Respiratory viruses, symptoms, and inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease.

The effects of respiratory viral infection on the time course of chronic obstructive pulmonary disease (COPD) exacerbation were examined by monitoring changes in systemic inflammatory markers in stable COPD and at exacerbation. Eighty-three patients with COPD (mean [SD] age, 66.6 [7.1] yr, FEV(1), 1.06 [0.61] L) recorded daily peak expiratory flow rate and any increases in respiratory symptoms. Nasal samples and blood were taken for respiratory virus detection by culture, polymerase chain reaction, and serology, and plasma fibrinogen and serum interleukin-6 (IL-6) were determined at stable baseline and exacerbation. Sixty-four percent of exacerbations were associated with a cold occurring up to 18 d before exacerbation. Seventy-seven viruses (39 [58.2%] rhinoviruses) were detected in 66 (39.2%) of 168 COPD exacerbations in 53 (64%) patients. Viral exacerbations were associated with frequent exacerbators, colds with increased dyspnea, a higher total symptom count at presentation, a longer median symptom recovery period of 13 d, and a tendency toward higher plasma fibrinogen and serum IL-6 levels. Non-respiratory syncytial virus (RSV) respiratory viruses were detected in 11 (16%), and RSV in 16 (23.5%), of 68 stable COPD patients, with RSV detection associated with higher inflammatory marker levels. Respiratory virus infections are associated with more severe and frequent exacerbations, and may cause chronic infection in COPD. Prevention and early treatment of viral infections may lead to a decreased exacerbation frequency and morbidity associated with COPD.     

Childhood respiratory infections and hospital admissions for COPD

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) exacerbations are associated with viral infections. We wished to determine if respiratory viral infection of children in the community was associated with hospital admissions of patients with exacerbations of COPD. METHODS: We collected data over a 45-month period from the Northern Ireland Regional Virus Laboratory and from a general hospital in the same locality. We studied the relationship between upper respiratory infections in children and COPD admissions. We also examined the role of school holidays. RESULTS: Correlations were seen between the frequency of all viral infections in children and the number of adult COPD hospitalizations (P<0.005). Subgroup analysis showed distinct relationships with epidemics of; influenza A (P<0.001), influenza B (P<0.05), adenovirus (P=0.05), respiratory syncytial virus (P<0.005) and hospital admissions of patients with COPD. There were significantly fewer COPD admissions in the week after the start of a school holiday period (P<0.05). CONCLUSIONS: When children are hospitalized with viral respiratory infection there is an associated rise in adult COPD admissions. This suggests exacerbations of COPD are associated with epidemics of respiratory viruses. When children are on school holidays there is a reduction in COPD admissions in the community. This provides further support for respiratory viruses in the pathogenesis of COPD exacerbations.     

Role of viruses in exacerbations of chronic obstructive pulmonary disease

Exacerbations of chronic obstructive pulmonary disease (COPD) are a major cause of morbidity and mortality and hospital admission. Respiratory viral infections, especially rhinoviruses, are a major cause of COPD exacerbations, with upper respiratory tract infections being associated with over 50% of COPD exacerbations. The presence of an upper respiratory tract infection leads to a more severe exacerbation and a longer symptom recovery time at exacerbation. Respiratory viral infections occurring during COPD exacerbations are more likely to lead to hospitalization. Sputum inflammatory markers were found to be higher in those patients with symptoms of a common cold or where rhinovirus was detected at exacerbation, thus suggesting that viral infections lead to greater airway inflammation and thus more severe exacerbations. COPD exacerbations are associated also with systemic inflammatory effects with increases in markers such as plasma fibrinogen and interleukin-6. Respiratory viruses have also been detected when the patients are stable, and this suggests that chronic viral infection may occur. Strategies to prevent viral infection will have a significant effect on the morbidity of COPD and will improve quality of life.     

