Recently, a group of experts from around the world defined bronchiectasis as a dilation of the airway lumen mainly produced by the destruction of the bronchial wall, secondary to the action of various proteolytic substances from local inflammation—usually neutrophilic inflammation,(1) although sometimes also eosinophilic inflammation,(2-4) and even with a systemic component(5,6)—and/or secondary bacterial products (usually as a chronic infection).(7-9) Furthermore, this radiological finding must be accompanied by symptoms related to it, especially productive cough (usually with a purulent component), with or without exacerbations.(10-12) Therefore, the definition of bronchiectasis must meet not only radiological criteria but also clinical criteria.(1,13) As a consequence, traction bronchiectasis (TBE) has been systematically excluded from diagnostic, prognostic, and therapeutic studies of bronchiectasis because it is not usually associated with a secondary clinical picture of airway inflammation or infection.(14)
 
It is true that TBE is usually due to dilation of the bronchial lumen caused by the destruction of the surrounding lung parenchyma. TBE is not usually accompanied by bronchial wall thickening related to excessive bronchial inflammation, and the probability of chronic infection with potentially pathogenic microorganisms is low. TBE is frequently observed in the context of advanced fibrotic processes secondary to interstitial diseases, after extensive infections or pulmonary emphysema, and, in general, after processes involving destruction of the lung parenchyma.(15)
 
In recent years, the presence of TBE has generated some particularly interesting questions about its ability to influence the prognosis of the underlying disease. Is TBE really as benign as we think? Could the presence of TBE influence the prognosis of patients, regardless of the usually associated interstitial pattern? Should the progression of TBE be monitored when it appears? Although the name bronchiectasis is still used for etymological reasons (bronkos = bronchus and ectasis = dilation), there is still no answer to these questions, since TBE has been systematically excluded, as mentioned above, from bronchiectasis studies of all types.
 
Recently, however, a study(16) involving 5,295 individuals with COPD (mean age = 59 years) seems to have indicated that the presence of TBE is not trivial at all and that TBE is capable of negatively impacting various important outcomes of COPD. In that study, Hata et al.(16) identified a subgroup of patients (n = 582) presenting interstitial abnormalities on CT scans. Those with associated TBE (n = 105) showed an adjusted linear correlation between greater radiological severity of TBE and poorer quality of life. Moreover, the patients with TBE presented an adjusted risk of death 3.8 times higher (95% CI: 2.6-5.6; p < 0.001) than did those without it.
 
These findings on the relationship between the presence of TBE and a poorer prognosis for the underlying disease are not new, having previously been described for various interstitial lung diseases such as idiopathic pulmonary fibrosis,(17) hypersensitivity pneumonitis,(18) and chronic eosinophilic pneumonia.(19) It is also a noteworthy fact that TBE has been shown to progress in most patients, resulting in a progressively worsening prognosis and greater severity of the underlying disease. The presence of TBE could therefore serve as a marker of the severity of interstitial diseases of any origin, which suggests—as it is already known—that early, intensified anti-inflammatory treatment during the inflammatory phase of the underlying disease is essential, before it progresses to an interstitial lesion and, consequently, to TBE. In fact, some authors have suggested the use of a TBE index(16,20) whose validity is distinguished by, among other things, excellent interobserver agreement for the diagnosis of TBE by chest CT (kappa index around 0.75). The TBE index classifies patients into four groups, according to the presence and type of TBE found in the interstitial process: type 1: no TBE; type 2: presence of bronchiolectasis; type 3: moderate TBE; and type 4: severe TBE. This classification system was used in the study by Hata et al,(16), as well as in another population-based study conducted in Iceland.(20) In the latter study, CT scanning was performed at baseline and 5 years after the inclusion of 3,167 participants in the study, 327 of whom had some type of interstitial alteration. The authors observed not only that TBE progressed in most individuals over time, but also that this progression was associated with an increased probability of death (hazard ratio = 1.68; 95% CI: 1.21-2.34; p < 0.001), adjusted for age, sex, BMI, and smoking habit after 11.5-14.0 years of follow-up.
 
