systemic inflammation response index

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<p>Systemic inflammation response index predicts prognosis in patients with clear cell renal cell carcinoma: a propensity score-matched analysis</p>

<p>Systemic inflammation response index predicts prognosis in patients with clear cell renal cell carcinoma: a propensity score-matched analysis</p>

SIRI, which is defined based on peripheral blood counts of neutrophils, monocytes, and lymphocytes, has been found to be an independent risk factor for survival among patients with pancreatic cancer. SIRI is considered to be better than MLR and NLR in terms of predictive accuracy, and it is able to reflect the status of local immune response and systemic inflammation in patients with pancreatic cancer. 14

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<p>Pretreatment Systemic Inflammation Response Index in Patients with Breast Cancer Treated with Neoadjuvant Chemotherapy as a Useful Prognostic Indicator</p>

<p>Pretreatment Systemic Inflammation Response Index in Patients with Breast Cancer Treated with Neoadjuvant Chemotherapy as a Useful Prognostic Indicator</p>

A novel and integrated indicator that named Systemic In fl ammation Response Index (SIRI), which is based on neutrophil (N), monocyte (M), and lymphocyte (L) counts, is reported to be associated with clinical outcomes and predict the survival of patients with gastric cancer. 17 This integrated indicator may comprehensively re fl ect the bal- ance of host immune and in fl ammatory status compared with NLR, LMR, and PLR. Nevertheless, the SIRI has been studied rarely in breast cancer patients with treated NACT. Therefore, our study aims to evaluate the prognos- tic signi fi cance of SIRI in patients with breast cancer receiving NACT.
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<p>The systemic inflammation response index predicts survival and recurrence in patients with resectable pancreatic ductal adenocarcinoma</p>

<p>The systemic inflammation response index predicts survival and recurrence in patients with resectable pancreatic ductal adenocarcinoma</p>

risk for local recurrence, distant metastasis, and short survival. Cancer-related in fl ammation is recognized as the seventh hallmark of cancer, and it has a close relation- ship with carcinogenesis and tumor progression. 5 Many studies have proved that in fl ammatory scores based on circulating immune and in fl ammatory cells, such as NLR and PLR, can improve the accuracy of survival prediction. 20,21 A novel in fl ammation-based index, SIRI, fi rst described by Qi et al, showed its prognostic value in advanced pancreatic cancer patients who received pallia- tive chemotherapy. 10 After that, several studies reported Table 2 Univariate analysis for survival of patients in the training cohort and validation cohort
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<p>Systemic immune-inflammation index and ultrasonographic classification of breast imaging-reporting and data system predict outcomes of triple-negative breast cancer</p>

<p>Systemic immune-inflammation index and ultrasonographic classification of breast imaging-reporting and data system predict outcomes of triple-negative breast cancer</p>

tigating the association between SII and OS and treatment response in patients with non-small-cell lung cancer at stage III. Furthermore, we found that tumor stage, BI-RADS, and histological grade also independently predicted poor DFS, while the same factors, alongside lympho-vascular invasion and lymph node status were independently associated with poor OS for patients with TNBC.

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Preoperative systemic immune-inflammation index predicts prognosis of patients with non-metastatic renal cell carcinoma: a propensity score-matched analysis

Preoperative systemic immune-inflammation index predicts prognosis of patients with non-metastatic renal cell carcinoma: a propensity score-matched analysis

The potential mechanism for the prognostic signifi- cance of this combination might be explained by the functions of neutrophil, platelet, and lymphocyte. Neu- trophils promote angiogenesis and inhibit anti-tumor immune system response, leading to tumor development [9, 12, 28]. Neutrophils also play an important role in the lymphangiogenesis [29]. Furthermore, neutrophils could secret circulating growth factors such as vascular endothelial growth factor, facilitating adhesion and tumor seeding [29, 30]. Huang et al. Observed that neutrophilia is an independent predictor of recurrence in patients with RCC [31]. Besides, the intratumoral neutrophil is associated with poor prognosis in patients with local- ized and metastatic RCC [32, 33]. Platelet could protect circulating tumor cells (CTCs) during circulation, induce CTC epithelial-mesenchymal transition, and facilitate the extraction of tumor cells, leading to the metastasis of tumor cells [34]. Moschini et al. revealed that the platelet count was associated with survival in patients with blad- der carcinoma [35]. Yun et al. also found that decreased mean platelet volume was independently associated with RCC [36]. Lymphocyte plays an important role in anti- tumor immunity. Lymphocyte could induce cytotoxic cell death and inhibit tumor proliferation and migration by secreting cytokines, leading to a host immune response to malignancy [8]. A decreased lymphocyte count might result in the attenuation of immunological anti-tumor response. Lymphopenia was found to be associated with lower survival in patients with advanced bladder can- cer and RCC [37, 38]. Besides, higher tumor-infiltrating
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Prognostic nutritional index serves as a predicative marker of survival and associates with systemic inflammatory response in metastatic intrahepatic cholangiocarcinoma

