Shpagina L A, Kotova O S, Shpagin I S, Karmanovskaya S A, Loktin E M, Rukavitsyna A A, Kuznetsova G V, Gerasimenko D A, Anikina E V
Novosibirsk State Medical University.
Ter Arkh. 2023 Apr 26;95(3):217-222. doi: 10.26442/00403660.2023.03.202086.
To establish symptoms, lung function and to evaluate subsequent exacerbations of chronic obstructive pulmonary disease (COPD) during a year after virus-induced COPD exacerbations.
Patients hospitalized with viral (=60), bacterial (=60) and viral-bacterial (=60) COPD exacerbations were enrolled to single-center prospective observational study. COPD was diagnosed according spirography criteria. Viral infection was established in bronchoalveolar lavage fluid or sputum by real-time reverse transcription-polymerase chain reaction for RNA of influenza A and B virus, rhinovirus, respiratory syncytial virus and SARS-CoV-2. Symptoms, lung function, COPD exacerbations were assessed. Patients were investigated at the hospitalization onset and then 4 and 52 weeks following the discharge from the hospital.
After 52 weeks in viral and viral-bacterial COPD exacerbations groups the rate of forced expiratory volume in one second (FEV1) decline were maximal - 71 (68; 73) ml/year and 69 (67; 72) ml/year versus 59 (55; 62) ml/year after bacterial exacerbations. Low levels of diffusion lung capacity for carbon monoxide (DLco/Va) - 52.5% (45.1%; 55.8%), 50.2% (44.9%; 56.0%) and 75.3% (72.2%; 80.1%) respectively, of 6-minute walk distance; <0.001 in relation to bacterial exacerbations. In Cox proportional hazards regression analyses viral and viral-bacterial exacerbations were associated with increased risk of subsequent COPD exacerbations by 2.4 times independent of exacerbations rate before index event and FEV1. In linear regression models the relationships between airflow limitation and respiratory syncytial virus, rhinovirus and influenza virus infection, between low DLco/Va and rhinovirus, influenza virus and SARS-CoV-2 infection.
COPD after virus-induced exacerbations were characterized by progression of airflow limitation, low DLco/Va, low 6-minute walking test distance, subsequent COPD exacerbations risk.
在病毒诱发慢性阻塞性肺疾病（COPD）加重后的一年中，确定其症状、肺功能并评估后续病情加重情况。
将因病毒感染（=60例）、细菌感染（=60例）和病毒-细菌混合感染（=60例）导致COPD加重而住院的患者纳入单中心前瞻性观察研究。根据肺量计标准诊断COPD。通过实时逆转录聚合酶链反应检测支气管肺泡灌洗液或痰液中甲型和乙型流感病毒、鼻病毒、呼吸道合胞病毒和SARS-CoV-2的RNA，以确定病毒感染情况。评估症状、肺功能和COPD加重情况。在患者住院时以及出院后4周和52周进行调查。
在病毒感染和病毒-细菌混合感染导致COPD加重的组中，52周后一秒用力呼气量（FEV1）下降率最大，分别为71（68；73）ml/年和69（67；72）ml/年，而细菌感染加重后为59（55；62）ml/年。一氧化碳弥散肺容量（DLco/Va）水平较低，分别为6分钟步行距离的52.5%（45.1%；55.8%）、50.2%（44.9%；56.0%）和75.3%（72.2%；80.1%）；与细菌感染加重相比，差异<0.001。在Cox比例风险回归分析中，病毒感染和病毒-细菌混合感染导致的加重与后续COPD加重风险增加2.4倍相关，且独立于指数事件前的加重率和FEV1。在线性回归模型中，气流受限与呼吸道合胞病毒、鼻病毒和流感病毒感染之间，低DLco/Va与鼻病毒、流感病毒和SARS-CoV-2感染之间存在关联。
病毒诱发加重后的COPD具有气流受限进展、DLco/Va低、6分钟步行试验距离短、后续COPD加重风险高的特点。