呼吸道合胞病毒感染与慢性阻塞性肺疾病发病的免疫机制

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种常见的呼吸系统疾病.随着近年来对病毒导致慢性阻塞性肺疾病急性加重(AECOPD)机制的深入研究以及呼吸道病毒检出率的提高,病毒感染在COPD发病机制中的作用受到了更多关注.呼吸道合胞病毒(respiratory syncytial vius,RSV)是常见的呼吸道病毒.有关RSV与宿主的免疫学的研究提示了COPD中RSV的易感性,可能成为某些COPD患者防治疾病发展的新方向.本文对病毒感染在AECOPD中的作用以及RSV感染与COPD发病机制的免疫研究进展现状作一综述.     

The costs of exacerbations in chronic obstructive pulmonary disease (COPD)

Exacerbations are the key drivers in the costs of chronic obstructive pulmonary disease (COPD). The objective was to examine the costs of COPD exacerbations in relation to differing degrees of severity of exacerbations and of COPD. We identified 202 subjects with COPD, defined according to the BTS and ERS criteria. Exacerbations were divided into mild (self-managed), mild/moderate (telephone contact with a health-care centre and/or the use of antibiotics/systemic corticosteroids), moderate (health-care centre visits) and severe (emergency care visit or hospital admission). Exacerbations were identified by sending the subjects a letter inquiring whether they had any additional respiratory problems or influenza the previous winter. At least one exacerbation was reported by 61 subjects, who were then interviewed about resource use for these events. The average health-care costs per exacerbation were SEK 120 (95% C=39-246), SEK 354 (252-475), SEK 2111 (1673-2612) and SEK 21852 (14436-29825) for mild, mild/moderate, moderate and severe exacerbations, respectively. Subjects with impaired lung function experienced more severe exacerbations, which was also reflected in the cost of exacerbations per severity of the disease during the 4 1/2 month study period (ranging from SEK 224 for mild to SEK 13708 for severe cases, median SEK 940). Exacerbations account for 35-45% of the total per capita health-care costs for COPD. In conclusion, costs varied considerably with the severity of the exacerbation as well as with the severity of COPD. The prevention of moderate-to-severe exacerbations could be very cost-effective and improve the quality of life.     

Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease

There is increasing evidence that chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation in the airways and lung parenchyma; however, little is known about the inflammatory response during acute COPD exacerbation. The objectives of this study were (1) to determine if inflammatory markers associated with neutrophilic inflammation and activation increase at times of acute COPD exacerbation relative to the clinically stable state, and (2) to determine whether the presence of acute bacterial or viral infection at the time of COPD exacerbation could be correlated with increases in sputum markers of inflammation. Induced sputum was collected from patients with COPD when they were clinically stable, during the time of an acute exacerbation, and 1 mo later. Sputum was analyzed at each time point for soluble markers associated with neutrophilic inflammation; myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-alpha), and interleukin-8 (IL-8). Serologic assays on acute and convalescent sera were performed for respiratory viruses, and induced sputum was also subject to quantitative bacterial cultures, viral cultures, and polymerase chain reaction (PCR) for detection of respiratory viruses. Fourteen of the 50 patients enrolled in the study met predetermined criteria for an acute COPD exacerbation over the 15-mo study period. TNF-alpha and IL-8 were significantly elevated in the sputum of patients during acute COPD exacerbation compared with when they were clinically stable (p = 0.01 and p = 0.05, respectively). Concentrations of these cytokines declined significantly 1 mo after the exacerbation. Three of 14 patients (21%) had confirmed bacterial or viral respiratory tract infections. Patients with documented infection did not demonstrate greater increases in sputum levels of inflammatory cytokines during exacerbations compared with patients without demonstrable infection. We conclude that markers of airway neutrophilic inflammation increase at the time of acute COPD exacerbation and then decline 1 mo later, and that this acute inflammatory response appears to occur independently of a demonstrable viral or bacterial airway infection.     