Prognostic nutritional index serves as a predicative marker of survival and associates with systemic inflammatory response in metastatic intrahepatic cholangiocarcinoma

However, this study also has some limitations. First, some other parameters involving in inflammation such as CRP, TNF- α , and interleukins were not measured in our study because they are not routinely tested in clinical applica- tions. Second, being a retrospective research, it has its own flaws since it was conducted at a single medical center with a relatively smaller number of cases. Thus, more studies are warranted to further validate the role of PNI and the possible mechanism in determining the prognosis of ICC.

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Systemic immune-inflammation index predicts the clinical outcome in patients with metastatic renal cell cancer treated with sunitinib

Systemic immune-inflammation index predicts the clinical outcome in patients with metastatic renal cell cancer treated with sunitinib

The use of validated prognostic indices is essential in clinical practice to better make correct decisions on the use of high-cost drugs and to potentially reduce the impact of toxicities especially in more frail patients. In advanced RCC, the IMCD model is currently accepted as the reference in prognostic stratification and replaced in clinical practice the MSKCC criteria. In this paper we want to purpose SII as a new tool to define outcome stratification in renal cancer patients. SII changes could be able to predict response to treatment and clinical outcome of these patients, giving a potential simple tool to monitor the effect of treatment on the clinical outcome of these patients. In addition, this inflammatory index is of special interest in RCC, which is an immune-responsive disease, and new immune-oncologic agents, like checkpoint inhibitors are in active development as agents for the treatment of systemic disease [28].
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Prognostic value of the systemic immune-inflammation index in patients with breast cancer: a meta-analysis

Prognostic value of the systemic immune-inflammation index in patients with breast cancer: a meta-analysis

Tumor environment and inflammation play important roles in tumor development [4]. The components of the tumor microenvironment include the response cells, such as neutrophils, monocytes, lymphocytes, platelets, and cytokines. Several inflammatory cell parameters, including the neutrophil-lymphocyte ratio, platelet- lymphocyte ratio, C-reactive protein/albumin ratio, and systemic immune-inflammation index (SII), are derived using these meditators. The SII is an index that is cal- culated on the basis of the platelet, neutrophil, and lym- phocyte counts. The SII has been used to evaluate the pretreatment balance between inflammatory factors and immune status of patients with cancer [5–8]. The SII is associated with the prognosis of patients with breast can- cer, although the results are controversial [9–16]. There- fore, we performed the current meta-analysis to identify the prognostic impact of the SII in patients with breast cancer by aggregating all available data.
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<p>Prognostic significance of systemic immune-inflammation index in triple-negative breast cancer</p>

<p>Prognostic significance of systemic immune-inflammation index in triple-negative breast cancer</p>

Cancer-related in fl ammation has been found to play a signi fi cant part in the development and prognosis of cancer. 15–17 Some biochemical or hematological markers, such as increase in platelet, lymphocyte, neutrophil, white cell counts, C-reactive protein levels, and hypoalbumine- mia, could trigger a systemic in fl ammatory response. 18–21 A combination of these factors has been used to obtain prognostic scores for in fl ammation, for example, lympho- cyte ratio (PLR) for platelet, lymphocyte ratio (NLR) for neutrophil, and the Glasgow Prognostic Score. The adverse role of elevated NLR and PLR has already been studied intensely in various cancers, including non-small cell lung cancer, cervical cancer, gallbladder cancer, ovar- ian cancer, colorectal cancer, breast cancer, and gastric cancer. 19,22–30
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Neutrophil Lymphocyte Ratio (NLR) in Patients with Lung Cancer - An Index of Cancer Related Systemic Inflammation

