Cédric Daubin1, François Fournel2, Fabrice Thiollière3, Fabrice Daviaud4, Michel Ramakers5, Andréa Polito6,7, Bernard Flocard8, Xavier Valette9, Damien Du Cheyron9, Nicolas Terzi10,11, Muriel Fartoukh12, Stephane Allouche13, Jean-Jacques Parienti2,14. 1. Department of Medical Intensive Care, CHU de Caen, 14000, Caen, France. daubin-c@chu-caen.fr. 2. Department of Biostatistics and Clinical Research, CHU de Caen, 14000, Caen, France. 3. Intensive Care Unit, Centre Hospitalier Lyon Sud, Pierre Bénite, Hospices Civils de Lyon, France. 4. Department of Medial Intensive Care, Cochin University Hospital, Paris, France. 5. Department of Intensive Care Medicine, General Hospital, Saint Lô, France. 6. Service de Médecine Intensive Et Réanimation, General Intensive Care Unit, Hôpital Raymond Poincaré (APHP), Raymond Poincaré Hospital, Garches, France. 7. Laboratoire Infection & Inflammation, U1173 Université de Versailles SQY-Paris Saclay - INSERM, Garches, France. 8. Department of Anesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France. 9. Department of Medical Intensive Care, CHU de Caen, 14000, Caen, France. 10. Department of Medical Intensive Care, CHU de Grenoble Alpes, 38000, Grenoble, France. 11. INSERM, U1042, University of Grenoble-Alpes, HP2, 38000, Grenoble, France. 12. Service de Medecine Intensive Reanimation, AP-HP, Sorbonne université, Hôpital Tenon, Groupe de Recherche Clinique CARMAS, collegium Gallilée, Paris, France. 13. Universite Caen Normandie, Medical School, EA 4650, Signalisation, Electrophysiologie et Imagerie des lésions d'Ischemie-reperfusion Myocardique, 14000, Caen, France. 14. EA2656 Groupe de Recherche sur l'Adaptation Microbienne (GRAM 2.0), Université Caen Normandie, Caen, France.
Abstract
BACKGROUND: To assess the ability of procalcitonin (PCT) to distinguish between bacterial and nonbacterial causes of patients with severe acute exacerbation of COPD (AECOPD) admitted to the ICU, we conducted a retrospective analysis of two prospective studies including 375 patients with severe AECOPD with suspected lower respiratory tract infections. PCT levels were sequentially assessed at the time of inclusion, 6 h after and at day 1, using a sensitive immunoassay. The patients were classified according to the presence of a documented bacterial infection (including bacterial and viral coinfection) (BAC + group), or the absence of a documented bacterial infection (i.e., a documented viral infection alone or absence of a documented pathogen) (BAC- group). The accuracy of PCT levels in predicting bacterial infection (BAC + group) vs no bacterial infection (BAC- group) at different time points was evaluated by receiver operating characteristic (ROC) analysis. RESULTS: Regarding the entire cohort (n = 375), at any time, the PCT levels significantly differed between groups (Kruskal-Wallis test, p < 0.001). A pairwise comparison showed that PCT levels were significantly higher in patients with bacterial infection (n = 94) than in patients without documented pathogens (n = 218) (p < 0.001). No significant difference was observed between patients with bacterial and viral infection (n = 63). For example, the median PCT-H0 levels were 0.64 ng/ml [0.22-0.87] in the bacterial group vs 0.24 ng/ml [0.15-0.37] in the viral group and 0.16 ng/mL [0.11-0.22] in the group without documented pathogens. With a c-index of 0.64 (95% CI; 0.58-0.71) at H0, 0.64 [95% CI 0.57-0.70] at H6 and 0.63 (95% CI; 0.56-0.69) at H24, PCT had a low accuracy for predicting bacterial infection (BAC + group). CONCLUSION: Despite higher PCT levels in severe AECOPD caused by bacterial infection, PCT had a poor accuracy to distinguish between bacterial and nonbacterial infection. Procalcitonin might not be sufficient as a standalone marker for initiating antibiotic treatment in this setting.
BACKGROUND: To assess the ability of procalcitonin (PCT) to distinguish between bacterial and nonbacterial causes of patients with severe acute exacerbation of COPD (AECOPD) admitted to the ICU, we conducted a retrospective analysis of two prospective studies including 375 patients with severe AECOPD with suspected lower respiratory tract infections. PCT levels were sequentially assessed at the time of inclusion, 6 h after and at day 1, using a sensitive immunoassay. The patients were classified according to the presence of a documented bacterial infection (including bacterial and viral coinfection) (BAC + group), or the absence of a documented bacterial infection (i.e., a documented viral infection alone or absence of a documented pathogen) (BAC- group). The accuracy of PCT levels in predicting bacterial infection (BAC + group) vs no bacterial infection (BAC- group) at different time points was evaluated by receiver operating characteristic (ROC) analysis. RESULTS: Regarding the entire cohort (n = 375), at any time, the PCT levels significantly differed between groups (Kruskal-Wallis test, p < 0.001). A pairwise comparison showed that PCT levels were significantly higher in patients with bacterial infection (n = 94) than in patients without documented pathogens (n = 218) (p < 0.001). No significant difference was observed between patients with bacterial and viral infection (n = 63). For example, the median PCT-H0 levels were 0.64 ng/ml [0.22-0.87] in the bacterial group vs 0.24 ng/ml [0.15-0.37] in the viral group and 0.16 ng/mL [0.11-0.22] in the group without documented pathogens. With a c-index of 0.64 (95% CI; 0.58-0.71) at H0, 0.64 [95% CI 0.57-0.70] at H6 and 0.63 (95% CI; 0.56-0.69) at H24, PCT had a low accuracy for predicting bacterial infection (BAC + group). CONCLUSION: Despite higher PCT levels in severe AECOPD caused by bacterial infection, PCT had a poor accuracy to distinguish between bacterial and nonbacterial infection. Procalcitonin might not be sufficient as a standalone marker for initiating antibiotic treatment in this setting.
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