Benign diffuse pleural thickening (BDPT) results from a fibrosing process of the visceral pleura with fusion to the parietal pleura over a wide area . The pathophysiological mechanism is thought to be an intense and continuous inflammatory insult that drives an excessive deposition and abnormal turnover of fibrinous matrix in the pleural space, which in turn becomes obliterated and fibrosed .
CT criteria fulfilment implies visualization of a continuous and smooth sheet of pleural thickening of >3mm extending for more than 8 cm craniocaudally and 5 cm laterally [2, 3]. BDPT usually extends along the posterior and lateral surfaces of the lower hemithorax, and sometimes is accompanied by parenchymal bands or foci of round atelectasis . Almost always there is blunting of the costophrenic angles and volume loss on the affected lung . Thickening >10mm, nodular thickening, and mediastinal pleural involvement are findings not usually associated with BDPT and should raise concern for malignancy (such as mesothelioma) .
Multiple aetiologies of BDPT are recognized, such as infection (including tuberculosis), haemothorax, asbestos exposure, collagen vascular diseases (notably systemic lupus erythematosus and rheumatoid arthritis) and thoracic irradiation .
Since it can be a cause of significant restrictive lung disease, some authors recommend follow-up for BDPT patients with physical examination, chest imaging and pulmonary function tests to monitor and manage deteriorations of the lung function .