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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.

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.

We report a case of severe eosinophilic pneumonia induced by several antibiotics, requiring mechanical ventilation. A 44-year-old man had been admitted previously to a different hospital because of a high fever and dry cough continuing for a week. Although bacterial pneumonia was diagnosed and he had been treated with several antibiotics, his respiratory state worsened gradually and he was refered to our hospital with severe hypoxia. He needed mechanical ventilation on the fifth hospital day. TBLB identified eosinophilic pneumonia. Although we discontinued all antibiotics and started steroid therapy, he became feverish and his leukocyte count, which was neutrophil dominant, elevated again. We suspected bacterial pneumonia and administered antibiotics that he had never received before. However we had to discontinue these antibiotics soon because of a further inflammatory response. His condition then improved gradually and he was weaned from mechanical ventilation. It is rare for drug-induced eosinophilic pneumonia to become so severe that mechanical ventilation is necessary. We thought that an allergic reaction may have been induced by the series of several antibiotics, inducing severe pneumonia.

An 80-year-old man was admitted in October, 2002 with blood-tinged sputum. He had already been treated for hepatocellular carcinoma (HCC). The chest radiograph and chest CT scan showed a solitary pulmonary mass in the left lower lobe. The serum alpha fetoprotein (AFP) was elevated to 261 ng/ml. Fiberoptic bronchoscopy revealed an endobronchial tumor at left B8a and the results of brushing cytology were compatible with HCC. We confirmed the diagnosis by immunohistochemical staining using anti-AFP antibody. Endobronchial metastatis of HCC is rare and immunohistochemical staining was useful for diagnosis.

This patient was a 28-year-old man who had been treated with steroids for recurrent asthmatic attacks since around the age of 20. At one time the steroid therapy was discontinued and other treatments, including bronchodilator therapy and desensitization therapy, were substituted. At age 28, he first consulted our hospital due to the recurrence of attacks. We found peripheral eosinophlia and a cytologic examination revealed Curschmann spirals in his sputum. Migratory infiltrate recurred, and steroids and antibiotics were prescribed each time. A confirmed diagnosis of allergic bronchopulmonary aspergillosis was made at age 35. The patient was treated with continuous oral steroids for recurrent infiltrates. After the start of inhale steroid therapy at age 44, the frequency of attacks decreased and tapering of the oral steroids became possible. It is notable that lung tissue destruction progressed by recurrent pneumonia and emphysema extended into all portions of the lung. Furthermore, this case history is of value since it yields a series of images taken over a period of 27 years.

A 50-year-old woman had been treated with propylthiouracil (PTU) for hyperthyroidism. She was admitted to our hospital because of hemosputum, and severe hypoxemia developed. The CT scan showed diffuse infiltration in both lung fields, bronchoalveolar lavage fluid revealed diffuse alveolar hemorrhage, and the level of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) was high; and therefore diffuse alveolar hemorrhage associated with MPO-ANCA positive vasculitis induced by PTU was diagnosed. Following corticosteroid therapy initiated after the termination of PTU, the pulmonary infiltration rapidly improved and the patient's MPO-ANCA level returned to normal. Recrudescence of diffuse alveolar hemorrhage occurred following a reduction in steroids, but no recurrence was found after cyclophosphamide therapy was combined with steroid therapy. During the course of therapy, various cardiac conducting system abnormalities which correlate with the course of steroid therapy were found, indicating that cardiac conducting system abnormalities may be associated with MPO-ANCA-positive vasculitis.

A 22-year-old woman was referred to our hospital suffering from repeated exacerbation of infiltrates confined to the medial portion of the right lower lung lobe, suggestive of pulmonary sequestration. Angiography revealed an anomalous vessel originating from the left side of the descending aorta, flowing behind it into the right lower lobe, the blood being returned to the pulmonary veins. A resection of the right lower lobe was conducted via thoracotomy. However, since there was no clear normal lung-pleura interface, this was classified as Pryce II type intralobar sequestration. Epithelioid granulomas with associated caseation necrosis confined to the sequestrated lung were confirmed by a polymerase chain reaction as Mycobacterium tuberculosis. Following oral antituberculosis drug administration, the patient recovered uneventfully. Superimposition of tuberculosis confined to a sequestrated lung portion is extremely rare. The presence of the aberrant artery led us to conclude that the intralobar sequestration must have been congenital.

