Abstract
Asbestos-related diffuse pleural thickening (DPT), or extensive fibrosis of the visceral pleura secondary to asbestos exposure, is increasingly common due to the large number of workers previously exposed to asbestos. It may coexist with asbestos related pleural plaques but has a distinctly different pathology. The pathogenesis of this condition as distinct from pleural plaques is gradually becoming understood. Generation of reactive oxygen and nitrogen species, profibrotic cytokines and growth factors in response to asbestos is likely to play a role in the formation of a fibrinous intrapleural matrix. Benign asbestos related pleural effusions commonly antedate the development of diffuse pleural thickening. Environmental as well as occupational exposure to asbestos may also result in pleural fibrosis, particularly in geographic areas with naturally occurring asbestiform soil minerals. Pleural disorders may also occur after household exposure. High resolution computed tomography (CT) is more sensitive and specific than chest radiography for the diagnosis of diffuse pleural thickening, and several classification systems for asbestos-related disorders have been devised. Magnetic resonance imaging and fluorodeoxyglucose positron emission tomography (PET) scanning may be useful in distinguishing between DPT and malignant mesothelioma. DPT may be associated with symptoms such as dyspnoea and chest pain. It causes a restrictive defect on lung function and may rarely result in respiratory failure and death. Treatment is primarily supportive.
Highlights
Millions of people worldwide have been exposed to asbestos
Malignant mesothelioma of the pleura and diffuse pleural thickening (DPT) are less common than plaques, both conditions are likely to become more common in the future[1]
DPT may coexist with pleural plaques but has a distinctly different pathology, natural history and prognosis
Summary
Millions of people worldwide have been exposed to asbestos. The commonest manifestation of asbestos exposure is pleural disease, including pleural plaques and diffuse pleural thickening (DPT). There are several mechanisms by which diffuse pleural thickening has been postulated to develop: subsequent to benign asbestos-related pleural effusion, following recurrent bouts of acute pleuritis and/or extension of parenchymal fibrosis (asbestosis) to the visceral pleura [31]. Possible sequela of benign asbestos associated pleural effusion, recurrent bouts of asbestos related pleuritis or extension of parenchymal fibrosis into the pleura Usually bilateral, 1/3rd are unilateral Can extend to encase the lung, obliterating the pleural spaces, the fissures and the costophrenic recesses Arises from the visceral pleura. One Swedish study reported a higher age and gender associated prevalence of calcified pleural plaques in patients with coronary artery disease (35%) compared with those with lung cancer (19%)[44]. This has not, been formally studied for asbestos-related DPT
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