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John M. Wrightson, MA; Andrew E. Stanton, MD; Nicholas A. Maskell, DM; Robert J. O. Davies, DM; Y. C. Gary Lee, PhD, FCCP
Author and Funding Information

From the Oxford Pleural Unit (Drs Wrightson, Stanton, and Davies); the North Bristol Lung Centre, Bristol University (Dr Maskell); the Oxford NIHR Biomedical Research Centre (Drs Wrightson and Davies); and the School of Medicine, University of Western Australia (Dr Lee).

Correspondence to: John M. Wrightson, Oxford Pleural Unit, Oxford Centre for Respiratory Medicine, Churchill Hospital, Oxford, OX3 7LJ, England; e-mail: johnwrightson@thorax.org.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 (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(4):1005. doi:10.1378/chest.09-3062
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To the Editor:

We thank Dr Garcia-Zamalloa for his comments regarding our case series of patients with arthritis-associated pseudochylothorax who did not have significant pleural thickening (October 2009).1 We agree that the low number of reported cases has hitherto prevented a robust description of the pathogenesis and natural history of pseudochylothorax. Hopefully, our case series serves to add to our understanding of the disease.

Conventionally, pseudochylothorax is viewed as a single disease entity; this preconception should be challenged. The majority (54%) of the published cases of pseudochylothorax were associated with TB, followed by rheumatoid arthritis (9%).2 A large number of other conditions has also been implied, although each has been linked with very few cases of pseudochylothorax. Pseudochyle is defined by a high pleural fluid cholesterol composition (presence of cholesterol crystals on microscopic examination or cholesterol concentration > 200 mg/dL).3 This definition makes no assumption about the underlying pathogenetic mechanisms leading to pseudochyle formation. The previous literature has always associated pseudochylothorax with significant pleural thickening (a complication relatively common in TB) and assumed the fibrotic pleura plays a role in the accumulation of cholesterol within the pleural cavity. Our report of six cases of pseudochylothoraces—all associated with arthritis—without significantly thickened pleura contradicts such belief. Rather than one unifying mechanism resulting in pseudochyle formation, it is possible that pseudochyle actually represents a common end point of a variety of disease pathophysiologic conditions; those associated with TB may arise from a separate mechanism from those associated with arthritis. Expansion of such a theory could provide a plausible explanation for the diversity in rates of formation of pseudochyle and other pathologic findings (such as degree of pleural thickening), as seen in our series.

Differing pathogenetic mechanisms may also underlie the differing clinical outcomes. Regardless of underlying pathology, it would seem reasonable to propose better outcomes of pseudochylothoraces with nonfibrotic pleura, as seen in our cohort, over those with dense pleural thickening.

Like Dr Garcia-Zamalloa, we suspect that pseudochylothorax is underdiagnosed. Up to 20% of pleural effusions remain undiagnosed in routine clinical practice, and pleural fluid cholesterol concentration is infrequently evaluated, especially in the absence of extensive pleural thickening. A prospective study of pleural fluid cholesterol concentration (and cholesterol crystals) in undiagnosed pleural effusions will help determine the degree of underdiagnosis of this condition.

Specifically with regard to arthritis-associated pseudochylothoraces, our patients demonstrated pleural fluid volume control or reduction with intensified rheumatoid arthritis treatment. One could postulate that many patients with inflammatory arthritis may develop pseudochylothorax at some point during the evolution of their disease; the pseudochyle may remain uninvestigated and undiagnosed if subsequent intensification of arthritis treatment results in resolution of the pleural effusion.

Improved physician awareness of pseudochylothorax should improve rates of diagnosis. Cumulative knowledge may lead to new and testable hypotheses regarding the disease pathogenesis and, ultimately, much-needed studies on better treatment of pseudochylothorax.

Wrightson JM, Stanton AE, Maskell NA, Davies RJ, Lee YC. Pseudochylothorax without pleural thickening: time to reconsider pathogenesis? Chest. 2009;1364:1144-1147. [CrossRef] [PubMed]
 
Garcia-Zamalloa A, Ruiz-Irastorza G, Aguayo FJ, Gurrutxaga N. Pseudochylothorax. Report of 2 cases and review of the literature. Medicine (Baltimore). 1999;783:200-207. [CrossRef] [PubMed]
 
Hillerdal G. Chylothorax and pseudochylothorax. Eur Respir J. 1997;105:1157-1162. [CrossRef] [PubMed]
 

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References

Wrightson JM, Stanton AE, Maskell NA, Davies RJ, Lee YC. Pseudochylothorax without pleural thickening: time to reconsider pathogenesis? Chest. 2009;1364:1144-1147. [CrossRef] [PubMed]
 
Garcia-Zamalloa A, Ruiz-Irastorza G, Aguayo FJ, Gurrutxaga N. Pseudochylothorax. Report of 2 cases and review of the literature. Medicine (Baltimore). 1999;783:200-207. [CrossRef] [PubMed]
 
Hillerdal G. Chylothorax and pseudochylothorax. Eur Respir J. 1997;105:1157-1162. [CrossRef] [PubMed]
 
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