BACKGROUND: Chromogranin A (CGA), a stress marker released with catecholamines by the adrenal medulla, has never been associated with acute inflammation in critically ill patients. AIM: To determine evidence for a link between serum concentration of CGA, biomarkers of inflammation, and outcome inpatients admitted with or without the systemic inflammatory response syndrome (SIRS). METHODS: At admission, we measured in 53 patients and 14 healthy controls the serum concentrations of CGA,procalcitonin, and C-reactive protein. We also assessed the Simplified Acute Physiological Score (SAPS) in the patients. RESULTS: Serum CGA concentrations were significantly increased in SIRS patients with a median value of 115 microg/L (68.0-202.8), when compared to healthy controls (PB0.001). In cases where infection was associated with SIRS, patients had the highest increase in CGA with a median value of 138.5 microg/L (65-222.3) (PB0.001). CGA concentrations positively correlated with inflammation markers (procalcitonin, C-reactive protein), but also with SAPS. Receiver operating characteristic (ROC) analysis showed that CGA is equivalent to SAPS as an indicator for 28-day mortality (area under curve (AUC) for both: 0.810). CONCLUSIONS: Patients with CGA concentration superior to 71 microg/L have a significantly shorter survival. A Cox model confirmed that CGA and SAPS were independent predictors of outcome.
BACKGROUND:Chromogranin A (CGA), a stress marker released with catecholamines by the adrenal medulla, has never been associated with acute inflammation in critically illpatients. AIM: To determine evidence for a link between serum concentration of CGA, biomarkers of inflammation, and outcome inpatients admitted with or without the systemic inflammatory response syndrome (SIRS). METHODS: At admission, we measured in 53 patients and 14 healthy controls the serum concentrations of CGA,procalcitonin, and C-reactive protein. We also assessed the Simplified Acute Physiological Score (SAPS) in the patients. RESULTS: Serum CGA concentrations were significantly increased in SIRS patients with a median value of 115 microg/L (68.0-202.8), when compared to healthy controls (PB0.001). In cases where infection was associated with SIRS, patients had the highest increase in CGA with a median value of 138.5 microg/L (65-222.3) (PB0.001). CGA concentrations positively correlated with inflammation markers (procalcitonin, C-reactive protein), but also with SAPS. Receiver operating characteristic (ROC) analysis showed that CGA is equivalent to SAPS as an indicator for 28-day mortality (area under curve (AUC) for both: 0.810). CONCLUSIONS:Patients with CGA concentration superior to 71 microg/L have a significantly shorter survival. A Cox model confirmed that CGA and SAPS were independent predictors of outcome.
Authors: Chih-Hsin Hsu; Luis F Reyes; Carlos J Orihuela; Ricardo Buitrago; Antonio Anzueto; Nilam J Soni; Stephanie Levine; Jay Peters; Cecilia A Hinojosa; Stefano Aliberti; Oriol Sibila; Alejandro Rodriguez; James D Chalmers; Ignacio Martin-Loeches; Jose Bordon; Jose Blanquer; Francisco Sanz; Pedro J Marcos; Jordi Rello; Jordi Solé-Violán; Marcos I Restrepo Journal: Biomarkers Date: 2015-07-08 Impact factor: 2.658
Authors: Alessandro Bartolomucci; Roberta Possenti; Sushil K Mahata; Reiner Fischer-Colbrie; Y Peng Loh; Stephen R J Salton Journal: Endocr Rev Date: 2011-08-23 Impact factor: 19.871