Thank you for a well-reasoned explanation on the effect of yoga on
asthma.
The study quoted [1] which justifies the Buteyko technique was flawed
by:
* unequal groups in that the Buteyko group initially required 1½ times the
steroids of the control group
* the Buteyko group receiving seven times the follow-up phone calls as the
control group, plus extra breathin...
Thank you for a well-reasoned explanation on the effect of yoga on
asthma.
The study quoted [1] which justifies the Buteyko technique was flawed
by:
* unequal groups in that the Buteyko group initially required 1½ times the
steroids of the control group
* the Buteyko group receiving seven times the follow-up phone calls as the
control group, plus extra breathing classes.
Also, no significant difference was found in quality of life scores at the
end of the trial.
However, there is anecdotal evidence of excellent results in some
patients, representing the overlap of hyperventilation syndrome and asthma.[2] If patients with asthma are given the simple Nijmegen questionnaire [3] to identify coexisting hyperventilation syndrome, a chartered
physiotherapist can usually treat them successfully.[4]
References
(1) Bowler SD, Green A, Mitchell CA (1998) Buteyko breathing
techniques in asthma: a randomised controlled trial. Med.J.Aust, 169, 575-8.
(2) Demeter SL (1986) Hyperventilation syndrome and asthma. Am J Med 1986;81:989-94.
(3) Hough A. Physiotherapy in Respiratory Care, 3rd edition. (www.nelsonthornes.com), 2001.
“A good surgeon knows how to operate.
A better surgeon knows when to operate.
The best surgeon knows when not to operate.”
Clinical Surgery in General 3rd Edition
Royal College of Surgeons of England Course Manual
We found the article "Effect of comorbidity on the treatment and
prognosis of elderly patients with non-small cell lung cancer" by Janssen-
Heijnen et al [1] very interesti...
“A good surgeon knows how to operate.
A better surgeon knows when to operate.
The best surgeon knows when not to operate.”
Clinical Surgery in General 3rd Edition
Royal College of Surgeons of England Course Manual
We found the article "Effect of comorbidity on the treatment and
prognosis of elderly patients with non-small cell lung cancer" by Janssen-
Heijnen et al [1] very interesting, as it highlights the increasing clinical
problems health care professionals face within the changing demographics
of an ageing population. The concluding question of “whether the less
aggressive treatment of elderly patients with NSCLC is justified,” is most
thought provoking.
Traditionally, surgeons are keen to perform surgery even on high risk
patients because they have undergone lengthy surgical training, and are
usually itching to put their skills into practice. Furthermore, surgery
may be the only treatment available that offers a realistic chance of cure
for the disease. The decision not to operate on an individual is often
more difficult and painful, as well as requires more experienced clinical
judgement. However, more recently, a whole host of factors including
advances in non-surgical therapies, pressure from clinical performance
auditing and medicolegal litigations may have made decisions not to
operate on elderly patients much easier. Perhaps now the pendulum has
swung too much the other way.
The elderly population of Hong Kong (traditionally defined as 65
years and above) is on the rise from 2.8% in 1961 to 11.1% in 2001, and
such changes are by no means restricted to South East Asia. These patients
have less functional reserve, more associated chronic diseases, and are
more sensitive to anaesthetic agents and medications. There is little
margin, if any for error. In order not to exclude this population from
potential curative surgery, we must become better educated in basic
geriatric principles of care, surgical techniques must be refined, and
perioperative care meticulous. It is the elderly patient group that
minimal access surgery in the form of video-assisted thoracic surgery
(VATS) may confer its greatest benefits. VATS major lung resection is
associated with less access trauma [2] and immunosuppression, [3] better
preserved shoulder function [4] and less post-operative pain [5] as well as
parenteral narcotic requirement [6] compared with open thoracotomy.
Furthermore, post-operative pulmonary function is better preserved
following VATS lung resection. [5] The lowest limits in lung function
parameters that would still be considered acceptable for VATS lobectomy
have not been scientifically studied. [7] Nevertheless, surgeon’s judgement,
experience and technique; the contribution of the excised lobe to overall
lung function; as well as the exact location of the pathology (for
example, upper lobe lesions in patients with bullous emphysema and middle
lobe pathology are favourable candidates for resection) are important
considerations. We have performed lobectomy on a few patients whose FEV1
was less than 1 litre or less than 40% predicted with excellent outcome.[5]
Patients who are not candidates for an anatomical resection could still be
considered for VATS wedge resection.[8] Through these advantages, VATS
allows recruitment of older and sicker patients with multiple
comorbidities who would otherwise not be suitable candidates for lung
resection through a conventional thoracotomy approach.[9,10] A large scale
randomized clinical trial is currently being conducted to confirm this.
Charles Darwin said in the Evolution of the Species, “it is not the
strongest of the species that survives, nor the most intelligent, it is
the one most adaptable to change.” It is our responsibility to improve and
change the way we operate to suit the current times. We must not allow
ourselves to become “extinct” as surgeons, or physicians, in the
management of our patients. More importantly, our elderly patients deserve
the best; advanced age alone in this day and age, should not be a reason
to deny them of a potentially curative operation.
Yours sincerely,
Dr. Calvin S.H. Ng BSc(Hons) MBBS(Hons)(Lond) MRCS(Edin)
Dr. Song Wan MD PhD FRCS(Eng)
Professor Ahmed A. Arifi MD FRCS(CTh)(Edin)
Professor Anthony P.C. Yim MA(cantab) DM(oxon) FRCS(Eng,Glas,Edin) FACS
FCCP
References
(1) Janssen-Heijnen MLG, Smulders S, Lemmens VEPP, Smeenk FWJM, van
Geffen HJAA, Coebergh JWW. Effect of comorbidity on the treatment and
prognosis of elderly patients with non-small cell lung cancer. Thorax
2004;59:602-607
(3) Leaver HA, Craig SR, Yap PL, Walker WS. Lymphocyte responses following
open and minimally invasive thoracic surgery. Eur J Clin Invest
2000;30:230-238
(4) Li WWL, Lee RLM, Lee TW, Ng CSH, Sihoe ADL, Wan IYP, Arifi AA, Yim
APC. The impact of thoracic surgical access on early shoulder function:
video-assisted thoracic surgery versus posterolateral thoracotomy. Eur J
Cardiothorac Surg 2003;23:390-6
(5) Yim APC. VATS major pulmonary resection revisited – controversies,
techniques, and results. Ann Thorac Surg 2002;74:615-23
(6) Yim APC, Wan S, Lee TW, Arifi AA. VATS lobectomy reduces cytokine
responses compared with conventional surgery. Ann Thorac Surg 2000;70:243-
7
(8) Ginsberg RT, Rubinstein LV. Lung Cancer Study Group randomized trial
of lobectomy versus limited resection for T1N0 non-small cell lung cancer.
