sensitive, and specific detection of sepsis in burn patients, achieving 97.5% sensitivity and 90.0% specificity. Furthermore, spectral differences between septic and non-septic burn patient EVs could be traced to specific glycoconjugates of bacterial strains associated with sepsis morbidity. This work illustrates the potential application of EVs as biomarkers in clinical burn trauma care and establishes Raman analysis as a fast, label-free method to specifically identify features of bacterial EVs relevant to infection amongst the host background.

Impact on survival of sarcopenia, systemic inflammatory response and anthropometric factors after pancreatectomy for resectable pancreatic adenocarcinoma.

INTRODUCTION: Pancreatic adenocarcinoma (PDAC) is becoming a public health issue with a 5-years survival rate around 10%. Patients with PDAC are often sarcopenic, which impacts postoperative outcome. At the same time, overweight population is increasing and adipose tissue promotes tumor related-inflammation. With several studies supporting independently these data, we aimed to assess if they held an impact on survival when combined. METHODS: We included 232 patients from two university hospitals (CHU de Lille, Institut Paoli Calmette), from January 2011 to December 2018, who underwent Pancreaticoduodenectomy (PD) for resectable PDAC. Preoperative CT scan was used to measure sarcopenia and visceral fat according to international cut-offs. Neutrophil to lymphocyte (NLR) and platelet to lymphocyte ratios (PLR) were used to measure inflammation. For univariate and multivariate analyses, the Cox proportional-hazard model was used. P-values below 0.05 were considered significant. RESULTS: Sarcopenic patients with visceral obesity were less likely to survive than the others in multivariate analysis (OS, HR 1.65, p= 0.043). Cutaneous obesity did not influence survival. We also observed an influence on survival when we studied sarcopenia with visceral obesity (OS, p= 0.056; PFS, p = 0.014), sarcopenia with cutaneous obesity (PFS, p= 0.005) and sarcopenia with PLR (PFS, p= 0.043). This poor prognosis was also found in sarcopenic obese patients with high PLR (OS, p= 0.05; PFS, p= 0.01). CONCLUSION: Sarcopenic obesity was associated with poor prognosis after PD for PDAC, especially in patients with systemic inflammation. Pre operative management of these factors should be addressed in pancreatic cancer patients.

The systemic inflammatory response index is associated with chronic kidney disease in patients with hypertension: data from the national health and nutrition examination study 1999-2018.

BACKGROUND: Studies have shown that in hypertensive patients, chronic kidney disease (CKD) is associated with a poor prognosis. Inflammation is a highly important factor in the progression of CKD. Detecting systemic inflammation and intervening promptly in patients with hypertension may help reduce the risk of CKD. The systemic inflammatory response index (SIRI) is a tool used to measure the systemic inflammatory response, but its relationship with CKD in patients with hypertension remains uncertain. METHODS: We utilized data from the National Health and Nutrition Examination Survey (NHANES), which was conducted between 1999 and 2018. The analysis included a total of 20,243 participants, categorized into three groups based on SIRI tertiles. Logistic regression analysis and restricted cubic spline analysis were used to examine the relationship between the SIRI and CKD. RESULTS: In patients with hypertension, there was a notable relationship between the SIRI and the odds of developing CKD. After full adjustment, there was a 31% greater likelihood of developing CKD associated with each incremental increase of 1 unit in the SIRI (OR: 1.31, 95% CI: 1.24-1.39, p < 0.001). The groups with greater SIRI values exhibited greater odds of developing CKD than did the T1 group (T2: OR: 1.20, 95% CI: 1.04-1.38, p = 0.015; T3: OR: 1.69, 95% CI: 1.47-1.94, p < 0.001). CONCLUSION: A high SIRI is associated with an increased risk of CKD in hypertensive patients. The greater the SIRI is, the greater the risk of CKD in hypertensive patients.

Stored RBC transfusions leads to the systemic inflammatory response syndrome in anemic murine neonates.

