Malnutritions is one cause of exercise intolerance in patients with chronic obstructive pulmonary disease. We studied the relation between exercise limitation and body composition in 20 clinically stable patients with chronic obstructive pulmonary disease. Maximal work capacity was measured during incremental exercise on a cycle ergometer, along with maximal oxygen uptake. Anaerobic threshold was determined by the V-slope method. Bone mineral content, lean mass, and fat mass were assessed by dual-energy X-ray absorptiometry. Bone mineral content and lean mass were significantly lower in moderately malnourished patients (%IBW < 80) than in well-nourished patients (%IBW > or = 90). Fat mass was significantly lower in mildly malnourished patients than in well-nourished patients. Maximal work capacity, maximal oxygen uptake, and anaerobic threshold correlated significantly with lean mass, but not with fat mass. These data suggest that lean mass is one determinant of exercise capacity in patients with chronic obstructive pulmonary disease.
A 65-year-old man was admitted to our hospital because of mild dyspnea. A chest roentgenogram showed diffuse reticulonodular shadows in both lung fields. The concentration of CA19-9 in serum was high. Pancreatic cancer and other diseases were considered as causes, but no definitive diagnosis could be made. An open-lung biopsy was done, and examination of a specimen resulted in the diagnosis of idiopathic interstitial pneumonia (chronic type). Immunohistochemical staining with anti-CA19-9 antibody was positive. The lumens of microscopic honeycomb structures and fibrotic areas were covered with flattened and cuboidal metaplastic epithelial cells, which stained positively for anti-CA19-9 antibody.
We encountered two patients with pulmonary hemorrhage who had high levels of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA). Patient 1 was a 69-year-old woman. Both were admitted to our hospital complaining of hemoptysis. Microscopic hematuria was detected in patient 1, and proteinuria and renal insufficiency were detected in patient 2. Chest X-ray films showed bilateral patchy infiltrates in patient 1, and right middle-lower infiltrates in patient 2. In both patients the levels of MPO-ANCA were high and the results of tests for anti-basement membrane antibodies were negative. These patients were suspected to have pulmonary-renal vasculitic syndrome with a high level of MPO-ANCA. In patient 1, because the level of MPO-ANCA decreased after treatment with steroid therapy, we believe that measuring the level of MPO-ANCA was useful in the management of the disease. Rapidly progressive glomerulonephritis developed in patient 2, and was exacerbated despite hemodialysis, steroid therapy, and plasma exchange therapy. Use of the term microscopic polyangiitis (MPA) was first proposed by yhe Chapel Hill Consensus Conference in 1993. MPA, which was formerly called microscopic polyarteritis nodosa, connotes pauci-immune necrotizing vasculitis affecting arterioles, venules, or capillaries, and this condition is strongly associated with ANCA. Patients with pulmonary-renal vasculitic syndrome who have MPO-ANCA may be given a diagnosis of MPA. Therefore, we diagnosed MPA in these two patients. Testing for ANCA may be useful in patients with pulmonary hemorrhage and renal involvement.
We report a case of intrapulmonary hematoma in which magnetic resonance imaging was useful in establishing the diagnosis. A 53-year-old man had bronchial asthma that was well controlled with inhaled beclomethasone dipropionate and salbutamol, and with oral theophylline. A spherical mass was found in the right lower lung field on a chest radiograph taken during a regular physical examination. A CT scan showed a well circumscribed spherical mass, which was attached to an intrapulmonary bullae. Magnetic resonance imaging showed a well-circumscribed mass in the superior segment of the right lower lobe. On a T1-weighted image the mass was hyperintense and had a higher-intensity rim. On a T2-weighted image the mass was hyperintense and had some hypointense areas. We therefore diagnosed intrapulmonary hematoma. Chest radiography 6 months later revealed a substantial decrease in the size of the mass, which supported the diagnosis. As in this case, intrapulmonary hematoma can be difficult to diagnose because of the lack of a history of injury and because of the slow regression. In this case, magnetic resonance imaging was useful in making the diagnosis.
