Interleukin-2 receptor expression (IL-2R) on monocytes and alveolar macrophages (AM) was determined in patients with sarcoidosis and pulmonary tuberculosis. In sarcoidosis and tuberculosis, IL-2R on monocytes was detectable, while it was undetectable in healthy controls. IL-2R on AM in sarcoidosis and tuberculosis was significantly increased as compared to healthy controls. IFN-γ, which has been shown to be increased in sarcoidosis and tuberculosis as compared to healthy controls, induced IL-2R on monocytes in healthy controls, suggesting that IFN-γ is at least in part responsible for the induction or enhancement of IL-2R on monocytes or AM in sarcoidosis and tuberculosis. Phorbol myristate acetate which is known to be protein kinase C (PKC) activator induced IL-2R on monocytes, and PKC inhibitor, H7, inhibited IFN-γ-induced IL-2R on monocytes in healthy controls. Calcium ionophore, A23187, induced IL-2R on monocytes and calmodulin antagonist, W7, inhibited IFN-γ-induced IL-2R on monocytes. Based on these results, it seems that not only the PKC pathway but also the calcium-calmodulin pathway is involved in IFN-γ-induced IL-2R.

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In order to clarify whether repirinast, an inhibitor of chemical mediator release, could influence the pharmacokinetics of theophylline, a loading test using intravenous injection of aminophylline was performed in 10 subjects with bronchial asthma before and after treatment with 300mg/day of repirinast. There was no significant difference in theophylline half-life before treatment (7.25±2.43hr) and after treatment (7.82±3.35hr). There was no significant difference in theophylline clearance before treatment (0.047±0.018L/kg/hr) and after treatment (0.047±0.020L/kg/hr). These results demonstrated that repirinast does not modify theophylline pharmacokinetics significantly.

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A total of 32 patients with mycoses other than cavity-formed aspergilloma were reviewed. The main pathogenic fungi were Aspergillus in 14, Candida in 8, Cryptococcus in 4, Trichosporon in 4 and Mucor in 2. Coinfection by two species was detected in 3 cases: Trichosporon and Aspergillus in 2 and Aspergillus and Candida in 1. The underlying diseases were hematologic malignancies in all cases except 1 case of lung cancer. The hematologic malignancies were mostly leukemias of various types. Cryptococcosis developed in patients given long-term corticosteroid treatment but not in leukemic patients. All cases of aspergillosis, candidiasis and mucormycosis were due to nosocomial infection. On the other hand, 3 of 4 cases of cryptococcosis or trichosporonosis were attributable to community-acquired infection. Two of 4 trichosporonosis cases were considered to have been acquired during 2-day home stays. The diagnosis of pulmonary mycosis was made pathologically in 18 and clinically in 14 cases. Of the latter, 6 cases had an air-crescent sign on chest X-ray films and 8 cases were culture-positive. Extrapulmonary involvement was seen in all 16 cases of candidiasis, cryptococcosis and trichosporonosis but not in 10 of 14 aspergillosis cases. Severe granulocytopenia was present in all cases except 4 cases of cryptococcosis and 3 cases of aspergillosis. Chest X-ray findings of aspergillosis were of two types: one was an air-crescent sign which was noted in the recovery phase from leukopenia and the other was gradually enlarging consolidation which was bounded by the interlobar fissure and progressed to lobar penumonia. A diffuse granular shadow was not characteristic of any fungus species. Amphotericin B should be prescribed in cases with a characteristic shadow of aspergillosis, while miconazole or fluconazole should be considered when a diffuse granular shadow was found, especially in cases of community-acquired fungal infection often associated with Trichosporon.

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The area of upper airway (from the nasopharynx to the hypopharynx) was measured by means of computed tomography (CT) scan in 15 confirmed cases of obstructive sleep apnea (OSA) and in 4 normal controls while they were awake. The minimum cross-sectional area (MA) of the upper airway was 14.7±20.0mm² in OSA patients and 80.0±33.1mm² in normal controls and the difference was statistically significant (p<0.01). In OSA patients, MA did not correlate with age, body weight, apnea index, desaturation index, mean nadir-SO₂ and lowest SO₂. MA was also measured with OSA patients while nasal continuous positive airway pressure (NCPAP) of 10cmH₂O was applied and it was found that MA was significantly widened when NCPAP therapy was performed. We conclude that upper airway narrowing is consistent finding in OSA patients but the degree of narrowing does not correlate with parameters of apnea and gas exchange during sleep, and NCPAP is effective to widen the area of upper airway in OSA patients.