OBJECTIVE: RBC transfusions (RBCT) are life-saving treatment for premature and critically ill infants. However, the procedure has been associated with the development of systemic inflammatory response syndrome (SIRS) and potentially multiple organ dysfunction syndrome (MODS) in neonates. The present study aimed to investigate the mechanisms of RBCT-related SIRS in severely anemic murine neonates. METHODS: C57BL/6 (WT), TLR4-/- and myeloid-specific triggered myeloid receptor-1 (trem1)-/- mouse pups were studied in 4 groups (n = 6 each): (1) naïve controls, (2) transfused control, (3) anemic (hematocrit 20-24%) and (4) anemic with RBC transfused using our established murine model of phlebotomy-induced anemia (PIA) and RBC transfusion. Plasma was measured for quantifying inflammatory cytokines (IFN-γ, IL-1ß, TNF-α, IL-6, MIP-1α, MIP-1ß, MIP2 and LIX) using a Luminex assay. In vitro studies included (i) sensitization by exposing the cells to a low level of lipopolysaccharide (LPS; 500 ng/ml) and (ii) trem1-siRNA transfection with/without plasma supernatant from stored RBC to assess the acute inflammatory response through trem1 by qRT-PCR and immunoblotting. RESULTS: Anemic murine pups developed cytokine storm within 2 h of receiving stored RBCs, which increased until 6 h post-transfusion, as compared to non-anemic mice receiving stored RBCTs ("transfusion controls"), in a TLR4-independent fashion. Nonetheless, severely anemic pups had elevated circulating endotoxin levels, thereby sensitizing circulating monocytes to presynthesize proinflammatory cytokines (IFN-γ, IL-1ß, TNF-α, IL-6, MIP-1α, MIP-1ß, MIP2, LIX) and express trem1. Silencing trem1 expression in Raw264.7 cells mitigated both endotoxin-associated presynthesis of proinflammatory cytokines and the RBCT-induced release of inflammatory cytokines. Indeed, myeloid-specific trem1-/- murine pups had significantly reduced evidence of SIRS following RBCTs. CONCLUSION: Severe anemia-associated low-grade inflammation sensitizes monocytes to enhance the synthesis of proinflammatory cytokines and trem1. In this setting, RBCTs further activate these monocytes, thereby inducing SIRS. Inhibiting trem1 in myeloid cells, including monocytes, alleviates the inflammatory response associated with the combined effects of anemia and RBCTs in murine neonates.

Molecular and Functional Alterations in the Cerebral Microvasculature in an Optimized Mouse Model of Sepsis-Associated Cognitive Dysfunction.

Systemic inflammation has been implicated in the development and progression of neurodegenerative conditions such as cognitive impairment and dementia. Recent clinical studies indicate an association between sepsis, endothelial dysfunction, and cognitive decline. However, the investigations of the role and therapeutic potential of the cerebral microvasculature in sepsis-induced cognitive dysfunction have been limited by the lack of standardized experimental models for evaluating the alterations in the cerebral microvasculature and cognition induced by the systemic inflammatory response. Herein, we validated a mouse model of endotoxemia that recapitulates key pathophysiology related to sepsis-induced cognitive dysfunction, including the induction of an acute systemic hyperinflammatory response, blood-brain barrier (BBB) leakage, neurovascular inflammation, and memory impairment after recovery from the systemic inflammation. In the acute phase, we identified novel molecular (e.g., upregulation of plasmalemma vesicle-associated protein, PLVAP, a driver of endothelial permeability, and the procoagulant plasminogen activator inhibitor-1, PAI-1) and functional perturbations (i.e., albumin and small-molecule BBB leakage) in the cerebral microvasculature along with neuroinflammation. Remarkably, small-molecule BBB permeability, elevated levels of PAI-1, intra-/perivascular fibrin/fibrinogen deposition, and microglial activation persisted 1 month after recovery from sepsis. We also highlight molecular neuronal alterations of potential clinical relevance following systemic inflammation including changes in neurofilament phosphorylation and decreases in postsynaptic density protein 95 and brain-derived neurotrophic factor, suggesting diffuse axonal injury, synapse degeneration, and impaired neurotrophism. Our study serves as a standardized mouse model to support future mechanistic studies of sepsis-associated cognitive dysfunction and to identify novel endothelial therapeutic targets for this devastating condition.

Multiple site inflammation and acute kidney injury in crush syndrome.

