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Conclusions Previous non-multiparametric studies might have reached inappropriate conclusions.
Introduction Despite rapid improvement in health care over the past decades, sepsis continues to be a major life-threatening condition in acute care patients [1]. Data collection Data collected at enrollment included patient characteristics, comorbidities, vital signs, respiratory parameters, routine blood tests, suspected source of infection, microbiological culture results, patient's severity according to the Mortality in Emergency Department Sepsis score MEDS [19] , treatments and final diagnosis.
Statistical analysis Quantitative data were expressed as median minimum-maximum values and qualitative data as numbers and percentages. Results Patients characteristics We included consecutive patients 71 men and 55 women with a median age of 54 years range: 19—96 years table 1. Download: PPT. Figure 1.
Table 2. Serum concentrations of cytokines in patients with and without SIRS.
Figure 2. Table 3. Serum concentrations of cytokines in patients with and without severe sepsis. Figure 3. Table 4. Serum concentrations of cytokines in patients with and without septic shock.
Figure 4. Table 5. Serum concentrations of cytokines in febrile patients with and without bacterial infection. Figure 5. Figure 6. Table 6. Serum concentrations of cytokines in patients with and without bacterial infection. Table 7. Comparison of serum concentrations of cytokines between patients with proven bacterial infection and without bacterial infection. Discussion In this study, we have quantitatively analyzed 22 cytokines, chemokines and growth factors in serum samples obtained from a single-center cohort of consecutive patients with acute onset diseases attending the ED of a single tertiary-care center.
Conclusion Altogether, our results suggest that previous studies aiming at identifying serum cytokines that could be relevant in sepsis could have used an inappropriate methodology. Key messages Previous studies aiming at identifying serum cytokines in sepsis have likely used an inappropriate methodology. No individual cytokine biomarker is associated with severe sepsis and septic shock. Cytokine profiles corresponding to SIRS, severe sepsis and septic shock cannot be identified in this large cohort of patients.
Multiplex cytokine profiling may yet be of limited interest for the pragmatic staging of septic patients in routine ED setting. References 1. N Engl J Med — View Article Google Scholar 2. Clin Infect Dis — View Article Google Scholar 3. Aalto H, Takala A, Kautiainen H, Repo H Laboratory markers of systemic inflammation as predictors of bloodstream infection in acutely ill patients admitted to hospital in medical emergency. View Article Google Scholar 4.
View Article Google Scholar 5. Crit Care Med 28 8 : — View Article Google Scholar 6. Crit Care R View Article Google Scholar 7. Crit Care Med — View Article Google Scholar 8. Crit Care Med 25 3 : — View Article Google Scholar 9. Chest — View Article Google Scholar Dinarello CA Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock.
Chest S—S. J Infect Dis — Clin Chem — Intensive Care Med — Trends Mol Med 56— APMIS — Ward J Hierarchical grouping to optimize an objective function. J Am Stat Assoc — Ann Intern Med — Relation to multiple-system organ failure and mortality.
Fundamentals of hierarchical linear and multilevel modeling. Septic shock is a subclass of distributive shock , a condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate blood supply to the body tissues , resulting in ischemia and organ dysfunction. Endothelial injury, which is strongly associated with the progression of sepsis 33 , can proliferate to generate cytokines such as IL-6, IL-8 and MCP Lancet Infect. Nature, , pp. Sign up now. Cytokines are a group of endogenous inflammatory and immunomodulating proteins, which mainly mediate the patho-physiology of the systemic inflammatory response syndrome SIRS associated with sepsis.
Lancet — Shock — Nat Med — Log in to view full text. If you're not a subscriber, you can:. Colleague's E-mail is Invalid. Your message has been successfully sent to your colleague. Save my selection.
You may be trying to access this site from a secured browser on the server. Please enable scripts and reload this page. Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining your privacy and will not share your personal information without your express consent. For more information, please refer to our Privacy Policy. Subscribe to eTOC. Based on that understanding, previous clin- ical studies have been designed to include only patients with positive blood cultures [1, 2].
However, the frequent occurrence of a septic response without the demon- stration of microorganisms in the circulation has led to a new definition and under- standing of sepsis, mainly as the systemic response of the host to an often unde- tectable microbiological or non-microbiological process [3]. The general consensus is that cytokines are central to the inflammatory response, particularly in sepsis.
It is now known that not only Gram-negative but also Gram- positive, viral, and fungal infections initiate the complex cascades of cytokine release. Probably the most important aspect of bacterial action is the release of toxic bacterial products.