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Serum lipid levels of 60 cases of bronchial asthma (males 30, females 30) were compared with 161 (males 91, females 70) controls. Serum cholesterol, triglyceride, Apo A1, A2, B, HDL-cholesterol (HDL-C), LDL VLDL, and atherosclerotic index (T-chol. HDL-chol/T-chol.) were measured.
Asthma cases slowed low levels of serum cholesterol, triglyceride, LDL, VLDL and Apo B compared to the control group, while HDL-C, ApoA2 were higher than the control group. (p<0.05). The atherosclerotic index was low in the asthma group. A patient who had a 9-year history of asthma showed decreased HDL-C and increased T-cholesterol, on improvement of asthma attack and body weight loss.

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Balloon occlusion pulmonary angiography was used to assess the frequency of pulmonary vascular thrombosis in five patients suffering from ARDS of diverse causes. Pulmonary hypertension, elevated pulmonary vascular resistance and disseminated intravascular coagulation were observed in all patients. Pulmonary artery filling defects (PAFD) were found in four of five patients. The results suggest that PAFD can be detected in a large proportion of patients in ARDS. It was therefore speculated that the detection of PAFD is a sign of severe lung injury.
Urokinase, heparin and protease inhibitor were infused to test the potential reversibility of pulmonary vascular thrombosis in four patients. After infusion, we found angiographic evidence of clearing of obstruction in arteries in three of four patients. We conclude that anticoagulant-antithrombotic therapy can improve hemodynamics in ARDS-associated pulmonary vascular thrombosis.

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Immunohistochemical analysis was performed in a case of pulmonary cryptococcosis that showed granulomatous pneumonia. The patient had no immunologic defects or other diseases. To cryostat sections, the immunocytes in granulomatous lesion were examined by application of monoclonal antibodies for T-lymphocytes, B-lymphocyte, macrophage series cells, lymphokines containing gamma interferon (γIFN), interleukin 1 (IL-1) and interleukin 2 (IL-2), and interleukin 2 receptor (IL-2R).
CD2⁺ cells, CD3⁺ cells and CD4⁺ cells were in and around the granulomas. On the other hand, CD8⁺ cells were around the granulomas. In granulomatous lesions, the CD4/CD8 ratio was 2.0. Some T-lymphocytes were considered as activated lymphocytes showing OKDR⁺, IL-2⁺, γIFN⁺ or IL-2R⁺. The lymphoid cells that aggregated near the granulomas were B-lymphocytes showing CD21⁺, CD24⁺, s-IgD⁺, s-IgM⁺, OKDR⁺. According to these results they were mature B lymphocytes. Alveolar macrophages (AMs) were CD11⁺, CD36⁺, IL-1⁺, OKDR⁺. Epithelioid cells were CD4⁺, CD11⁺, CD36⁺, OKDR⁺, IL-1⁺, IL-2R⁺. CD1⁺ cells showing dendritic forms were scattered in granulomas. They were recognized to be Langerhans giant cells.
These results suggest that in pulmonary cryptococcosis the formation of epithelioid cell granulomas is mainly induced by CD4⁺ cells (helper/inducer T-lymphocytes). Additionally, Langerhans giant cells and mature B lymphocytes may be related to humoral immunity in pulmonary cryptococcosis.

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The phase difference between mouth flow and chest flow in cases of pulmonary diseases measured using a body box was compared with those in normal subjects. Phase differences in chronic pulmonary emphysema (CPE) and diffuse panbronchiolitis (DPB) patients increased compared to normal subjects, but remained normal in interstitial pnemonitis patients (Normal: 3.76±1.71, CPE: 10.70±4.93, DPB: 10.81±3.15, PF: 3.83±0.15^°). In addition, there was a good correlation with FEV1.0, FEV1.0% and RV/TLC (r: -0.634, -0.610 and 0.803). The analysis of phase differences during rest breathing is clinically useful because it is non-effort dependent and can evaluate the degree of airway disorders.