Crush syndrome, which frequently occurs in earthquake disasters, often leads to rhabdomyolysis induced acute kidney injury (RIAKI). Recent findings indicate that systemic inflammatory response syndrome (SIRS) exacerbates muscle collapse, contributing to RIAKI. The purpose of this study is to investigate the involvement of multiple site inflammation, including intraperitoneal, in crush syndrome. In a mouse model of RIAKI, elevated levels of inflammatory mediators such as TNFα, IL-6, myoglobin, and dsDNA were observed in serum and the peritoneal cavity, peaking earlier in the intraperitoneal cavity than in serum or urine. Our previously developed novel peptide inhibiting leukocyte extracellular traps was administered intraperitoneally and blocked all of these mediators in the intraperitoneal cavity and serum, ameliorating muscle damage and consequent RIAKI. Although further studies are needed to determine whether intraperitoneal inflammation associated with muscle collapse can lead to systemic inflammation, resulting in more severe and prolonged muscle damage and renal injury, early suppression of multiple site inflammation, including intraperitoneal, might be an effective therapeutic target.

Association of Systemic Inflammation Level on Admission with Total and Cardiovascular­Specific Death in Heart Failure with Preserved Ejection Fraction: A Large Multi­Center Retrospective Longitudinal Study.

Purpose: Heart failure with preserved ejection fraction (HFpEF) is inherently a complex inflammatory syndrome, and heightened inflammation is strongly associated with an increased risk of death. However, the association of systemic inflammation levels with total and cardiovascular death among patients with HFpEF remains unknown. We aimed to investigate the prognostic impact of systemic inflammation on all-cause and cardiovascular death among patients with HFpEF. Patients and Methods: Patients with HFpEF were included in this study. Systemic inflammation response index (SIRI) is defined as the multiplication of neutrophil and monocyte divided by lymphocyte count, and patients were divided into four groups based on SIRI quartiles. Cox regression models and competing risk models were used to examine the relationships between SIRI and total and cardiovascular­specific mortality, respectively. Results: 9,986 patients with HFpEF were included in five tertiary hospitals. During a median follow-up period of 4.4 years, a total of 2004 patients died, of which 965 were cardiovascular deaths. After fully adjusting for confounders, elevated SIRI level was significantly related to the increased risk of all-cause death (Q2, Q3, Q4: adjusted hazard ratio (aHR) [95 confidence interval (CI)%] =1.17[1.01-1.35], 1.31[1.13-1.52], 1.51[1.30-1.76], respectively; P for trend <0.001). The elevated quartile of SIRI showed higher risks of cardiovascular death, but there was no statistically significant increased risk of cardiovascular death across the lower SIRI quartile (model 3: Q2, Q3, Q4: aHR [95CI%] =1.22[0.99-1.51], 1.50[1.20-1.86], 1.73[1.37-2.18], respectively; P for trend <0.001). Conclusion: Elevated systemic inflammation level on admission was correlated with an increased risk of all-cause and cardiovascular death among patients with HFpEF. The SIRI may serve as a promising marker of risk stratification for patients with HFpEF.

A systematic review of the role of systemic inflammation-based prognostic scores in patients with abdominal aortic aneurysm.

BACKGROUND AND AIMS: Activation of the systemic inflammatory response (SIR) is associated with inferior outcomes across a spectrum of disease. Routinely available measures of the SIR (neutrophil:lymphocyte ratio (NLR), platelet:lymphocyte ratio (PLR), systemic immune-inflammatory index (SII), systemic inflammatory grade (SIG)) have been shown to provide prognostic value in patients undergoing surgical intervention. The present study aimed to review the literature describing the prognostic association of NLR, PLR, SII and SIG in patients undergoing intervention for abdominal aortic aneurysm (AAA). METHODS: This PRISMA guidelines were followed. The MEDLINE database was interrogated for relevant studies investigating the effect of peri-operative systemic inflammation-based prognostic systems on all-cause mortality in patients undergoing OSR and EVAR for AAA. Inter-study heterogeneity precluded meaningful meta-analysis; qualitative analysis was instead performed. RESULTS: There were 9 studies included in the final review reporting outcomes on a total of 4571 patients; 1256 (27 %) patients underwent OSR, and 3315 (73 %) patients underwent EVAR. 4356 (95 %) patients underwent a procedure for unruptured AAA, 215 (5 %) patients underwent an emergency procedure for ruptured AAA0.5 studies reported early (inpatient or 30-day) mortality; 2 of these found that elevated NLR predicted inferior survival, however PLR did not provide prognostic value. 6 studies reported long-term mortality; elevated NLR (5 studies), PLR (1 study), and SIG (1 study) predicted inferior survival. CONCLUSIONS: It appears that activation of the SIR is associated with inferior prognosis in patients undergoing intervention for AAA, however the evidence is limited by heterogenous methodology and lack of consensus regarding optimal cutoff. PROSPERO DATABASE REGISTRATION NUMBER: CRD42022363765.

