廣島 健三

In order to compare the activity of lung cancer cells in the central zones of lesions with cells in the peripheral zones of the tumor, we examined 29 resected specimens of primary lung cancer in terms of argyrophilic nucleolar organizer regions (AgNORs) and immunoreactivity of proliferating cell nuclear antigen (PCNA). The 29 resected specimens consisted of 9 squamous cell carcinomas, 10 papillary adenocarcinomas, and 10 tubular adenocarcinomas. © 1993, The Japan Lung Cancer Society. All rights reserved.

A 34-year-old man with persistant cough was admitted to our hospital. Bronchoscopic examination revealed a polypoid tumor with smooth surface which almost completely obstructed the right main bronchus. The tumor was removed by transbronchial snaring forceps and histologically confirmed as neurofibroma. Residual tumor was excised by biopsy forceps and further endoscopic Nd-YAG laser vaporization was performed. This is the first case in our country in which bronchoscopic treatment was performed for bronchial neurofibroma. Bronchoscopic removal might be the preferred treatment in the present case, although long-term follow-up is also required.

We report a 60-year-old man, who was admitted to the hospital with complaints of cough and sputum. His chest x ray showed an abnormal mass in the right upper lobe. After admission he noticed the painful gingival tumor. Right upper lobectomy and resection of the gingival tumor were performed. Their histological features showed that the tumor consisted of a papillary and tubular adenocarcinoma mixed with a component of spindle cells. Immunohistochemical study demonstrated a positive reaction in the epithelial component for keratin and epithelial membrane antigen, and not only these epithelial markers but also vimentin were expressed in some spindle tumor cells. Electron microscopic study confirmed the biphasic pattern, showing gland formation and undifferentiated cells. We diagnose this case as adenocarcinoma of the lung with a spindle cell component and the gingival tumor was metastatic. Autopsy showed that metastatic lesions were found in the left adrenal gland and in the left kidney. The tumor cells in the left adrenal gland were composed of spindle cells and the tumor in the left kidney showed gland formation. Immunohistochemical and electron microscopic findings of surgical and autopsy specimen suggest that this tumor is of epithelial origin, and the spindle cells are derived from immature mesenchymal cell transformation of epithelial cells.

A 39-year-old male was admitted complaining of nonproductive cough and dyspnea on exertion. Death occurred eight months after onset of the symptoms. Autopsy examination showed that the pulmonary trunk and left main pulmonary artery were markedly dilated and completely occluded by a tumor. The tumor had infiltrated into the left upper lobe and mediastinal lymph nodes, and metastatic nodules were found in both lungs and in the left adrenal gland. Small foci of infarction were noted in the lower lobes of both lungs. The tumor cells were of two types; pleomorphic spindle cells and bizarre multinucleated giant cells. Immunohistochemically, they were positive for vimentin, myosin, and lysozyme, but negative for desmin and muscle-specific actin. The cytoplasm of the tumor cells was showed by electron microscopy to contain microfilaments, dense bodies, and pinocytotic vesicles. We diagnosed this case as undifferentiated sarcoma of the pulmonary artery. Approximately 100 cases of pulmonary artery sarcoma have been reported. Histopathologically, almost all of the reported cases showed both spindle cells and pleomorphic giant cells, indicating a biologically anaplastic neoplasm.

大気汚染物質のうち, 最も一般的に存在するオゾン (O₃) と生活と密接に関連したタバコ煙の複合作用が, 呼吸器系にどのような影響を引き起こすか明らかにする目的で動物実験を行った。5週令のWistar系雄ラットを用い, 週5回タバコ煙暴露を行った群, 0.5 ppm O₃に1日8時間, 週6回暴露した群, 0.5 ppm O₃に1日8時間, 週6回暴露し, 同時に週5回タバコ煙暴露を行つた群および対照群を作成した。この条件を継続して行い, 2, 4, 8, 16, 20, 24, 36, 52週後に屠殺し, 病理組織学的に検索した。<BR>タバ切煙とO₃の複合暴露により, 気管, 気管支の障害と肺胞の障害がいずれも単独暴露肺よりも早期に起こる。気管では4週後に局所的に上皮が増生し, 数層をなすものがみられ, 気管支壁では浮腫や膠原線維の増生がみられた。また24週後の7例中1例に気管上皮の扁平上皮化生が認められた. 細気管支, 肺胞では4週後から, 細気管支上皮細胞の腫大と肺胞側への増生が認められた。このalveolar bronchiolizationを呈する過形成巣の細胞は2～3層をなし, 線毛上皮細胞や無線毛上皮細胞からなっていた。また, 扁平上皮化生を示すものもみられた。これらの変化は52週まで認められたが, 20週以後は線維化を伴い, 上皮細胞が単層となるものが増加し, 腫瘍の発生はみられなかった。

A 72-year-old female was admitted to our hospital because of bronchorrhea and diffuse infiltrative shadows on chest x-ray. The TBLB specimens suggested adenocarcinoma with a bronchiolo-alveolar pattern. This case was clinically diagnosed as bronchiolo-alveolar cell carcinoma. Corticosteroids were not effective and she died of respiratory failure about 3 months after the admission. Autopsy findings showed a 5 X 4 x 2cm mass at the tail of the pancreas. The specimens obtained from the lung tissue showed tumor cells growing as a single layer along alveolar walls. The features of the lesion in the lung were pathologically similar to those of the lesion in the tail of the pancreas. Further examination revealed metastatic pulmonary adenocarcinoma of pancreatic origin. Comparative analyses of biochemical components in sputum in this case and previous reports showed that levels of fucose, albumin, and DNA were low in this case. It was suggested that this excessive production of sputum was due to abnormal secretion of tumor cells rather than exudation of plasma constituents and inflammatory change in the airways. © 1991, The Japan Lung Cancer Society. All rights reserved.

