- Email: [email protected]
What Is in a Name?
12. Campo A, Mathai SC, Le Pavec J, et al. Hemodynamic predictors of survival in scleroderma-related pulmonary arterial hypertension. Am J Respir Crit Care Med. 2010;182(2):252-260. 13. Avouac J, Airò P, Meune C, et al. Prevalence of pulmonary hypertension in systemic sclerosis in European Caucasians and metaanalysis of 5 studies. J Rheumatol. 2010;37(11):2290-2298. 14. Zhai Z, Wang J, Zhao L, Yuan JX, Wang C. Pulmonary hypertension in China: pulmonary vascular disease: the global perspective. Chest. 2010;137(suppl 6):69S-77S. 15. Barboza D. China passes Japan as second-largest economy. New York Times. August 15, 2010. 16. Simonneau G, Robbins IM, Beghetti M, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol. 2009;54(suppl 1):S43-S54.
What Is in a Name? The Dilemma of “Prebronchiectasis” “When I use a word,” Humpty Dumpty said, in a rather scornful tone, “it means just what I choose it to mean— nothing more nor less.” Lewis Carroll, Through the Looking Glass1
are powerful. They can topple political Words regimes, polarize discourse, and frame our
thoughts. It was not long ago that physicians often called asthma “reactive airways disease.”2 An unfortunate result of this was that many considered asthma to be a disease of airway smooth muscle, characterized by bronchodilator deficiency and diagnosed using bronchial provocation testing, which has a strong negative predictive value but is not a robust diagnostic test to confirm the clinical diagnosis of asthma.3 We face a similar confusion of words today. Flexible bronchoscopy has safely facilitated spelunking in an ever-increasing number of airways, and highresolution CT scanning using low radiation doses and incremental scanning has increased resolution while decreasing radiation exposure to levels comparable to a standard chest radiograph,4 making high-resolution CT scanning almost a routine diagnostic test in some patients with chronic lung disease. We are recognizing that more airways than we suspected contain bacteria, inflammatory cells, or both and that more patients with chronic lung problems and relatively normal chest radiographs have high-resolution CT scanning evidence of bronchiectasis. In this issue of CHEST (see page 317), Douros and colleagues5 report a study of nearly 100 children (mean age 5.8 years) who had chronic wet cough and were evaluated using high-resolution CT scanning and flexible bronchoscopy.5 They determined that most of these children had a condition they name “chronic suppurative lung disease” (CSLD). Although many of these children had visual signs of inflammation at bronchoscopy and bacteria in their bronchial washings, only one-half of these children had an
increased number of neutrophils in their BAL fluid. The authors conclude that CSLD is part of a continuum starting in the young child with protracted bacterial bronchitis,6 which can become CSLD and finally progress to bronchiectasis. They also speculate that early therapy with antibiotics can stop this progression. The data suggesting that chronic wet cough is associated with protracted bacterial bronchitis and CSLD are strongest for the youngest of children. In the study by Douros and colleagues,5 nearly two-thirds of the children were under the age of 6 years, and the mean age of the children studied by Marchant and colleagues6 was 3.2 years. Older children and adolescents appear to have causes and natural histories of chronic cough that are more similar to those of adults.7 These studies raise several questions. If there is truly a spectrum from protracted bacterial bronchitis to bronchiectasis that progresses if untreated, why is non-cystic fibrosis bronchiectasis so uncommon in children?8 If many of these children have chronic wet cough that resolves spontaneously, can this truly be considered a “prebronchiectasis” lesion? At what age do we evaluate the child for protracted bacterial bronchitis or CSLD, and at what age do we begin to rigorously test for gastroesophageal reflux or asthma? When are children like small adults? Does the child’s age matter, or only the characteristic wet or dry cough? It is not clear why so many of the children with CSLD did not have more neutrophils in their airway. Our knowledge of the airway microbiome is evolving. While the airways were once thought to be sterile when healthy, culture-independent techniques have shown that even “healthy” lungs are not free of bacteria.9 What then are we to make of the presence of bacteria without neutrophils in children who have wet cough? We face a dilemma of both nomenclature and clinical consequences. Undoubtedly, some children with protracted bacterial bronchitis or CSLD do progress to bronchiectasis. In those children, early diagnosis and appropriate intervention using antibiotics is likely to halt this progression before permanent lung damage develops. On the other hand, non-cystic fibrosis bronchiectasis is rare in children, and the overly ambitious use of antibiotics to treat the possibility of bronchiectasis developing can lead to increased health-care costs, risks of antibiotic interaction or side effects, and the public health concern of overuse of antibiotics leading to bacterial resistance. Douros and colleagues5 have done a great service by expanding our awareness of CSLD in children. We now need controlled prospective studies with sufficiently long observation periods and unambiguous end points in order to better identify which of these children can truly
