Fine structural changes in cryptogenic fibrosing alveolitis and asbestosis

Our plain-English summary of Fine structural changes in cryptogenic fibrosing alveolitis and asbestosis, by B. Corrin, A. Dewar, R. Rodriguez-Roisin, et al (The Journal of Pathology, 1985).

The study

• Authors: B. Corrin, A. Dewar, R. Rodriguez-Roisin, M. Turner-Warwick
• Journal: The Journal of Pathology
• Published: 1985;147(2):107-19
• Cited by: 65 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Lung biopsies from 17 patients with cryptogenic fibrosing alveolitis of a cellular rather than fibrotic pattern were examined by transmission electron microscopy in the hope that such cases would show features of pathogenetic significance. Further selection was made by choosing minimally affected areas. There was no ultrastructural evidence of immune complex deposition but alveolar epithelial and capillary damage was frequently found (17 and 14 of the 17 cases respectively). Alveolar epithelial injury consisted of patchy necrosis and regenerative hyperplasia. Alveolar capillary injury consisted of cytoplasmic swelling and basement membrane thickening and reduplication. Many of these features have not been emphasized in previous reports and their prominence in early stages of the disease suggest that they may have pathogenetic significance, possible mechanisms of which are discussed. Similar findings identified during the course of this study in 8 asbestos workers suggest that similar pathogenetic mechanisms may operate in asbestosis.

In plain English

The authors examined lung biopsy tissue with an electron microscope, looking for early cell changes that might explain how lung scarring develops. They studied biopsies from 17 patients at the Brompton Hospital, London, with cryptogenic fibrosing alveolitis (lung scarring with no known cause), choosing the least affected areas. They also included eight Spanish asbestos workers with heavy asbestos exposure. The fiber type was not stated. In the alveolitis patients, no deposits suggesting immune complexes were found. Swelling of the cells lining the small blood vessels was seen in 13 of the 17 patients, and focal loss of the cells lining the air sacs in 13 of the 17. The asbestos workers showed similar changes, apart from fewer inflammatory cells and the presence of asbestos. Patchy loss of air-sac lining was found in six of the eight. The authors concluded that, in both diseases, they believed inflammatory mediators promote scarring by continually damaging susceptible lung cells. They also stated that they did not know the cause of the cell loss.

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: Prospective electron microscopy study of open lung biopsies (descriptive case series), begun in 1975, with a small group of asbestos workers presented alongside
• Who was studied: 17 patients with cryptogenic fibrosing alveolitis who had open lung biopsy at the Brompton Hospital, London, since 1975, selected because the tissue looked cellular rather than fibrotic. Also included were 8 Spanish asbestos workers whose biopsy tissue reaction ranged from no change to severe interstitial fibrosis with honeycombing.
• Exposure: The asbestos workers all had heavy asbestos exposure, and open lung biopsy showed asbestos in the lung. Fiber types, jobs and doses are not given. The alveolitis patients had no known cause.
• Main results:
  • Fibrosing alveolitis patients: no electron-dense deposits suggesting immune complexes were found in any case
  • Fibrosing alveolitis patients: swelling of capillary lining (endothelial) cells was found in 13 of the 17 patients
  • Fibrosing alveolitis patients: the capillary basement membrane was diffusely thickened or reduplicated in seven patients
  • Fibrosing alveolitis patients: focal loss of air-sac lining (epithelium) was seen in 13 of the 17 cases. Hyperplasia of type II pneumocytes or intermediate cells was seen in 16 of the 17. Overall, epithelial damage was found in 17 of 17 and capillary damage in 14 of 17.
  • Asbestos workers: changes were similar to those in fibrosing alveolitis, except for fewer interstitial inflammatory cells and the presence of asbestos. Patchy loss of alveolar epithelium was found in six of the eight cases.
• The authors' conclusion: The authors believed that in both fibrosing alveolitis and asbestosis, inflammatory mediators promote fibrosis by continually damaging susceptible lung cells. They postulated that long-standing interstitial oedema and loss of epithelial inhibitors of connective tissue growth are important factors, and suggested that the two diseases may share common mechanisms despite different causes.
• Limitations the authors state:
  • The authors state they do not know the cause of the epithelial cell loss they observed
  • The authors note that the apparent finding of type II pneumocytes free of the alveolar wall could be explained by tangential sectioning
  • The authors state they have no firm evidence that one proposed mechanism, the organization of intra-alveolar exudates, is important in their cases

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Transmission Electron Microscopy (TEM), Deposition, Necrosis.

Related studies

• British Thoracic Society study of cryptogenic fibrosing alveolitis: current presentation and initial management. Fibrosing Alveolitis Subcommittee of the Research Committee of the British Thoracic Society — I.D. Johnston, R.J. Prescott, et al. (1997)
• Desquamative interstitial pneumonitis. Cellular phase of fibrosing alveolitis — R.R. Tubbs, S.P. Benjamin, et al. (1977)
• Cryptogenic fibrosing alveolitis and lung cancer: the BTS study — J.M. Harris, I.D. Johnston, et al. (2010)
• Electron microscopic studies in desquamative interstitial pneumonia associated with asbestos — B. Corrin, A.B. Price (1972)
• Cryptogenic Fibrosing Pleuritis — A. Manco, V. Alfieri, et al. (2021)
• Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis — R. Day, S. Lemaire, et al. (1987)

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