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Cases of chronic pulmonary emphysema accompanied with paroxysmal dyspnea attacks are often misdiagnosed as bronchial asthma. These patients repeatedly fall into a state of life-threatening respiratory failure. We must make an accurate diagnosis of emphysema to provide care of them. To clarify the possibility of doing this, we investigated the clinical and physiological features (primarily respiratory function) of emphysema. We observed twenty-five patients with chronic pulmonary emphysema and with chronic bronchial asthma, previously confirmed by selective alveolo-bronchogram (SAB); this technique reliably diagnoses emphysema, but often induces dyspnea attacks due to the stimulation resulting from intratracheal and intrabronchial procedures. In eight patients, chronic pulmonary emphysema was accompanied by an attack of paroxysmal wheezing and dyspnea; chronic pulmonary emphysema with wheezing (WPE). In eight other patients, chronic pulmonary emphysema was present without such attacks; usual pulmonary emphysema (UPE). In the final nine patients, chronic bronchial asthma (CBA) was present, while emphysema was ruled out by means of SAB. In all patients, we measured respiratory function before and after the combination therapy of intravenous aminophylline and subcutaneous epinephrine, which followed daily oral administration of prednisolone (PAE-treatment).
In the WPE group, significant increases in measurement of various respiratory functions, including VC, RV, RV/TLC%, FVC, FEV1.0, PFR and V75 (p<.05 excluded in FEV1.0 and PFR were p<.01), were found after the PAE-treatment, compared with the values revealed before the treatment. In the UPE group, there were few changes in respiratory function. In the WPE group, significant lower values in several parameters of respiratory function, including %-FEV1.0, FEV1.0%, %-MMF, %V75, %V50, %-V25, %-DLco and %-DLco/VA (p<.01 excluded in %-FEV1.0 was p<.05 and in %-V75 and %-DLco/VA were p<.001) were demonstrated after the PAE-treatment, compared with the results from the CBA group. Therefore, we concluded that there is a reversibility, similar to that of asthma, in the airway obstruction in patients with WPE; however, it might be possible to distinguish WPE from CBA, based on several respiratory function parameters, including %-DLco and especially %-DLco/VA, FEV1.0%, %-PFR, %-V75, %-MMF and %-V50, after the recovery from dyspnea attacks. An additional study on a larger number of cases will be required to establish an accurate method to diagnose such cases.

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A 70-year-old woman complained of cough, sputum and fever. Chest roentgenogram showed a mass-like lesion with pleural effusion in the left thorax. Bronchoscopy revealed a polypoid lesion at the orifice of left B10 and mucosal swelling of the left lower lobe bronchi. The biopsied material of the polypoid lesion was diagnosed as malignant lymphoma (diffuse small cell type by LSG classification) and the immunohistochemical examination showed monoclonal proliferation of T lymphocytes. The atypical lymphocytes which were positive for T lymphocyte surface marker were detected in the pleural effusion. There was no evidence of metastasis in any part of the body under clinical examinations, and the lung was thought to be a primary site of the lymphoma. The doubling time of tumor was estimated to be 134 days. Four-drug combination chemotherapy resulted in a marked decrease of the tumor size.
Immunohistochemical study to determine the subpopulation of lymphoma cells are required for diagnosis of pulmonary lymphoma, because the biological characters of T cell lymphoma might differ from those of B cell lymphoma.

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The patient was a 51-year-old woman who had no history of asbestos exposure and showed left pneumothorax with a small amount of pleural effusion. On admission to our hospital, she showed clinical and laboratory data similar to that of spontanous pneumothorax except for a high concentration of hyaluronic acid in pleural fluid. After treatment of pneumothorax, pleural effusion appeared to decrease on chest X-ray. After 3 months, however, pleural effusion again increased, in spite of the improvement of pneumothorax. The patient received open lung biopsy and the histological examination showed mixed type malignant pleural mesothelioma.

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A 51-year-old female was admitted with high grade fever, cyanosis and hypoxemia. The chest X-ray showed nodular shadows on bilateral lung fields. β-streptococci were found on culture from the blood, and the fever fell after administration of both antibiotics and corticosteroid. Pulmonary angiography revealed four arteriovenous fistulae on bilateral lung fields. On abdominal ultrasonography and CT scan, a hypoechoic lesion with an irregular wall and varying internal echogenicity was detected within the spleen. This lesion changed in size and shape during the clinical course and diminished with improvement in the patient's condition. These findings were compatible with splenic abscess. Splenic abscess with pulmonary arteriovenous fistulae is rare.