Two cases of asthmatic exacerbation caused by parainfluenza virus 3 infection]

Although viral respiratory tract infections are considered to be the most frequent causes of asthmatic exacerbation, respiratory viruses can rarely be detected in the adult population. We describe 2 cases, in a 43-yr-old man with severe atopic asthma and in a 69-yr-old man with moderate non-atopic asthma. After the onset of nasal discharge, sore throat and fever, the asthma had become exacerbated in both cases during the summer of 2002. In both cases, parainfluenza virus (PIV) 3 viral RNA could be detected from oral gargling by RT-PCR, and the serum viral antibody titer against PIV 3 increased significantly. These cases were therefore diagnosed as undergoing asthmatic exacerbation caused by PIV 3 infection and were successfully treated with systemic steroids. During summer, 2002, in our outpatient clinic, PIV 3 infection was demonstrated in approximately half of the asthmatic exacerbations associated with upper respiratory symptoms, including the present cases. Collectively, PIV 3 seems to represent an important viral cause of asthma exacerbation in summer.     

COPD assessment tests scores are associated with exacerbated chronic obstructive pulmonary disease in Japanese patients

BackgroundGuidelines recommend chronic obstructive pulmonary disease (COPD) assessment tests (CATs) for evaluation of symptoms and management risks. To investigate whether CAT can predict moderate or severe exacerbations in Japanese COPD patients, a single-blinded prospective study was performed.MethodsA 123 Japanese COPD patients were classified into high-CAT (n=64) and low-CAT (n=59) groups. The frequencies and periods of moderate or severe exacerbation and hospitalization were compared between the two groups. Multivariate logistic regression analysis was performed to investigate whether CAT could predict exacerbations. A receiver operating characteristic (ROC) curve analysis was employed to find an appropriate CAT score for exacerbation.ResultsThe high-CAT group was significantly older, had a lower body mass index, and had a lower airflow obstruction as compared to the low CAT group. The frequency of moderate or severe exacerbation (1.3±1.3 events per patient per year, p<0.0001) and hospitalizations (0.2±0.4, p=0.0202) in the high-CAT group was significantly higher than in the low-CAT group (0.4±0.7 and 0.0±0.1, respectively). Multivariate logistic regression analysis showed that both high CAT score and low airflow obstruction were independently predictive of frequent moderate or severe COPD exacerbation. ROC analysis showed that the best cut-off CAT score for moderate or severe COPD exacerbation was 8 points.ConclusionOur present results indicate that COPD Japanese patients showing high CAT scores have a poor prognosis, and that the CAT score is able to predict exacerbation in Japanese COPD.     

儿科重症监护室先天性心脏病合并呼吸道感染患儿的病毒性病原学研究

目的：总结儿科重症监护室中先天性心脏病合并呼吸道感染患儿的病毒性病原谱。方法收集2010年6月至2012年6月因呼吸道感染入住本院儿科重症监护室的患儿咽拭子标本622份,其中先天性心脏病合并呼吸道感染患儿咽拭子34份。应用多重聚合酶链反应(PCR)技术对呼吸道病毒进行检测,并对照分析合并先天性心脏病患儿的病毒性病原学特点。结果①34份先天性心脏病组咽拭子标本中,呼吸道病毒检测阳性20份(58.8%),588份非先天性心脏病组咽拭子标本中,呼吸道病毒检测阳性368份(62.6%)。②先天性心脏病组中,最常见的病毒分别为人鼻病毒(human rhinovirus,HRV)8份,呼吸道合胞病毒(respiratory syncytial virus, RSV)6份,人博卡病毒(human bocavirus,HBoV)4份,腺病毒(adenovirus,ADV)2份;非先天性心脏病组中,最常见的病毒分别为 HRV 160份,RSV 104份,ADV 72份,HBoV50份;其他病毒阳性率较低。③先天性心脏病组中,混合病毒感染有2份(2/20,10.0%),非先天性心脏病组中,混合病毒感染有110份(110/368,29.9%)。结论本地区儿科重症监护室中先天性心脏病合并呼吸道感染患儿的病原体中病毒性病原体检出率高,以鼻病毒、呼吸道合胞病毒、人博卡病毒和腺病毒最常见,病毒谱和非先天性心脏病组相似。     

Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease

Although exacerbations of chronic obstructive pulmonary disease (COPD) are associated with symptomatic and physiological deterioration, little is known of the time course and duration of these changes. We have studied symptoms and lung function changes associated with COPD exacerbations to determine factors affecting recovery from exacerbation. A cohort of 101 patients with moderate to severe COPD (mean FEV(1) 41.9% predicted) were studied over a period of 2.5 yr and regularly followed when stable and during 504 exacerbations. Patients recorded daily morning peak expiratory flow rate (PEFR) and changes in respiratory symptoms on diary cards. A subgroup of 34 patients also recorded daily spirometry. Exacerbations were defined by major symptoms (increased dyspnea, increased sputum purulence, increased sputum volume) and minor symptoms. Before onset of exacerbation there was deterioration in the symptoms of dyspnea, sore throat, cough, and symptoms of a common cold (all p < 0.05), but not lung function. Larger falls in PEFR were associated with symptoms of increased dyspnea (p = 0.014), colds (p = 0.047), or increased wheeze (p = 0.009) at exacerbation. Median recovery times were 6 (interquartile range [IQR] 1 to 14) d for PEFR and 7 (IQR 4 to 14) d for daily total symptom score. Recovery of PEFR to baseline values was complete in only 75.2% of exacerbations at 35 d, whereas in 7.1% of exacerbations at 91 d PEFR recovery had not occurred. In the 404 exacerbations where recovery of PEFR to baseline values was complete at 91 d, increased dyspnea and colds at onset of exacerbation were associated with prolonged recovery times (p < 0.001 in both cases). Symptom changes during exacerbation do not closely reflect those of lung function, but their increase may predict exacerbation, with dyspnea or colds characterizing the more severe. Recovery is incomplete in a significant proportion of COPD exacerbations.     

The similarities and differences of epidemic cycles of chronic obstructive pulmonary disease and asthma exacerbations

The majority of chronic obstructive pulmonary disease (COPD) and asthma exacerbations in both children and adults are associated with respiratory viral infections and are cyclic in nature. Some variation in these cycles is associated with the timing of the appearance of respiratory viruses, particularly influenza and respiratory syncytial virus. Much more, however, is associated with signal events that are of either fixed or predictable timing. In children, asthma exacerbations reach epidemic levels following school return after the summer vacation and these are predominantly associated with rhinovirus infections. Although younger adults experience a rise in asthma exacerbations at this time, these are secondary to the epidemic in children. Older adults with either COPD or asthma experience only a slightly elevated risk of exacerbations after school return, and hospital presentations for pneumonia in any age group show only marginal increases at that time. Exacerbations of both COPD and adult asthma, with increasing risk with age, are at their highest average annual levels during the Christmas period. This effect appears to be independent of the timing of above average levels of influenza, RSV, parainfluenza, or adenovirus detections; however, hospitalization for respiratory tract infections in all age groups reaches high levels at the same time. Both the post-summer vacation asthma epidemic and the Christmas epidemic of COPD, asthma, and pneumonia are synchronous with the timing of signal events, the day of school return for the former and Christmas Day for the latter, and have been for several years. The agents responsible for the Christmas epidemic of respiratory diseases have not yet been identified. The differences between age and disease exacerbation patterns after school return and at Christmas suggest that either different agents are involved or that the response to a common agent is different between the two signal events.     

Viral infections in obstructive airway diseases

The most common syndromes associated with obstructive lung disease are asthma and chronic obstructive pulmonary disease (COPD). Evidence for a viral etiology of asthmatic exacerbations is well known, but evidence for a role for viruses in COPD exacerbation is just emerging. Viruses may cause chronic infection in both diseases. This paper reviews some studies on the effects of respiratory viruses on asthma and COPD published in 2002 and discusses their relevance to current thinking in pulmonary medicine.     

