The presentation and natural history of asbestos-induced diffuse pleural thickening

Quoted from http://occmed.oxfordjournals.org/content/early/2012/04/26/occmed.kqs028.abstract?maxtoshow=&HITS=10&hits=3&RESULTFORMAT=&andorexacttitle=or&andorexacttitleabs=and&fulltext=asbestos&andorexactfulltext=and&searchid=1&usestrictdates=yes&resourcetype=HWCIT&ct

The presentation and natural history of asbestos-induced diffuse pleural thickening

  1. V. Jeebun1 and
  2. S. C. Stenton2
  1. ? 1Department of Respiratory Medicine, University Hospital of North Tees, Stockton on Tees, TS19 8PE, UK
  2. ? 2Regional Unit for Occupational Lung Disease, Royal Victoria Infirmary, Newcastle Upon Tyne, NE1 4AP, UK.
  • Received September 26, 2011.
  • Revision received January 15, 2012.
  • Accepted January 26, 2012.

Abstract

Background Three forms of asbestos-related benign pleural disease are recognized: discrete pleural plaques, pleural effusions and diffuse pleural fibrosis. Of these, diffuse pleural fibrosis is the most significant on account of its chronicity and associated morbidity.

Aims The objectives of this study were to determine the latency of asbestos-induced diffuse pleural fibrosis, its presenting features and its clinical course once established.

Methods We conducted a retrospective review of 75 patients with asbestos-induced diffuse pleural fibrosis referred for assessment at our institution from 1992 to 2007. Diffuse pleural fibrosis was considered to be present if there was obliteration of the costophrenic angle in continuity with at least 3-mm pleural thickening, in accordance with the International Labour Organization 2000 Classification.

Results The median latency for development of diffuse pleural fibrosis from first asbestos exposure was 34 years. Seventy-three per cent of patients had unilateral disease at presentation and 24% of these were observed to develop contralateral disease after a median of 2 years. Unilateral pleural disease was commonest on the right. Forty per cent of patients presented with pleural effusions preceding the development of diffuse pleural thickening. The median latency for development of pleural effusions from onset of exposures was 38 years. Eighty per cent of the pleural effusions were unilateral. Once established, pleural thickening was reported to have remained stable in 91% on the ipsilateral side.

Conclusions The findings of this study may help in providing further insight into the natural history of diffuse pleural fibrosis to guide the clinician in the management of this condition.

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