Neutrophil Lymphocyte Ratio (NLR) in Patients with Lung Cancer - An Index of Cancer Related Systemic Inflammation

suicidal programmes in tumor microenvironment that has major implications in pathogenesis of neutrophil mediated chronic inflammatory diseases, which remainas major hurdles in understanding thepathogenesis of cancer related inflammation. Neutrophils that have phagocytosed the pathogens are removed by macrophages by a process called efferocytosis. Neutrophil macrophage interaction in tumor micro environment is mediated via various inter cellular signals. A neutrophilic response is having worse prognosis by inhibiting the immune system by way of suppression of cytotoxic T cells. Tissue infiltration is accompanied by leucocytosis. Neutrophil lifespan is altered in cancer, extending from 7 hin normal conditions to 17 h in cancer (4) . The immune infiltrating cells in the tumorstroma is critical in tumor behaviour, and response to therapy. The prognostic value of absence, presence or abundance of tumor associated neutrophils (TANs)
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Systemic immune-inflammation index, thymidine phosphorylase and survival of localized gastric cancer patients after curative

Systemic immune-inflammation index, thymidine phosphorylase and survival of localized gastric cancer patients after curative

Tumor-associated platelets release ATP into the blood and facilitate tumor metastasis by relaxing endothelial barrier function [5]. Platelets have direct contact with tumor cells, synergistically activate the TGFbeta/Smad and NF- kappaB pathways in cancer cells, induce an epithelial- mesenchymal-like transition and promote metastasis [4]. Thus, an elevated SII, due to high levels of neutrophils and platelets while low level of lymphocytes, usually suggests a stronger inflammatory and a weaker immune response in patients. It may be associated with invasion and metastasis of cancer cells and hence lead to poor survival.
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The impact of the systemic inflammatory response on hepatic bacterial elimination in experimental abdominal sepsis

The impact of the systemic inflammatory response on hepatic bacterial elimination in experimental abdominal sepsis

The mechanisms underlying decreased bacterial elimination by the liver in systemic inflammation seen in our study are unclear. Several mechanisms in the liver are affected by sepsis [36]. In mice, hepatic bacterial clearance decreased during severe bacteraemia and mild bacteraemia developed into severe bacteraemia with increased mortality in the setting of Kupffer cell ablation. Similarly to our findings, decreased Kupffer cell function has been associated with increased systemic endotoxemia [37]. These findings illustrate the importance of these resident macrophages for bacterial elimination and that decreased hepatic bacterial elimination can affect outcome in bacteraemia [38]. We assessed liver function by ICG clearance [28], finding no signs of decreased liver function in animals exposed to endotoxin compared with the previously healthy ones before the E. coli infusion was started. This finding suggests that decreased hepatic bacterial elimination during systemic inflammation is most likely not explained by liver failure.
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Brain Injury and Inflammation and Placental Inflammation in Response to Repetitive Umbilical Cord Occlusions in the Near Term Ovine Fetus

Brain Injury and Inflammation and Placental Inflammation in Response to Repetitive Umbilical Cord Occlusions in the Near Term Ovine Fetus

