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Editorials |

Elastic Recoil RevisitedElastic Recoil FREE TO VIEW

Klaus F. Rabe, MD, PhD
Author and Funding Information

From the LungenClinic Grosshansdorf, member of the German Center for Lung Research (DZL); and Department of Medicine, Christian-Albrechts-Universität zu Kiel, member of the German Center for Lung Research (DZL), Kiel, Germany.

CORRESPONDENCE TO: Klaus F. Rabe, MD, PhD, LungenClinic Grosshansdorf, Woehrendamm 80, D-22927 Grosshansdorf, Germany; e-mail: k.f.rabe@lungenclinic.de


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST the following conflicts of interest: Prof Rabe has served as a consultant to, participated in advisory board meetings with, and received lecture fees from AstraZeneca, Boehringer Ingelheim GmbH, Chiesi Farmaceutici SpA, Pfizer Inc, Novartis AG, Takeda Pharmaceutical Company Limited/Nycomed, Merck Sharp & Dohme Corp, and GlaxoSmithKline plc. He has received research funding from Altana Pharma, Novartis AG, AstraZeneca, Boehringer Ingelheim GmbH, F. Hoffmann-La Roche Ltd, and GlaxoSmithKline plc.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(2):297-298. doi:10.1378/chest.15-0786
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In this issue of CHEST (see page 313), readers will find one of those increasingly rare essays on the principles of pathophysiology of chronic lung diseases, in this case, asthma and COPD.1 What is probably even more remarkable though is the fact that the article is largely based on a 1967 paper from the Journal of Applied Physiology2 whose senior author is also senior author of the current commentary—chapeau Prof Jay Nadel!

The concept of the reversible loss of elastic recoil in asthma was the subject of a study by Gold et al2 almost 50 years ago, was later confirmed in patients with stable asthma with airflow limitation, and has since been discussed as an important factor contributing to airflow limitation in case of peripheral airway narrowing in asthma.2-4 So far, some pathologic evidence has been published5 supporting the concept of the loss of alveolar attachments in fatal asthma that would result in loss of recoil, potentially contributing to the catastrophic events preceding death in these patients. It was speculated that inflammation involving neutrophil and mast cell activation, as well as remodeling processes, might be involved in this loss of attachments5,6 and the observed concomitant fragmentation of elastic fibers in the airway wall.7 However, a direct causal relation has not been established thus far, partly due to the absence of physiologic measurements in such patients when they were clinically more stable. Additionally, in the case of fatal asthma, loss of tethering attachments due to final massive hyperinflation, rather than a chronic inflammatory response including elastolysis, could not completely be ruled out.

Gelb et al8 recently discussed their findings on patients with long-standing asthma and very little signs of emphysema in CT scan scanning. The image analysis was done following standard procedures—and seemingly in-line with the overall concept of the present article1—using the Thurlbeck score from 1970.9 Patients were all treated according to clinical standards and had a decreased FEV1 of 69% predicted with markedly reduced specific airway conductance. Notably, diffusion capacity was normal or increased, and all 10 patients with asthma exhibited a loss of static lung elastic recoil compared with matched control subjects. In the small cohort that was observed for > 10 years, the authors curiously can now provide evidence from four autopsies that significant amounts of mild, diffuse centrilobular emphysema do exist in these patients, despite largely normal CT scans. Of note, and somewhat reassuringly, almost all tissues investigated demonstrated pathologic features of long-standing asthma.

The authors present their findings and discuss the available literature in light of the ongoing and rather fashionable debate on asthma and COPD overlaps.10,11 While I personally believe that the concept of asthma and COPD overlaps is somewhat premature and not all too helpful for the practicing clinician (especially in light of a lack of definition, the lack of a defined pathology, and the huge variability in epidemiology dependent on disease chronicity and patient age), I also agree that patients, on superficial observation, may share characteristics of both diseases. For the pulmonary specialist, however, I would insist that everything should be tried diagnostically (as in the present article) to identify the leading component of the condition at a patient’s presentation rather than lumping very different and by definition heterogeneous disease items together because this might inevitably lead to overtreatment of many patients with drugs, inhaled corticosteroids in particular.

The interesting and thus far unique data by Gelb and colleagues1 are, therefore (in my view), of more general importance for chronic asthma as they lead the way to understanding the structure and function relation in these patients who are asthmatic and remain asthmatic even though they demonstrate the presence of emphysema.12,13 Obviously, the present report is a starting point and needs reconfirmation in more cases, and CT scan assessments would probably be more accurately performed using image analysis software including densitometry. Another intriguing question is related to the apparent reversibility of the loss of elastic recoil which would require a cofactor outside structural and irreversible (?) emphysematous changes in the lung periphery.

Trials like the present one by Gelb and colleagues1 are difficult to perform; they require patience and the unbending desire to study tangible mechanisms to understand human disease. At the very least, such studies are enormously helped by long-standing scientific experience and a living memory of where we came from in clinical lung research. Finally, articles like this one should remind all of us about the importance of understanding lung physiology in this Omics world of complex biologic systems. Thank you!

References

Gelb AF, Yamamoto A, Verbeken EK, Nadel JA. Unraveling the pathophysiology of the asthma-COPD overlap syndrome: unsuspected mild centrilobular emphysema is responsible for loss of lung elastic recoil in never smokers with asthma with persistent expiratory airflow limitation. Chest. 2015;148(2):313-320.
 