Inflammatory Response in Acute Viral Exacerbations of COPD

Background  Respiratory viruses are important triggers of acute exacerbations of COPD (AE-COPD). However, the inflammatory response in virus-positive exacerbations is still not fully understood. Methods  We investigated CRP, IL-6, IL-8, IL-10, IFN-γ, blood and sputum cells in patients with acute exacerbation (n = 36) and in stable disease (n = 20) and correlated these parameters to virus detection in respiratory secretions. Results  Similar to other studies we found a significant increase in systemic CRP and absolute numbers of blood leukocytes in AE-COPD patients. Sputum IL-6 levels and sputum eosinophils tended to be higher during exacerbation. In patients with detection of respiratory viruses in nasal lavage, local IL-6 production in sputum was significantly increased; FEV₁ was significantly decreased and both parameters were inversely correlated to each other. Conclusion  This study supports previous findings of both, increased local and systemic inflammation in acute exacerbation of COPD. In virus-associated exacerbations, IL-6 is significantly increased and negatively correlated to FEV₁ indicating a relation between virus-induced inflammation and airway obstruction. However, regarding our finding and previous data, it is becoming increasingly clear that the mediators investigated so far do not permit identifying the etiology of AE-COPD. Hence, further studies are needed to better define the inflammatory response in AE-COPD in general and in viral exacerbations in particular. Supported by Bundesministerium für Bildung und Forschung (BMBF) grant #01GC0101.     

A Two-Stage Logistic Model Based on the Measurement of Pro-Inflammatory Cytokines in Bronchial Secretions for Assessing Bacterial,Viral, and Non-Infectious Origin of COPD Exacerbations

Exacerbations often complicate the progressive course of chronic obstructive pulmonary disease (COPD), mainly due to infectious agents. The precise role of bacterial infections in the course and the pathogenesis of COPD has been a source of controversy for decades. Also viruses and other non-infectious causes of exacerbation play a relevant role and also contribute to persisting airway inflammation. Usually, the etiologic identification of the infective causes of COPD require considerable time and costs. The development of more rapid, reliable, and widely applicable methods to promptly define the etiology of COPD exacerbations should represent a relevant issue in devising earlier and more specific strategies for their effective therapeutic control. Aim: of the study was to assess the predictive role of some pro-inflammatory cytokines measured in spontaneous bronchial secretions in discriminating the main infectious causes of COPD exacerbations. Methods: 124 subjects with moderate COPD (51–79 y; mean basal FEV₁ = 49.6% pred. ± 4.6 sd; FEV1 reversibility + 3.9% from baseline ± 4.8 sd after salbutamol 200 mcg) were studied during acute exacerbation. Respiratory viruses were isolated from bronchial secretions in 21 cases; common bacteria (CFU ≥ 10⁶/ml) in 28 cases; Pseudomonas Aeruginosa (Ps.Ae.; CFU ≥ 10⁶/ml) in 20 cases. The cytokines IL1β, IL8, and TNFα (pg/ml; Immulite; Diagnostic Product Corp, Los Angeles, CA, USA), and neutrophils (% total count) were measured in bronchial secretions of all patients. Statistics: a two-stage logistic model was chosen for discriminating the different causes of COPD exacerbations (such as: non-infectious, or viral, bacterial, or due to Ps.Ae.). Results: At the first decisional step, the two-stage logistic model proved that TNFα levels in bronchial secretions recognise clearly patients belonging to the Ps.Ae. group from those of all othergroups (Area under ROC curve = 0.96; 95% CI = 0.91–0.99), and that, at the second decisional step, IL8 + IL1β levels discriminate patients with bacterial causes (such as all bacteria) from the non-infected ones and from those with a viral cause of exacerbation (Area under ROC curve = 0.87; 95% CI = 0.77–0.94). Neutrophil percent count did not support any contribution in discriminating the different subgroups of COPD subjects. Conclusions: when exacerbated, COPD subjects express different patterns of pro-inflammatory mediators in bronchial secretions, which appear modulated according to the etiological cause of the exacerbation. In particular, TNFα concentration per se enables recognition of COPD exacerbations due to Ps.Ae., while IL8 + IL1β levels prove helpful in discriminating those to common bacteria from those to viral agents and to non-infectious causes. When present data are further confirmed, the use of a decisional rule based on cytokine measurements might be regarded as a helpful predictive tool. As measures of pro-inflammatory cytokines are low-cost, simple, and faster to perform, they could support rapid clinical decision making at the bedside regarding therapeutic strategy for COPD exacerbations, in particular when they are needed for severe COPD patients.     

