Pathogenesis of pleurisy, pleural fibrosis, and mesothelial proliferation

Our plain-English summary of Pathogenesis of pleurisy, pleural fibrosis, and mesothelial proliferation, by A. Herbert (Thorax, 1986).

The study

• Author: A. Herbert
• Journal: Thorax
• Published: 1986;41(3):176-89
• Type of article: Review
• Cited by: 59 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 001210).

In plain English

This was a narrative review, not a new study, of published research on how the pleura (the lining of the lungs and chest wall) responds to injury. The author described pleural structure, mesothelial repair, and the causes of pleural effusion, fibrosis and mesothelial proliferation. On asbestos, the review stated that diffuse pleural fibrosis may follow acute asbestos pleurisy with effusion, probably through direct damage to the mesothelium, while pleural plaques probably arise by a different mechanism. It cited necropsy series reporting plaques in 11-12% of people in urban communities and almost 40% in a Finnish mining community. It also cited lung fibre counts showing relatively more crocidolite and amosite in people with plaques, compared with mainly chrysotile in controls. It also cited a survey that did not find a significant association between radiographic pleural thickening and asbestos exposure. The author stressed that reactive mesothelial cells can closely mimic cancer and cautioned against a certain cytological diagnosis of mesothelioma without close clinical correlation. The author concluded that the mesothelial response to injury must be distinguished from fibrous repair.

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: Narrative review of published literature on pleural anatomy, mesothelial injury and repair, pleural effusion, pleural fibrosis and mesothelial proliferation; no new data
• Who was studied: No study population; the review drew on previously published human and animal studies
• Exposure: Many causes of pleural disease. Asbestos-related sections covered benign asbestos pleural effusion and fibrosis, pleural plaques (with fibre types crocidolite, amosite, chrysotile and tremolite discussed) and folded lung (rounded atelectasis)
• Main results:
  • The review stated that diffuse pleural fibrosis may follow acute asbestos pleurisy with effusion and is probably caused by direct damage to the mesothelium
  • The review stated that the way asbestos fibres reach the pleural space is unknown
  • Citing a published series, the review stated that a considerable number of patients with benign asbestos effusions later develop mesothelioma or lung cancer
  • Cited necropsy series found hyaline pleural plaques in 11-12% of routine necropsies in urban communities and almost 40% in a mining community in Finland
  • Cited lung fibre counts showed a relative predominance of commercial amphiboles (crocidolite and amosite) in patients with pleural plaques, compared with a predominance of chrysotile in controls
  • A cited study showed plaques develop beneath an intact mesothelium, which the review took to suggest that direct mesothelial damage does not play a part in plaque formation
  • In a cited rabbit experiment, asbestos fibres placed directly into the pleural space produced extensive plaques, but plaques did not form in animals first treated with nitrogen mustard
  • A cited survey of patients with radiographic pleural thickening did not show a significant association with asbestos exposure
  • Folded lung was first described in three patients, all with some occupational asbestos exposure; later cases confirmed an association with pleural plaques, but not all patients had a history of asbestos exposure
  • The review described localised fibrous mesothelioma as a rare group of primary pleural tumours unrelated to asbestos exposure
  • Because reactive mesothelial cells can mimic malignancy, the review stated it is unwise to give a certain cytological diagnosis of mesothelioma without close clinical correlation
• The authors' conclusion: The author concluded that the mesothelial response to injury must be distinguished from the fibrous repair that takes over when the mesothelium is irreversibly destroyed

Topics

Medical terms in this study, explained in our Lexicon: Pleurisy, Fibrosis.

Related studies

• Evidence of a role for mesothelial cell-derived interleukin 8 in the pathogenesis of asbestos-induced pleurisy in rabbits — A.M. Boylan, C. Rüegg, et al. (1992)
• Benign asbestos pleurisy in the rabbit. A model for the study of pathogenesis — B.L. Shore, C.C. Daughaday, et al. (1983)
• Mesothelial cell proliferation: a nonspecific response to lung injury associated with fibrosis — I.Y. Adamson, J. Bakowska, et al. (1994)
• Cause of Asbestos-Induced Pleurisy Forgotten — E. Böhm (2019)
• How useful is GLUT-1 in differentiating mesothelial hyperplasia and fibrosing pleuritis from epithelioid and sarcomatoid mesotheliomas? An international collaborative study — A.N. Husain, M.K. Mirza, et al. (2014)
• Ventilatory failure due to asbestos pleurisy — A. Miller, A.S. Teirstein, et al. (1983)

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