Systemic Inflammatory Response Index and the Short-Term Functional Outcome of Patients with Acute Ischemic Stroke: A Meta-analysis.

INTRODUCTION: The systemic inflammatory response index (SIRI) is a novel indicator of systemic inflammation derived from the absolute counts of neutrophils, monocytes, and lymphocytes. The aim of this meta-analysis was to evaluate the association between SIRI and functional outcome in patients with acute ischemic stroke (AIS). METHODS: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed in this meta-analysis. Relevant cohort studies were retrieved by a search of electronic databases including PubMed, Web of Science, Embase, Wanfang, and China National Knowledge Infrastructure from database inception to February 9, 2024. A poor functional outcome was defined as a modified Rankin Scale ≥ 3 within 3 months after disease onset. A random-effects model was used to combine the data by incorporating the influence of between-study heterogeneity. The protocol of the meta-analysis was not prospectively registered in PROSPERO. RESULTS: Fourteen cohort studies were included. Pooled results showed that a high SIRI at admission was associated with increased risk of poor functional outcome within 3 months (odds ratio [OR]: 1.57, 95% confidence interval: 1.39 to 1.78, p < 0.001; I2 = 0%). Results of the meta-regression analysis suggested that the cutoff for defining a high SIRI was positively related to the OR for the association between SIRI and the risk of poor functional outcome (coefficient = 0.13, p = 0.03), while other variables including sample size, mean age, severity of stroke at admission, percentage of men, current smokers, or patients with diabetes did not significantly modify the results. Subgroup analyses according to study design, main treatments, and study quality scores showed similar results. CONCLUSION: A high SIRI may be associated with a poor functional outcome in patients after AIS.

The role of sarcopenia in pre- and postoperative inflammation: implications of outcomes in patients with colorectal cancer.

BACKGROUND: Patients with colorectal cancer (CRC) with sarcopenia often have a poor prognosis, and the timing of preoperative intervention to improve sarcopenia is unclear. Sarcopenia can affect the body's overall inflammatory status. This study aimed to investigate whether sarcopenia exacerbates the inflammatory response in patients with CRC after surgical stimulation and its effect on the prognosis. METHODS: A retrospective analysis was conducted on a cohort of 215 patients with CRC who were categorized into either the sarcopenia group or the nonsarcopenia group based on their skeletal muscle index values. Inflammation-related indicators were collected from patients before and after surgery, allowing for the calculation of the differences in preoperative and postoperative changes. In addition, the correlation between inflammatory markers and postoperative complications was assessed. All patients were followed up for a period ranging from 2 to 5 years, with an average follow-up duration of 3 years, during which their recurrence and mortality rates were recorded. In addition, the relationship between inflammation indicators was explored. RESULTS: Of note, 45 of 215 patients with sarcopenia had higher levels of preoperative baseline inflammation markers, such as C-reactive protein (P = .002), immune-inflammation index (IBI; P < .001), systemic inflammatory response index (SIRI; P = .009), and systemic immune-inflammation index (SII; P = .002) than patients without sarcopenia. There was a significant difference in inflammatory indicators before and after surgery between dIBI, dSIRI, and dSII, with the largest effect observed. In addition, the predictive capabilities of dIBI, dSIRI, and dSII for postoperative complications, as measured using the area under the receiver operating characteristic curve, were found to be 0.938, 0.877, and 0.818, respectively. Furthermore, survival analysis indicated that the differences in preoperative and postoperative alterations in IBI (dIBI), SIRI (dSIRI), and SII (dSII) were effective in predicting long-term postoperative mortality. CONCLUSION: Our findings suggest that sarcopenia plays a significant role in exacerbating postoperative inflammatory response in patients with CRC, leading to an increased risk of postoperative complications and influencing long-term survival outcomes.

