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10.1097/CCM.0000000000004724

http://scihub22266oqcxt.onion/10.1097/CCM.0000000000004724
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33181590!ä!33181590

suck abstract from ncbi


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pmid33181590      Crit+Care+Med 2021 ; 49 (2): 228-239
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  • Inflammatory Response and Phenotyping in Severe Acute Respiratory Infection From the Middle East Respiratory Syndrome Coronavirus and Other Etiologies #MMPMID33181590
  • Arabi YM; Jawdat D; Hajeer AH; Sadat M; Jose J; Vishwakarma RK; Almashaqbeh W; Al-Dawood A
  • Crit Care Med 2021[Feb]; 49 (2): 228-239 PMID33181590show ga
  • OBJECTIVES: In this study, we evaluated the inflammatory response in patients with severe acute respiratory infection due to the Middle East respiratory syndrome and non-Middle East respiratory syndrome and assessed the presence of distinct inflammatory subphenotypes using latent class analysis. DESIGN: Prospective cohort study. SETTING: A tertiary care ICU in Riyadh, Saudi Arabia. PATIENTS: Consecutive critically ill patients with laboratory-confirmed Middle East respiratory syndrome severe acute respiratory infection and non-Middle East respiratory syndrome severe acute respiratory infection. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: We measured cytokines on days 1, 3, 7, and 14 of ICU stay. We included 116 patients (40 with Middle East respiratory syndrome severe acute respiratory infection and 76 with non-Middle East respiratory syndrome severe acute respiratory infection). On ICU day 1, both patients with Middle East respiratory syndrome severe acute respiratory infection and non-Middle East respiratory syndrome severe acute respiratory infection had higher levels of interleukin-3, interleukin-4, interleukin-6, interleukin-8, interleukin-17A, eotaxin, and epidermal growth factor compared with healthy controls. There were no differences in cytokines over time between patients with Middle East respiratory syndrome severe acute respiratory infection and non-Middle East respiratory syndrome severe acute respiratory infection. Using day 1 cytokine levels, latent class analysis categorized patients into two subphenotypes: subphenotype 1 (n = 74 [64%]) and subphenotype 2 (n = 42 [36%]); the latter had significantly higher levels of interleukin-1beta, interleukin-1ra, interleukin-2, interleukin-6, interleukin-7, interleukin-8, interleukin-10, interleukin-12p70, interleukin-15, interleukin-17A, inducible protein-10, monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor, granulocyte-colony stimulating factor, interferon-alpha, and interferon-gamma. Although baseline characteristics were not different between the two subphenotypes, patients in the subphenotype 2 had higher ICU mortality compared with the subphenotype 1 (18/42 [43%] vs 17/74 [23%]; p = 0.03). CONCLUSIONS: One third of critically ill patients with Middle East respiratory syndrome severe acute respiratory infection and non-Middle East respiratory syndrome severe acute respiratory infection demonstrated a subphenotype characterized by increased proinflammatory cytokines, consistent with cytokine storm. Further research is needed to examine whether immunomodulators have differential effects based on inflammatory subphenotypes.
  • |*Critical Illness[MESH]
  • |Adult[MESH]
  • |COVID-19/complications/*immunology[MESH]
  • |Cytokine Release Syndrome/complications/*immunology[MESH]
  • |Cytokines/*immunology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Middle East Respiratory Syndrome Coronavirus/*immunology[MESH]
  • |Prospective Studies[MESH]


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