Cryptogenic Fibrosing Pleuritis

We report the case of a 46-year-old male patient who was referred for chest pain and bilateral pleural effusion. Despite treatment with antibiotics and steroids, the pleural effusion worsened over a few months until pulmonary function was halved. The CT scan showed bilateral pleural thickening with right basal opacity. Histology revealed extensive fibrotic tissue with focal collections of lymphocytes and giant cells without traces of asbestos bodies. Since no evidence of an infectious, embolic or occupational aetiology was found, this bilateral pleural effusion progressing to diffuse pleural thickening was diagnosed as cryptogenic fibrosing pleuritis, a rare pleural disease.

Sarcomatoid Mesothelioma: A Clinicopathological and Immunohistochemical Study of 64 Cases

Sixty-four cases of sarcomatoid pleural mesothelioma represent the basis of this study. The patients are 51 men and 13 women between the ages of 42 and 79 years, who presented with symptoms of chest pain, cough, and weight loss. Diagnostic imaging showed the presence of diffuse pleural thickening with encasement of the lung parenchyma in all the cases. All patients had surgical resection via extrapleural pneumonectomy. By immunohistochemistry, all cases were positive for cytokeratin AE1/AE3; however, reactivity with other markers including keratin 5/6, calretinin, and D2-40 was seen in different proportions, whereas a few cases showed positive staining for GATA3, WT1, and p40. All tumors were negative for carcinomatous epitopes (carcinoembryonic antigen, CD15, and TTF1). Our findings show that even though the use of immunohistochemical stains plays an important role in the final interpretation, the best results are accomplished by a global interpretation of clinical, radiographical, and immunohistochemical findings. It is also important to highlight that it does not seem to be a single immunohistochemical stain that is pathognomonic of sarcomatoid mesothelioma and that some other stains that are commonly used for other tumors may also show positive staining in a small percentage of sarcomatoid mesotheliomas.

Fatal diffuse pleural calcification due to Tuberculosis- An unexplained entity

Diffuse pleural thickening has many causes and often need to be diagnosed early as delay in treatment can be lethal. Diffuse pleural thickening can be due to calcifications and may occur as a result of chronic infections including Tuberculous effusion. Primary pleural calcification due to Tuberculosis is extremely rare. A 28 year old patient was presented with exertional dyspnea, chronic cough and pleuritic type chest pain for a period of 4 months. CXR showed left sided diffuse pleural calcifications and ultrasonography showed calcified pleura with thick echogenic material suggestive of an empyema. Further evaluation with a CECT showed left sided diffusely calcified, septated pleura with empyema and contralateral early pleural and peritoneal calcification. Pleural aspiration showed a hemorrhagic exudative lymphocytic effusion with high ADA titer. Cytology did not reveal malignant cells. His serum calcium level was normal. He was diagnosed to have extra-pulmonary tuberculosis and was treated with standard anti TB treatment with an intercostal tube drainage. Despite TB treatment he passed away due to respiratory distress caused by pleural thickening. This case highlights the importance of timely initiation of anti TB treatment and the capacity of Tuberculosis to cause diffuse pleural calcification which can be fatal in an untreated setting.

Diffuse pleural thickening and thoracic contraction: An indistinguishable case from malignant pleural mesothelioma

The differential diagnosis of reactive mesothelial hyperplasia and mesothelioma is difficult. We present a rare case of diffuse pleural thickening with thoracic contraction that was indistinguishable from mesothelioma. A 66-year-old woman with no history of asbestos exposure visited our hospital with a complaint of dyspnea. The clinical findings included circumferential pleural thickening on chest computed tomography image and a high concentration of hyaluronic acid in the pleural fluid. Pleural biopsies obtained by thoracoscopy under local anesthesia were pathologically consistent with mesothelioma, but the patient refused to take any kind of mesothelioma treatments. Four months later, she consented to a surgical pleural biopsy under general anesthesia to obtain larger tissue samples, which included typical proliferating polygonal cells positive for CAM5.2, calretinin, WT-1, D2-40, CK5/6, epithelial membrane antigen, and glucose transporter-1 and negative for carcinoembryonic antigen, BerEP4, and MOC31. The analysis was consistent with diagnosis of epithelioid mesothelioma. Fluorescence in situ hybridization, however, showed the presence of p16 gene, and the expression of BRCA1-associated protein-1 was detected by immunohistochemistry. Our final diagnosis was diffuse pleural thickening unrelated to asbestos exposure. Differential diagnosis of diffuse pleural thickening and malignant mesothelioma is thus difficult and routine immunohistochemical examinations are often insufficient for accurate diagnosis. Multiple diagnostic methods are required for correct diagnosis in a clinically marginal case.

Pleural Thickening and Calcification

Pleural thickening and calcification discusses the radiographic and computed tomography (CT) manifestations of benign pleural thickening and pleural calcification. Benign pleural thickening must be differentiated from malignant pleural thickening and their differentiating characteristics will be discussed. Pleural plaque is the most common manifestation of asbestos exposure and carries no risk of malignant degeneration. The most common imaging appearance is bilateral sharply demarcated, multifocal areas of discontinuous pleural thickening that often calcifies over time. Pleural plaques spare the apical and costophrenic sulcus pleura and has a predilection for the diaphragmatic pleura. Diffuse pleural thickening is associated with hemothorax, empyema, connective tissue disorders, and asbestos exposure. It is generally unilateral, causes blunting of the costophrenic angle, spans multiple rib interspaces, and is irregular in shape. When diffuse pleural thickening calcifies and is associated with volume loss in the affected lung, it is termed fibrothorax.

Yellow Nail Syndrome with Bilateral Pleural Plaques and Diffuse Pleural Thickening: A Mimic of Asbestos Related Disease

Yellow nail syndrome is a rare acquired condition of unknown aetiology associated with distinct nail discolouration/xanthonychia, pulmonary manifestations, and lymphoedema. Pleural plaques and diffuse pleural thickening are typically, although not exclusively, recognised as markers of prior commercial asbestos exposure. The presence of such biomarkers may assist an asbestos personal injury evaluation. A postmortem examination performed on a 72-year-old man with known long-standing yellow nail syndrome identified pleural plaques and diffuse pleural thickening. An evaluation of the occupational history identified no known asbestos exposure. Electron microscopic mineral fibre analysis detected no asbestos fibres. To the best of our knowledge, this is the only case of yellow nail syndrome in which these benign pleural changes are reported ex asbestos. Alternate causes for such pleural pathology were absent. There is merit in physicians and pathologists having an awareness of these new manifestations when considering claimed asbestos related changes during life and at postmortem.

Occupational lung disease

Some occupational lung diseases are defined by their clinical or pathological nature (e.g. occupational asthma or mesothelioma), while others are defined by their specific etiology (e.g. silicosis, farmer’s lung). Most fall into one of three categories. The first is airways disease, including occupational asthma (induced by a workplace agent), work-exacerbated asthma (preexisting asthma provoked by one or more agents at work), and irritant-induced asthma (initiated by a single, toxic exposure to a respiratory irritant); COPD and obliterative bronchiolitis may arise from workplace exposures, and around 10% of lung cancers have an occupational etiology. The second is parenchymal diseases, incorporating the many types of pneumoconiosis, differentiated by the dust that caused them, and the many types of extrinsic allergic alveolitis (or hypersensitivity pneumonia) categorized by the occupations in which they arise. The third is pleural diseases comprising pleural plaques, diffuse pleural thickening, and mesothelioma.