nCD64 index as a prognostic biomarker for mortality in acute exacerbation of chronic obstructive pulmonary disease

Abstract

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality and morbidity worldwide. However, there are still no easily obtained biomarkers for prognosis. As a high-affinity Fc receptor, CD64 is an early marker of immune response to bacterial infection, but its role in acute exacerbation of COPD (AECOPD) remains incompletely understood. OBEJECTIVE: We investigated the prognostic role of the neutrophial CD64 (nCD64) index in AECOPD patients. DESIGN: Retrospective cross-sectional study of all patient admitted between January 2013 to May 2014. SETTING: Provincial hospitals affiliated with a university. PATIENTS AND METHODS: Clinical and laboratory data were collected in patients admitted for AECOPD and stable COPD patients, in whom nCD64 index was obtained. A receiver operating characteristics curve was used to determine the optimal cut-off levels for the nCD64 index that discriminated survivors versus nonsurvivors during index hospitalization, and during a post-discharge period of 12 months. MAIN OUTCOME MEASURES: nCD64 index level. RESULTS: The white blood cell count, CRP (C-reactive protein (CRP) and PCT (procalcitonin) in AECOPD subjects (n=31) were all significantly higher than in controls (n=18) (P=≤.01). The mean nCD64 index in AECOPD subjects was significantly higher than in control subjects (2.84% [1.0%] vs. 1.50% [0.5%], P=3.3 predicted in-hospital mortality with a sensitivity and specificity of 80% and 83%, respectively (area under the ROC=0.887; 95% confidence interval [CI]=0.721–0.972, P<.001). An nCD64 index of 3.3 upon admission as the optimal cut-off level to predict post-discharge mortality had a sensitivity and specificity of 83% and 75%, respectively (area under the ROC=0.842; 95% confidence interval [CI]=0.667–0.948, P<.001). CONCLUSIONS: An elevated nCD64 index was a reliable prognostic biomarker for both short-term and long-term mortality in patients admitted for AECOPD. LIMITATIONS: Retrospective design prevented collection of enough evidence to demonstrate infectious origin for COPD in every patient. Unsure whether nCD64 differed between bacterial and viral exacerbation.