Ann Thorac Surg 1995;60:615-23
(9) Yim APC. Thoracoscopic surgery in the elderly population. Surg Endosc
1996;10:880-82
(10) Demmy TL, Curtis JJ. Minimally invasive lobectomy directed toward
frail and high-risk patients: a case control study. Ann Thorac Surg
1999;68:194-200
Controversy exists as to the role of modern histamine H1-receptor
antagonists in the treatment of atopic asthma.
Forty-nine patients with atopic asthma were evaluated from three
randomised double-blind placebo-controlled cross-over studies assessing
the anti-inflammatory effects of desloratadine, fexofenadine, and
levocetirizine at clinically recommended doses.
Controversy exists as to the role of modern histamine H1-receptor
antagonists in the treatment of atopic asthma.
Forty-nine patients with atopic asthma were evaluated from three
randomised double-blind placebo-controlled cross-over studies assessing
the anti-inflammatory effects of desloratadine, fexofenadine, and
levocetirizine at clinically recommended doses.
Desloratadine, fexofenadine, and levocetirizine significantly
improved (p <0.05) the provocative concentration of adenosine
monophosphate producing a 20% fall in forced expiratory volume in one
second by 142% compared to placebo. There was a significant improvement (p
<0.05) of 15% in forced expiratory flow at 25% to 75% of maximal lung
volume compared to placebo with desloratadine, fexofenadine, and
levocetirizine. Fexofenadine significantly improved (p <0.05) exhaled
nitric oxide, domiciliary peak expiratory flow, and albuterol rescue use
by 27%, 4%, and 83% respectively compared to placebo. There were no
significant differences in all outcomes among the modern histamine H1-
receptor antagonists.
Modern histamine H1-receptor antagonists improve airway
hyperresponsiveness, small-airways caliber, surrogate inflammatory
markers, and asthma diary outcomes in patients with atopic asthma. Further
studies are required to evaluate the effects of modern histamine H1-
receptor antagonists on asthma exacerbations.
We read with interest McGroder et al’s study on the radiographic findings of patients four months after severe COVID-19 and the associated risk factors. Hürsoy and colleagues’ comment (1) on the paper was equally thought-provoking. We would like to further this discussion by contributing some of our observations from the pulmonology clinic at a major academic medical center in South East Asia.
It has been tremendously challenging globally to achieve precision in the diagnosis of Interstitial Lung Disease (ILD) post-COVID as invasive testing such as lung biopsies are performed sparingly. Histopathological pulmonary findings have largely remained inaccessible since COVID survivors are hypoxic so biopsies pose a high risk for the patient, and healthcare personnels are reluctant to perform such high-risk procedures. Hence, we are left to derive our diagnosis from radiological data and pulmonary function tests (PFTs) of the patient.
We propose that a consensus definition be reached for the diagnosis of post-COVID ILD, one that incorporates well-accepted radiological terms (used to represent any interstitial lung disease). We recommend that lung fibrosis only be classified as ILD if the lung parenchymal abnormalities persist for a minimum of six months after the COVID infection has resolved. Post-COVID ILD should then be further subclassified based on distinct radiological patterns. In our retrospective cohort study, four patterns of post-COV...
We read with interest McGroder et al’s study on the radiographic findings of patients four months after severe COVID-19 and the associated risk factors. Hürsoy and colleagues’ comment (1) on the paper was equally thought-provoking. We would like to further this discussion by contributing some of our observations from the pulmonology clinic at a major academic medical center in South East Asia.
It has been tremendously challenging globally to achieve precision in the diagnosis of Interstitial Lung Disease (ILD) post-COVID as invasive testing such as lung biopsies are performed sparingly. Histopathological pulmonary findings have largely remained inaccessible since COVID survivors are hypoxic so biopsies pose a high risk for the patient, and healthcare personnels are reluctant to perform such high-risk procedures. Hence, we are left to derive our diagnosis from radiological data and pulmonary function tests (PFTs) of the patient.
We propose that a consensus definition be reached for the diagnosis of post-COVID ILD, one that incorporates well-accepted radiological terms (used to represent any interstitial lung disease). We recommend that lung fibrosis only be classified as ILD if the lung parenchymal abnormalities persist for a minimum of six months after the COVID infection has resolved. Post-COVID ILD should then be further subclassified based on distinct radiological patterns. In our retrospective cohort study, four patterns of post-COVID lung parenchymal changes were exhibited by patients with no preexisting lung disease: persistent ground-glass opacities; interlobular septal thickening; reticulation and honeycombing; interlobular septal thickening and reticulations; and patchy consolidation with or without ground-glass opacity (2).
In terms of outcome, within our cohort of severe to critically ill patients, most developed persistent ground-glass opacities or patchy consolidation (with or without ground-glass opacity); a majority of these participants significantly improved (clinically and radiologically) upon administration of corticosteroids (2). Radiological improvement was defined as clearance of at least 50% of lung infiltrates. Reiterating our findings, Han et al. reported ground-glass opacities as the predominant pattern observed in follow-up CT scans of patients with fibrotic-like changes within six months of disease onset (3). Three of the five patients in our study who died had progressive disease with reticulation and honeycombing. To achieve greater accuracy in disease severity assessment and risk stratification, we suggest employing PFTs, particularly to obtain diffusion capacity of the lungs for carbon monoxide (DLCO) and forced vital capacity (FVC) measurements. For the eight out of thirty patients in our cohort who had significant HRCT findings, PFTs were ordered to assess physiological function; three presented with low FVCs (2). In Han et al’s study, abnormal DLCO (less than 80%) at 6-month follow up was a common occurrence in those with fibrotic-like changes (3).
Similar to McGroder et al’s findings, we concluded that the male gender was a significant predisposing factor for post-COVID pulmonary fibrosis. Moreover, like Li et al. and Han et al., we found diabetes mellitus and hypertension to be prevalent comorbidities in patients who developed fibrotic changes (2-4). Interestingly, in our cohort, disease severity did not significantly influence the development of any particular pattern of lung parenchymal abnormality. In light of these observations, we can conclude that the reported lung microstructure changes are not only a ramification of post-ARDS fibrosis or ventilator-induced lung damage but also a consequence of direct virus attack and aberrant local immune response. This is further evidenced by the finding that the Coronavirus induced fibrosis even in moderately ill patients who did not require invasive mechanical ventilation or ICU stay (2).
