Diffuse interstitial pneumonia of unknown etiology has been subclassified into two groups on the patho-histological basis by the study group under the sponsorship of the Japanese Ministry of Health and Welfare. One is Group A, typical idiopathic subtype, fundamentally corresponding to UIP (usual interstitial pneumonia, Liebow) and the other is Group B, closely similar to Group A but possibly modified by respiratory infection. As the clinical features of Group B have not been clarified so far, we investigated them in 8 cases of Group B (M:F=7:1, 56.7 years at first visit) and 5 cases of Group A (M:F=4:1, 54.4 years), all of which were pathologically diagnosed by open lung biopsy and/or autopsy. Only in Group B, there were 3 cases with occupations related to dust exposure, and 7 cases with intermittent but persistent mucus expectoration. The duration of symptoms before the first presentation to hospital was longer in Group B than in Group A (1.6 years vs. 0.6 years). Clubbed fingers were more frequently observed in Group B (n=6 vs. n=1), but induration in the tuberculin test was less frequent in Group B (n=1 vs. n=5). In the chest X-ray findings, pleural thickening was frequent in Group B (n=6 vs. n=0), but elevation of the diaphragm was unusual in Group B (n=2 vs. n=5). At the end of the observation period (1968-1990), 4 of 8 cases in Group B were alive and their mean survival period was 6.9 years (in cases of death, 8.8 years), longer than in Group A (all 5 dead, 3.5 years). In conclusion, Group B has a better prognosis and is possibly connected with respiratory infection. At the time of the first presentation to hospital, Group B is likely to be distinguishable from Group A both by frequent findings of persistent productive cough, clubbed fingers, pleural thickening and by unusual occurrences of diaphragmatic elevation and induration in the tuberculin test.

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We determined the effects of Pseudomonas aeruginosa on transport of protein and liquid across the alveolar epithelium in anesthetized rabbits. Following the injection of 3μCi of ¹³¹I-albumin in anesthetized rabbits as a vascular marker, we instilled 3ml/kg of 5% albumin solution with 10⁷ or 10⁹ CFU P. aeruginosa, 3μCi of ¹²⁵I-albumin and 3mg of Evans blue into the alveolar spaces of the right lung. The rabbits were ventilated with 60-100% oxygen and 1-2% halothane over 8h. We removed the lungs and aspirated the alveolar fluid 8h after instillation. We measured protein concentration in instilled and aspirated alveolar fluid, and radioisotope counts in alveolar fluid, homogenized lung and plasma. Then we calculated the influx and efflux of radioisotope across the alveolar epithelium. Liquid clearance from the alveolar spaces and the lungs was calculated using protein concentration of alveolar fluid and extravascular lung water. In the experiments with 10⁹ CFU P. aeruginosa, we found that ¹²⁵I-albumin remaining in the lungs decreased and ¹²⁵I-albumin in plasma increased. Lung liquid clearance decreased by 15%. However, protein and liquid clearance in the experiments with 10⁷ CFU P. aeruginosa or autologous serum were not different from those in the control experiments. P. aeruginosa was cultured from blood, right pleural effusion, and liver in the experiments with 10⁹ CFU P. aeruginosa, but not in the experiments with 10⁷ CFU P. aeruginosa. We conclude that P. aeruginosa increases the influx and efflux of protein across the alveolar epithelium, but decreases clearance of liquid from the alveolar spaces. The effect of P. aeruginosa on permeability across the alveolar epithelium depends on the inoculum size of P. aeruginosa in the lung.

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Between January 1988 and December 1992, 68 patients admitted to our Department of Internal Medicine with hematological malignancies or solid tumors showed colonization of the respiratory tract with Xanthomonas maltophilia (X. maltophilia). To characterize the significance of respiratory tract colonization by X. maltophilia, we retrospectively reviewed the medical records of the 68 patients colonized with this organism. Twenty-seven of these 68 patients developed pneumonia, with X. maltophilia being implicated in 10 cases. The majority of the 10 patients showed lobular infiltration on chest X-ray. Pleural effusion was observed in 2 (20%) of the 10 patients. All 68 strains of X. maltophilia were resistant to imipenem/cilastatin. Most strains (98.5%) were sensitive to latamoxef, while all strains were sensitive to minocycline. This report describes the clinical features of nosocomial X. maltophilia pneumonia in immunocompromised patients.