Two cases showed multiple coin lesions on chest X-ray. Case 1, a 61-year-old woman, had multiple lung nodules which were detected 18 years after hysterectomy for leiomyoma. The lesions were composed of monotonous smooth muscle cells and intermingled with glandular structures of bronchiolar appearance. There was no morphologic evidence of malignancy in these components. Cases 2, a 45-year-old woman, was under therapy for uterine leiomyosarcoma for 2 years. The tumor cells of the lung were apparently similar to those in case 1 but were more pleomorphic and hyper-chromatic. Multinucleated bizarre cells were also found. Most lesions of case 2 included no glandular structures except for a tiny lesion less than 2 mm. Concerning those morphologic feature the lesions of case 1 differ from those of case 2, which are considered to be metastatic from uterine leiomyosarcoma. We diagnosed case 1 as benign metastasizing leiomyoma. © 1991, The Japan Lung Cancer Society. All rights reserved.

検査室内における環境汚染状況把握のため, 21名の呼吸器疾患患者を対象に気管支鏡検査の前後で室内および気管支鏡表面定点において付着菌を検出し, その菌量および菌種について比較検討を行った。その結果, 透視台天板頭部, 同部下床, 術者プロテクター, 気管支鏡把持部および先端部に付着細菌の有意な増加を認めた。多量に検出された菌でみると, 気管支鏡先端部および把持部では口腔由来と思われるGPCおよびGNCが多く, 透視台頭部下床では環境に存在するGPRおよびGNRが主に検出された。また透視台天板頭部ではGPR, GPC, GNRがほぼ同等に検出された。今回の検出菌は口腔常在菌と環境に存在する細菌が主であったが, 被験者から病原性細菌の飛散が予想される場合には, 環境汚染に十分配慮する必要がある。

Administration of monocrotaline in rats causes hypertensive changes in the pulmonary vasculature, focal pneumonitis and mast cell hyperplasia in the lung. In order to investigate the role of mast cell hyperplasia in monocrotaline-induced pulmonary changes, changes of mast cell density and histamine content in rat lung were studied after monocrotaline administration (40 mg/kg, s.c.) with or without ketotifen treatment (2 mg/kg, every 8 hours). After monocrotaline administration, mast cell density in lung tissue decreased at 1 wk (0.67 ± 0.41/mm2), but increased by 4 wk (307.4 ± 152.6/mm2) 136 times control value (2.25 ± 1.5/mm2). Histamine content in lung tissue (control: 0.6 ± 0.23 mcg/g wet weight) increased as much as 144-fold in 4 weeks (86.7 ± 50.5 mcg/g). There was significant correlation between the degree of right ventricular hypertrophy (RV/LV + S) to histamine content in lung tissue and to mast cell density in relation to the various types of treatment. Ketotifen treatment did not prevent the development of pulmonary hypertension which was evaluated by the elevation of right ventricular systolic pressure in right heart catheterization, but significantly reduced right ventricular hypertrophy. Ketotifen treatment did not significantly inhibit the increase of mast cell denstiy and serum histamine content, but decreased the histamine content in lung tissue significantly by 4 wk. Because of the anti-histamine activity of ketotifen, the present data revealed that histamine contained in mast cell has no pathogenetic role in the development of monocrotaline-induced pulmonary hypertension. We consider that pronounced mast cell hyperplasia probably reflects the existence of hyperplastic stimulation for lung cells which was topically shown as pneumonitis.

Administration of monocrotaline in rats causes hypertensive changes in the pulmonary vasculature, focal pneumonitis and mast cell hyperplasia in the lung. In order to investigate the role of mast cell hyperplasia in monocrotaline-induced pulmonary changes, changes of mast cell density and histamine content in rat lung were studied after monocrotaline administration (40 mg/kg, s.c.) with or without ketotifen treatment (2 mg/kg, every 8 hours). After monocrotaline administration, mast cell density in lung tissue decreased at 1 wk (0.67 ± 0.41/mm2), but increased by 4 wk (307.4 ± 152.6/mm2) 136 times control value (2.25 ± 1.5/mm2). Histamine content in lung tissue (control: 0.6 ± 0.23 mcg/g wet weight) increased as much as 144-fold in 4 weeks (86.7 ± 50.5 mcg/g). There was significant correlation between the degree of right ventricular hypertrophy (RV/LV + S) to histamine content in lung tissue and to mast cell density in relation to the various types of treatment. Ketotifen treatment did not prevent the development of pulmonary hypertension which was evaluated by the elevation of right ventricular systolic pressure in right heart catheterization, but significantly reduced right ventricular hypertrophy. Ketotifen treatment did not significantly inhibit the increase of mast cell denstiy and serum histamine content, but decreased the histamine content in lung tissue significantly by 4 wk. Because of the anti-histamine activity of ketotifen, the present data revealed that histamine contained in mast cell has no pathogenetic role in the development of monocrotaline-induced pulmonary hypertension. We consider that pronounced mast cell hyperplasia probably reflects the existence of hyperplastic stimulation for lung cells which was topically shown as pneumonitis.