278
Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on August 3, 2011 © 2011 American College of Chest Physicians
benefit from early intervention. This is a dilemma that cannot be solved by words alone. Bruce K. Rubin, MD, FCCP Richmond, VA Affiliations: From the Virginia Commonwealth University School of Medicine and the Children’s Hospital of Richmond. Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Correspondence to: Bruce K. Rubin, MD, FCCP, Department of Pediatrics, Virginia Commonwealth University School of Medicine, 1001 E Marshall St, PO Box 980646, Richmond, VA 23284; e-mail: [email protected] © 2011 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/ site/misc/reprints.xhtml). DOI: 10.1378/chest.11-0666
References 1. Carroll L. Through the Looking Glass. Raleigh, NC: Hayes Barton Press; 1872:72. 2. Fahy JV, O’Byrne PM. “Reactive airways disease.” A lazy term of uncertain meaning that should be abandoned. Am J Respir Crit Care Med. 2001;163(4):822-823. 3. Busse WW. The relationship of airway hyperresponsiveness and airway inflammation: airway hyperresponsiveness in asthma: its measurement and clinical significance. Chest. 2010; 138(suppl 2):4S-10S. 4. O’Connor OJ, Vandeleur M, McGarrigle AM, et al. Development of low-dose protocols for thin-section CT assessment of cystic fibrosis in pediatric patients. Radiology. 2010;257(3): 820-829. 5. Douros K, Alexopoulou E, Nicopoulou A, et al. Bronchoscopic and high-resolution CT scan findings in children with chronic wet cough. Chest. 2011;140(2):317-323. 6. Marchant JM, Masters IB, Taylor SM, Cox NC, Seymour GJ, Chang AB. Evaluation and outcome of young children with chronic cough. Chest. 2006;129(5):1132-1141. 7. Khoshoo V, Edell D, Mohnot S, Haydel R Jr, Saturno E, Kobernick A. Associated factors in children with chronic cough. Chest. 2009;136(3):811-815. 8. Redding GJ. Bronchiectasis in children. Pediatr Clin North Am. 2009;56(1):157-171. 9. Erb-Downward JR, Thompson DL, Han MK, et al. Analysis of the lung microbiome in the “healthy” smoker and in COPD. PLoS ONE. 2011;6(2):e16384.
Survival and Physical Activity in COPD A Giant Leap Forward! decades, cardiopulmonary exercise testing Forhasmany been considered essential to make the correct
diagnosis of exercise limitation and to plan rational treatment in patients with COPD. Indeed, laboratory exercise testing offers clinicians and researchers the unique opportunity to study simultaneously the cellular, cardiovascular, and ventilatory system responses under conditions of precisely controlled metabolic www.chestpubs.org
stress. Maximum incremental exercise testing is still widely performed in the respiratory and cardiovascular evaluation of symptoms and disability, and exercise physiologic examination is dominated by the assessment of maximum oxygen uptake, maximum exercise heart rate, or maximum exercise ventilation. During the last decade, interest has moved from exercise capacity to daily physical activity, which is defined as any bodily movement produced by the contraction of skeletal muscles that increases energy expenditure.1 Indeed, reduced levels of regular physical activity have been associated with increased lung function decline and COPD risk among smokers.2 Moreover, people diagnosed with COPD were shown to be healthy subjects who are elderly: Walking time, standing time, and movement intensity were all reduced.3 In fact, Pitta et al4 showed that about one-half of the patients with COPD walked , 30 min per day, which is the amount of daily physical activity recommended by the American College of Sports Medicine to maintain or develop fitness.1 Moreover, reductions in physical activity are not restricted only to the patients with more severe COPD, but have already been reported in patients with mild COPD according to GOLD (the Global Initiative for Chronic Obstructive Lung Disease).5 Reductions in daily physical activity levels are related to clinically relevant outcomes in patients with COPD, such as concurrent cardiometabolic morbidities,5,6 reduced health status,7 and hospital admissions and readmissions.8,9 Moreover, patients with COPD who had low to very low levels of daily physical activity had higher mortality rates compared with patients with COPD who were physically active to some extent.9 In this issue of CHEST (see page 331), Waschki and colleagues10 also report an association between baseline levels of physical activity and the probability of 4-year survival in 169 patients with mild to very severe COPD. Physically inactive patients with COPD have the worst prognoses. Even though the studied sample is relatively small for a survival study, this study adds significantly to the existing literature. First, Waschki et al10 used accelerometerderived data to assess daily physical activity levels in patients with COPD, while others used data from a physical activity questionnaire,9 which is known to lack precision. Second, Waschki et al10 included multiple pulmonary and nonpulmonary outcomes that had been related individually (eg, degree of dyspnea, static hyperinflation, cardiac function, systemic biomarkers of inflammation, mood status, health status, body composition, and 6-min walk distance test) or in combination (eg, the BODE [BMI, airflow obstruction, dyspnea, and exercise capacity] index and the ADO [age, dypsnea, and airflow obstruction] index) with survival in patients with COPD. Still, baseline levels of daily physical activity were the strongest predictors CHEST / 140 / 2 / AUGUST, 2011