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We evaluated bronchial arterial hemodynamics after thoracic irradiation therapy. We performed bronchial arteriography in 9 patients (8 males and 1 female) with lung cancer who received thoracic irradiation (58-72 Gy). Three patients had adenocarcinoma, 3 squamous cell carcinoma, 2 small cell carcinoma and 1 large cell carcinoma. Their clinical stages were 6 in stage III_B and 3 in stage IV. Eight of these cases also received chemotherapy by intra-bronchial arterial infusion of anti-cancer agents (Carboplatin and/or Cisplatin).
The bronchial arterial supply was patent except in the one complete remission case (small cell carcinoma of stage III_B). In the five cases developing radiation pneumonitis, bronchial arteries demonstrated angiogenesis in the radiation fields, despite which pulmonary arteriography and/or pulmonary perfusion scintigrams showed a decreased pulmonary arterial supply. Bronchial arterial hemodynamics demonstrated no significant damage in the bronchial arteries by the thoracic irradiation therapy and/or bronchial arterial infusion of anti-cancer agents. It is suggested that patent bronchial arteries after radiation therapy promote local recurrences of lung cancer. In 5 cases, including 2 local relapsed cases and 3 cases showing no remarkable response to radical radiation therapy, we performed bronchial arterial infusion of anti-cancer agents after radiation therapy, with good responses obtained.
We conclude that thoracic irradiation did not damage bronchial arteries as compared with pulmonary arteries, and that in local relapsed and radio-resistant cases bronchial arterial infusion of anti-cancer agents after radiation therapy is a useful approach.

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We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60mM KCl. Preincubation with either meclofenamate (31μM), a cyclooxygenase inhibitor, or L-N^G-nitroarginine (100μM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

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Here we report a new type of hypersensitivity pneumonitis caused by inhalation of spores of Pholiota nameko. P. nameko is a kind of mushrrom which is a of Japanese delicacy. Among people who are working in nameko cultivation, we found three patients suffering from hypersensitivity pneumonitis, and identified that it was caused by inhalation of spores of P. nameko. Every patient was engaged in indoor nameko cultivation inside a building equipped with a air and moisture conditioning system for two to ten years. In the indoor environment, it was thought that they were exposed to and inhaled a high density of nameko spores. Among 15 healthy indoor nameko growers, we found 6 who had precipitating antibody against extracts from nameko spores; however, there were no antibody positive people in 17 outdoor nameko growers. As seen in dairy farmers, it was clarified that there is a percentage of precipitin positive nameko growers who are asymptomatic. This is concrete evidence that changes of mushroom cultivation style can induce a new type of hypersensitivity pneumonitis. These findings were considered to be an important experience from the view points of environmental pulmonary diseases and industrial medicine.

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A 65-year-old woman being treated under the diagnosis of pneumonia was subjected to further evaluation for right back tenderness. Chest radiography revealed a granular, net-like shadow in the right lower lung field, and right pleural thickening with pleural fluid retention. Ultrasonography demonstrated a cystic mass of uniformly low echo density, corresponding to the site of tenderness. This lesion was located on the right renal dorsal, right iliopsoas muscle ventral side. Based on CT findings of internal water density and marginal enhancemant, the lesion was diagnosed as an abscess. With the suspicion of right tuberculous pyothorax with retroperitoneal gravitation abscess, puncture was attemped. The diagnosis was confirmed by the presence of Mycobacterium tuberculosis in the specimen. Antituberculosis chemotherapy was initiated, with drainage for symptom relief and lesion range definition. The abscess cavity communicated with the right pleural cavity via s stalk. The stalk path was confirmed by CT, and surgical curettage was performed. Tuberculous pyothorax with retroperitoneal gravitation abscess is rare and is not discussed in standard textbooks. In large series of cases it is not mentioned. In this patient we assumed that retroperitoneal gravitation abscess occurred as a result of the advanced state of tuberculous pyothorax.

