Assessing available information on the burden of sepsis: global estimates of incidence, prevalence and mortality

Jawad, Issrah; Lukšić, Ivana; Rafnsson, Snorri Björn

doi:10.7189/jogh.01.010404

Cited by 269 publications

(162 citation statements)

References 26 publications

(31 reference statements)

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“…2 T he incidence of severe sepsis and septic shock in adults is estimated to range from 56 to 91 per 100,000 population per year. 1 Affected patients have high rates of death, complications, and resource utilization. [2][3][4][5] Since 2002, the Surviving Sepsis Campaign (SSC) has promoted best practice, including early recognition, source control, appropriate and timely antibiotic administration, and resuscitation with intravenous fluids and vasoactive drugs.…”

Section: Discussionmentioning

confidence: 99%

Trial of Early, Goal-Directed Resuscitation for Septic Shock

Mouncey¹,

Osborn

Power³

et al. 2015

N Engl J Med

1,304

899

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Section: Discussionmentioning

confidence: 99%

Trial of Early, Goal-Directed Resuscitation for Septic Shock

Mouncey¹,

Osborn

Power³

et al. 2015

N Engl J Med

1,304

899

View full text Add to dashboard Cite

Section: Introduction Heart Failurementioning

confidence: 99%

“…26 In the Western world, more than 1 in 1000 people are estimated to have sepsis each year, with 30-50% of cases progressing to more severe stages. 26 Characterized by uncontrolled inflammation, sepsis is, among other severe organ dysfunctions, associated with impaired systolic and diastolic function. [27][28][29] Importantly, it is the overstimulated immune response, and not the infection in itself, that predominantly contributes to the cardiodepressant effects.…”

Section: Introduction Heart Failurementioning

confidence: 99%

Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart

et al. 2013

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Sustained pressure overload induces heart failure, the main cause of mortality in the Western world. Increased understanding of the underlying molecular mechanisms is essential to improve heart failure treatment. Despite important functions in other tissues, cardiac proteoglycans have received little attention. Syndecan‐4, a transmembrane heparan sulfate proteoglycan, is essential for pathological remodeling, and we here investigated its expression and shedding during heart failure. Pressure overload induced by aortic banding for 24 h and 1 week in mice increased syndecan‐4 mRNA, which correlated with mRNA of inflammatory cytokines. In cardiac myocytes and fibroblasts, tumor necrosis factor‐α, interleukin‐1β and lipopolysaccharide through the toll‐like receptor‐4, induced syndecan‐4 mRNA. Bioinformatical and mutational analyses in HEK293 cells identified a functional site for the proinflammatory nuclear factor‐κB transcription factor in the syndecan‐4 promoter, and nuclear factor‐κB regulated syndecan‐4 mRNA in cardiac cells. Interestingly, tumor necrosis factor‐α, interleukin‐1β and lipopolysaccharide induced nuclear factor‐κB‐dependent shedding of the syndecan‐4 ectodomain from cardiac cells. Overexpression of syndecan‐4 with mutated enzyme‐interacting domains suggested enzyme‐dependent heparan sulfate chains to regulate shedding. In cardiac fibroblasts, lipopolysaccharide reduced focal adhesion assembly, shown by immunohistochemistry, suggesting that inflammation‐induced shedding affects function. After aortic banding, a time‐dependent cardiac recruitment of T lymphocytes was observed by measuring CD3, CD4 and CD8 mRNA, which was reduced in syndecan‐4 knockout hearts. Finally, syndecan‐4 mRNA and shedding were upregulated in failing human hearts. Conclusively, our data suggest that syndecan‐4 plays an important role in the immune response of the heart to increased pressure, influencing cardiac remodeling and failure progression.

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“…Research on eicosanoids, resolvins and protectins has provided diagnostics, therapies and preventive strategies remain elusive. To date, clinical interventions include vaccination, broad-spectrum antibiotics, cytokine therapy and respiratory and metabolic support (2); however, mortality rates are still high at 30% for sepsis, 50% for severe sepsis and 80% for septic shock among patients (3). Identification of key molecular mediators…”

mentioning

confidence: 99%