We hope that prospective studies will further enrich and broaden the global dialogue on post-COVID lung fibrosis.
References:
1. Hürsoy et al. 2021. e-letter https://thorax.bmj.com/eletters
2. Zubairi ABS, Shaikh A, Zubair SM, Ali AS, Awan S, Irfan M. Persistence of post-COVID lung parenchymal abnormalities during the three-month follow-up. Adv Respir Med. 2021;89(5):477–83. Available from: https://pubmed.ncbi.nlm.nih.gov/34612504/
3. Han X, Fan Y, Alwalid O, Li N, Jia X, Yuan M, et al. Six-month Follow-up Chest CT Findings after Severe COVID-19 Pneumonia. Radiology. 2021;299(1):E177-E186.
4. Li Y, Wu J, Wang S, Li X, Zhou J, Huang B, et al. Progression to fibrosing diffuse alveolar damage in a series of 30 minimally invasive autopsies with COVID-19 pneumonia in Wuhan, China. Histopathology. 2021;78(4):542-55.
We thank A. Raja and colleagues for their interest in our article on risk factors for fibrotic-like changes after severe COVID-19 infection (1). We agree that identification and management of post-COVID fibrosis continues to be impeded by the lack of consensus definitions and we look forward to further studies that help describe the natural history of post-COVID pulmonary manifestations.
The authors propose that lung fibrosis be classified into different ILDs by the pattern of lung parenchymal abnormalities six months after the initial COVID illness has resolved. We agree with the authors that persistent radiographic abnormalities are an adverse outcome of COVID that deserve future study, but we disagree with their proposed classification of patterns. We believe that recognition of fibrotic interstitial lung abnormalities (ILAs), as opposed to non-fibrotic ILAs, help prognosticate which abnormalities are less likely to resolve over time (2). Han et al (3) recently demonstrated that individuals with post-COVID fibrotic ILAs at six months had persistent fibrosis at 1-year, suggesting that fibrotic ILAs rarely resolve completely. Ultimately, serial imaging, quantitative measures of fibrosis (4), and assessment of pharmaceutical interventions (5), will be key to fully understanding the trajectory of post-COVID fibrosis.
Secondly, the authors report that disease severity did not significantly impact the development of particular parenchymal abnormalities on CT...
We thank A. Raja and colleagues for their interest in our article on risk factors for fibrotic-like changes after severe COVID-19 infection (1). We agree that identification and management of post-COVID fibrosis continues to be impeded by the lack of consensus definitions and we look forward to further studies that help describe the natural history of post-COVID pulmonary manifestations.
The authors propose that lung fibrosis be classified into different ILDs by the pattern of lung parenchymal abnormalities six months after the initial COVID illness has resolved. We agree with the authors that persistent radiographic abnormalities are an adverse outcome of COVID that deserve future study, but we disagree with their proposed classification of patterns. We believe that recognition of fibrotic interstitial lung abnormalities (ILAs), as opposed to non-fibrotic ILAs, help prognosticate which abnormalities are less likely to resolve over time (2). Han et al (3) recently demonstrated that individuals with post-COVID fibrotic ILAs at six months had persistent fibrosis at 1-year, suggesting that fibrotic ILAs rarely resolve completely. Ultimately, serial imaging, quantitative measures of fibrosis (4), and assessment of pharmaceutical interventions (5), will be key to fully understanding the trajectory of post-COVID fibrosis.
Secondly, the authors report that disease severity did not significantly impact the development of particular parenchymal abnormalities on CT scan. The authors do not provide analyses in their study to support this statement. Their cohort was sampled from survivors with a persistent need for oxygen therapy, was not sampled randomly from the larger acute COVID population, and only included two subjects who required invasive mechanical ventilation. While we agree that an interplay of many factors contribute to pattern and extent of parenchymal lung disease, we believe that greater severity of illness, as determined by need for invasive mechanical ventilation, should be recognized as a risk factor for persistent fibrotic abnormalities. This conclusion is supported by our study as well as others (1, 6, 7).
Claire McGroder, MD
Mary Salvatore, MD
Eric A. Hoffman, PhD
Matthew Baldwin, MD
Christine Kim Garcia, MD, PhD
REFERENCES
1. McGroder CF, Zhang D, Choudhury MA, Salvatore MM, D'Souza BM, Hoffman EA, Wei Y, Baldwin MR, Garcia CK. Pulmonary fibrosis 4 months after COVID-19 is associated with severity of illness and blood leucocyte telomere length. Thorax 2021.
2. Putman RK, Gudmundsson G, Axelsson GT, Hida T, Honda O, Araki T, Yanagawa M, Nishino M, Miller ER, Eiriksdottir G, Gudmundsson EF, Tomiyama N, Honda H, Rosas IO, Washko GR, Cho MH, Schwartz DA, Gudnason V, Hatabu H, Hunninghake GM. Imaging Patterns Are Associated with Interstitial Lung Abnormality Progression and Mortality. Am J Respir Crit Care Med 2019; 200: 175-183.
3. Han X, Fan Y, Alwalid O, Zhang X, Jia X, Zheng Y, Shi H. Fibrotic Interstitial Lung Abnormalities at 1-year Follow-up CT after Severe COVID-19. Radiology 2021; 301: E438-E440.
4. Nagpal P, Motahari A, Gerard SE, Guo J, Reinhardt JM, Comellas AP, Hoffman EA, Kaczka DW. Case Studies in Physiology: Temporal Variations of the Lung Parenchyma and Vasculature in Asymptomatic COVID-19 Pneumonia: A Multi-Spectral CT Assessment. J Appl Physiol (1985) 2021.
5. Myall KJ, Mukherjee B, Castanheira AM, Lam JL, Benedetti G, Mak SM, Preston R, Thillai M, Dewar A, Molyneaux PL, West AG. Persistent Post-COVID-19 Inflammatory Interstitial Lung Disease: An Observational Study of Corticosteroid Treatment. Ann Am Thorac Soc 2021.
6. Francone M, Iafrate F, Masci GM, Coco S, Cilia F, Manganaro L, Panebianco V, Andreoli C, Colaiacomo MC, Zingaropoli MA, Ciardi MR, Mastroianni CM, Pugliese F, Alessandri F, Turriziani O, Ricci P, Catalano C. Chest CT score in COVID-19 patients: correlation with disease severity and short-term prognosis. Eur Radiol 2020; 30: 6808-6817.