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on August 3, 2011 © 2011 American College of Chest Physicians
279
What Is in a Name? The Dilemma of “Prebronchiectasis” “When I use a word,” Humpty Dumpty said, in a rather scornful tone, “it means just what I choose it to mean— nothing more nor less.” Lewis Carroll, Through the Looking Glass1
are powerful. They can topple political Words regimes, polarize discourse, and frame our
thoughts. It was not long ago that physicians often called asthma “reactive airways disease.”2 An unfortunate result of this was that many considered asthma to be a disease of airway smooth muscle, characterized by bronchodilator deficiency and diagnosed using bronchial provocation testing, which has a strong negative predictive value but is not a robust diagnostic test to confirm the clinical diagnosis of asthma.3 We face a similar confusion of words today. Flexible bronchoscopy has safely facilitated spelunking in an ever-increasing number of airways, and highresolution CT scanning using low radiation doses and incremental scanning has increased resolution while decreasing radiation exposure to levels comparable to a standard chest radiograph,4 making high-resolution CT scanning almost a routine diagnostic test in some patients with chronic lung disease. We are recognizing that more airways than we suspected contain bacteria, inflammatory cells, or both and that more patients with chronic lung problems and relatively normal chest radiographs have high-resolution CT scanning evidence of bronchiectasis. In this issue of CHEST (see page 317), Douros and colleagues5 report a study of nearly 100 children (mean age 5.8 years) who had chronic wet cough and were evaluated using high-resolution CT scanning and flexible bronchoscopy.5 They determined that most of these children had a condition they name “chronic suppurative lung disease” (CSLD). Although many of these children had visual signs of inflammation at bronchoscopy and bacteria in their bronchial washings, only one-half of these children had an
increased number of neutrophils in their BAL fluid. The authors conclude that CSLD is part of a continuum starting in the young child with protracted bacterial bronchitis,6 which can become CSLD and finally progress to bronchiectasis. They also speculate that early therapy with antibiotics can stop this progression. The data suggesting that chronic wet cough is associated with protracted bacterial bronchitis and CSLD are strongest for the youngest of children. In the study by Douros and colleagues,5 nearly two-thirds of the children were under the age of 6 years, and the mean age of the children studied by Marchant and colleagues6 was 3.2 years. Older children and adolescents appear to have causes and natural histories of chronic cough that are more similar to those of adults.7 These studies raise several questions. If there is truly a spectrum from protracted bacterial bronchitis to bronchiectasis that progresses if untreated, why is non-cystic fibrosis bronchiectasis so uncommon in children?8 If many of these children have chronic wet cough that resolves spontaneously, can this truly be considered a “prebronchiectasis” lesion? At what age do we evaluate the child for protracted bacterial bronchitis or CSLD, and at what age do we begin to rigorously test for gastroesophageal reflux or asthma? When are children like small adults? Does the child’s age matter, or only the characteristic wet or dry cough? It is not clear why so many of the children with CSLD did not have more neutrophils in their airway. Our knowledge of the airway microbiome is evolving. While the airways were once thought to be sterile when healthy, culture-independent techniques have shown that even “healthy” lungs are not free of bacteria.9 What then are we to make of the presence of bacteria without neutrophils in children who have wet cough? We face a dilemma of both nomenclature and clinical consequences. Undoubtedly, some children with protracted bacterial bronchitis or CSLD do progress to bronchiectasis. In those children, early diagnosis and appropriate intervention using antibiotics is likely to halt this progression before permanent lung damage develops. On the other hand, non-cystic fibrosis bronchiectasis is rare in children, and the overly ambitious use of antibiotics to treat the possibility of bronchiectasis developing can lead to increased health-care costs, risks of antibiotic interaction or side effects, and the public health concern of overuse of antibiotics leading to bacterial resistance. Douros and colleagues5 have done a great service by expanding our awareness of CSLD in children. We now need controlled prospective studies with sufficiently long observation periods and unambiguous end points in order to better identify which of these children can truly
278
Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on August 3, 2011 © 2011 American College of Chest Physicians