Acetylene rebreathing was used to measure pulmonary tissue volume in 10 normal subjects and in 15 patients undergoing hemodialysis. A mixture containing 0.65% acetylene and 10% argon was rebreathed from the end-tidal level, and gas concentrations were measured with a mass spectrometer. Pulmonary tissue volume was computed from the difference between the argon equilibrium concentration and the corrected acetylene concentration, under the assumption that FAr was constant. Measured tissue volumes per unit lung volume (at functional residual capacity) in the normal subjects, before hemodialysis, and after hemodialysis were 0.204 +/- 0.042, 0.334 +/- 0.100, and 0.282 +/- 0.074, respectively. Tissues volumes per unit lung volume were significantly higher in the patients than in the normal subjects, even after hemodialysis. Tissues volumes per unit of lung volume decreased significantly during hemodialysis. Pulmonary blood flows per unit of body surface area of normal subjects, before hemodialysis and after hemodialysis were 3.004 +/- 0.791, 2.790 +/- 1.007, and 2.399 +/- 0.781 (l/min/m2), respectively. These volumes did not differ significantly between normal subjects and patients, and they decreased significantly during hemodialysis. Measured tissue volumes per unit of pulmonary blood flow for normal subjects, before hemodialysis, and after hemodialysis were 0.119 +/- 0.034, 0.167 +/- 0.024, and 0.166 +/- 0.030 (1/1/min), respectively. The values in the patients did not change during hemodialysis, but they were significantly higher than the volumes in the normal subjects.
A 44-year-old Japanese man who had suffered from bronchial asthma since childhood was given the diagnosis of chronic eosinophilic pneumonia because of his symptoms, chest roentgenographic findings, and the results of a transbronchial lung biopsy. At the time of the onset of the disease, the pleural effusion contained 73% eosinophils. Symptoms were relieved and the laboratory findings returned forward normal after a short course of high-dose corticosteroids. The concentrations of IL-5, IL-6, and G-CSF in pleural fluid and in serum were very high; the concentrations of these cytokines were 3 times to 35 times higher in pleural fluid than in serum. In contrast, no IL-3 or GM-CSF was detected in any of these samples. The precise etiology of chronic eosinophilic pneumonia is still unclear, but this case suggests that inappropriate production of IL-5, IL-6 and G-CSF in the lung play a pivotal role in this disease. Inhibition of the production of these cytokines may be another therapeutic approach to this disease.
A 56-year-old man was admitted to our hospital because of hemoptysis, and dyspnea. Breathing sounds decreased and rhonchi was audible in the right lung. Chest X-ray and Chest CT showed infiltrative shadows in the bilateral lower lobes. He was intubated and bronchofiberscopy revealed mucosal necrosis and hemorrhage of the lower trachea and the bilateral bronchi. MRSA was isolated from sputum and bronchial lavage fluids. He was diagnosed as NTB caused by MRSA. On the 7th day in hospital, he suffocated by the necrotic tissue and autopsy was performed. NTB is a very uncommon disease in adults, especially ones who are not under mechanical ventilation.
Bronchial asthma has been identified as a chronic inflammatory airway disorder associated with cell infiltration (mainly eosinophils) and airway epithelial cell detachment caused by the activation of infiltrated cells. Interleukin-5 (IL-5), a cytokine closely related to the production and activation of eosinophils, has been shown to induce the proliferation and differentiation of eosinophils, prolong their survival, and to enhance the functions of mature eosinophils. We monitored clinically the changes in serum IL-5 concentrations in patients with bronchial asthma both during and after asthma attacks. The relationship serum IL-5 concentrations and the type and severity of bronchial asthma, as well as eosinophil counts in sputum, was investigated. We also measured changes in IL-5 concentrations during steroid therapy. IL-5 concentrations were significantly decreased during asthma attacks and after their relief (p < 0.001). An analysis of blood samples taken from 55 patients suffering asthma attacks showed that serum IL-5 concentrations were significantly higher in non-atopy-type asthma than in atopy-type asthma (p < 0.05). Serum IL-5 levels are highest in severe asthma, followed by moderate asthma (p < 0.001) and mild asthma (p < 0.001). Serum IL-5 concentrations during asthma attacks and eosinophil counts in sputum were closely correlated (r = 0.85). Serum IL-5 concentrations were below the limit of determination and decrease the number of eosinophils in sputum was noted in 15 patients whose asthma was well-controlled by the long-term inhalation of beclometasone. Serum IL-5 concentrations did not decrease below the limit of determination (even during attack-free periods) in patients whose disease could not be well controlled by 6-month inhalation therapy with beclometasone. In patients with major and moderate bronchial asthma attacks, serum IL-5 concentrations decreased as symptoms improved over time following the i.v. infusion of steroids, suggesting that steroids are effective in inhibiting the production of IL-5. Measurement serum IL-5 concentrations could be clinically useful in the determination of the pathology (e.g., severity) of bronchial asthma could serve as an index for the degree of control of asthma, and may be useful in determining the disease's long-term prognosis.