7. Han X, Fan Y, Alwalid O, Li N, Jia X, Yuan M, Li Y, Cao Y, Gu J, Wu H, Shi H. Six-month Follow-up Chest CT Findings after Severe COVID-19 Pneumonia. Radiology 2021; 299: E177-E186.
We thank N. Hürsoy and colleagues for their interest in our study of patients four months after severe COVID-19 [1]. We agree that there needs to be continued development of terms describing the radiographic appearance of post-COVID fibrotic-like patterns. We acknowledge that without the benefit of histopathology or serial imaging, our ability to define pulmonary fibrosis is limited.
The authors posit that parenchymal bands, irregular densities, and ground glass opacities, may be considered fibrotic-like patterns. We have included irregular densities, characterized as reticulations or traction bronchiectasis, as fibrotic-like changes. We did not include parenchymal bands [2], as these can be associated with atelectasis, which is common in COVID and can disappear over time [3]. Similarly, we did not include isolated ground glass opacities as fibrotic-like changes, as these have been found to decrease over time in CT lung cancer screening cohorts [4] and in other post COVID-19 cohorts [5, 6].
A priori, we evaluated for both previously established interstitial lung abnormality categories [7], as well as categories of radiographic abnormalities reported in Acute Respiratory Distress Syndrome (ARDS) survivors using an established scoring system [8]. This inclusive approach should facilitate meta-analyses and comparisons with future studies of COVID-19 survivors, interstitial lung disease studies, and studies of non-COVID ARDS survivors. Fu...
We thank N. Hürsoy and colleagues for their interest in our study of patients four months after severe COVID-19 [1]. We agree that there needs to be continued development of terms describing the radiographic appearance of post-COVID fibrotic-like patterns. We acknowledge that without the benefit of histopathology or serial imaging, our ability to define pulmonary fibrosis is limited.
The authors posit that parenchymal bands, irregular densities, and ground glass opacities, may be considered fibrotic-like patterns. We have included irregular densities, characterized as reticulations or traction bronchiectasis, as fibrotic-like changes. We did not include parenchymal bands [2], as these can be associated with atelectasis, which is common in COVID and can disappear over time [3]. Similarly, we did not include isolated ground glass opacities as fibrotic-like changes, as these have been found to decrease over time in CT lung cancer screening cohorts [4] and in other post COVID-19 cohorts [5, 6].
A priori, we evaluated for both previously established interstitial lung abnormality categories [7], as well as categories of radiographic abnormalities reported in Acute Respiratory Distress Syndrome (ARDS) survivors using an established scoring system [8]. This inclusive approach should facilitate meta-analyses and comparisons with future studies of COVID-19 survivors, interstitial lung disease studies, and studies of non-COVID ARDS survivors. Furthermore, it allows for future post-hoc analyses if alternate definitions of fibrotic-like patterns in COVID-19 survivors are established. Additionally, we showed that objective quantitative analyses closely agreed with visual assessments (Figure S2). These types of quantitative imaging analyses may facilitate the convergence of data from multiple centers if imaging protocols become more standardized [9].
Efforts are underway to characterize pulmonary impairments and radiographic abnormalities in our cohort over time in order to assess longitudinal evolution. We acknowledge that our findings do not exclude the possibility of pre-existing lung disease and we therefore look forward to reviewing independent studies, such as the Collaborative Cohort of Cohorts for COVID-19 Research (C4R) [10] project, which will provide better understanding of radiographic changes by comparing chest imaging studies before and after SARS-CoV-2 infection.
1. McGroder, C.F., et al., Pulmonary fibrosis 4 months after COVID-19 is associated with severity of illness and blood leucocyte telomere length. Thorax, 2021.
2. Pulmonary Parenchymal Band. Available from: https://www.ncbi.nlm.nih.gov/medgen/978776.
3. Kong, M., et al., Evolution of chest CT manifestations of COVID-19: a longitudinal study. J Thorac Dis, 2020. 12(9): p. 4892-4907.
4. Jin, G.Y., et al., Interstitial lung abnormalities in a CT lung cancer screening population: prevalence and progression rate. Radiology, 2013. 268(2): p. 563-71.
5. Nagpal, P., et al., Case Studies in Physiology: Temporal Variations of the Lung Parenchyma and Vasculature in Asymptomatic COVID-19 Pneumonia: A Multi-Spectral CT Assessment. J Appl Physiol (1985), 2021.
6. Liu, D., et al., The pulmonary sequalae in discharged patients with COVID-19: a short-term observational study. Respir Res, 2020. 21(1): p. 125.
7. Hatabu, H., et al., Interstitial lung abnormalities detected incidentally on CT: a Position Paper from the Fleischner Society. Lancet Respir Med, 2020. 8(7): p. 726-737.
8. Burnham, E.L., et al., Chest CT features are associated with poorer quality of life in acute lung injury survivors. Crit Care Med, 2013. 41(2): p. 445-56.
9. Nagpal, P., et al., Quantitative CT imaging and advanced visualization methods: potential application in novel coronavirus disease 2019 (COVID-19) pneumonia. BJR Open, 2021. 3(1): p. 20200043.
10. Collaborative Cohort of Cohorts for COVID-19 Research. Available from: https://c4r-nih.org/content/overview.
We have read with great interest the article investigating the relationship between computed tomography (CT) findings of the patients with fibrotic-like patterns and telomere length after four months of acute COVID-19 infection. According to the literature and our experience, post-COVID interstitial lung disease is a potential public health problem. Thus, we aimed to share our concerns about the fibrotic-like patterns in this group of patients.
Post-COVID fibrosis is not as the same as the other interstitial lung diseases. In the article, the authors describe CT findings of fibrotic-like patterns as limited to reticulation, honeycomb cysts, and traction bronchiectasis. However, post-COVID fibrosis CT findings were shown to be more varied and may include parenchymal bands, irregular densities, and ground-glass areas (1–3). As we move towards the future, all of us need to create a common language, a lingua franca in the definition of post-COVID fibrosis. To achieve this, we need brainstorming and close cooperation.
It will also be helpful to elaborate the characteristics of the non-fibrotic pattern in the table. The clinical importance of the ground glass areas, which persist four months after active infection but not defined as fibrotic, is unknown. We consider that these patterns cannot be separated from fibrotic-like patterns precisely. Additionally, we can also classify parenchymal bands as fibrosis-like appearance. In our experience...
