The natural history of idiopathic pulmonary fibrosis in a large European population: the role of age, sex and comorbidities

Author(s):  
Antonella Caminati ◽  
Fabiana Madotto ◽  
Sara Conti ◽  
Giancarlo Cesana ◽  
Lorenzo Mantovani ◽  
...  
Thorax ◽  
2017 ◽  
Vol 73 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Lucile Sesé ◽  
Hilario Nunes ◽  
Vincent Cottin ◽  
Shreosi Sanyal ◽  
Morgane Didier ◽  
...  

IntroductionIdiopathic pulmonary fibrosis (IPF) has an unpredictable course corresponding to various profiles: stability, physiological disease progression and rapid decline. A minority of patients experience acute exacerbations (AEs). A recent study suggested that ozone and nitrogen dioxide might contribute to the occurrence of AE. We hypothesised that outdoor air pollution might influence the natural history of IPF.MethodsPatients were selected from the French cohort COhorte FIbrose (COFI), a national multicentre longitudinal prospective cohort of IPF (n=192). Air pollutant levels were assigned to each patient from the air quality monitoring station closest to the patient’s geocoded residence. Cox proportional hazards model was used to evaluate the impact of air pollution on AE, disease progression and death.ResultsOnset of AEs was significantly associated with an increased mean level of ozone in the six preceding weeks, with an HR of 1.47 (95% CI 1.13 to 1.92) per 10 µg/m3 (p=0.005). Cumulative levels of exposure to particulate matter PM10 and PM2.5 were above WHO recommendations in 34% and 100% of patients, respectively. Mortality was significantly associated with increased levels of exposure to PM10 (HR=2.01, 95% CI 1.07 to 3.77) per 10 µg/m3 (p=0.03), and PM2.5 (HR=7.93, 95% CI 2.93 to 21.33) per 10 µg/m3 (p<0.001).ConclusionThis study suggests that air pollution has a negative impact on IPF outcomes, corroborating the role of ozone on AEs and establishing, for the first time, the potential role of long-term exposure to PM10 and PM2.5 on overall mortality.


Thorax ◽  
2016 ◽  
Vol 71 (Suppl 3) ◽  
pp. A13.1-A13
Author(s):  
V Navaratnam ◽  
AW Fogarty ◽  
T McKeever ◽  
N Thompson ◽  
G Jenkins ◽  
...  

CHEST Journal ◽  
1990 ◽  
Vol 98 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Hubert De Cremoux ◽  
Jean-François Bernaudin ◽  
Philippe Laurent ◽  
Patrick Brochard ◽  
Jean Bignon

2021 ◽  
Vol 08 (02) ◽  
pp. 16-26
Author(s):  
Naresh Kumar ◽  

Coronavirus disease 2019 (COVID-19) is caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The most common cause of hospitalisation for COVID-19 is interstitial pneumonia that may be complicated by Acute Respiratory Distress Syndrome (ARDS). With an increasing magnitude of COVID-19 survivors, post-COVID interstitial lung disease and pulmonary vascular disease are likely to be the most important long term respiratory complications. Data from previous coronavirus infections such as Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), as well as emerging data from the COVID-19 pandemic, suggest that there could be substantial pulmonary fibrotic consequences following SARS-CoV-2 infection. Thus, the long-term consequences of COVID-19 appear crucial. Here, we have discussed the pathogenesis, natural history, and radiological aspects of such patients and the possible predictors which might lead to the development of lung fibrosis. Older age, severity of illness, prolonged ICU stay, history of smoking and alcoholism are few of the risk factors for the development of post-COVID-19 pulmonary fibrosis. Therapeutic options like antifibrotic drugs such as pirfenidone, nintedanib, pulmonary rehabilitation, SARS-COV-2 vaccine etc. have been described. The role of steroids and antifibrotics in the prevention of post-COVID fibrosis is still controversial. Careful longitudinal follow-up of multiple cohorts of post-COVID-19 survivors with serial lung function testing and imaging is required to complete the knowledge about natural history of the disease and the response to various therapies.


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