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The patient was a 71-year-old man with dyspnea and bilateral leg edema. He was admitted to our hospital with worsening of dyspnea and had received therapy for chronic heart failure in another hospital. On admission, chest X-ray film revealed dilatation of the cardiac silhouette (CTR: 58%). Electrocardiogram showed atrial fibrillation and negative T wave in II, III, and _aV_F. Cardiac arteriogram showed no organic lesions, but pulmonary hypertension, pulmonary artery pressure of 60/21/34mmHg, right ventricular pressure of 40/9/20mmHg were recongnized in pulmonary hemodynamics. The diagnosis of chronic pulmonary thromboembolism was made on the basis of pulmonary arteriogram findings and multiple defects of lung perfusion scintigram. After administration of oral PGI₂ analogue for one month, lung perfusion scintigram and right cardiac pressure were markedly improved.

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We report a case of minocycline-induced pneumonitis. A 30-year-old woman was treated with minocycline for mycoplasma pneumonia of the right upper lobe. About 15 days after starting treatment, she developed a productive cough, stridor, and dyspnea. The chest X-ray film showed pulmonary infiltration in the left middle lung field. Based on the clinical history and the detection of eosinophilia in the bronchoalveolar fluid, drug-induced pneumonitis was suspected. Treatment with minocycline was discontinued and prednisolone (20mg/day) was started, after which her symptoms subsided and there was marked regression of the pulmonary infiltrates on chest X-ray films. The lymphocyte stimulation test for minocycline was negative, but the diagnosis was confirmed by a positive oral provocation test.

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We report the first case of pulmonary actinomycosis that was diagnosed by histological findings of transbronchial lung biopsy specimen. A 60-year-old man was admitted because of cough and bloody sputa. His chest roentgenogram and CT scan revealed a cavitary opacity in the apex of the left lung. Histological findings of the biopsy specimen showed multiple basophilic actinomyces granules accompanied by an acute inflammatory exudate, comfirming the diagnosis of pulmonary actinomycosis. We prescribed antibiotic treatment and a good response was obtained.

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An asymptomatic 26-year-old male was admitted to our hospital for examination of an abnormal mediastinal shadow on chest X-ray. Chest CT showed a large mass in the anterior mediastinum with marked para-aortic lymph node enlargement. The mass consisted mostly of multiloculated low-density areas surrounded by a rim of enhancing parenchymal tissue. Both the cystic tumor and surrounding lymphnodes were resected. The tumor measured 18×10×2cm and contained about 450ml of straw colored fluid. Pathological examination revealed a thymic cyst, the wall of which was composed of Hodgkin's lymphoma cells and nodular sclerotic lesions containing many lacunar cells and Reed-Sternberg cells.

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A 17-year-old female with anorexia nervosa developed pneumomediastinum, subcutaneous emphysema, retroperitoneal emphysema, interstitial pulmonary emphysema and epidural emphysema (epidural emphysema; air between the dura mater and the vertebral arch). She had no history of bronchial asthma. The mechanism was presumed to be weakness of the alveolar wall due to malnutrition, leading to rupture of alveoli, followed by air entering the interstitium and dissecting along perivascular sheaths (interstitial pulmonary emphysema) into the mediastinum. A further increase in mediastinal pressure may bring about opening of the fascial planes along great vessels and allow air to penetrate into subcutaneous tissues and the spinal canal. These types of emphysema have been reported in bronchial asthma cases and in those on positive pressure breathing. To our knowledge, there are no previous reports of anorexia nervosa associated with these phenomena.

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A 59-year-old woman complaining of progressive dyspnea on exertion was admitted to our hospital in August 1992. In 1983 she had experienced exertional dyspnea from August to November, then improved spontaneously. In August 1984, she was admitted to our hospital due to the recurrence of the symptom. She was diagnosed as summer type hypersensitivity pneumonitis based on the following findings, 1) detection of non-caseous granuloma by transbronchial lung biopsy, 2) detection of precipitating antibody to Trichosporon cutaneum in the serum, 3) induction of the symptom by provocation test with the fungi, 4) isolation of the fungi from her house. In spite of moving from her house after discharge, she continued to visit her former house once a week to clean it. During the period, fibrotic changes on the chest roentgenogram were slowly progressive. In august 1992, ten years after the onset, she was re-admitted to our hospital with a complaint of exacerbated dyspnea on exertion. Open lung biopsy revealed granulomatous lesions with fibrotic changes, which was compatible with chronic type hypersensitivity pneumonitis. This patient was diagnosed as a chronic case of summer type hypersensitivity pneumonitis because of the clinical course and findings of open lung biopsy as well as laboratory data at the first admission.
We consider that this case offers various information in considering the mechanism of chronic progress of summer type hypersensitivity pneumonitis.