We have read with great interest the article investigating the relationship between computed tomography (CT) findings of the patients with fibrotic-like patterns and telomere length after four months of acute COVID-19 infection. According to the literature and our experience, post-COVID interstitial lung disease is a potential public health problem. Thus, we aimed to share our concerns about the fibrotic-like patterns in this group of patients.
Post-COVID fibrosis is not as the same as the other interstitial lung diseases. In the article, the authors describe CT findings of fibrotic-like patterns as limited to reticulation, honeycomb cysts, and traction bronchiectasis. However, post-COVID fibrosis CT findings were shown to be more varied and may include parenchymal bands, irregular densities, and ground-glass areas (1–3). As we move towards the future, all of us need to create a common language, a lingua franca in the definition of post-COVID fibrosis. To achieve this, we need brainstorming and close cooperation.
It will also be helpful to elaborate the characteristics of the non-fibrotic pattern in the table. The clinical importance of the ground glass areas, which persist four months after active infection but not defined as fibrotic, is unknown. We consider that these patterns cannot be separated from fibrotic-like patterns precisely. Additionally, we can also classify parenchymal bands as fibrosis-like appearance. In our experience, subpleural parenchymal bands are not uncommon. Furthermore, respiratory symptoms may persist in patients with parenchymal bands. So, this pattern should be considered as a part of fibrotic-like pattern.
Another challenge is the lack of proof regarding fibrosis development due to COVID-19 infection. For example, honeycomb cysts are an indicator of irreversible fibrosis, and it is uncertain whether they are present in the previous CT images or not. A similar condition may apply to irregular reticulation and traction bronchiectasis. The development of fibrotic patterns may also differ from the images during the active infection (4). It may be instructive to examine the process by which signs of active involvement evolve into fibrosis, as well as the development of a fibrotic-like pattern.
We need a more precise interpretation of the development of fibrotic-like patterns. Therefore, we suggest analysing subtypes of post-COVID fibrosis, compare present findings on CT with long-term follow-up images. Also, it might be beneficial to show, if possible, that there is no fibrotic pattern in the CTs before acute Covid 19 infection.
References
1. Huang W, Wu Q, Chen Z, Xiong Z, Wang K, Tian J, et al. The potential indicators for pulmonary fibrosis in survivors of severe COVID-19. Vol. 82, Journal of Infection. 2021.
2. Myall KJ, Mukherjee B, Castanheira AM, Lam JL, Benedetti G, Mak SM, et al. Persistent Post-COVID-19 Interstitial Lung Disease. An Observational Study of Corticosteroid Treatment. Ann Am Thorac Soc. 2021;18(5).
3. Shah AS, Wong AW, Hague CJ, Murphy DT, Johnston JC, Ryerson CJ, et al. A prospective study of 12-week respiratory outcomes in COVID-19-related hospitalisations. Vol. 76, Thorax. 2021.
4. Guan CS, Wei LG, Xie RM, Lv Z Bin, Yan S, Zhang ZX, et al. CT findings of COVID-19 in follow-up: Comparison between progression and recovery. Diagnostic Interv Radiol. 2020;26(4):301–7.
We thank Dr Abdulqawi for interest in our work (1). He comments that the referral, uptake and completion rates for pulmonary rehabilitation in the current study were lower than in a previous study by Jones and colleagues (2). We would caution against retrospective comparison with unmatched historical controls due to confounding factors such as differences in patient characteristics and practice pathways that may contribute to inaccurate point estimates.
We hypothesised that the COPD discharge bundle would impact on referral rates. Strengths of the current work include the prospective real-world nature of the study, with the research team having no involvement in treatment allocation. The clinical team delivering the bundle were blinded to the study objectives, thus minimising any Hawthorne effect.
Dr Abdulqawi raises the point that pulmonary rehabilitation completion rates were low in the current study (albeit based on a low denominator). The reasons for non-completion of PR are often complex and multi-factorial (3) and may not be directly related to referral source. However, what is clear is that without a referral for pulmonary rehabilitation, uptake and completion rates are zero.
1. Barker RE BL, Maddocks M, Nolan CM, Patel S, Walsh JA, Polgar O, Wenneberg J, Kon SSC, Wedzicha JA, Man WDC, Farquhar M. Integrating Home-Based Exercise Training with a Hospital at Home Service for Patients Hospitalised with Acute Exacerbations of COPD: Developing the M...
We thank Dr Abdulqawi for interest in our work (1). He comments that the referral, uptake and completion rates for pulmonary rehabilitation in the current study were lower than in a previous study by Jones and colleagues (2). We would caution against retrospective comparison with unmatched historical controls due to confounding factors such as differences in patient characteristics and practice pathways that may contribute to inaccurate point estimates.
We hypothesised that the COPD discharge bundle would impact on referral rates. Strengths of the current work include the prospective real-world nature of the study, with the research team having no involvement in treatment allocation. The clinical team delivering the bundle were blinded to the study objectives, thus minimising any Hawthorne effect.
Dr Abdulqawi raises the point that pulmonary rehabilitation completion rates were low in the current study (albeit based on a low denominator). The reasons for non-completion of PR are often complex and multi-factorial (3) and may not be directly related to referral source. However, what is clear is that without a referral for pulmonary rehabilitation, uptake and completion rates are zero.
1. Barker RE BL, Maddocks M, Nolan CM, Patel S, Walsh JA, Polgar O, Wenneberg J, Kon SSC, Wedzicha JA, Man WDC, Farquhar M. Integrating Home-Based Exercise Training with a Hospital at Home Service for Patients Hospitalised with Acute Exacerbations of COPD: Developing the Model Using Accelerated Experience-Based Co-Design. Int J Chron Obstruct Pulmon Dis. 2021;16:1035-49.
2. Jones SE, Green SA, Clark AL, Dickson MJ, Nolan AM, Moloney C, et al. Pulmonary rehabilitation following hospitalisation for acute exacerbation of COPD: Referrals, uptake and adherence. Thorax. 2014;69(2):181-2.
3. Jones SE, Barker RE, Nolan CM, Patel S, Maddocks M, Man WD. Pulmonary rehabilitation in patients with an acute exacerbation of chronic obstructive pulmonary disease. J Thorac Dis. 2018;1(1):S1390-S9.
We have read the paper by Barker et al. (1) with interest. We congratulate the authors for conducting and publishing their prospective cohort study evaluating the effect of COPD discharge bundle on pulmonary rehabilitation (PR) referral and uptake following hospitalisation for acute exacerbation of COPD (AECOPD).