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A 69-year-old man was admitted with general fatigue, dyspnea, cough, fever and right pulmonary infiltrations on a chest X-ray films. He had suffered from myocardial infarction 8 years before. Since September 1987, he had been given Aprindine in addition to previous drugs. In early November 1987, he developed dyspnea. Antibiotics were not effective. He was hospitalized on Nov. 13, '87 when crepitations were audible on his right chest. Methylprednisolone pulse therapy was effective, however right pneumothorax developed. He underwent right thoracotomy and lung biopsy. Lung biopsy specimens showed pathological features of bronchiolitis obliterans organizing pneumonia (BOOP).
Corticosteroid therapy yielded a remarkable clinical, physiological and roentgenographic recovery. However, approximately two years later during prednisolone maintenance therapy, BOOP recurred. He responded again to corticosteroid treatment, however he died of hepatic failure on Dec. 17, '89. “Idiopathic” rather than “drug induced” was suggested for the cause of BOOP in this case.

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A 50-year-old man was admitted for evaluation of an abnormal shadow on a chest X-ray. He had experienced pain and swelling in his fingers for three years. He had also noticed that he is impotent. The diagnosis of Klinefelter syndrome and rheumatoid arthritis (RA) was established by clinical findings and chromosamal analysis.
Transbronchial biopsy revealed adenocarcinoma and right upper lobectomy was performed. Open lung biopsy showed interstitial penumonia. In conclusion, we reported a rare case of lung cancer, rheumatoid arthritis and RA lung associated with Klinefelter syndrome.

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A case of pulmonary sarcoidosis (stage III), in which the abnormal chest shadow disappeared within two weeks was reported. A 35-year-old male was admitted for further examination of bronchial asthma.
He stayed overnight at home after he received inhalation provocation test of sulpyrin. Returning to the hospital, he had a fever (38°C) with diffuse small nodular shadows on the chest roentgenogram. The onset and clinical features of the disease suggested hypersensitivity or drug induced pneumonitis rather than sarcoidosis. Bronchoalveolar lavage fluid (BALF) analysis showed an increase of total cell counts and lymphocytes. The surface marker of lymphocytes in BALF revealed that the CD4/8 ratio was remarkably elevated to 6.2. Both transbronchial lung and scalene node biopsy specimens revealed numerous noncaseous granulomas, and a diagnosis of sarcoidosis was confirmed. The chest infiltrates disappeared spontaneously within two weeks. This case was reported because of its rare natural course as stage III pulmonary sarcoidosis.

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A 39-year-old man with a history of repeated attacks of acute bronchitis and pneumonia since childhood was admitted complaining of cough, sputum, and a high fever. A diagnosis of Kartagener's syndrome was made because of the presence of mirror-image dextrocardia with complete situs inversus, bronchiectasis in right B⁶ and B¹⁰, and chronic sinusitis. Examination of the ciliary ultrastructure of the bronchial epithelium showed defective inner dynein arms and impaired nasal clearance was suggested by the saccharin particle method. Contrast venography of great veins revealed a McCotter type II bilateral superior vena cava and an absent inferior vena cava with (hemi-) azygos continuation. A search to find a similar case in the literature failed. Abnormal ciliary movement from the embryonic period was implicated as a causative factor in Kartagener's triad and the morphological abnormalities of the great veins.

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A 63-year-old female, who had been suffering from idiopathic interstitial pneumonia (IIP) since two years and four months previously, was admitted with general fatigue, body weight loss, bloody sputum and progression of dyspnea. Chest roentgenogram on admission showed diffuse coarse ring shadows in the right middle and lower lung fields and in the left middle lung filed. Chest CT clearly showed honeycombing in bilateral dorso-basal segments of the lung. Serum CA19-9 level was elevated, and continued to increase during her clinical course. Sputum cytology was positive. Autopsy showed papillary adenocarcinoma of the lung (alveolar cell type). Immunohistochemical study of lung tissue showed positive CA19-9 staining on the surface of adenocarcinoma cells.

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