Acute exacerbation of COPD

The literature of acute exacerbation of chronic obstructive pulmonary disease (COPD) is fast expanding. This review focuses on several aspects of acute exacerbation of COPD (AECOPD) including epidemiology, diagnosis and management. COPD poses a major health and economic burden in the Asia‐Pacific region, as it does worldwide. Triggering factors of AECOPD include infectious (bacteria and viruses) and environmental (air pollution and meteorological effect) factors. Disruption in the dynamic balance between the ‘pathogens’ (viral and bacterial) and the normal bacterial communities that constitute the lung microbiome likely contributes to the risk of exacerbations. The diagnostic approach to AECOPD varies based on the clinical setting and severity of the exacerbation. After history and examination, a number of investigations may be useful, including oximetry, sputum culture, chest X‐ray and blood tests for inflammatory markers. Arterial blood gases should be considered in severe exacerbations, to characterize respiratory failure. Depending on the severity, the acute management of AECOPD involves use of bronchodilators, steroids, antibiotics, oxygen and noninvasive ventilation. Hospitalization may be required, for severe exacerbations. Nonpharmacological interventions including disease‐specific self‐management, pulmonary rehabilitation, early medical follow‐up, home visits by respiratory health workers, integrated programmes and telehealth‐assisted hospital at home have been studied during hospitalization and shortly after discharge in patients who have had a recent AECOPD. Pharmacological approaches to reducing risk of future exacerbations include long‐acting bronchodilators, inhaled steroids, mucolytics, vaccinations and long‐term macrolides. Further studies are needed to assess the cost‐effectiveness of these interventions in preventing COPD exacerbations.     

AECOPD对肱动脉内皮功能的影响

目的 探讨AECOPD对肱动脉内皮功能的影响.方法 78例AECOPD患者根据严重度分为COPDⅠ组(轻度和中度,共38人)及COPDⅡ组(重度和极重度,共40人),同时选取30例健康对照,测定急性加重期及稳定期肱动脉内皮功能.结果 COPD患者急性加重期FMD均减低,Ⅱ组减低更加明显,COPDⅡ组稳定期FMD仍显著减低;COPDⅠ组急性加重期及稳定期NMD正常,COPDⅡ组急性加重期及稳定期NMD均减低.结论 COPD急性加重对肱动脉内皮功能的损伤更加明显.     

Evaluation of Respiratory Viral Pathogens in Acute Asthma Exacerbations during Childhood

Objective. Common upper respiratory tract viruses are the most frequent and important causes of asthma exacerbations in both children and adults. Prospective epidemiologic studies report that up to 80% of childhood exacerbations are associated with viral upper respiratory tract infections. Materials and methods. The study group consisted of 104 children with asthma aged 3–17 years who received treatment for asthma exacerbations in our clinic between September 2009 and 2010. Nasopharyngeal and nasal swabs were obtained from all patients during an acute attack, and from the control group (31 subjects). These specimens were investigated for the presence of viral respiratory pathogens using a real-time multiplex PCR method. The patients were compared for the presence of respiratory pathogens and factors related to the severity of the asthma exacerbation. Results. A pathogenic respiratory virus was detected in 53.8% of patients in the acute exacerbation group. The most commonly encountered viral agent was Rhinovirus (35.6%). Patients who had an acute exacerbation with or without a detectable viral pathogen were compared according to the severity of the exacerbation, the need for systemic steroids, and hospitalization rates. No statistically significant difference was found. Conclusion. Although viral upper respiratory tract infections are the most common cause of asthma exacerbations, the severity level of the exacerbation seems to be independent of whether a respiratory virus has been detected.     