A 58-year-old man, a carpenter, had been suffering from cough, rhinorrhea, wheezing, dyspnea and ocular itching a few minutes after each exposure to the sawdust of "Ayous" wood (Obeche, Triplochiton scleroxylon) since starting to work on this imported wood in 1998. Although his symptoms improved soon after exposure, he had a secondary response several hours later. He had no symptoms when working with any other woods. In January, 2001, he came to our hospital, and occupational asthma was suspected. Peak flow monitoring revealed immediate- and late-type responses when he was exposed to Ayous wood dust. Non-specific bronchial hyperresponsiveness to acetylcholine was positive. An immediate skin test with Ayous wood extract was positive. In the RAST inhibition test, his serum revealed specific IgE antibody to Ayous extract. Bronchoprovocation with Ayous wood extract demonstrated immediate and later type responses (dual response). Occupational asthma caused by Ayous wood dust was confirmed. This is the first case report of occupational asthma caused by Ayous wood in Japan.

We report a case of pulmonary eosinophilic granuloma with the latest onset ever reported in Japan. A 72-year-old woman, a current smoker, developed dyspnea and dry cough in late January 2001. Chest radiography and CT examinations revealed numerous small nodular lesions and multiple cysts in both upper lung fields. A thoracoscopic lung biopsy revealed a granulomatous lesion composed of eosinophils and large histiocytic cells with pale eosinophilic cytoplasms and large cleaved nuclei. These cells gave a positive reaction for S-100 protein. These findings led to a diagnosis of pulmonary eosinophilic granuloma. This disease is generally reported in much younger subjects, and few cases are known in those over 60-years old. No Japanese report of histologically confirmed pulmonary eosinophilic granuloma in an older patient has previously appeared, but it may now be prudent to take this disease into consideration when diagnosing pulmonary disease in older subjects.

A 68-year-old man had been suffering from swelling and deformation of both auricles, hoarseness, hearing loss, and a productive cough since November, 1999. Elevation of the inflammatory reaction was noted, together with swelling of the glottis and inflammation of the bronchial mucosa on bronchoscopy. Relapsing polychondritis was diagnosed when an auricle biopsy specimen demonstrated auricle chondritis. The laboratory findings revealed high titers of anti-type II collagen antibody. After steroid treatment, the symptoms improved and the titer of anti-type II collagen antibody decreased. The measurement of this antibody was useful for the diagnosis and follow-up of this disease. To prevent the impairment of organs and sudden death, early diagnosis involving the use of anti-type II collagen antibody and the commencement of therapy are important in this disease.

In August, 1999, a 46-year-old man with fever, cough, and dyspnea was admitted to a hospital. On the basis of the clinical and radiographic findings, bacterial pneumonia was suspected. Antibiotics were not effective, because of atypical lymphocytes in the peripheral blood and positive anti-human T-cell leukemia virus antibody, and he was transferred to our hospital. A chest radiograph and a CT scan revealed bilateral ground-glass opacities with huge multiple cysts. Intensive treatment of Pneumocystis carinii pneumonia associated with human T-cell leukemia was unsuccessful. Pneumocystis carinii was found in the bronchoalveolar lavage fluid. Human T-cell leukemia and Pneumocystis carinii pneumonia were diagnosed. In this case, numerous pulmonary cysts were progressing rapidly, the largest cyst being 8.7 cm in diameter, and the largest cyst in our experience either in clinical practice or in reading of the literature in Pneumocystis carinii pneumonia. The maximum serum KL-6 was markedly increased to 15,200 U/ml, which is the highest level reported for Pneumocystis carinii pneumonia.