Association of Systemic Inflammatory Response Index and Neutrophil-to-Lymphocyte Ratio on Unfavorable Functional Outcomes in Acute Ischemic Stroke Patients After Endovascular Therapy.

BACKGROUND: Inflammatory markers for the prognosis of acute ischemic stroke (AIS) with endovascular therapy remain unclear. The purpose of this study was to investigate the association between the systemic inflammatory response index (SIRI) and neutrophil-to-lymphocyte ratio (NLR) with unfavorable functional outcomes at 90-day in individuals of AIS who underwent endovascular therapy. METHODS: A total of 128 AIS patients who had endovascular therapy were enrolled from the Nanjing Stroke Registry between September 2019 and November 2022. Peripheral venous blood was collected from patients within 24 h of admission for information on the following parameters: neutrophil count, lymphocyte count, and monocyte count. Then, the SIRI and NLR values were calculated and the association among SIRI, NLR, and modifled Rankin Scale scores 90 days after endovascular therapy was examined via univariate and multivariate logistic analyses. Receiver operating characteristic curves were utilized to determine the best threshold for SIRI and NLR in predicting negative neurological outcomes following endovascular treatment for patients with AIS. RESULTS: A total of 128 participants were evaluated, among which 50% had unfavorable outcomes. Linear regression analysis showed that the best threshold for SIRI was >1.407 (odds ratio = 1.265; 95% confidence interval, 1.071-1.493; P = 0.006), and for NLR it was >5.347 (odds ratio = 1.088; 95% confidence interval, 1.007-1.175; P = 0.033). These results revealed NLR and SIRI as significant predictors of unfavorable outcomes at 90 days. The area under the curve for SIRI and NLR in predicting 90-day adverse outcomes was 0.643 and 0.609, respectively. CONCLUSIONS: Higher SIRI and NLR levels at admission may lead to unfavorable outcomes at 90 days for AIS patients with endovascular therapy.

Investigation of Predictors of Systemic Inflammatory Response Syndrome After Endourological Procedure of Upper Urinary Tract Stones.

Background: In order to prevent infectious complications following endourological procedure of upper urinary tract stones, it is essential to determine which patients are at high risk of developing this complication. We aimed to identify predictors that may cause systemic inflammatory response syndrome (SIRS) after the endourological procedure of upper urinary tract stones. Materials and Methods: Patients who underwent percutaneous nephrolithotomy (PNL), flexible ureteroscopy (F-URS), or semirigid ureteroscopy (SR-URS) in our center between January 2011 and June 2020 were evaluated retrospectively. After surgery, patients were pursued for SIRS criteria. Logistic regression analyses were applied to identify predictors of SIRS. Results: A total of 1471 patients were included in the study. The rates of SIRS after PNL, F-URS, and SR-URS were 12.9%, 6.3%, and 1.7%, respectively. In multivariate analysis, predictors for SIRS were determined to be stone volume, operative time, and history of recurrent urinary tract infection (UTI) in the PNL group; ipsilateral stone surgery history, stone volume, and operative time in the F-URS group; and stone volume, operative time, and history of recurrent UTI in the SR-URS group. Conclusion: Stone volume and operative time were determined to be independent predictors of SIRS in endourological surgery of upper urinary tract stones.

State of the art of sepsis care for the emergency medicine clinician.

Sepsis impacts 1.7 million Americans annually. It is a life-threatening disruption of organ function because of the body's host response to infection. Sepsis remains a condition frequently encountered in emergency departments (ED) with an estimated 850,000 annual visits affected by sepsis each year in the United States. The pillars of managing sepsis remain timely identification, initiation of antimicrobials while aiming for source control and resuscitation with a goal of restoring tissue perfusion. The focus herein is current evidence and best practice recommendations for state-of-the-art sepsis care that begins in the ED.