Plasma tumor necrosis factor and mortality in critically ill septic patients

Debets, J. M. H.; Kampmeijer, R.; Linden, Margareta; Buurman, Wim A.; Linden, C. J. Van Der

doi:10.1097/00003246-198906000-00001

Cited by 296 publications

(98 citation statements)

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“…13 TNF-a is widely reported to be a pivotal mediator of sepsis, septic shock, and multiple organ failure, and high circulating plasma levels of TNF-a have been found to correlate with poor outcome in patients with meningococcal shock 8, 14,15 and in patients with other forms of sepsis. 16,17 IL-1b, an agonist, is a potent proinflammatory cytokine, 18 whereas IL-1Ra, an antagonist, inhibits the activities of IL-1b by binding to the IL-1 receptor and blocking signal transduction. 19,20 As with TNF-a and IL-6, levels of IL-1b are associated with the outcome in meningococcal disease.…”

Section: Introductionmentioning

confidence: 99%

Genomic polymorphic profiles in an Irish population with meningococcaemia: is it possible to predict severity and outcome of disease?

et al. 2003

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Section: Introductionmentioning

confidence: 99%

Genomic polymorphic profiles in an Irish population with meningococcaemia: is it possible to predict severity and outcome of disease?

et al. 2003

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“…Together with other cytokines, it appears to orchestrate the response to an inflammatory stimulus. Many features of septic shock [10][11][12][13] and ARDS [14,15] have been ascribed to TNF-α, but measurements of this cytokine under such clinical conditions (serum and lavage fluid) have produced inconsistent results [16][17][18][19][20][21][22][23][24]. Interleukin-6 (IL-6) is produced by a variety of inflammatory cells in response to other cytokines or bacterial agents.…”

mentioning

confidence: 99%

Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Schütte¹,

Lohmeyer²,

Rosseau³

et al. 1996

Eur Respir J

207

130

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B Br ro on nc ch ho oa al lv ve eo ol la ar r a an nd d s sy ys st te em mi ic c c cy yt to ok ki in ne e p pr ro of fi il le es s i in n p pa at ti ie en nt ts s w wi it th h A AR RD DS S, ,s se ev ve er re e p pn ne eu um mo on ni ia a a an nd d c ca ar rd di io og ge en ni ic c p pu ul lm mo on na ar ry y o oe ed de em ma a (PN) and a combined group (PN+ARDS).In all patients with ARDS and/or PN, markedly elevated BAL levels of IL-6 and IL-8 were detected, which were significantly greater than levels in CPO and healthy controls. Absolute quantities and time-course of these cytokines did not differentiate between the absence and presence of lung infection, or different categories of PN. Similarly, circulating IL-6 levels were comparably elevated in patients with ARDS and/or PN, whereas circulating IL-8 concentrations were inconsistently increased. TNF-α was rarely detected in BAL samples, but increased serum concentrations were measured in ARDS and/or PN patients.Bronchoalveolar lavage levels of interleukin-6 and interleukin-8, but not tumour necrosis factor-α, and serum concentrations of interleukin-6 are consistently elevated in acute respiratory distress syndrome and/or severe pneumonia, discriminating these entities from cardiogenic pulmonary oedema. Alveolar and systemic cytokine profiles do not differentiate between acute respiratory distress syndrome in the absence of lung infection and states of severe primary or secondary pneumonia, which evidently present with comparable local and systemic inflammatory sequelae.

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“…TNF-a was assayed using a solid-phase double-ligand ELISA system [20] and IL-8 was assayed using a solid-phase double-ligand ELISA [21].…”

Section: Methodsmentioning

confidence: 99%

Anti‐TNF Treatment of Baboons with Sepsis Reduces TNF‐α, IL‐6 and IL‐8, but not the Degree of Complement Activation

et al. 1998

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The activation of complement and the release of TNF‐α, IL‐6 and IL‐8 are important pathogenic factors behind organ dysfunction in sepsis. The aim of this study was to determine whether infusion of anti‐TNF antibodies alters complement activation and plasma concentrations of pro‐inflammatory cytokines at high doses of Escherichia coli. Six baboons received intravenously 2 × 109 live E. coli bacteria per kg body weight (group 1), in addition five received pretreatment with 1 mg per kg body weight anti‐TNF antibodies (group 2), and seven received 5 × 108 live E. coli bacteria per kg body weight (group 3). Two hours after the start of infusion of the bacteria, plasma concentrations of C3 activation products, C5a and the terminal SC5b‐9 complement complex were increased in groups 1 and 2 (P < 0.05), but there was no significant difference between the groups. At 2 h the levels of TNF‐α, IL‐6 and IL‐8 were lower in group 2 compared with group 1 (P < 0.05). In group 2 compared with group 1 the TNF‐α concentrations were, however, higher at 4, 8 and 24 h. The explanation for this phenomenon is probably that TNF‐α binds to the anti‐TNF antibody complex and is released slowly after it has been bound. The study showed that infusion of anti‐TNF antibodies reduced the concentrations of TNF‐α, IL‐6 and IL‐8, without any detectable influence on complement activation.

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Plasma tumor necrosis factor and mortality in critically ill septic patients

Cited by 296 publications

References 0 publications

Genomic polymorphic profiles in an Irish population with meningococcaemia: is it possible to predict severity and outcome of disease?

Genomic polymorphic profiles in an Irish population with meningococcaemia: is it possible to predict severity and outcome of disease?

Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Anti‐TNF Treatment of Baboons with Sepsis Reduces TNF‐α, IL‐6 and IL‐8, but not the Degree of Complement Activation

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