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Lymphomatoid granulomatosis (LG) is an angiocentric and angiodestructive lymphoproliferative disease that mainly involves the lung. Thirty percent of patients with LG have neurological symptoms. We report serial changes in MRI of a patient with LG of the brain. Postcontrast MRI demonstrated multiple punctate and linear areas that preceded hemorrhage, as indicated by hypointensity with surrounding hyperintensity on subsequent T2-weighted images. The diagnostic value of these lesions observed with contrast MR images is discussed. We consider that enhancing areas correspond to walls of small vessels affected by LG.

We describe a case of bilateral chylothorax with malignant pleural mesothelioma. A 41-year-old woman was admitted to our hospital because of dyspnea. She had no history of exposure to asbestos. A chest radiograph and chest computed tomogram (CT) on admission revealed massive bilateral pleural effusion and a large tumor with pleural thickening in the left lateral and anterior parts of the pleura and mediastinum. Biochemical tests of pleural fluid revealed chyle. Two years before, she had been diagnosed through histological and histochemical examinations as having diffuse malignant pleural mesothelioma of the epithelial type. Chest-tube drainage was performed, and pleurodesis was induced by the intrathoracic injection of OK-432 at 10 KE per dose. The chylothorax disappeared after pleurodesis. To date, reports of malignant mesothelioma with nontraumatic chylothorax have been rare.

We encountered a case of pulmonary eosinophilic granuloma complicated with pneumothorax. A 24-year-old man was admitted to our department because of respiratory difficulty. Chest radiography on admission showed a right pneumothorax. A thoracic catheter was therefore inserted, and the pneumothorax was improved. A chest radiograph obtained after treatment showed diffuse linear reticular shadows; and a chest CT scan showed starlike nodular lesions and multiple cysts in the lungs, and a large nodule in the left rib. Because an ulcer had been diagnosed in the oral cavity 1 year previously, a mandible biopsy was performed, and a granulomatous lesion consisting of eosinophils was recognized. Taken together with the pulmonary findings, an eosinophilic granuloma was diagnosed. The patient was instructed not to smoke and the clinical course was observed. The pulmonary, mandibular, and costal lesions improved.

While Nocardial infections are being diagnosed with increasing frequency, infection with Nocardia otitidiscaviarum remains relatively uncommon. We report a case of pulmonary Nocardia otitidis-caviarum infection in a 35-year-old man with Cushing's disease. This work describes the first case of nocardiosis in Japan caused by Nocardia otitidis-caviarum in Cushing's disease. The patient was admitted to our department because of edema. A diagnosis of Cushing's disease was made on the basis of elevated serum levels of cortisol and adrenocorticotropic hormone (ACTH) and pituitary adenoma was found in a cranial CT scan. One month after admission, chest radiographs showed a large bilateral mass on the lung fields. Nocardia otitidis-caviarum was isolated from the sputum. The patient responded poorly to intravenous PAPM/BP, but later improved after treatment with trimethoprim-sulfamethoxazole, but he died of heart failure and respiratory failure after the initiation of this therapy. This case demonstrated that nocardiosis must be considered in differential diagnosis as an opportunistic infection.

Sarcoidosis is known to be a disease characterized by high familial aggregations. We reported on the genealogy of sarcoidosis in a man and his identical twin sons. The patient we encountered was a 49-year-old man admitted to our hospital because of abnormal chest X-ray findings observed during a medical checkup. Cervical and hilar lymph nodes were swollen on both sides, and lesions were observed in the right lung field. Biopsy specimens from cervical lymph nodes disclosed epithelioid cell granuloma without caseous necrosis. A diagnosis of sarcoidosis was made. The disease had also been diagnosed in the patient's identical twin sons 2 years earlier. They had been successfully treated and no recurrence has been observed. HLA typing disclosed that the father and his twin sons had identical A 33 (19), B 44 (12), DR 2, and DR 12 genes. This finding suggested that genetic factors are involved in the onset of this disease.