apoptotic cell death within the developing brain as noted. While it has been held that brain injury in response to hypoxia is more likely to be apoptotic with milder insult and necrotic with severe insult, it is becoming evident that both occur as a continuum of cell death in proportion to the severity of hypoxic insult. 55 As such, the adaptive metabolic mechanisms enacted to protect against necrotic cell death are also likely to protect against apoptotic cell death in the normoxic- and hypoxic-UCO groups as studied. Moreover, the balance in the expression of anti- and pro-apoptotic genes determines apoptotic triggering in response to hypoxia, and it is possible that the mild- and moderate-partial UCOs have altered this in favour of anti-apoptotic gene expression by hypoxic conditioning, thereby increasing tolerance to the severe-complete UCOs. 55 However, the number of TUNEL positive cells was increased in the hippocampal CA1 and dentate gyrus regions for the LPS-UCO group animals compared to respective control values. While these animals did not show any evidence of a brain inflammatory response as studied, they did show an increase in plasma and amniotic fluid inflammatory cytokines that related to the degree of UCO-induced acidemia and indicating a fetal/placental inflammatory response. 26 Accordingly, it is likely that the LPS- and UCO-induced systemic inflammation together with the fetal hypoxic-acidemia contributed to the increased brain apoptosis with the relative expression of anti- and pro- apoptotic genes accounting for the regional differences in vulnerability. 55 This conjecture is also consistent with the synergistic interaction between inflammation and hypoxia in the pathogenesis of perinatal brain injury reported by others. 9,12,13 However, intra-amniotic LPS dosing alone similar to the present study has shown apoptotic cell counts in the ovine fetal brain to be selectively increased at 48 hours, 59 although a second study with lower LPS dosing but over 28 days showed no impact here. 60 Since the effects of intra-amniotic LPS alone were not studied which is a limitation, it is possible the apoptotic changes seen were primarily the result of the LPS, although it seems likely that the repetitive UCOs were also contributory given the relationship to the degree of resultant acidemia as noted.
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Traumatic Injury as the Inciting Event of Inflammation leading to Sepsis and Cardiovascular Disease: Review of the Literature Frieri M 1*, Kumar K2 , Boutin A 2and Makaryus AN3

Traumatic Injury as the Inciting Event of Inflammation leading to Sepsis and Cardiovascular Disease: Review of the Literature Frieri M 1*, Kumar K2 , Boutin A 2and Makaryus AN3

Inflammation, autoimmunity and cardiovascular disease The pathogenesis of many autoimmune diseases is based on prolonged activation of the innate immune system [29]. Excessive activation of innate immunity is often the result of a chronic inflammatory process and this inflammation can be induced by exogenous and endogenous alarm factors. Recent discoveries implicate neutrophils as important regulators of both innate and adaptive immunity and in the development of organ damage in systemic autoimmune diseases, including SLE [30]. Thus, recent discoveries support the notion that neutrophils, low-density granulocytes and aberrant NET formation and clearance play important roles in lupus pathogenesis. Future studies should focus on how to selectively target these immunostimulatory pathways in this disease [30].
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Longitudinal association of C-reactive protein and Haemoglobin A1c over 13 years: the European Prospective Investigation into Cancer - Norfolk study

Longitudinal association of C-reactive protein and Haemoglobin A1c over 13 years: the European Prospective Investigation into Cancer - Norfolk study

Serum C-reactive protein (CRP) is a marker of systemic inflammation and has been shown to be associated with incident type 2 diabetes [1,2]. Patients with type 2 dia- betes are also at risk of developing micro-vascular and macro-vascular complications such as diabetic retinop- athy, nephropathy, neuropathy, atherosclerosis, and car- diovascular diseases. The potential etiologic role of chronic systemic inflammation in the pathogenesis of type

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Personality, Sex and Systemic Inflammation

Personality, Sex and Systemic Inflammation

For more than sixty years, personality has been known to influence both positive and negative health outcomes (Segerstrom et al., 1998; Steptoe & Molloy, 2007; Temoshok, Wald, Synowski, & Garzino-Demo, 2008). Certain personality traits have been associated with increased risk of chronic systemic inflammation. We examined whether the Big 5 personality dimensions were associated with IL6 in healthy males and females, and the extent to which physical activity and sex might explain this association. Our findings were that personality phenotype had a greater impact on systemic inflammation than physical activity, and the impact differed between men and women according to different personality characteristics. Controlling for age and BMI, higher scores of Openness have more of an impact on IL6 than physical activity among males than females and lower scores of Agreeable- ness have more of an impact on IL6 than physical activity among females than males. The finding of a weaker influence of physical activity on inflammation was surprising, but reinforces the importance of personality with regards to potentially harmful immune system activity.
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Unique patterns of lower respiratory tract microbiota are associated with inflammation and hospital mortality in acute respiratory distress syndrome

Unique patterns of lower respiratory tract microbiota are associated with inflammation and hospital mortality in acute respiratory distress syndrome