The authors have shown that the COPD discharge bundle had a positive effect on PR referral compared with a no bundle (17.5% (40 of 228) referral rate vs 0%(0 of 63)). This figure is lower than the expected 30% referral rate to PR following AECOPD (2). However, the paper offers no potential reasons for the lower referral rate.
The study had two bundle groups:
• COPD discharge bundle delivered by a current PR practitioner
• COPD discharge bundle delivered by a practitioner with no involvement in PR
Compared to delivery by a practitioner with no PR involvement, completion of the bundle delivery by a current PR practitioner resulted in higher referral and pick-up rates (60% vs 12% and 40% vs 32%, respectively). These results support the concept of integrating PR and hospital services.
Unfortunately, the completion rate (number of subjects who completed PR divided by the number of referrals) was disappointingly low. Also, there was no difference between the two bundle groups (13% (2 of 15) vs 12% (3 of 25)), as stated in the supplementary data.
It seems that patients' willingness or ability to complete PR is not af...
We have read the paper by Barker et al. (1) with interest. We congratulate the authors for conducting and publishing their prospective cohort study evaluating the effect of COPD discharge bundle on pulmonary rehabilitation (PR) referral and uptake following hospitalisation for acute exacerbation of COPD (AECOPD).
The authors have shown that the COPD discharge bundle had a positive effect on PR referral compared with a no bundle (17.5% (40 of 228) referral rate vs 0%(0 of 63)). This figure is lower than the expected 30% referral rate to PR following AECOPD (2). However, the paper offers no potential reasons for the lower referral rate.
The study had two bundle groups:
• COPD discharge bundle delivered by a current PR practitioner
• COPD discharge bundle delivered by a practitioner with no involvement in PR
Compared to delivery by a practitioner with no PR involvement, completion of the bundle delivery by a current PR practitioner resulted in higher referral and pick-up rates (60% vs 12% and 40% vs 32%, respectively). These results support the concept of integrating PR and hospital services.
Unfortunately, the completion rate (number of subjects who completed PR divided by the number of referrals) was disappointingly low. Also, there was no difference between the two bundle groups (13% (2 of 15) vs 12% (3 of 25)), as stated in the supplementary data.
It seems that patients' willingness or ability to complete PR is not affected by the referral source, i.e. whether the referral was received by a practitioner involved in PR or not. A previous publication has demonstrated a 47% completion rate for PR referrals following AECOPD, with a 72% completion rate for those who started the programme (2).
We are curious whether the authors have explored the potential reasons for the lower completion rate in their study. Causes could include dissatisfaction with the provided programme, a patient’s anxiety, and lack of perceived benefit from PR participation.
References
1. Barker RE, Kon SS, Clarke SF, et alCOPD discharge bundle and pulmonary rehabilitation referral and uptake following hospitalisation for acute exacerbation of COPDThorax Published Online First: 02 March 2021. doi: 10.1136/thoraxjnl-2020-215464
2. Jones SE, Green SA, Clark AL, et alPulmonary rehabilitation following hospitalisation for acute exacerbation of COPD: referrals, uptake and adherenceThorax 2014;69:181-182.
The paper by Hopkinson et al (1) provides unique and important data on smoking prevalence and COVID-19 symptoms, but their conclusion does not reflect the data well. The authors conclude “these data are consistent with people who smoke being at an increased risk of developing symptomatic COVID-19”. The study includes over 150,000 people with self-reported COVID-19 symptoms and over two million without such symptoms. It also includes data on over 25,000 people who were tested for SARS-CoV-2 and their test results. Based on our analysis of these more relevant data, we interpret the study differently. Our conclusion would be “these data are consistent with smokers having an increased risk of symptoms such as cough and breathlessness, but a decreased risk of having SARS-CoV-2 infection”.
The difficulty in interpreting these results is that both symptoms and testing are likely colliders in a causal model of smoking and COVID-19. The data reported on SARS-CoV-2 test results make it possible to compare smoking prevalence by age-group and sex in three groups: those who tested positive for SARS-CoV-2 (n=7,123); those who tested negative (n=16,765); and untested asymptomatic users (n=2,221,088, called “standard users” by the authors). Overall smoking prevalence was less in those tested (8.9%) than in all users of the app (11.0%). This might be thought of as a surprising finding – smoking-related symptoms should lead to testing – but can probably be explained by most asymptom...
The paper by Hopkinson et al (1) provides unique and important data on smoking prevalence and COVID-19 symptoms, but their conclusion does not reflect the data well. The authors conclude “these data are consistent with people who smoke being at an increased risk of developing symptomatic COVID-19”. The study includes over 150,000 people with self-reported COVID-19 symptoms and over two million without such symptoms. It also includes data on over 25,000 people who were tested for SARS-CoV-2 and their test results. Based on our analysis of these more relevant data, we interpret the study differently. Our conclusion would be “these data are consistent with smokers having an increased risk of symptoms such as cough and breathlessness, but a decreased risk of having SARS-CoV-2 infection”.
The difficulty in interpreting these results is that both symptoms and testing are likely colliders in a causal model of smoking and COVID-19. The data reported on SARS-CoV-2 test results make it possible to compare smoking prevalence by age-group and sex in three groups: those who tested positive for SARS-CoV-2 (n=7,123); those who tested negative (n=16,765); and untested asymptomatic users (n=2,221,088, called “standard users” by the authors). Overall smoking prevalence was less in those tested (8.9%) than in all users of the app (11.0%). This might be thought of as a surprising finding – smoking-related symptoms should lead to testing – but can probably be explained by most asymptomatic testing being in healthcare workers among whom smoking is less common. Importantly, smoking prevalence was appreciably lower in those who tested positive for SARS-CoV-2 (7.4%) than in both those who tested negative (9.3%) and in untested users (10.8%). The lower prevalence of smokers in app-users who tested positive was observed in all but one age-sex strata. In Table 1 https://shorturl.at/ovDL1 we reproduce the stratum-specific prevalence and provide two sets of odds ratios: one relative to participants who tested negative; and the other relative to standard users. If smoking causes similar symptoms to COVID-19 (e.g. persistent cough and shortness of breath) then using symptoms as a “test” for COVID-19 will more often lead to a false-positive in smokers than in non-smokers. This would explain the finding that the authors focus on, but it also means that one might expect lower prevalence of smoking in true-positives (i.e. those who test positive for SARS-CoV-2) than in false-positives (i.e. those who test negative). However, a different explanation is needed to explain the lower prevalence in test positive than in untested asymptomatic users. That might be because current smokers are at lower risk of SARS-CoV-2 infection, or it might be because asymptomatic smokers were less likely to be tested than asymptomatic non-smokers.
