Kawamatawong Theerasuk, Apiwattanaporn Apitch, Siricharoonwong Warisara
Division of Pulmonary and Critical Care Medicine.
Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Int J Chron Obstruct Pulmon Dis. 2017 May 31;12:1625-1630. doi: 10.2147/COPD.S132132. eCollection 2017.
COPD exacerbation is characterized by worsening of symptoms, warranting change in treatment. Systemic and airway inflammation play roles in the pathogenesis of COPD exacerbation. We hypothesized whether increased serum inflammatory biomarkers are associated with the clinical outcomes of COPD exacerbation caused by different infectious pathogens.
COPD patients with exacerbation were recruited from a hospital emergency department during 2014-2015. Serum procalcitonin (PCT) and C-reactive protein (CRP) were measured. Dyspnea, eosinopenia, consolidation, acidemia, and atrial fibrillation (DECAF) score was calculated for predicting mortality. Multiplex polymerase chain reaction was carried out for respiratory viral assay from nasopharyngeal swabs, and sputum bacterial culture was also performed. Hospital mortality, invasive mechanical ventilation requirement, and length of hospital stay (LOS) were evaluated, and their associations with clinical characteristics, DECAF score, and serum biomarkers were examined.
A total of 62 COPD patients were enrolled. These patients were classified as Global Initiative for Obstructive Lung Disease (GOLD) stage 2, 3, and 4 in 12.9%, 6.4%, and 80.7% of cases, respectively. Isolated bacterial exacerbation was recovered in 30.6% of exacerbation episodes: was the most commonly identified bacteria. Viral pathogens and coinfections were noted in 9.6% and 16.1% of exacerbated patients, respectively. Influenza was the most commonly detected viral pathogen. Serum biomarkers and DECAF score for viruses, bacteria, coinfection, and noninfectious causes of exacerbations were similar. Neither DECAF score nor serum biomarkers were able to differentiate patients with and without mortality or requiring mechanical ventilation. Increased serum PCT was noted in patients with LOS ≥7 days when compared with those with LOS <7 days (0.38 ng/mL vs 0.1 ng/mL; =0.035).
Increased serum PCT is associated with longer LOS in COPD exacerbation. However, CRP and DECAF score play limited roles in predicting clinical outcome and lack an association with causes of exacerbation.
慢性阻塞性肺疾病（COPD）急性加重的特征是症状恶化，需要改变治疗方案。全身和气道炎症在COPD急性加重的发病机制中起作用。我们推测血清炎症生物标志物升高是否与不同感染病原体引起的COPD急性加重的临床结局相关。
2014年至2015年期间，从医院急诊科招募COPD急性加重患者。检测血清降钙素原（PCT）和C反应蛋白（CRP）。计算呼吸困难、嗜酸性粒细胞减少、实变、酸血症和心房颤动（DECAF）评分以预测死亡率。对鼻咽拭子进行多重聚合酶链反应以检测呼吸道病毒，并进行痰细菌培养。评估医院死亡率、有创机械通气需求和住院时间（LOS），并检查它们与临床特征、DECAF评分和血清生物标志物的关联。
共纳入62例COPD患者。这些患者分别有12.9%、6.4%和80.7%被分类为慢性阻塞性肺疾病全球倡议（GOLD）2期、3期和4期。30.6%的急性加重发作中分离出细菌感染： 是最常鉴定出的细菌。分别有9.6%和16.1%的急性加重患者检测到病毒病原体和合并感染。流感是最常检测到的病毒病原体。病毒、细菌、合并感染和非感染性急性加重原因的血清生物标志物和DECAF评分相似。DECAF评分和血清生物标志物均无法区分有或没有死亡或需要机械通气的患者。与住院时间<7天的患者相比，住院时间≥7天的患者血清PCT升高（0.38 ng/mL对0.1 ng/mL； =0.035）。
COPD急性加重时血清PCT升高与住院时间延长有关。然而，CRP和DECAF评分在预测临床结局方面作用有限，且与急性加重原因无关。
