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Impaired Quality of Life in Chronic Hypersensitivity PneumonitisQuality of Life in Hypersensitivity Pneumonitis FREE TO VIEW

Christopher M. Barber, MD; Ruth E. Wiggans, MD; David Fishwick, MD
Author and Funding Information

From the Centre for Workplace Health, Health and Safety Laboratory.

CORRESPONDENCE TO: Christopher M. Barber, MD, Centre for Workplace Health, Health and Safety Laboratory, Buxton, SK17 9JN, England; e-mail: chris.barber@hsl.gsi.gov.uk


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

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


Chest. 2015;147(6):e230. doi:10.1378/chest.15-0198
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To the Editor:

We read with interest in an issue of CHEST (June 2014) the article by Lubin et al,1 who compared Short Form-36 quality of life (QOL) among patients with idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis (CHP). The authors noted that they were surprised to find that QOL scores were significantly better in IPF than CHP in seven of eight domains. They demonstrated that this finding did not relate to age or severity of lung function impairment, and they discussed possible explanations.

We would like to offer a further possible explanation as to why QOL scores may be worse in those with CHP in comparison with IPF. CHP, unlike IPF, is an allergic lung disease predominantly caused by occupational or environmental exposure.2 In a variable proportion of cases, no cause is easily demonstrated, following a careful clinical evaluation, measurement of precipitins, and occupational/domestic hygiene assessment. There is evidence that prognosis is worse in this group, as avoiding further exposure to a cause is not possible.3

The article by Lubin et al1 does not present data relating to the cause of CHP in their series, but common causes in other series include domestic exposure to birds kept as pets and for hobbies and microbial contamination of damp buildings, air conditioners, humidifiers, and hot tubs.4,5 Common occupational causes also include exposures to birds and microbial contamination of organic dusts and water-containing mists/aerosols.4-6

The main aim of treatment in hypersensitivity pneumonitis is to identify and avoid further exposure to the cause.3 In our clinical experience, this may involve relocating a loved family pet, discontinuing an enjoyable hobby, carrying out building work to remediate a home or moving house, removing a hot tub, changing a work role, or losing employment. However, in IPF, a disease with no known cause, patients with a similar level of respiratory impairment will not be advised to make such changes. This raises the possibility that exposure-avoidance measures in CHP may have a negative impact in many of the Short Form-36 domains, where questions specifically inquire about mental health, social functioning, vitality, and physical impact on work.1

We would be interested to see more information from this case series as to the causes of CHP and whether such advice to avoid exposures had been given. It may also be of interest to compare QOL in CHP, between individuals with and without an identifiable inciting agent, to identify whether there is any evidence to support this hypothesis.

References

Lubin M, Chen H, Elicker B, Jones KD, Collard HR, Lee JS. A comparison of health-related quality of life in idiopathic pulmonary fibrosis and chronic hypersensitivity pneumonitis. Chest. 2014;145(6):1333-1338. [CrossRef] [PubMed]
 
Lacasse Y, Girard M, Cormier Y. Recent advances in hypersensitivity pneumonitis. Chest. 2012;142(1):208-217. [CrossRef] [PubMed]
 
Fernández Pérez ER, Swigris JJ, Forssén AV, et al. Identifying an inciting antigen is associated with improved survival in patients with chronic hypersensitivity pneumonitis. Chest. 2013;144(5):1644-1651. [CrossRef] [PubMed]
 
Hanak V, Golbin JM, Ryu JH. Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis. Mayo Clin Proc. 2007;82(7):812-816. [CrossRef] [PubMed]
 
Selman M, Pardo A, King TE Jr. Hypersensitivity pneumonitis: insights in diagnosis and pathobiology. Am J Respir Crit Care Med. 2012;186(4):314-324. [CrossRef] [PubMed]
 
Barber CM, Burton CM, Hendrick DJ, et al. Hypersensitivity pneumonitis in workers exposed to metalworking fluids. Am J Ind Med. 2014;57(8):872-880. [CrossRef] [PubMed]
 

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Tables

References

Lubin M, Chen H, Elicker B, Jones KD, Collard HR, Lee JS. A comparison of health-related quality of life in idiopathic pulmonary fibrosis and chronic hypersensitivity pneumonitis. Chest. 2014;145(6):1333-1338. [CrossRef] [PubMed]
 
Lacasse Y, Girard M, Cormier Y. Recent advances in hypersensitivity pneumonitis. Chest. 2012;142(1):208-217. [CrossRef] [PubMed]
 
Fernández Pérez ER, Swigris JJ, Forssén AV, et al. Identifying an inciting antigen is associated with improved survival in patients with chronic hypersensitivity pneumonitis. Chest. 2013;144(5):1644-1651. [CrossRef] [PubMed]
 
Hanak V, Golbin JM, Ryu JH. Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis. Mayo Clin Proc. 2007;82(7):812-816. [CrossRef] [PubMed]
 
Selman M, Pardo A, King TE Jr. Hypersensitivity pneumonitis: insights in diagnosis and pathobiology. Am J Respir Crit Care Med. 2012;186(4):314-324. [CrossRef] [PubMed]
 
Barber CM, Burton CM, Hendrick DJ, et al. Hypersensitivity pneumonitis in workers exposed to metalworking fluids. Am J Ind Med. 2014;57(8):872-880. [CrossRef] [PubMed]
 
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