All of these findings open up a timely topic of great relevance related to sequelae in the lung parenchyma of patients who have had SARS-CoV-2-related pneumonia. Various follow-up studies based on CT data have shown that a high proportion of such patients have suffered from chronic interstitial damage (especially after having severe pneumonia), often associated with TBE.(21,22) Will TBE even further worsen the prognosis or clinical severity in patients with interstitial alterations, in comparison with those without TBE? The answer to this question is still unknown, but it should certainly be a subject for research because an early aggressive treatment during the inflammatory phase of the disease would probably be the best option to prevent interstitial sequelae and the subsequent appearance of TBE. Moreover, it is also unknown whether, in addition to TBE, clinically active bronchiectasis might result in chronic infection with pathogenic microorganisms as a consequence of a vicious circle of excessive inflammation/infection over time. This situation cannot be ruled out since it is known that one of the most common etiologies of symptomatic bronchiectasis is after an infection, including viral infections.
 
In short, the supposed benignity attributed to TBE as part of an interstitial process within different underlying lung diseases (including both interstitial and non-interstitial disorders) does not seem to be confirmed in the literature. The presence of TBE could in fact worsen the prognosis and the clinical severity of the underlying disease responsible for it, over and above the prognosis resulting from the interstitial alteration itself. Another very important question remains to be clarified, which has already been generating a field of research of great interest: what will be the future impact of bronchiectasis associated with interstitial patterns in patients who have overcome COVID-19 pneumonia? There is still no answer to this question, but the data available so far indicate that a long-term follow-up period is required for such patients; if necessary, imaging techniques and even clinical monitoring should be used, including microbiological data, wherever possible.
 
CONFLICTS OF INTEREST
 
None declared.
 