benefit from early intervention. This is a dilemma that cannot be solved by words alone. Bruce K. Rubin, MD, FCCP Richmond, VA Affiliations: From the Virginia Commonwealth University School of Medicine and the Children’s Hospital of Richmond. Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Correspondence to: Bruce K. Rubin, MD, FCCP, Department of Pediatrics, Virginia Commonwealth University School of Medicine, 1001 E Marshall St, PO Box 980646, Richmond, VA 23284; e-mail: [email protected] © 2011 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/ site/misc/reprints.xhtml). DOI: 10.1378/chest.11-0666
References 1. Carroll L. Through the Looking Glass. Raleigh, NC: Hayes Barton Press; 1872:72. 2. Fahy JV, O’Byrne PM. “Reactive airways disease.” A lazy term of uncertain meaning that should be abandoned. Am J Respir Crit Care Med. 2001;163(4):822-823. 3. Busse WW. The relationship of airway hyperresponsiveness and airway inflammation: airway hyperresponsiveness in asthma: its measurement and clinical significance. Chest. 2010; 138(suppl 2):4S-10S. 4. O’Connor OJ, Vandeleur M, McGarrigle AM, et al. Development of low-dose protocols for thin-section CT assessment of cystic fibrosis in pediatric patients. Radiology. 2010;257(3): 820-829. 5. Douros K, Alexopoulou E, Nicopoulou A, et al. Bronchoscopic and high-resolution CT scan findings in children with chronic wet cough. Chest. 2011;140(2):317-323. 6. Marchant JM, Masters IB, Taylor SM, Cox NC, Seymour GJ, Chang AB. Evaluation and outcome of young children with chronic cough. Chest. 2006;129(5):1132-1141. 7. Khoshoo V, Edell D, Mohnot S, Haydel R Jr, Saturno E, Kobernick A. Associated factors in children with chronic cough. Chest. 2009;136(3):811-815. 8. Redding GJ. Bronchiectasis in children. Pediatr Clin North Am. 2009;56(1):157-171. 9. Erb-Downward JR, Thompson DL, Han MK, et al. Analysis of the lung microbiome in the “healthy” smoker and in COPD. PLoS ONE. 2011;6(2):e16384.
Survival and Physical Activity in COPD A Giant Leap Forward! decades, cardiopulmonary exercise testing Forhasmany been considered essential to make the correct
diagnosis of exercise limitation and to plan rational treatment in patients with COPD. Indeed, laboratory exercise testing offers clinicians and researchers the unique opportunity to study simultaneously the cellular, cardiovascular, and ventilatory system responses under conditions of precisely controlled metabolic www.chestpubs.org
stress. Maximum incremental exercise testing is still widely performed in the respiratory and cardiovascular evaluation of symptoms and disability, and exercise physiologic examination is dominated by the assessment of maximum oxygen uptake, maximum exercise heart rate, or maximum exercise ventilation. During the last decade, interest has moved from exercise capacity to daily physical activity, which is defined as any bodily movement produced by the contraction of skeletal muscles that increases energy expenditure.1 Indeed, reduced levels of regular physical activity have been associated with increased lung function decline and COPD risk among smokers.2 Moreover, people diagnosed with COPD were shown to be healthy subjects who are elderly: Walking time, standing time, and movement intensity were all reduced.3 In fact, Pitta et al4 showed that about one-half of the patients with COPD walked , 30 min per day, which is the amount of daily physical activity recommended by the American College of Sports Medicine to maintain or develop fitness.1 Moreover, reductions in physical activity are not restricted only to the patients with more severe COPD, but have already been reported in patients with mild COPD according to GOLD (the Global Initiative for Chronic Obstructive Lung Disease).5 Reductions in daily physical activity levels are related to clinically relevant outcomes in patients with COPD, such as concurrent cardiometabolic morbidities,5,6 reduced health status,7 and hospital admissions and readmissions.8,9 Moreover, patients with COPD who had low to very low levels of daily physical activity had higher mortality rates compared with patients with COPD who were physically active to some extent.9 In this issue of CHEST (see page 331), Waschki and colleagues10 also report an association between baseline levels of physical activity and the probability of 4-year survival in 169 patients with mild to very severe COPD. Physically inactive patients with COPD have the worst prognoses. Even though the studied sample is relatively small for a survival study, this study adds significantly to the existing literature. First, Waschki et al10 used accelerometerderived data to assess daily physical activity levels in patients with COPD, while others used data from a physical activity questionnaire,9 which is known to lack precision. Second, Waschki et al10 included multiple pulmonary and nonpulmonary outcomes that had been related individually (eg, degree of dyspnea, static hyperinflation, cardiac function, systemic biomarkers of inflammation, mood status, health status, body composition, and 6-min walk distance test) or in combination (eg, the BODE [BMI, airflow obstruction, dyspnea, and exercise capacity] index and the ADO [age, dypsnea, and airflow obstruction] index) with survival in patients with COPD. Still, baseline levels of daily physical activity were the strongest predictors CHEST / 140 / 2 / AUGUST, 2011
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on August 3, 2011 © 2011 American College of Chest Physicians
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