A 72-year-old man who had worked as a coal worker for 28 years and as a tunnel construction worker for 18 years was admitted because of fever, dyspnea, and appetite loss. Pneumoconiosis had been diagnosed when he was 64 years old and myelodysplastic syndrome at 71 years of age. After admission, the patient was treated with antibiotics and anti-fungal drugs but did not respond. Respiratory failure gradually worsened and he died. Autopsy specimens revealed that the cause of death was exacerbation of respiratory failure due to pulmonary proteinosis rather than pulmonary infection. This is a case of pulmonary proteinosis complicated with pneumoconiosis and myelodysplastic syndrome which, to our knowledge, is rare. We also considered the possibility that defective pulmonary macrophage function due to myelodysplastic syndrome and long-term silica inhalation played a part in the development of pulmonary alveolar proteinosis in this case.

A 66-year-old woman had a history of partial gastrectomy and resection of the residual stomach because of early gastric cancer and its recurrence. She had been suffering from dyspnea on effort, hemosputum, and cough since the age of 52 years. Chronic pulmonary emphysema and bronchial asthma were diagnosed when she was 59. On January 31, 1996, she was admitted to UOEH hospital with a complaint of increased dyspnea. In spite of treatment with oxygen, steroid, and inhaled anti-cholinergic agent, her condition deteriorated. Subsequently, she had DIC, respiratory failure and reticulolinear opacities were seen on chest radiographs, and she died 2 weeks after admission. At autopsy, the lung specimen revealed numerous cystic spaces surrounded by a proliferation of smooth muscle cells. Immunohistological examination showed these cells to be positive for HMB-45. Signet cells were seen in the lymphatics and vessels, and hemosiderin-laden macrophages were found in the alveolar spaces. This was a rare case of lymphangioleiomyomatosis with carcinomatous lymphangiosis.

We report a case of severe pulmonary fibrosis in a patient exposed to asbestos and other natural and man-made mineral fibers (MMMF) over a period of time. A 63-year-old man was admitted to our hospital because of progressive dyspnea and severe hypoxemia with hypercapnea. Mineral fibers recovered by bronchoalveolar lavage were analyzed by scanning electron microscope (SEM) and energy-dispersive x-ray spectroscopy (SEM-EDS). The bronchoalveolar lavage fluid (BALF) included a large number of asbestos bodies (116,000/ml). The cores of the asbestos fibers were crocidolite, and no vitreous fibers nor other kinds of man-made mineral fibers (MMMFs) were identified. To our knowledge, the number of asbestos bodies per ml of this patient's BALF is the greatest ever reported. Insufficient personal protection of the airways, high concentrations of inhaled fibers, co-exposure to cigarette smoke, and prolonged biopersistence of crocidolite asbestos fibers are presumed to be the causes of such severe asbestosis.

We encountered a 55-year-old man with pulmonary involvement in acute febrile neutrophilic dermatosis (Sweet's syndrome). He had been treated with steroids for Sweet's syndrome for 2 years, and on September 17, 1998 presented with a cough and a fever of 38.9 degrees C. Physical examination revealed fine crackles at the bases of both lungs. Chest radiography and computed tomography demonstrated reticular and nodular infiltrates in both lungs. Treatment with a variety of antibiotic agents and an antifungal agent was not effective. Sputum culture was sterile and bronchial washings were negative for infectious pathogens. Transbronchial biopsy revealed a mild chronic interstitial infiltrate and an inflammatory exudate in bronchiolo-alveolar tissue. The pulmonary lesions and cutaneous lesions were resolved by intradermal injections of triamcinolone acetonide in addition to oral prednisolone. Although the apparent neutrophilic infiltrates cited by earlier reports were not observed in transbronchial biopsy specimens, the clinical course in this case suggested that our patient had Sweet's syndrome with pulmonary involvement.