REFERENCES
 
1.            Aliberti S, Goeminne PC, O’Donnell AE, Aksamit TR, Al-Jahdali H, Barker AF, et al. Criteria and definitions for the radiological and clinical diagnosis of bronchiectasis in adults for use in clinical trials: international consensus recommendations. Lancet Respir Med. 2022;10(3):298-306. https://doi.org/10.1016/S2213-2600(21)00277-0
2.            Martínez-García MÁ. Bronchiectasis and Eosinophils. Arch Bronconeumol. 2021;57(11):671-672. https://doi.org/10.1016/j.arbres.2021.08.001
3.            Shoemark A, Shteinberg M, De Soyza A, Haworth CS, Richardson H, Gao Y, et al. Characterization of Eosinophilic Bronchiectasis: A European Multicohort Study. Am J Respir Crit Care Med. 2022;205(8):894-902. https://doi.org/10.1164/rccm.202108-1889OC
4.            Martinez-Garcia MA, Posadas T, Sotgiu G, Blasi F, Saderi L, Aliberti S. Repeteability of Circulating Eosinophil Measures and Inhaled Corticosteroids Effect in Bronchiectasis. A Post Hoc Analysis of a Randomized Clinical Trial. Arch Bronconeumol (Engl Ed). 2020;56(10):681-683. https://doi.org/10.1016/j.arbr.2020.06.003
5.            Saleh AD, Chalmers JD, De Soyza A, Fardon TC, Koustas SO, Scott J, et al. The heterogeneity of systemic inflammation in bronchiectasis. Respir Med. 2017;127:33-39. https://doi.org/10.1016/j.rmed.2017.04.009
6.            Posadas T, Oscullo G, Zaldivar E, Villa C, Dobarganes Y, Girón R, et al. C-Reactive Protein Concentration in Steady-State Bronchiectasis: Prognostic Value of Future Severe Exacerbations. Data From the Spanish Registry of Bronchiectasis (RIBRON). Arch Bronconeumol (Engl Ed). 2021;57(1):21-27. https://doi.org/10.1016/j.arbr.2019.12.022
7.            de la Rosa Carrillo D, López-Campos JL, Alcázar Navarrete B, Calle Rubio M, Cantón Moreno R, García-Rivero JL, et al. Consensus Document on the Diagnosis and Treatment of Chronic Bronchial Infection in Chronic Obstructive Pulmonary Disease. Arch Bronconeumol (Engl Ed). 2020;56(10):651-664. https://doi.org/10.1016/j.arbr.2020.08.006
8.            Figueiredo MR, Lomonaco I, Araújo AS, Lundgren F, Pereira EDB. Isolation of and risk factors for airway infection with Pseudomonas aeruginosa in patients with non-cystic fibrosis bronchiectasis. J Bras Pneumol. 2021;47(3):e20210017. https://doi.org/10.36416/1806-3756/e20210017
9.            Monsó E. Look at the wood and not at the tree: The Microbiome in Chronic Obstructive Lung Disease and Cystic Fibrosis. Arch Bronconeumol (Engl Ed). 2020;56(1):5-6. https://doi.org/10.1016/j.arbr.2019.04.014
10.          Martinez-García MA, Villa C, Dobarganes Y, Girón R, Maíz L, García-Clemente M, et al. RIBRON: The spanish Online Bronchiectasis Registry. Characterization of the First 1912 Patients. Arch Bronconeumol (Engl Ed). 2021;57(1):28-35. https://doi.org/10.1016/j.arbr.2020.11.010
11.          Amati F, Simonetta E, Gramegna A, Tarsia P, Contarini M, Blasi F, et al. The biology of pulmonary exacerbations in bronchiectasis. Eur Respir Rev. 2019 Nov 20;28(154):190055. https://doi.org/10.1183/16000617.0055-2019
12.          Chen CL, Huang Y, Yuan JJ, Li HM, Han XR, Martinez-Garcia MA, et al. The Roles of Bacteria and Viruses in Bronchiectasis Exacerbation: A Prospective Study. Arch Bronconeumol (Engl Ed). 2020;56(10):621-629. https://doi.org/10.1016/j.arbr.2019.12.014
13.          Nucci MCNM, Fernandes FLA, Salge JM, Stelmach R, Cukier A, Athanazio R. Characterization of the severity of dyspnea in patients with bronchiectasis: correlation with clinical, functional, and tomographic aspects. J Bras Pneumol. 2020;46(5):e20190162. https://doi.org/10.36416/1806-3756/e20190162
14.          Crichton ML, Aliberti S, Chalmers JD. A systematic review of pharmacotherapeutic clinical trial end-points for bronchiectasis in adults. Eur Respir Rev. 2019;28(151):180108. https://doi.org/10.1183/16000617.0108-2018
15.          Piciucchi S, Tomassetti S, Ravaglia C, Gurioli C, Gurioli C, Dubini A, et al. From “traction bronchiectasis” to honeycombing in idiopathic pulmonary fibrosis: A spectrum of bronchiolar remodeling also in radiology?. BMC Pulm Med. 2016;16(1):87. https://doi.org/10.1186/s12890-016-0245-x
16.          Hata A, Hino T, Putman RK, Yanagawa M, Hida T, Menon AA. Traction Bronchiectasis/Bronchiolectasis on CT Scans in Relationship to Clinical Outcomes and Mortality: The COPDGene Study [published online ahead of print, 2022 May 31]. Radiology. 2022;212584. https://doi.org/10.1148/radiol.212584
17.          Desai SR, Wells AU, Rubens MB, du Bois RM, Hansell DM. Traction bronchiectasis in cryptogenic fibrosing alveolitis: associated computed tomographic features and physiological significance. Eur Radiol. 2003;13(8):1801-1808. https://doi.org/10.1007/s00330-002-1779-2
18.          Jacob J, Bartholmai BJ, Egashira R, Brun AL, Rajagopalan S, Karwoski R, et al. Chronic hypersensitivity pneumonitis: identification of key prognostic determinants using automated CT analysis. BMC Pulm Med. 2017;17(1):81. https://doi.org/10.1186/s12890-017-0418-2
19.          Takei R, Arita M, Kumagai S, Ito Y, Takaiwa T, Tokioka F, et al. Traction bronchiectasis on high-resolution computed tomography may predict fatal acute eosinophilic pneumonia. Respir Investig. 2019;57(1):67-72. https://doi.org/10.1016/j.resinv.2018.09.005
20.          Hino T, Hida T, Nishino M, Lu J, Putman RK, Gudmundsson EF, et al. Progression of traction bronchiectasis/bronchiolectasis in interstitial lung abnormalities is associated with increased all-cause mortality: Age Gene/Environment Susceptibility-Reykjavik Study. Eur J Radiol Open. 2021;8:100334. https://doi.org/10.1016/j.ejro.2021.100334
21.          Martinez-Garcia MA, Aksamit TR, Aliberti S. Bronchiectasis as a Long-Term Consequence of SARS-COVID-19 Pneumonia: Future Studies are Needed. Arch Bronconeumol. 2021;57(12):739-740. https://doi.org/10.1016/j.arbres.2021.04.021
22.          Ding X, Xu J, Zhou J, Long Q. Chest CT findings of COVID-19 pneumonia by duration of symptoms. Eur J Radiol. 2020;127:109009. https://doi.org/10.1016/j.ejrad.2020.109009