Infections and airway inflammation in chronic obstructive pulmonary disease severe exacerbations

RATIONALE: Severe exacerbations of chronic obstructive pulmonary disease (COPD) are major causes of health care costs mostly related to hospitalization. The role of infections in COPD exacerbations is controversial. OBJECTIVES: We investigated whether COPD exacerbations requiring hospitalization are associated with viral and/or bacterial infection and evaluated relationships among infection, exacerbation severity, assessed by reduction of FEV1, and specific patterns of airway inflammation. METHODS: We examined 64 patients with COPD when hospitalized for exacerbations, and when in stable convalescence. We measured lung function, blood gases, and exhaled nitric oxide, and examined sputum for inflammation and for viral and bacterial infection. RESULTS: Exacerbations were associated with impaired lung function (p < 0.01) and increased sputum neutrophilia (p < 0.001). Viral and/or bacterial infection was detected in 78% of exacerbations: viruses in 48.4% (6.2% when stable, p < 0.001) and bacteria in 54.7% (37.5% when stable, p = 0.08). Patients with infectious exacerbations (29.7% bacterial, 23.4% viral, 25% viral/bacterial coinfection) had longer hospitalizations (p < 0.02) and greater impairment of several measures of lung function (all p < 0.05) than those with noninfectious exacerbations. Patients with exacerbations with coinfection had more marked lung function impairment (p < 0.02) and longer hospitalizations (p = 0.001). Sputum neutrophils were increased in all exacerbations (p < 0.001) and were related to their severity (p < 0.001), independently of the association with viral or bacterial infections; sputum eosinophils were increased during (p < 0.001) virus-associated exacerbations. CONCLUSIONS: Respiratory infections are associated with the majority of COPD exacerbations and their severity, especially those with viral/bacterial coinfection. Airway neutrophilia is related to exacerbation severity regardless of viral and/or bacterial infections. Eosinophilia is a good predictor of viral exacerbations.     

The Christmas season as a risk factor for chronic obstructive pulmonary disease exacerbations

BACKGROUND

Epidemics of hospitalization for chronic obstructive pulmonary disease (COPD) occur annually during the Christmas holidays, and COPD exacerbations commonly coincide with respiratory viral infections.

OBJECTIVE

To compare the incidence and determinants of COPD exacerbations occurring between the Christmas holiday period and the remainder of the winter season.

METHODS

Seventy-one subjects with COPD of mixed severity faxed daily symptom diaries to a computer monitoring system from December 1, 2006, to April 30, 2007. Possible exacerbations prompted a home visit for assessment, spirometry and specimen collection for virological testing.

RESULTS

Study subjects submitted a total of 95.4% of possible daily symptom diary sheets by fax. Of 114 possible COPD exacerbations detected using the faxed diaries, 110 met the Anthonisen criteria for true exacerbations. A total of 47 exacerbations (mean 6.7/week) occurred during the Christmas holiday period, while 63 exacerbations (mean 4.3/week) occurred during the remainder of winter. Of the Christmas period exacerbations and of those in the balance of winter, 21 (44%) and 20 (32%), respectively, coincided with respiratory viral infections.

CONCLUSIONS

The incidence of COPD exacerbations during the Christmas period was greater than during the rest of winter in 2006/2007 and peaked immediately before Christmas – in contrast to hospital presentation for COPD, which peaked during the Christmas week. No clear role of respiratory viral infections in the increased rate of exacerbations during the Christmas period was established in the present study. COPD patients were highly compliant with daily symptom reporting using faxed daily diaries, which permitted nearly complete detection of all exacerbations that occurred at incidence.