The role of viral infection in pulmonary exacerbations of bronchiectasis in adults: a prospective study.

The role of viral infection in pulmonary exacerbations of bronchiectasis in adults: a prospective study.
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病毒感染在成人支气管扩张的肺部加剧中的作用:一项前瞻性研究。

DOI:
10.1378/chest.14-1961
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发表时间:
2015-06
期刊:
影响因子:
9.6
通讯作者:
Chen RC
Chen RC
中科院分区:
医学1区
文献类型:
--
作者:
Gao YH;Guan WJ;Xu G;Lin ZY;Tang Y;Lin ZM;Gao Y;Li HM;Zhong NS;Zhang GJ;Chen RC

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尽管病毒感染是慢性气道疾病患者病情加重的主要原因,但其在引发成人支气管扩张加重中的作用仍不清楚。因此,我们前瞻性地研究了支气管扩张加重成人中病毒感染的发生率和临床影响。研究队列对 119 名患有支气管扩张症的成年人进行了为期 12 个月的前瞻性随访。使用聚合酶链反应检测鼻咽拭子和痰样本中的 16 种呼吸道病毒。在稳态支气管扩张和恶化期间评估症状、肺活量测定、生活质量、细菌培养和炎症标志物。在 1 年的随访期间,共记录了 58 名患者的 100 次病情加重。支气管扩张恶化期间(100 例中有 49 例,49.0')鼻咽拭子和痰液中呼吸道病毒的发现率高于稳定状态期间(58 例中的 11 例,18.9';P < .001)。在病情恶化的患者中发现的最常见病毒是冠状病毒(65 例中的 19 例,39.2')、鼻病毒(65 例中的 16 例,24.6')和甲型/乙型流感病毒(65 例中的 16 例,24.6')。与病毒阴性恶化相比,病毒阳性恶化与全身和气道炎症标志物(血清IL-6和肿瘤坏死因子-α;痰IL-1β和肿瘤坏死因子-α)的增加更大相关,但肺活量指数、生活质量和细菌密度的差异并不显着。在受试者操作特征分析中,血清干扰素 γ 诱导蛋白 10 的曲线下面积为 0.67(95' CI,0.53-0.77;P = .018)。此外,更大比例的病毒阳性病情加重的患者接受了静脉注射抗生素。通过聚合酶链反应检测发现,支气管扩张加重病例中病毒感染的患病率高于稳态支气管扩张病例,这表明呼吸道病毒在引发支气管扩张加重中发挥着至关重要的作用。病毒引起的支气管扩张恶化的潜在机制值得进一步研究。临床试验.gov;编号:NCT01801657; www.clinicaltrials.gov
Although viral infections are a major cause of exacerbations in patients with chronic airway diseases, their roles in triggering bronchiectasis exacerbations in adults remain unclear. Therefore, we prospectively investigated the incidence and clinical impacts of viral infection in adults with bronchiectasis exacerbations. The study cohort of 119 adults with bronchiectasis was followed up prospectively for 12 months. Nasopharyngeal swabs and sputum samples were assayed for 16 respiratory viruses, using polymerase chain reaction assays. Symptoms, spirometry, quality of life, bacterial cultures, and inflammatory markers were assessed during steady-state bronchiectasis and exacerbations. A total of 100 exacerbations were captured from 58 patients during 1-year follow-up. Respiratory viruses were found more frequently in nasopharyngeal swabs and sputum during bronchiectasis exacerbations (49 of 100, 49.0') than during steady state (11 of 58, 18.9'; P < .001). The most common viruses found in patients experiencing exacerbations were coronavirus (19 of 65, 39.2'), rhinovirus (16 of 65, 24.6'), and influenza A/B viruses (16 of 65, 24.6'). Virus-positive exacerbations were associated with a greater increase in markers of systemic and airway inflammation (serum IL-6 and tumor necrosis factor-α; sputum IL-1β and tumor necrosis factor-α) compared with virus-negative exacerbations, but the differences in spirometric indexes, quality of life, and bacterial density were unremarkable. In receiver operating characteristics analysis, serum interferon-γ-induced protein 10 yielded an area under curve of 0.67 (95' CI, 0.53-0.77; P = .018). Furthermore, a greater proportion of patients with virus-positive exacerbations received IV antibiotics. Prevalence of viral infections, detected by polymerase chain reaction assay, is higher in cases of bronchiectasis exacerbations than in steady-state bronchiectasis, suggesting that respiratory viruses play crucial roles in triggering bronchiectasis exacerbations. The potential mechanisms of virus-induced bronchiectasis exacerbations merit further investigations. ClinicalTrials.gov; No.: NCT01801657; www.clinicaltrials.gov
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发表时间: 2012-09
期刊: Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society
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发表时间: 2007-09
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