Our plain-English summary of Coexistent atypical adenomatous hyperplasia, primary lung adenocarcinoma and pleural mesothelioma in an asbestos-exposed subject, by D.H. Thomas, R.L. Attanoos, A.R. Gibbs (Histopathology, 2004).
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The study
- Authors: D.H. Thomas, R.L. Attanoos, A.R. Gibbs
- Journal: Histopathology
- Published: 2004;45(5):540-2
- Type of article: Case report, Letter
- Cited by: 2 articles, as counted by NIH iCite
- Read it: PubMed · Publisher
In plain English
This letter to the journal was a case report about one man. He was 62, had worked at a thermoelectric power station in the 1970s alongside asbestos laggers, and was an ex-smoker with a 30 pack-year smoking history. Surgery on his right upper lung removed two tumours: a 20-mm moderately differentiated acinar adenocarcinoma (a lung cancer) and an epithelioid malignant mesothelioma of the pleura. In the surrounding lung there was also a 2-mm focus of atypical adenomatous hyperplasia (AAH), a lesion described as a precursor of lung adenocarcinoma. The lung showed no diffuse interstitial fibrosis (asbestosis). Fibre analysis found 2.73 million amphibole fibres per gram of dry lung tissue, all amosite. The authors described this as above the range for unexposed people but below the level considered enough to cause asbestosis. Chrysotile was within the control range. The authors asked whether asbestos might cause lung cancer through AAH without asbestosis. They noted the AAH could be an unrelated finding in an ex-smoker, and said a formal study controlling for smoking was needed.
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 (letter to the journal) of a single patient
- Who was studied: One 62-year-old man, an ex-smoker for 8 years with a cumulative 30 pack-year history, who presented with 2 months of increasing breathlessness on exertion. The authors were based at Llandough Hospital, Cardiff, Wales, UK. No dates for the case were given.
- Exposure: Occupational: worked at a thermoelectric power station in the 1970s alongside asbestos laggers. Lung fibre analysis by transmission electron microscopy with energy dispersive X-ray spectrometry found amosite as the only amphibole, plus small quantities of chrysotile.
- Main results:
- The lung tumour was a 20-mm nodule, subtyped as a moderately differentiated acinar adenocarcinoma.
- The pleural tumour was a malignant mesothelioma of epithelioid subtype.
- A 2-mm focus of atypical adenomatous hyperplasia was found in a random section of background lung.
- The lung showed no diffuse interstitial fibrosis (no asbestosis).
- Two classical asbestos bodies were seen in 35 square millimetres of background lung section.
- Total amphibole content was 2.73 × 10 to the sixth (2.73 million) fibres per gram dry lung tissue, all amosite. Chrysotile was present in small quantities, within the background control range.
- In the authors' Cardiff laboratory, the amphibole fibre content was above the control range for non-asbestos-exposed subjects but below the level deemed sufficient to cause asbestosis.
- A chest X-ray showed calcification of both diaphragms consistent with asbestos-related pleural plaques.
- The authors' conclusion: The authors raised the question of whether, without asbestosis, lung cancer might arise through asbestos-induced AAH. They also said the AAH in this person could be interpreted as a concurrent but unrelated finding. They concluded that a formal study of AAH in asbestos-exposed people with and without fibrosis, controlling for smoking, is needed before definitive conclusions can be made.
- Limitations the authors state:
- The patient was an ex-smoker, and in an individual case it is not possible to determine whether the lung cancer would have developed without asbestos exposure.
- AAH is more often found in people with invasive lung adenocarcinoma, so its presence here may be unrelated to asbestos.
- There are no data on how often AAH occurs in asbestos-exposed people with or without asbestosis.
Topics
The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.
Medical terms in this study, explained in our Lexicon: Lung Adenocarcinoma, Pleural Mesothelioma.
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- Analysis of microRNA expression signatures in malignant pleural mesothelioma, pleural inflammation, and atypical mesothelial hyperplasia reveals common predictive tumorigenesis-related targets — E.G. Ramírez-Salazar, L.C. Salinas-Silva, et al. (2014)
- Malignant mesothelioma eight years after a diagnosis of atypical mesothelial hyperplasia — J. Scurry, M.A. Duggan (1999)
- Case reports of primary pulmonary adenocarcinoma with pleural spread: so-called pseudomesotheliomatous adenocarcinoma — R. Saito, A. Kasajima, et al. (2012)
- Reactive mesothelial hyperplasia vs mesothelioma, including mesothelioma in situ: a brief review — D.W. Henderson, K.B. Shilkin, et al. (1998)
Browse more research in Histopathology, or return to medical research.
Cited on this site
How to cite it
Cite the study
D.H. Thomas, R.L. Attanoos, A.R. Gibbs. Coexistent atypical adenomatous hyperplasia, primary lung adenocarcinoma and pleural mesothelioma in an asbestos-exposed subject. Histopathology 2004;45(5):540-2. doi:10.1111/j.1365-2559.2004.01939.x. PMID: 15500660.
Cite our summary
“Coexistent atypical adenomatous hyperplasia, primary lung adenocarcinoma and pleural mesothelioma in an asbestos-exposed subject.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/coexistent-atypical-adenomatous-hyperplasia-primary-lung.
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