We examined a 72-year-old man suffering from chronic interstitial pneumonia with crescentic glomerulonephritis associated with perinuclear antineutrophil cytoplasmic antibodies (P-ANCA). Ten years before admission, he was given a diagnosis of interstitial pneumonia, but received no medication. He was admitted to our hospital because of a high fever and back pain. Antibiotics were used, but without success. The serum P-ANCA titer was high, and examination of a kidney biopsy specimen showed crescentic glomerulonephritis. Computed tomography of the chest showed that the lungs had a honecomblike appearance, and examination of a specimen obtained by transbronchial lung biopsy showed interstitial fibrosis. This case shows that interstitial pneumonia can be associated with P-ANCA. It is important to be a wore that crescentic glomerulonephritis associated with P-ANCA can develop in patients with interstitial pneumonia.
We measured lung lobar volume by using helical computed tomography (HCT) in 23 patients with idiopathic interstitial pneumonia (IIP), 7 patients with chronic interstitial pneumonia associated with collagen vascular disease (CVD-IP), and 5 healthy volunteers. HCT scanning was done at the maximal inspiratory level and the resting end-expiratory level. To measure lung lobar volume, we traced the lobar margin on HCT images with a digitizer and calculated the lobar volume with a personal computer. The lower lobar volume and several factors influencing it in chronic interstitial pneumonia were studied. At the maximal inspiratory level, the lower lobar volume as a percent of the whole lung volume was 46.8 +/- 4.13% (mean +/- SD) in the volunteers, 39.5 +/- 6.19% in the patients with IIP, and 27.7 +/- 7.86% in the patients with CVD-IP. The lower lobar volumes in the patients were significantly lower than in the volunteers. Patients with IIP in whom autoantibody tests were positive had lower lobar volumes that were very low and were similar to those of patients with CVD-IP. These data suggest that collagen vascular disease may develop in patients with interstitial pneumonia. The patients with IIP who had emphysematous changes on the CT scans had smaller decreases in total lung capacity and lower ratios of forced expiratory volume in one second to forced vital capacity than did those who had no emphysematous changes, those two groups did not differ in the ratio of lower lobar volume to whole lung volume. This suggests that emphysematous change is not factor influencing lower lobar volume in patients with chronic interstitial pneumonia. We conclude that chronic interstitial pneumonia together with very low values for lower lobar volume may be a pulmonary manifestation of collagen vascular disease.
A 40-year-old woman who worked as a nurse and had suffered from progressive exertional dyspnea for about 14 years underwent open lung biopsy with surgical treatment for pneumothorax. The diagnosis was lymphangiomyomatosis and she was treated with danazol to suppress ovarian function. Her condition improved temporarily, but she died of respiratory failure when she was 47 years old. The survival time after the onset of respiratory symptoms was 21 years, and after the biopsy it was 8 years. At autopsy a retroperitoneal cystic tumor was found (9 x 7 x 5 cm), which had been evident clinically. Histologic examination showed that the tumor was an extrapulmonary manifestation of the lumphangiomyomatosis lesion. Some paraaortic lymph nodes has similar lesions. Aggregates of small red spots were seen on acute surface of the liver. These were diagnosed as peliosis hepatis, they may have been caused by the danazol.
In order to obtain normal values and 95% confidence limits of various CT indices, healthy adult subjects with no history of smoking (n = 36) underwent CT scanning under a variety of conditions. By then applying the normal limits thus obtained to CT images of COPD patients (n = 45), we examined the sensitivity for detecting abnormal emphysematous changes in the lung fields. To measure emphysematous alterations, we used the average value of lung CT densities (ROI), the maximally appearing value in a CT histogram (Hist. Peak), the relative area with low CT densities below -910 HU (%LDA) and the total cross-sectional area (Area) in each lung section. Regardless of the section thickness (10 mm or 1 mm), the lung volume level at which the breath was held or the site from which CT images were taken (upper, middle or lower lung field), no significant correlation was observed between the CT indices associated with emphysematous changes and the subjects' age. This allowed us to define, independently of the subjects' age, normal values and 95% confidence limits for the CT indices. Among the CT indices surveyed, %LDA was found to be the most sensitive indicator for detecting emphysematous abnormalities. In so far as the extent of emphysema may be determined by lung CT density, classical CT images of 10-mm section thickness appear to have a sufficiently high sensitivity for the detection of emphysematous abnormalities, such that high-resolution CT may be unnecessary.
