Clinical Investigation of Benign Asbestos Pleural Effusion

Our plain-English summary of Clinical Investigation of Benign Asbestos Pleural Effusion, by N. Fujimoto, K. Gemba, K. Aoe, et al (Pulmonary Medicine, 2015).

The study

• Authors: N. Fujimoto, K. Gemba, K. Aoe, K. Kato, T. Yokoyama, I. Usami, K. Onishi, K. Mizuhashi, T. Yusa, T. Kishimoto
• Journal: Pulmonary Medicine
• Published: 2015;2015:416179
• Cited by: 21 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

There is no detailed information about benign asbestos pleural effusion (BAPE). The aim of the study was to clarify the clinical features of BAPE. The criteria of enrolled patients were as follows: (1) history of asbestos exposure; (2) presence of pleural effusion determined by chest X-ray, CT, and thoracentesis; and (3) the absence of other causes of effusion. Clinical information was retrospectively analysed and the radiological images were reviewed. There were 110 BAPE patients between 1991 and 2012. All were males and the median age at diagnosis was 74 years. The median duration of asbestos exposure and period of latency for disease onset of BAPE were 31 and 48 years, respectively. Mean values of hyaluronic acid, adenosine deaminase, and carcinoembryonic antigen in the pleural fluid were 39,840 ng/mL, 23.9 IU/L, and 1.8 ng/mL, respectively. Pleural plaques were detected in 98 cases (89.1%). Asbestosis was present in 6 (5.5%) cases, rounded atelectasis was detected in 41 (37.3%) cases, and diffuse pleural thickening (DPT) was detected in 30 (27.3%) cases. One case developed lung cancer (LC) before and after BAPE. None of the cases developed malignant pleural mesothelioma (MPM) during the follow-up.

In plain English

This retrospective study reviewed records and chest images of 110 patients diagnosed with benign asbestos pleural effusion (BAPE), a non-cancerous fluid build-up around the lung, at 9 Japanese hospitals between 1991 and 2012. All were men; median age was 74. Of 109 with exposure details, 108 were exposed at work, most often in shipbuilding or construction, and one environmentally. Median exposure lasted 31 years; median latency before BAPE was 48 years. The fluid was exudative in all cases and bloody in 75 of 104. Pleural plaques were found in 98 patients (89.1%), rounded atelectasis in 41 (37.3%), diffuse pleural thickening in 30 (27.3%) and asbestosis in 6. Among 70 patients followed at one hospital, median overall survival was 104.2 months (95% confidence interval 67.3 to 141.0); 17 had died; causes were known for 11, including 7 from respiratory failure. One patient had lung cancer before and after BAPE; none had developed malignant pleural mesothelioma at analysis. The authors concluded that BAPE develops after a long latency and that thoracoscopy with pleural biopsy should be performed to confirm the diagnosis.

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: Retrospective clinical case series based on medical records and centrally reviewed radiological images
• Who was studied: 110 patients diagnosed with BAPE at 9 institutions (Rosai Hospital and affiliated hospitals) in Japan, 1991 to 2012. All were male, with a median age of 74 (range 36 to 90).
• Exposure: Asbestos exposure was assessed from work, family and residential histories. Fiber types were not reported. Of 109 patients with exposure information, 108 had occupational exposure and 1 had environmental exposure. Leading occupations were shipbuilding (25), construction (20), chemical facility (10), asbestos products manufacturing (8) and electrical work (8). The median age at first exposure was 21.5 years (range 14 to 58).
• Main results:
  • Median duration of asbestos exposure was 31 years (range 0.75 to 50). Median latency for onset of BAPE was 48 years (range 17 to 76).
  • Of 104 cases with pleural fluid information, the fluid was bloody in 75 and light yellow in 27. Effusions were exudative in all cases.
  • In 57 cases with cell classification, the median proportion of lymphocytes in the fluid was 77.7%.
  • In pleural fluid, mean hyaluronic acid (measured in 106 cases) was 39,840 ng/mL (standard deviation 40,228). Mean adenosine deaminase was 23.9 IU/L (SD 24.9). Mean carcinoembryonic antigen was 1.8 ng/mL (SD 1.3).
  • Pleural plaques were found in 98 cases (89.1%), 76 of them calcified. Asbestosis was found in 6 cases, rounded atelectasis in 41 (37.3%) and diffuse pleural thickening in 30 (27.3%).
  • One patient had lung cancer two years before and another lung cancer two years after the BAPE diagnosis.
  • Thoracoscopic exploration was done in 78 patients to exclude carcinomatous pleuritis or malignant pleural mesothelioma.
  • Among 70 patients with survival data from Okayama Rosai Hospital, median overall survival was 104.2 months (95% CI 67.3 to 141.0).
  • 17 of the 70 patients had died, and causes of death were determined in 11, including 7 from respiratory failure.
  • 9 of the 17 who died had developed diffuse pleural thickening, including all 7 respiratory failure deaths.
  • No patient had developed malignant pleural mesothelioma at the time of analysis.
• The authors' conclusion: The authors concluded that BAPE develops after a long latency period after past asbestos exposure and that diagnosis should rest on excluding other pleural diseases. Markers such as hyaluronic acid, adenosine deaminase and carcinoembryonic antigen might help. In their view, thoracoscopic exploration and pleural biopsy should be performed to confirm the diagnosis. They proposed diagnostic criteria on that basis.
• Limitations the authors state:
  • The study was retrospective.
  • Pathological analyses, including immunohistochemistry, were not reviewed.
  • The relationship between the amount of exposure and development of BAPE is unclear.
  • Most patients also had other asbestos-related lesions, so BAPE may have developed earlier than detected. This could explain the longer latency than previously published.

Topics

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

Medical terms in this study, explained in our Lexicon: Benign Asbestos Pleural Effusion, Asbestos Exposure, Pleural Effusion, Chest X-Ray, Thoracentesis, Latency, Hyaluronic Acid, Carcinoembryonic Antigen (CEA).

Related studies

• Retrospective investigation on diagnostic process for benign asbestos pleural effusion (BAPE) using checklist — T. Kishimoto, N. Fujimoto, et al. (2020)
• Pleural irregularities and mediastinal pleural involvement in early stages of malignant pleural mesothelioma and benign asbestos pleural effusion — K. Kato, K. Gemba, et al. (2016)
• 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)
• Clinical investigation of malignant mesothelioma in Japan — N. Fujimoto, K. Aoe, et al. (2010)
• Predicting Malignant and Paramalignant Pleural Effusions by Combining Clinical, Radiological and Pleural Fluid Analytical Parameters — S. Herrera Lara, E. Fernández-Fabrellas, et al. (2017)
• Significance of secretory leukocyte peptidase inhibitor in pleural fluid for the diagnosis of benign asbestos pleural effusion — T. Kishimoto, Y. Kojima, et al. (2021)

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