Gold WM, Kaufman HS, Nadel JA. Elastic recoil of the lungs in chronic asthmatic patients before and after therapy. J Appl Physiol. 1967;23(4):433-438. [PubMed]
 
Woolcock AJ, Read J. The static elastic properties of the lungs in asthma. Am Rev Respir Dis. 1968;98(5):788-794. [PubMed]
 
McFadden ER Jr, Lyons HA. Serial studies of factors influencing airway dynamics during recovery from acute asthma attacks. J Appl Physiol. 1969;27(4):452-459. [PubMed]
 
Mauad T, Silva LF, Santos MA, et al. Abnormal alveolar attachments with decreased elastic fiber content in distal lung in fatal asthma. Am J Respir Crit Care Med. 2004;170(8):857-862. [CrossRef] [PubMed]
 
Saetta M, Ghezzo H, Kim WD, et al. Loss of alveolar attachments in smokers. A morphometric correlate of lung function impairment. Am Rev Respir Dis. 1985;132(4):894-900. [PubMed]
 
Dolhnikoff M, da Silva LF, de Araujo BB, et al. The outer wall of small airways is a major site of remodeling in fatal asthma. J Allergy Clin Immunol. 2009;123(5):1090-1097. [CrossRef] [PubMed]
 
Gelb AF, Yamamoto A, Mauad T, Kollin J, Schein MJ, Nadel JA. Unsuspected mild emphysema in nonsmoking patients with chronic asthma with persistent airway obstruction [published correction appears inJ Allergy Clin Immunol. 2014;133(4):1232]. J Allergy Clin Immunol. 2014;133(1):263-265. [CrossRef] [PubMed]
 
Thurlbeck WM, Dunnill MS, Hartung W, Heard BE, Heppleston AG, Ryder RC. A comparison of three methods of measuring emphysema. Hum Pathol. 1970;1(2):215-226. [CrossRef] [PubMed]
 
Mattes J, Gibson PG. The early origins of COPD in severe asthma: the one thing that leads to another or the two things that come together? Thorax. 2014;69(9):789-790. [CrossRef] [PubMed]
 
Gibson PG, Simpson JL. The overlap syndrome of asthma and COPD: what are its features and how important is it? Thorax. 2009;64(8):728-735. [CrossRef] [PubMed]
 
Gelb AF, Zamel N. Unsuspected pseudophysiologic emphysema in chronic persistent asthma. Am J Respir Crit Care Med. 2000;162(5):1778-1782. [CrossRef] [PubMed]
 
Gelb AF, Zamel N, Hogg JC, Müller NL, Schein MJ. Pseudophysiologic emphysema resulting from severe small-airways disease. Am J Respir Crit Care Med. 1998;158(3):815-819. [CrossRef] [PubMed]
 

Figures

Tables

References

Gelb AF, Yamamoto A, Verbeken EK, Nadel JA. Unraveling the pathophysiology of the asthma-COPD overlap syndrome: unsuspected mild centrilobular emphysema is responsible for loss of lung elastic recoil in never smokers with asthma with persistent expiratory airflow limitation. Chest. 2015;148(2):313-320.
 
Gold WM, Kaufman HS, Nadel JA. Elastic recoil of the lungs in chronic asthmatic patients before and after therapy. J Appl Physiol. 1967;23(4):433-438. [PubMed]
 
Woolcock AJ, Read J. The static elastic properties of the lungs in asthma. Am Rev Respir Dis. 1968;98(5):788-794. [PubMed]
 
McFadden ER Jr, Lyons HA. Serial studies of factors influencing airway dynamics during recovery from acute asthma attacks. J Appl Physiol. 1969;27(4):452-459. [PubMed]
 
Mauad T, Silva LF, Santos MA, et al. Abnormal alveolar attachments with decreased elastic fiber content in distal lung in fatal asthma. Am J Respir Crit Care Med. 2004;170(8):857-862. [CrossRef] [PubMed]
 
Saetta M, Ghezzo H, Kim WD, et al. Loss of alveolar attachments in smokers. A morphometric correlate of lung function impairment. Am Rev Respir Dis. 1985;132(4):894-900. [PubMed]
 
Dolhnikoff M, da Silva LF, de Araujo BB, et al. The outer wall of small airways is a major site of remodeling in fatal asthma. J Allergy Clin Immunol. 2009;123(5):1090-1097. [CrossRef] [PubMed]
 
Gelb AF, Yamamoto A, Mauad T, Kollin J, Schein MJ, Nadel JA. Unsuspected mild emphysema in nonsmoking patients with chronic asthma with persistent airway obstruction [published correction appears inJ Allergy Clin Immunol. 2014;133(4):1232]. J Allergy Clin Immunol. 2014;133(1):263-265. [CrossRef] [PubMed]
 
Thurlbeck WM, Dunnill MS, Hartung W, Heard BE, Heppleston AG, Ryder RC. A comparison of three methods of measuring emphysema. Hum Pathol. 1970;1(2):215-226. [CrossRef] [PubMed]
 
Mattes J, Gibson PG. The early origins of COPD in severe asthma: the one thing that leads to another or the two things that come together? Thorax. 2014;69(9):789-790. [CrossRef] [PubMed]
 
Gibson PG, Simpson JL. The overlap syndrome of asthma and COPD: what are its features and how important is it? Thorax. 2009;64(8):728-735. [CrossRef] [PubMed]
 
Gelb AF, Zamel N. Unsuspected pseudophysiologic emphysema in chronic persistent asthma. Am J Respir Crit Care Med. 2000;162(5):1778-1782. [CrossRef] [PubMed]
 
Gelb AF, Zamel N, Hogg JC, Müller NL, Schein MJ. Pseudophysiologic emphysema resulting from severe small-airways disease. Am J Respir Crit Care Med. 1998;158(3):815-819. [CrossRef] [PubMed]
 
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