A 29-year-old man was referred to our hospital because of exertional dyspnea and progressive eruption on the buttocks and the lower extremities. Chest roentgenograms and computed tomograms taken at that time revealed diffuse fibrotic changes accompanied by multiple cavities and bullae in the lungs. There were no signs of mediastinal or hilar lymphadenopathy. A chest roentgenogram taken 7 years before admission showed no abnormalities. Serum ACE and lysozyme levels were high: 29.9 IU/l and 14.1 micrograms/ml, respectively. 67Ga scintigraphy showed diffuse uptake in both lung fields. The PPD skin test was negative, and repeated sputum smears and cultures were negative for pyogenic bacteria and acid-fast bacilli. Examination of transbronchial lung biopsy and skin biopsy specimens confirmed the diagnosis--they showed noncaseating epithelioid granulomas with giant cells and a negative reaction of the stain to acid-fast bacilli, which are compatible with sarcoidosis. The patient was given 30 mg/d of prednisone orally. The dyspnea and eruption were clearly alleviated, although there was little roentgenographic regression of cystic or fibrotic changes. There have been only a few reports of cystic and fibrotic changes early in the course of sarcoidosis. The cystic lesions in this case were probably secondary pulmonary cavities caused by the contracting and obstructive changes related to pulmonary fibrosis.

A 36-year-old man with hemophilia A was admitted to hospital because of otalgia, hearing loss, nasal obstruction, nonproductive cough, and high fever. His laboratory data showed high-grade acute inflammatory reactions. His chest X-ray and CT films showed multiple cavitary masses in the right lower lung field. Bronchoscopy performed at our institution revealed bronchial nodules in the intermediate truncus, and BAL revealed increases in the neutrophils and an IgG index (BAL IgG/albumin divided by serum IgG/albumin). Biopsy specimens obtained from nasal mucosa showed epithelioid granulomas with Langerhans' giant cells and necrotizing vasculitis. Antineutrophil cytoplasmic antibodies were also positive, but no evidence of glomerulonephritis was observed. The diagnosis of limited Wegener's granulomatosis was thus made. He was treated with standard therapy (daily cyclophosphamide and glucocorticoids), but within 1 month he had complications of empyema with herpes zoster, and bronchopleural fistula. The complications resolved with appropriate treatment.

A 54-year-old female was admitted to our hospital because of abnormal shadows on chest X-ray at annual checkup. She complained of dyspnea on exertion. Chest X-ray findings showed an increase in density at the bilateral lower lung fields and unclearness of the silhouette of the heart and the diaphragm. CT scan findings revealed irregular opacities of various density with many small cystic changes and air bronchograms and air bronchiolograms. The pulmonary function test showed restrictive ventilatory disturbance and reduced diffusing capacity. BALF findings revealed an increase in the total cell count, an increase in the percentage of lymphocytes and a decrease in the OKT4+/OKT8+ ratio. TBLB specimen showed infiltration of mononuclear cells in alveolar septa and organizing exudate in alveolar ducts. These findings suggested a diagnosis of BOOP rather than IPF, and an open lung biopsy was performed. Open lung biopsy specimen showed obstructive bronchiolitis with polypoid granulation tissue and thickening of alveolar septa with infiltration of mononuclear cells, and she was diagnosed as having BOOP. She responded well to corticosteroid and is free from any abnormalities on chest X-ray, CT scan and pulmonary function test at present. Analysis of BALF and CT scan findings are useful for the differential diagnosis of BOOP and IPF.

We report two cases of pulmonary lymphangioleiomyomatosis with recurrent spontaneous pneumothorax. The cases were diagnosed by open lung biopsy. Case 1 was a 38-year-old woman, whose chest X-ray showed linear and reticular shadows. Lung tissue was negative for hormone receptors. She was treated with tamoxifen, but developed allergic symptoms. Her condition gradually deteriorated despite oxygen and progesterone therapy. Case 2 was a 41-year-old woman, whose chest X-ray showed a reticular shadows and slight overinflation. Hormone receptors were not examined, but the disease did not progress with oxygen, progesterone and GnRH agonist (Sprecur) therapy.

We report three cases of pulmonary cryptococcosis in which one community acquired and two nosocomial infections were suspected. Clinical studies were focused on histological and immunological diagnosis and antifungal chemotherapy. The first case was initially suspected of having primary cryptococcosis. The second case was first suspected to have BOOP on the basis of clinical and radiological findings. The third was initially suspected of having lung cancer because of an enlarging mass lesion in fibrotic lung and elevated tumor markers. All cases were treated with antifungal agents. Two cases were treated with fluconazole alone, the other case with fluconazole and 5-fluorocytosine. In all cases, the abnormal shadows on chest X-ray demonstrated 50 to 90 percent improvement within 6 months, and cryptococcal antigen in the serum decreased. There were no side effects from the drugs.