Continuous microaspiration and an impaired natural air- way clearance contributed to this increase in patients on mechanical ventilation [22]. Nevertheless, the bacterial copy numbers in the BALF in ARDS patients tended to be increased compared with those of the control patients on mechanical ventilation, even if the number of the control patients were limited. Moreover, bacterial pneu- monia, as cause of ARDS, did not affect the bacterial burden. In this study, we judged this difference of the bacterial copy number had an important meaning in the pathogenesis. Increased bacterial loads in the BALF were observed in a lipopolysaccharide-induced mouse model of ARDS [23]. This indicates a possible mechanism for the lung bacterial burden in ARDS patients other than via the respiratory tract. An anaerobic zone caused by inflammation of the alveolar epithelial cells promotes bacterial growth in injured lungs [24]. Our controls in- cluded a patient with heart failure; however, alveolar epi- thelial cells are not typically injured in heart failure. Several studies have indicated that increased lung and gut permeability may induce bacterial migration via gut- draining lymphatics and the portal or systemic circula- tion [11, 25, 26]. These mechanisms, which occur in the ARDS pathophysiology, could contribute to the in- creased bacterial numbers and increased morbidity.
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Sarcopenia correlates with systemic inflammation in COPD

Sarcopenia correlates with systemic inflammation in COPD

Materials and methods: In a cross-sectional design, muscle strength and muscle mass were measured by handgrip strength (HGS) and bioelectrical impedance analysis in 80 patients with stable COPD. Patients ($40 years old) diagnosed with COPD were recruited from outpatient clinics, and then COPD stages were classified. Sarcopenia was defined as the presence of both low muscle strength (by HGS) and low muscle mass (skeletal muscle mass index [SMMI]). Levels of circulating inflammatory biomarkers (IL-6 and high-sensitivity TNFα [hsTNFα]) were measured.

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The digestive tract as the origin of systemic inflammation

The digestive tract as the origin of systemic inflammation

this model [74]. Thus, physiological amounts of bacterial ligands arriving at the liver from the gut can contribute to maintain systemic immune homeostasis through the in- duction of STAT3 activity. However, gut alterations and excessive microbiota-dependent liver inflammation may shift this balance towards a more proinflammatory phenotype, leading to damage in remote organs such as brain, lung, pancreas, and heart [75]. A good example of this crosstalk is the gut–liver–lung axis during acute pancreatitis, leading to the acute respiratory distress syndrome (ARDS) and MODS. In this scenario, severe pancreatitis triggers intestinal barrier dysfunction and gut inflammation. Translocated microbial products and inflammatory mediators produced in the gut (e.g., tumor necrosis factor (TNF)-α, IL-6, and IL-1β) then arrive at the liver via the portal vein and activate KCs, which produce more pro-inflammatory cytokines that amplify the inflammatory response [76]. These cytokines released by the liver are then transported via the systemic circulation to the lung, where they cause acute hemorrhagic necrosis of lung epithelial cells and activation of pulmonary monocytes and macrophages, ultimately contributing to ARDS and MODS [77, 78]. Indeed, inhib- ition of KCs has been shown to reduce pancreatitis- associated remote organ injury [78, 79]. Together, these studies suggest that failure of the gut barrier may consti- tute a fatal event in patients with end-stage liver disease and that the “gut–liver inflammation” axis may play an important role in the balance between tolerance and systemic inflammation in critical illness.
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Extracorporeal life support and systemic inflammation

Extracorporeal life support and systemic inflammation

Although the impact of protective MV during CPB on cytokine levels, pulmonary func- tion, and clinical outcomes is still controversial [129 – 131], most studies described its beneficial effect on post-CPB systemic inflammatory response [132 – 135] and lung function [74, 136], thereby potentially improving clinical outcomes [74]. For example, in adult patients undergoing CPB, IL-6 and IL-8 levels in the bronchoalveolar lavage fluid and plasma were higher with high tidal volume/low positive end-expiratory pres- sure than with low tidal volume/high positive end-expiratory pressure [132]. However, the interesting results of a pilot randomized controlled trial, comparing MV versus no MV during CPB, showed that the group treated with MV had less pulmonary edema and shorter overall duration of MV [74]. It has been proposed that this benefit derives from the partial preservation of bronchial arterial flow. Despite a recent meta-analysis of randomized controlled trials showing that ventilation during CPB may improve post-CPB oxygenation and gas exchange [137], the positive effects of the designated MV techniques are probably short-term and with a questionable impact on the clinical outcome [137, 138].
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