Diffuse pleural thickening following heart failure-related pleural effusions in an asbestos exposed patient

Our plain-English summary of Diffuse pleural thickening following heart failure-related pleural effusions in an asbestos exposed patient, by M. Evison, P. Barber (International Journal of Occupational and Environmental Health, 2015).

The study

• Authors: M. Evison, P. Barber
• Journal: International Journal of Occupational and Environmental Health
• Published: 2015;21(2):169-71
• Type of article: Case report
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Diffuse pleural thickening (DPT) is a well-recognized consequence of asbestos exposure and often follows a benign asbestos-related pleural effusion. At our tertiary center, in the North West of England where the prevalence of asbestos-related pleural disease is high, we have encountered a series of patients that have had led us to consider a new hypothesis in DPT. We postulate that non-asbestos-related pleural effusions, particularly transudative pleural effusions, caused by heart failure can trigger the development of DPT. We present one such case, discuss the limitations of our temporal observations, and invite further discussions from readers.

In plain English

This perspective article described one patient seen at a tertiary respiratory center in North West England and used the case to propose a hypothesis. The patient had worked as a joiner cutting asbestos sheets for roofing daily for 5 years. The patient developed breathlessness and was found to have pleural effusions on both sides, larger on the right. A chest X-ray 12 months earlier had been normal. The fluid was a transudate with no malignant cells, and the diagnosis was decompensated heart failure linked to atrial fibrillation and aortic stenosis. Over the next 6 months, the patient developed right-sided pleural thickening with CT features that the authors described as consistent with asbestos-related diffuse pleural thickening (DPT). The patient later died after heart valve surgery. The authors suggested that heart failure-related effusions might trigger DPT in asbestos-exposed people, but called this purely speculative. Their observations concerned timing only and gave no evidence on causation, and the effusion might have been a benign asbestos effusion that coincided with the heart disease.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Case report (one patient) presented in a perspective article proposing a hypothesis
• Who was studied: One patient ('Patient X') seen at the University Hospital of South Manchester, a tertiary respiratory center in North West England. The authors say they have seen a series of similar patients, but only this one is described. No dates are given.
• Exposure: Work as a joiner cutting asbestos sheets for roofing daily for 5 years. The fiber type is not stated. The patient was also an ex-smoker, with the history printed as '65-packs per year'.
• Main results:
  • A chest X-ray taken 12 months before presentation showed no pleural disease.
  • At presentation, thoracic ultrasound showed pleural effusions on both sides, larger on the right.
  • Fluid from the right effusion was a transudate: fluid protein 28 g/l, serum protein 71 g/l, fluid LDH 165 IU/l and serum LDH 339 IU/l. Cytology showed no malignant cells.
  • The diagnosis was decompensated heart failure precipitated by atrial fibrillation on a background of aortic stenosis.
  • Over the next 6 months, the patient developed right-sided smooth pleural thickening with rounded atelectasis and linear bands on CT, which the authors described as consistent with asbestos-related DPT.
  • After about 12 months of radiological stability, the patient underwent aortic valve replacement, developed widespread small bowel ischemia after the operation, and died.
• The authors' conclusion: The authors proposed, as a purely speculative hypothesis, that pleural effusions of any cause, including transudative effusions from heart failure, might trigger DPT in asbestos-exposed people. They said the hypothesis rests on a temporal observation but warrants further discussion.
• Limitations the authors state:
  • The observations are temporal and provide no evidence on causation.
  • It is not possible to know whether the DPT would have developed without the cardiac disease.
  • The effusion could have been a benign asbestos-related pleural effusion (BAPE) that simply coincided with the heart disease.
  • If the hypothesis were true, a sizeable number of such patients would be expected, given how common heart failure effusions are.
  • DPT can occur without a preceding effusion.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Diffuse Pleural Thickening, Pleural Effusion, Asbestos Exposure, Asbestos-Related Pleural Disease.

Related studies

• Natriuretic peptides in pleural effusions: Beyond a diagnosis of heart failure — J.M. Porcel (2020)
• Occult primary cardiac lymphomas causing unexpected/sudden death or acute heart failure — A. De Martino, F. Del Re, et al. (2020)
• Predicting Malignant and Paramalignant Pleural Effusions by Combining Clinical, Radiological and Pleural Fluid Analytical Parameters — S. Herrera Lara, E. Fernández-Fabrellas, et al. (2017)
• A retrospective study on radiological findings of diffuse pleural thickening with benign asbestos pleural effusion in Japanese cases — T. Kishimoto, K. Kato, et al. (2022)
• Diffuse thickening superimposed on circumscribed pleural thickening related to asbestos exposure — A. Miller, J.A. Miller (1993)
• Asbestos-related diffuse pleural thickening — N. Fujimoto, K. Kato, et al. (2014)

Browse more research in International Journal of Occupational and Environmental Health, or return to medical research.