We note that the numbers of prevalent smokers in the authors’ Table 1 do not correspond to the percentages. This presumably is due to some users not completing the question regarding smoking. It is interesting to note that there were more people tested than those with either a positive or negative result. If, by subtraction, one calculates the prevalence of smoking among those tested who do not have a result, one finds that the prevalence of smoking is significantly (P<0.05) greater than amongst both those with a negative result (risk ratio 1.14) and those with a positive result (risk ratio 1.45).
These data are consistent with the unexpected observation made across a considerable number of studies that smokers have a decreased risk of COVID-19 (2). As with these previous observations, the results of this study could be an artefact of reporting and selection biases, but they certainly do not disprove the ‘protection’ hypothesis. The authors state that they have data to differentiate ex-smokers from current smokers, but unfortunately do not present them. Others have reported higher risk of COVID-19 in ex-smokers than in never smokers but also higher than in current smokers (2). As ex-smokers can be expected to lose the hypothetical protective effect of smoking but retain the health impact of their previous smoking, this makes the hypothesis more plausible. The fact that studies using similar approaches have detected a much higher risk in smokers to develop laboratory-confirmed influenza than non-smokers (3) also suggest that the finding of lower incidence of COVID-19 in smokers may not be just a methodological artefact. Several tentative hypotheses were proposed to explain the possible protective effect of smoking, including effects of nicotine on ACE receptors (4), effects on immune system of tobacco mosaic virus that typically colonizes airways of smokers (5), and thermic effects of regular inhalation of hot smoke on virus replication (2, 6).
There is no doubt that the harms of smoking hugely outweigh any benefits and that efforts to help smokers quit are important even in the time of pandemic. However, if current smoking causes a lowering of risk, then it is imperative to understand the mechanisms, because a better understanding could lead to new ways to reduce the risk of infection in the general population. Better data are urgently needed to clarify this potentially very important issue.
References:
1. Hopkinson NS, Rossi N, El-Sayed_Moustafa J, et al. Thorax Epub ahead of print. doi:10.1136/thoraxjnl-2020-216422
2. David Simons, Lion Shahab, Jamie Brown, Olga Perski. (2020). The association of smoking status with SARS-CoV-2 infection, hospitalisation and mortality from COVID-19: A living rapid evidence review with Bayesian meta-analyses (version 9). Qeios. doi:10.32388/UJR2AW.10.
3. Lawrence H, Hunter A, Murray R, Lim WS, McKeever T. Cigarette smoking and the occurrence of influenza - Systematic review. J Infect. 2019 Nov;79(5):401-406. doi: 10.1016/j.jinf.2019.08.014. Epub 2019 Aug 26. PMID: 31465780.
4. Farsalinos K, Angelopoulou A, Alexandris N, et al. COVID-19 and the nicotinic cholinergic system. Eur Respir J 2020 56: 2001589; DOI: 10.1183/13993003.01589-2020
5. de Bernardis E, Busà L. A putative role for the tobacco mosaic virus in smokers' resistance to COVID-19. Med Hypotheses. 2020;143:110153. doi:10.1016/j.mehy.2020.110153
6. Conti C, de Marco A, Mastromarino P, Tomao P, Santoro MG. Antiviral Effect of Hyperthermic Treatment in Rhinovirus Infection. Antimicrob Agents Chemother 1999; 43: 822–9.
Dear Editor
Thank you for a well-reasoned explanation on the effect of yoga on asthma.
The study quoted [1] which justifies the Buteyko technique was flawed by:
* unequal groups in that the Buteyko group initially required 1½ times the steroids of the control group
* the Buteyko group receiving seven times the follow-up phone calls as the control group, plus extra breathin...
Dear Editor
“A good surgeon knows how to operate. A better surgeon knows when to operate. The best surgeon knows when not to operate.”
Clinical Surgery in General 3rd Edition Royal College of Surgeons of England Course Manual
We found the article "Effect of comorbidity on the treatment and prognosis of elderly patients with non-small cell lung cancer" by Janssen- Heijnen et al [1] very interesti...
Dear Editor,
Controversy exists as to the role of modern histamine H1-receptor antagonists in the treatment of atopic asthma.
Forty-nine patients with atopic asthma were evaluated from three randomised double-blind placebo-controlled cross-over studies assessing the anti-inflammatory effects of desloratadine, fexofenadine, and levocetirizine at clinically recommended doses.
Desloratadine, fexo...
Dear Editor,
We read with interest McGroder et al’s study on the radiographic findings of patients four months after severe COVID-19 and the associated risk factors. Hürsoy and colleagues’ comment (1) on the paper was equally thought-provoking. We would like to further this discussion by contributing some of our observations from the pulmonology clinic at a major academic medical center in South East Asia.
It has been tremendously challenging globally to achieve precision in the diagnosis of Interstitial Lung Disease (ILD) post-COVID as invasive testing such as lung biopsies are performed sparingly. Histopathological pulmonary findings have largely remained inaccessible since COVID survivors are hypoxic so biopsies pose a high risk for the patient, and healthcare personnels are reluctant to perform such high-risk procedures. Hence, we are left to derive our diagnosis from radiological data and pulmonary function tests (PFTs) of the patient.
We propose that a consensus definition be reached for the diagnosis of post-COVID ILD, one that incorporates well-accepted radiological terms (used to represent any interstitial lung disease). We recommend that lung fibrosis only be classified as ILD if the lung parenchymal abnormalities persist for a minimum of six months after the COVID infection has resolved. Post-COVID ILD should then be further subclassified based on distinct radiological patterns. In our retrospective cohort study, four patterns of post-COV...
Show MoreWe thank A. Raja and colleagues for their interest in our article on risk factors for fibrotic-like changes after severe COVID-19 infection (1). We agree that identification and management of post-COVID fibrosis continues to be impeded by the lack of consensus definitions and we look forward to further studies that help describe the natural history of post-COVID pulmonary manifestations.
The authors propose that lung fibrosis be classified into different ILDs by the pattern of lung parenchymal abnormalities six months after the initial COVID illness has resolved. We agree with the authors that persistent radiographic abnormalities are an adverse outcome of COVID that deserve future study, but we disagree with their proposed classification of patterns. We believe that recognition of fibrotic interstitial lung abnormalities (ILAs), as opposed to non-fibrotic ILAs, help prognosticate which abnormalities are less likely to resolve over time (2). Han et al (3) recently demonstrated that individuals with post-COVID fibrotic ILAs at six months had persistent fibrosis at 1-year, suggesting that fibrotic ILAs rarely resolve completely. Ultimately, serial imaging, quantitative measures of fibrosis (4), and assessment of pharmaceutical interventions (5), will be key to fully understanding the trajectory of post-COVID fibrosis.