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A 65-year-old man was admitted to Oita Medical University Hospital with complaints of right back pain, diplopia and vertigo. A tumor, 33×25mm, was found on the right lateral chest wall on admission. Chest X-ray film and chest CT scan showed a tumor, 50×30mm, in the right posterior mediastinum. The chest wall tumor was diagnosed as malignant hemangiopericytoma by biopsy, and the same diagnosis was made for the mediastinal lesion by aspiration cytology. Brain MRI showed a mass at the skull base, which was found to be a metastatic bone tumor from the mediasinal malignant hemangiopericytoma. Abdominal CT scan showed a massive tumor, 65×60mm, in the right lobe of the liver. The liver tumor was diagnosed as hepatocellular carcinoma by biopsy.
Combination chemotherapy, employing cyclophosphamide, vincristin, pirarubicin and dacarvazine (DYVADIC), in conjunction with radiation therapy, produced no response. The patient died 5 months after admission.
Malignant hemangiopericytoma arising from the mediastinum is uncommon. Thus, the clinical features of our case, as well as those of previously reported cases in Japan, are discussed herein.

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A 76-year-old man was admitted to our hospital in December of 1990, for investigation of progressive dyspnea on exertion over the previous 3 months. Physical examination revealed cyanosis, but no edema. Cardiomegaly was seen on chest X-ray, and findings compatible with right-sided congestive heart failure were revealed by ECG and echocardiography. Lung perfusion scintigrams showed multiple defects in both lungs, but no abnormal findings were detected on a ventilation study. Venograms of the lower extremities disclosed thrombosis of the right femoral vein. Therefore, a diagnosis of recurrent pulmonary thromboembolism was made. Furthermore, lupus anticoagulant and IgG-class anticardiolipin antibody were noted in the serum. The patient was treated with intravenous heparin, long-term warfarin, and transvenous placement of a Greenfield filter in the inferior vena cava. The clinical symptoms and signs improved, and no recurrence has been seen during the 13 months since the onset. On discharge, both antiphospholipid antibodies were negative. This case of primary antiphospholipid syndrome without autoimmune disease, with transiently positive antibodies only in the exacerbation phase, is discussed herein.

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A 49-year-old man was admitted to our hospital for dyspnea. Chest X-ray examination showed a massive right pleural effusion. Using intrathoracic tube drainage, a large quantity of chocolate-like pleural effusion was removed. Laboratory data demonstrated severe anemia and hypoproteinemia, and TPHA was positive. Antiameba antibody in blood was high, and a liver abscess was demonstrated on abdominal CT scan. Amebic liver abscess and amebic empyema were thus diagnosed. With pleural tube drainage and percutaneous liver abscess drainage, metronidazole (1.5g/day) was administered. After administering this drug, the high temperature normalized and the patient's general condition improved significantly.
Recently, amebic infections have been reported in increased numbers, especially in male homosexuals and immunocompromised patients. Henceforth amebic infection should be considered when pleural effusion and empyema are suspected.

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A 49-year-old man was admitted to our hospital because of hemosputum, left chest pain and an abnormal shadow on chest X-ray. Computed tomography of the chest revealed a tumor-like shadow with a low density area in the left lower lung field. Ga scintigraphy revealed strong Ga uptake in the left lower lung. Fiberoptic bronchoscopy showed obstruction of subsegmental bronchi of lt. B⁹⁺¹⁰. Neither transbronchial biopsy nor sputum cytology showed any malignant cells. Transcutaneous lung biopsy showed infiltration of foamy macrophages in alveolar spaces and lymphocytes and plasma cells in alveolar septa. Since there was a possibility of complicating lung cancer, and because of refractory hemosputum, the patient underwent left lower lobectomy. The cut surface of the resected left lobe showed the features of golden pneumonia with cavitation. The histological features of the resected specimen were those of lipoid pneumonia, and no cancer cells were detected.

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