Visfatin Serum Levels Predict Mortality in Critically Ill Patients

Koch, Alexander; Weiskirchen, Ralf; Krusch, Alexander; Bruensing, Jan; Buendgens, Lukas; Herbers, Ulf; Yagmur, Eray; Koek, Ger H.; Tacke, Frank

doi:10.1155/2018/7315356

Cited by 15 publications

(15 citation statements)

References 33 publications

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“…In our study, we found no associations between resistin levels in patients with CA and history of coronary artery disease, stroke, diabetes mellitus, obesity, smoking or alcoholic beverages. This reinforces the idea that in an acute critical illness high levels of resistin (or other adipokines) are mostly due to inflammatory status and not to adipose tissue mass or pre-existing unhealthy lifestyle [32].…”

Section: Discussionsupporting

confidence: 83%

Resistin and Cardiac Arrest—A Prospective Study

Tat

Golea

Rahaian

et al. 2019

JCM

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The systemic response to ischemia-reperfusion that occurs after a cardiac arrest (CA) followed by the return of spontaneous circulation leads to endothelial toxicity and cytokine production, both responsible for the subsequent occurrence of severe cardiocirculatory dysfunction and early death. Resistin is emerging as a biomarker of proinflammatory status and myocardial ischemic injury and as a mediator of endothelial dysfunction. The study aimed to analyze the possible associations between several clinical and biological variables and the serum levels of resistin in CA survivors. Forty patients with out-of-hospital resuscitated CA, were enrolled in the study. Demographic, clinical and laboratory data (including serum resistin measurements at admission and at 6, 12, 24, 48 and 72 h) were recorded. For resistin, we calculated the area under the curve (AUC) using the trapezoidal method with measurements from 0 to 12 h, 0 to 24 h, 0 to 48 h and 0 to 72 h. Fifteen (37.5%) patients died in the first 72 h after CA. Cardiovascular comorbidities were present in 65% of patients. The majority of patients had post-CA shock (29 (72.5%)). Resistin serum levels rose in the first 12–24 h and decreased in the next 48–72 h. In univariate analysis, advanced age, longer duration of resuscitation, high sequential organ failure assessment score, high lactate levels, presence of cardiovascular comorbidities and the post-CA shock were associated with higher resistin levels. In multivariate analysis, post-CA shock or cardiovascular comorbidities were independently associated with higher AUCs for resistin for 0–12 h and 0–24 h. The only identified variable to independently predict higher AUCs for resistin for 0–48 h and 0–72 h was the presence of post-CA shock. Our data demonstrate strong independent correlation between high serum resistin levels, cardiac comorbidities and post-CA shock. The impact of the post-CA shock on serum concentration of resistin was greater than that of cardiac comorbidities.

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Section: Discussionsupporting

confidence: 83%

Resistin and Cardiac Arrest—A Prospective Study

Tat

Golea

Rahaian

et al. 2019

JCM

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“…63 High eNAMPT levels at the time of admission to the intensive care unit correlate with disease severity and may predict mortality in patients with sepsis and ARDS. 76,77 Unfortunately, no single biomarker has been shown to reliably provide information about the patient's overall disease outcome and thus stratify patients for enrollment in clinical trials. However, recent efforts to combine biomarkers demonstrate that prognostic ability can be greatly enhanced.…”

Section: Ards Biomarkers By Categorymentioning

confidence: 99%

The acute respiratory distress syndrome biomarker pipeline: crippling gaps between discovery and clinical utility

Bime

Camp

Casanova

et al. 2020

Translational Research

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Recent innovations in translational research have ushered an exponential increase in the discovery of novel biomarkers, thereby elevating the hope for deeper insights into "personalized" medicine approaches to disease phenotyping and care. However, a critical gap exists between the fast pace of biomarker discovery and the successful translation to clinical use. This gap underscores the fundamental biomarker conundrum across various acute and chronic disorders: how does a biomarker address a specific unmet need? Additionally, the gap highlights the need to shift the paradigm from a focus on biomarker discovery to greater translational impact and the need for a more streamlined drug approval process. The unmet need for biomarkers in acute respiratory distress syndrome (ARDS) is for reliable and validated biomarkers that minimize heterogeneity and allow for stratification of subject selection for enrollment in clinical trials of tailored therapies. This unmet need is particularly highlighted by the ongoing SARS-CoV-2/COVID-19 pandemic. The unprecedented numbers of COVID-19-induced ARDS cases has strained health care systems across the world and exposed the need for biomarkers that would accelerate drug development and the successful phenotyping of COVID-19infected patients at risk for development of ARDS and ARDS mortality. Accordingly, this review discusses the current state of ARDS biomarkers in the context of the drug development pipeline and highlight gaps between biomarker discovery and clinical implementation while proposing potential paths forward. We discuss potential ARDS biomarkers by category and by context of use, highlighting progress in the development continuum. We conclude by discussing challenges to successful translation of biomarker candidates to clinical impact and proposing possible novel strategies.

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“…The accumulation of ECM proteins including collagen in the early stages of obesity contributes to tissue remodeling through which fibrosis and infiltration of proinflammatory leukocytes into the AT are promoted [26]. AT produces a wide range of adipokines that play key roles in the regulation of glucose and lipid metabolism [27], and their dysregulation has been linked to systemic inflammation [28]. (Table 1).…”

Section: Adipose Tissue Structure and Biologymentioning

confidence: 99%

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Komi

Shafaghat

Christian

2020

Clinic Rev Allerg Immunol

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Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing proinflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these cells play a critical role in the regulation of AT homeostasis and inflammation.

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Visfatin Serum Levels Predict Mortality in Critically Ill Patients

Cited by 15 publications

References 33 publications

Resistin and Cardiac Arrest—A Prospective Study

Resistin and Cardiac Arrest—A Prospective Study

The acute respiratory distress syndrome biomarker pipeline: crippling gaps between discovery and clinical utility

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

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