A 61-year-old man was admitted to our hospital on October 8, 1991 because of abnormal shadows on chest X-ray at annual checkup at his company. Chest X-ray and CT on admission showed diffuse reticular shadows in bilateral lower lung fields and a nodular opacity approximately 10 mm in diameter in the right lower lung. Since transbronchial lung biopsy was not diagnostic, an open lung biopsy was performed on October 28, 1991. The lung specimens showed diffuse pulmonary fibrosis compatible with usual interstitial pneumonia and an intrapulmonary lymph node containing silicotic nodules. Only 29 cases (including the present case) of intrapulmonary lymph nodes have been reported. Although the causes of intrapulmonary lymph nodes are not clear, smoking is considered to play an important role in the development of pulmonary lymphoid tissue. In our case, the intrapulmonary lymph node contained silicotic nodules. Only several case have been reported to have silicotic nodules in the lymph nodes. As suggested by Kradin, they may be induced by relatively low levels of exposure to dust. Our case also had pulmonary fibrosis (IIP), and is the first reported case of intrapulmonary lymph node associated with IIP. Although it is difficult to determine these two diseases occurred coincidently or not, it is possible that a low level of dust exposure may have contributed to both silicotic nodules in the lymph node and IIP.

A 60-year-old man was admitted to our hospital on January 29, 1991 with dry cough, shortness of breath on exertion, appetite loss and abnormal shadows on chest X-ray. Chest X-ray on admission showed marked vascular shadows in both lung fields accompanied by left interlobar effusion. Chest CT showed thickening of vessels and bronchial walls with prominent interlobular septa in the subpleural regions. These findings suggested that the lesions were located in the peribronchial and perivascular interstitium and interlobular septa. Biopsy specimens of bronchial epithelium, lung tissue and right supraclavicular lymph nodes revealed small cell carcinoma (intermediate cell type). Because of the absence of lesions in other organs, the initial diagnosis was carcinomatous lymphangiosis of small cell carcinoma of the lung. However, the mild symptoms, normal arterial blood gas and good response to chemotherapy suggested the possibility of extensive small cell carcinoma of longitudinal spread type. Although small cell carcinoma of the lung is not a rare disease, this case suggests two possibilities. 1) Carcinomatous lymphangiosis of small cell carcinoma may have different symptoms, clinical course and prognosis from that of non-small cell carcinoma. 2) Carcinomatous lymphangiosis of small cell carcinoma may not be a clinical entity and in fact may simply represent extensive small cell carcinoma of longitudinal spread type.

Marked obstructive ventilatory impairment and diffusion disturbance were noted in two intravenous methylphenidate (Ritalin) abusers. In one patient, chest radiogram demonstrated pulmonary emphysema accompanied by bullae and atelectasis, and spontaneous pneumothorax was also present. The primary finding in the other patient was interstitial shadows. Both patients began to note dyspnea during exertion after about 10 years of use. Since radiography also disclosed pulmonary emphysema in an ex-companion of Ritalin abuse, and since the onset was at relatively young ages, these pulmonary disorders are considered to have been a result of intravenous Ritalin abuse. Intravenous drug abuse should be considered in patients with precocious emphysema or obstructive ventilatory impairment accompanied by diffusion disturbance.