Secondly, the authors report that disease severity did not significantly impact the development of particular parenchymal abnormalities on CT...
Show MoreTo the editor,
We thank N. Hürsoy and colleagues for their interest in our study of patients four months after severe COVID-19 [1]. We agree that there needs to be continued development of terms describing the radiographic appearance of post-COVID fibrotic-like patterns. We acknowledge that without the benefit of histopathology or serial imaging, our ability to define pulmonary fibrosis is limited.
The authors posit that parenchymal bands, irregular densities, and ground glass opacities, may be considered fibrotic-like patterns. We have included irregular densities, characterized as reticulations or traction bronchiectasis, as fibrotic-like changes. We did not include parenchymal bands [2], as these can be associated with atelectasis, which is common in COVID and can disappear over time [3]. Similarly, we did not include isolated ground glass opacities as fibrotic-like changes, as these have been found to decrease over time in CT lung cancer screening cohorts [4] and in other post COVID-19 cohorts [5, 6].
A priori, we evaluated for both previously established interstitial lung abnormality categories [7], as well as categories of radiographic abnormalities reported in Acute Respiratory Distress Syndrome (ARDS) survivors using an established scoring system [8]. This inclusive approach should facilitate meta-analyses and comparisons with future studies of COVID-19 survivors, interstitial lung disease studies, and studies of non-COVID ARDS survivors. Fu...
Show MoreDear Editor,
We have read with great interest the article investigating the relationship between computed tomography (CT) findings of the patients with fibrotic-like patterns and telomere length after four months of acute COVID-19 infection. According to the literature and our experience, post-COVID interstitial lung disease is a potential public health problem. Thus, we aimed to share our concerns about the fibrotic-like patterns in this group of patients.
Post-COVID fibrosis is not as the same as the other interstitial lung diseases. In the article, the authors describe CT findings of fibrotic-like patterns as limited to reticulation, honeycomb cysts, and traction bronchiectasis. However, post-COVID fibrosis CT findings were shown to be more varied and may include parenchymal bands, irregular densities, and ground-glass areas (1–3). As we move towards the future, all of us need to create a common language, a lingua franca in the definition of post-COVID fibrosis. To achieve this, we need brainstorming and close cooperation.
It will also be helpful to elaborate the characteristics of the non-fibrotic pattern in the table. The clinical importance of the ground glass areas, which persist four months after active infection but not defined as fibrotic, is unknown. We consider that these patterns cannot be separated from fibrotic-like patterns precisely. Additionally, we can also classify parenchymal bands as fibrosis-like appearance. In our experience...
Show MoreWe thank Dr Abdulqawi for interest in our work (1). He comments that the referral, uptake and completion rates for pulmonary rehabilitation in the current study were lower than in a previous study by Jones and colleagues (2). We would caution against retrospective comparison with unmatched historical controls due to confounding factors such as differences in patient characteristics and practice pathways that may contribute to inaccurate point estimates.
We hypothesised that the COPD discharge bundle would impact on referral rates. Strengths of the current work include the prospective real-world nature of the study, with the research team having no involvement in treatment allocation. The clinical team delivering the bundle were blinded to the study objectives, thus minimising any Hawthorne effect.
Dr Abdulqawi raises the point that pulmonary rehabilitation completion rates were low in the current study (albeit based on a low denominator). The reasons for non-completion of PR are often complex and multi-factorial (3) and may not be directly related to referral source. However, what is clear is that without a referral for pulmonary rehabilitation, uptake and completion rates are zero.
1. Barker RE BL, Maddocks M, Nolan CM, Patel S, Walsh JA, Polgar O, Wenneberg J, Kon SSC, Wedzicha JA, Man WDC, Farquhar M. Integrating Home-Based Exercise Training with a Hospital at Home Service for Patients Hospitalised with Acute Exacerbations of COPD: Developing the M...
Show MoreWe have read the paper by Barker et al. (1) with interest. We congratulate the authors for conducting and publishing their prospective cohort study evaluating the effect of COPD discharge bundle on pulmonary rehabilitation (PR) referral and uptake following hospitalisation for acute exacerbation of COPD (AECOPD).
The authors have shown that the COPD discharge bundle had a positive effect on PR referral compared with a no bundle (17.5% (40 of 228) referral rate vs 0%(0 of 63)). This figure is lower than the expected 30% referral rate to PR following AECOPD (2). However, the paper offers no potential reasons for the lower referral rate.
The study had two bundle groups:
• COPD discharge bundle delivered by a current PR practitioner
• COPD discharge bundle delivered by a practitioner with no involvement in PR
Compared to delivery by a practitioner with no PR involvement, completion of the bundle delivery by a current PR practitioner resulted in higher referral and pick-up rates (60% vs 12% and 40% vs 32%, respectively). These results support the concept of integrating PR and hospital services.
Unfortunately, the completion rate (number of subjects who completed PR divided by the number of referrals) was disappointingly low. Also, there was no difference between the two bundle groups (13% (2 of 15) vs 12% (3 of 25)), as stated in the supplementary data.
It seems that patients' willingness or ability to complete PR is not af...
Show MoreThe paper by Hopkinson et al (1) provides unique and important data on smoking prevalence and COVID-19 symptoms, but their conclusion does not reflect the data well. The authors conclude “these data are consistent with people who smoke being at an increased risk of developing symptomatic COVID-19”. The study includes over 150,000 people with self-reported COVID-19 symptoms and over two million without such symptoms. It also includes data on over 25,000 people who were tested for SARS-CoV-2 and their test results. Based on our analysis of these more relevant data, we interpret the study differently. Our conclusion would be “these data are consistent with smokers having an increased risk of symptoms such as cough and breathlessness, but a decreased risk of having SARS-CoV-2 infection”.
The difficulty in interpreting these results is that both symptoms and testing are likely colliders in a causal model of smoking and COVID-19. The data reported on SARS-CoV-2 test results make it possible to compare smoking prevalence by age-group and sex in three groups: those who tested positive for SARS-CoV-2 (n=7,123); those who tested negative (n=16,765); and untested asymptomatic users (n=2,221,088, called “standard users” by the authors). Overall smoking prevalence was less in those tested (8.9%) than in all users of the app (11.0%). This might be thought of as a surprising finding – smoking-related symptoms should lead to testing – but can probably be explained by most asymptom...
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