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   <subfield code="a">Temporal trends of circulating nitric oxide and pro-inflammatory cytokine responses ex vivo in intra-abdominal sepsis: results from a cohort study</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Miriam Ojeda Ojeda, Hilev Larrondo Muguercia, Abel Magdariaga Figuerola, Alfredo Sánchez Valdivia, Ingrid Rodríguez Alonso, Carmen Valenzuela Silva, Elizeth García Iglesias, Emma Domínguez Alonso, Wim Buurman, Manuel Araña Rosaínz]</subfield>
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   <subfield code="a">Objective and design: To evaluate the association of pro-inflammatory mediators with organ dysfunction and adverse outcome in intra-abdominal sepsis patients. Subjects: Twenty-one patients admitted to the Intensive Care Unit (ICU) were prospectively included in the study. Only patients with surgical diagnosis of intra-abdominal sepsis were enrolled. Results: Tumor necrosis factor-α (TNFα) and interleukin (IL)-6 produced ex vivo were significantly lower in non-survivors on admission (p=0.021) and day 2 (p=0.013), respectively. Nitric oxide (NOx) levels were significantly higher in non-survivors from the onset of sepsis and until day 4 after diagnosis (p&lt;0.05). Circulating lymphocyte counts were lower in non-survivors after admission over time, but there was no association with impaired cytokine production in this group of patients during the entire follow-up. All non-survivors developed nosocomial pneumonia concomitantly with multiple organ dysfunction and septic shock. There was a significant correlation between nitric oxide (NOx) concentrations and the sequential organ failure assessment (SOFA) score at day 2 (r=0.598, p=0.009), and ICU stay (r=0.605, p=0.006). Continuously high NOx levels correlated with organ failure. The pro-inflammatory mediators TNFα, IL-6 and NOx, and also the Simplified Acute Physiology Score II (SAPS-II), discriminate survivors from non-survivors. According to logistic regression models, although these parameters are independently associated with the outcome, they do not improve the predictive power of the SAPS-II score for mortality risk. Conclusions: Disturbances in inflammatory responses and increase in NOx generation seem to characterize early intra-abdominal sepsis, in which immune suppression is associated with an increased susceptibility to nosocomial infections. Sequential NOx determinations could be a useful approach for improving the management of patients with intra-abdominal sepsis.</subfield>
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   <subfield code="a">Springer Basel AG, 2010</subfield>
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   <subfield code="a">Sepsis</subfield>
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   <subfield code="a">Peritonitis</subfield>
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   <subfield code="a">Intensive care</subfield>
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   <subfield code="a">Cytokines</subfield>
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   <subfield code="a">Markers</subfield>
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   <subfield code="a">Ojeda Ojeda</subfield>
   <subfield code="D">Miriam</subfield>
   <subfield code="u">Division of Pharmaceuticals, Center for Genetic Engineering and Biotechnology, Havana, Cuba</subfield>
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   <subfield code="a">Larrondo Muguercia</subfield>
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   <subfield code="u">Critical Care Unit, Hospital &quot;Hermanos Ameijeiras”, Havana, Cuba</subfield>
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   <subfield code="a">Magdariaga Figuerola</subfield>
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   <subfield code="u">Division of Pharmaceuticals, Center for Genetic Engineering and Biotechnology, Havana, Cuba</subfield>
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   <subfield code="a">Sánchez Valdivia</subfield>
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   <subfield code="a">Rodríguez Alonso</subfield>
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   <subfield code="a">Valenzuela Silva</subfield>
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   <subfield code="u">Division of Clinical Trials, Center for Genetic Engineering and Biotechnology, Havana, Cuba</subfield>
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   <subfield code="a">García Iglesias</subfield>
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   <subfield code="u">Division of Clinical Trials, Center for Genetic Engineering and Biotechnology, Havana, Cuba</subfield>
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   <subfield code="a">Domínguez Alonso</subfield>
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   <subfield code="u">Department of General Surgery, University of Maastricht, Maastricht, The Netherlands</subfield>
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   <subfield code="a">Araña Rosaínz</subfield>
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   <subfield code="u">Division of Pharmaceuticals, Center for Genetic Engineering and Biotechnology, Havana, Cuba</subfield>
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   <subfield code="t">Inflammation Research</subfield>
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   <subfield code="g">60/3(2011-03-01), 289-297</subfield>
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