A 23-year-old man was admitted to our hospital on June 24, 1991, because of worsening chest X-ray findings of sarcoidosis. In August 1990, he was referred to our outpatient office, because of BHL and nodular lesions on chest X-ray film performed at his company 4 months earlier. At that time, serum ACE was elevated to 34.0 IU/l, and Ga scintigraphy showed abnormal uptake in bilateral lacrimal and salivary glands, mediastinal and hilar lymph nodes, and in the lung fields. TBLB specimen showed noncaseating epithelioid granuloma with giant cells and negative stains for acid-fast bacilli. Although it was planned to follow this patient without medication, he did not return to our outpatient department. In June 1991, because of worsening of lesions in the lung at annual checkup at his company, he was referred and admitted for steroid therapy. Chest X-ray film on admission showed BHL, multiple nodular lesions in both lung fields, and bullous change in the left upper lobe. Chest CT on admission showed three cavitating lesions within preexisting nodules. PPD skin test was negative, and sputum smears and cultures were repeatedly negative for pyogenic bacteria and acid-fast bacilli. Therapy was initiated with prednisolone 30 mg daily. Four months later, there was marked resolution of BHL and nodular lesions, and the cavitating lesions were no longer visible on chest X-ray film. From the clinical and radiological observations, it is concluded that the cavitating lesions in the present case were primary acute pulmonary cavitation in sarcoidosis, distinct from infection, bullae, or cystic bronchiectasis which are seen in the chronic and fibrotic stages of sarcoidosis.

A 56-year-old man with fever, headache, cough and sputum was admitted to another clinic. Chest X-ray examination revealed infiltrates in the upper lobe of the right lung. Cefem and aminoglycoside therapy was not effective, and the infiltrates migrated from the right upper lobe to the right middle and lower lobes and then to the left lung. He was transferred to our clinic, and laboratory data showed that CRP was 6+; ESR, 119 mm/1 h; WBC, 3000/mm3; and CAR, 512. The tentative diagnosis of atypical pneumonia was based on the positive agglutination test for Legionella pneumophila, and treatment with erythromycin, minocycline and rifampicin resulted in alleviation of symptoms and resolution of the infiltrates in the lungs. Complement fixation titer for Chlamydia was 128 at admission and was elevated to 512 after 2 weeks. Indirect fluorescent antibody for Legionella was negative. Transient liver dysfunction was also observed.

An unusual case of a benign giant cell tumor of bone with pulmonary metastasis is reported. A 23-year-old man had a painful tumor in the right radial olecranon that proved to be a histologically benign giant cell tumor. Curettage and bone-grafting were performed, but the tumor recurred twice, 8 months and 20 months after initial treatment. Histological examination of biopsy materials from the recurring tumor showed typical benign giant cell tumors. Five years later, wedge resections were performed for bilateral pulmonary nodules, which had been detected by chance. The pulmonary nodules turned out to be histologically similar to the primary tumor of the olecranon. Almost 7 years later, he was asymptomatic and the chest radiograph was clear, and there was no local recurrence of the lesion.

In order to evaluate the role of membranous (MB) and respiratory bronchioles (RB) in patients with normal and mild airflow limitation, we quantitatively assessed the pathological change of MB, RB and alveoli in the pathological specimens of 42 patients who required surgery for removal of a solitary pulmonary nodule. We also measured the destructive index (DI), to evaluate the destruction of alveolar walls. High resolution CT scan and pulmonary function tests were performed within 1 month of resection. Results of the pulmonary function tests correlated with pathological changes of RB better than with MB. Significant correlation between the emphysema score of resected lung and the pathological change of MB and RB was observed. There was also significant correlations between the CT score or DI and RB changes. However, there was no significant correlation between the CT score or DI and the change of MB. There were significant differences between smokers and nonsmokers in the results of pulmonary function test, pathological changes of RB and severity of emphysema. We postulate that RB is responsible for subtle functional abnormalities in the early stages of chronic obstructive pulmonary disease.

To assess the ability of high resolution CT scan and pulmonary function tests in detecting and grading mild emphysema, we correlated the high resolution CT scan and pulmonary function tests with the pathologic grade of emphysema and the destructive index of lung specimens from 42 patients undergoing thoracotomy for solitary pulmonary nodules. Using the high resolution CT scan, we could identify the pathologic grade of mild and moderate emphysema. By measuring diffusing capacity per unit alveolar gas volume (DLco/VA), it seemed to be possible to detect the mildest degree of alveolar destruction assessed by the destructive index, which was not detected by high resolution CT scan. The reason for these results seemed to be that we assessed the severity of emphysema by detecting the air space enlargement on high resolution CT scan images caused by the destruction of alveolar walls, which were detectable by measuring DLco/VA. We conclude that it is possible to detect mild emphysema using the combination of high resolution CT scan and pulmonary function tests.