Detection of MALT1 gene rearrangements in BAL fluid cells for the diagnosis of pulmonary mucosa-associated lymphoid tissue lymphoma.

BACKGROUND: Mucosa-associated lymphoid tissue (MALT) lymphoma constitutes approximately 90% of primary pulmonary lymphoma, and the diagnosis of pulmonary MALT lymphoma often requires invasive methods such as surgical lung biopsy. Chromosomal rearrangements involving MALT lymphoma translocation gene 1 (MALT1) have been reported to be specific for MALT lymphoma. The combination of BAL and cytologic approaches with molecular methods is useful for the diagnosis of lymphoproliferative disorders. Therefore, we examined the detection of MALT1 gene rearrangements in BAL fluid (BALF) cells for the diagnosis of MALT lymphoma. METHODS: We determined the percentage of BALF cells with MALT1 gene rearrangements by using the fluorescence in situ hybridization (FISH) method in 10 patients suspected to have pulmonary MALT lymphoma. RESULTS: MALT1 gene rearrangements in BALF cells were found in four of five cases with pulmonary MALT lymphoma (percentage of BALF cells with MALT1 gene rearrangements: 21.8% ± 6.8%). On the other hand, MALT1 gene rearrangements in BALF cells were negative in the five cases without pulmonary MALT lymphoma and one case with pulmonary MALT lymphoma. CONCLUSION: These results suggest that the detection of MALT1 gene rearrangements in BALF cells is useful for the diagnosis of pulmonary MALT lymphoma, as it is a specific method that is less invasive than surgical biopsy. Because of the small number of patients in this study, further investigations are necessary to evaluate the detection rate of MALT1 gene rearrangements in BALF cells from patients with pulmonary MALT lymphoma.

[A case of rheumatoid arthritis with pneumothorax due to subpleural pulmonary rheumatoid nodules].

Pneumothorax secondary to nodular rheumatoid lung disease is a rare complication of rheumatoid arthritis. Here we report a case of rheumatoid arthritis with pneumothorax due to subpleural pulmonary rheumatoid nodule. A 74-year-old woman with a 14-year history of rheumatoid arthritis has admitted to our hospital due to dyspnea and right chest discomfort, and her chest X-ray film and computed tomography revealed right pneumothorax. Her chest X-ray and computed tomography findings before the onset of pneumothorax had demonstrated multiple subpleural cavitary nodules in both lungs. She had taken antifungal agents under a diagnosis of pulmonary fungal infection for a year without any change of her chest radiological findings. After incomplete reexpansion with sustained air leakage by right chest tube drainage, video-assisted thoracic surgery was performed. The pulmonary cavitary nodules of her right middle and lower lobes were with successfully excised. The histopathology of excised subpleural lung nodules showed typical features of rheumatoid nodules, and the cavitation of the rheumatoid nodule in right S5 had fistula formation to the pleural space, and thus was thought to have caused the pneumothorax.

[Early case of idiopathic pulmonary alveolar proteinosis positive for serum anti-GM-CSF antibody].

An asymptomatic 56-year-old woman who had never smoked and had been healthy was admitted to our hospital because of abnormal shadows on a chest X-ray film taken on a medical check-up. Chest CT showed ground-glass opacities in the right upper lung field. No abnormality on chest X-ray had been pointed out on any annual medical check up until then. As bronchofiberscopy (BAL and TBLB) could not reveal any diagnostic information, VATS biopsy was performed. Histological findings showed that alveolar spaces were filled with PAS-positive granular materials, and fused membrane structures and amorphous material were demonstrated by electron microscopy. Anti-GM-CSF antibody of serum was also positive (7.908 microg/ml). Based on these findings, we decided this was an early case of idiopathic pulmonary alveolar proteinosis.