Cutaneous Kaposi's sarcoma (KS) is a well-known manifestation of the acquired immunodeficiency syndrome, but pulmonary KS is very rare in Japan. We encountered a 27-year-old Japanese, homosexual man who had extensive pulmonary KS. He came to our hospital because of a cough and dyspnea. On admission, there were some small nodules on the skin, and examination of a biopsy specimen led to the diagnosis of KS. The test for the human immunodeficiency virus antibody was positive and the CD4+ cell count was 69 per cubic millimeter. A radiograph of the chest showed multiple diffuse nodules, linear opacities, and some pleural effusion. Computed tomography also revealed multiple nodules and linear densities distributed along the bronchovascular bundles. Bronchoscopic examination revealed diffuse erythematous changes of the bronchial mucosa with some red polypoid lesions, which was compatible with endobronchial KS. Hypoxia developed one month after bronchoscopy. Two courses of chemotherapy with bleomycin and vincristine were given, and resulted in temporary improvement. A definite diagnosis of KS was made by necropsy.
A 30-year-old woman with systemic lupus erythematosus was admitted to our hospital because of a slight fever and diffuse interstitial shadows on a chest X-ray film. She had taken prednisolone (60 mg per day) at another hospital for six weeks. At the time of admission to our hospital, she had been treated with antituberculosis drugs (streptomycin, isoniazid, and rifampicin) for two weeks because of suspected miliary tuberculosis. Chest radiography on admission revealed diffuse nodular and micronodular shadows in the middle and lower lung fields on both sides. Examination of transbronchial lung biopsy specimens revealed intranuclear viral inclusion bodies in infected alveolar epithelial cells, which suggested the diagnosis of cytomegalovirus infection. The elevation of serum IgM antibody to cytomegalovirus and positive results of in situ hybridization for cytomegalovirus DNA supported this diagnosis. The symptoms and radiographic abnormalities resolved completely without ganciclovir. Although we cannot exclude the possibility that the antituberculosis drugs caused the resolution of the cytomegalovirus pneumonia, it appears most probable that the cytomegalovirus pneumonia resolved spontaneously.
A 53-year-old woman was given a diagnosis of rheumatoid arthritis in 1988, and begun treatment with D-penicillamine in September 1992. She noticed dry coughing and exertional dyspnea that began in April 1993. Chest X-ray and CT films revealed no abnormal opacities. However, bronchiolitis obliterans was suspected because of a low FEV1% (23%). Examination of specimens obtained by thoracoscopic lung biopsy revealed constrictive obliteration by granulation tissue in proximal bronchioles and follicular bronchiolitis. Alveoli and respiratory bronchioles were intact. After corticosteroid and cyclophosphamide pulse therapy, FEV1% increased to 35%. At the time of this writing she was alive 2.5 years after hospitalization.
Pimobendan is a positive inotropic agent that dilates blood vessels and sensitizes the myocardium to calcium. We studied the clinical usefulness of single oral doses of pimobendan (2.5 mg) in 8 patients with pulmonary hypertension caused by chronic pulmonary emphysema. We measured the short-term effects of pimobendan on pulmonary hemodynamics and gas exchange. Pimobendan significantly decreased mean pulmonary artery pressure from 23.4 +/- 3.4 to 18.5 +/- 2.5 mmHg, and total pulmonary resistance from 383 +/- 111 to 281 +/- 81 dyne.sec.cm-5, while oxygen delivery and cardiac output increased significantly (oxygen delivery: from 81.8 +/- 10.2 to 93.5 +/- 16.2 ml O2/min. cardiac output: from 4.98 +/- 0.76 to 5.77 +/- 1.49 l/min, means +/- SD). Systemic vascular resistance was not significantly reduced. The ratio of pulmonary to systemic vascular resistance was reduced, but not significantly. Arterial oxygen tension (PaO2) and arterial carbon dioxide tension (PaCO2) did not change significantly. These results indicate that pimobendan may be useful in the treatment of patients with secondary pulmonary hypertension.
