[DIAGNOSIS OF LUNG DISEASES. LUNG DISEASES MISDIAGNOSED AS TUBERCULOSIS].
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Arterial PaO2 and some phonomechanographic indices were studied during and after a period of 40-60-100% oxygen breathing in fourteen patients (six with pulmonary insufficiency, four with cardiac disease and four with cardiorespiratory insufficiency). Arterial PaO2 was measured at the beginning, every five minutes during and many times after the ventilation. Myocardial performance was also measured by sistolic time: isovolumetric contraction time, left ventricular expulsive time, preejection pressure, deformation time. The authors discuss the modifications of these indices and the clinical involvement of O2 breathing.
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Inspiratory muscle fatigue and pulmonary edema are both known to cause rapid shallow breathing. It has been suggested that exercise tolerance in patients with pulmonary disease and cardiac disease may be limited by the development of inspiratory muscle fatigue and pulmonary edema, respectively, at maximal exercise. If these hypotheses are correct, breathing pattern during recovery from maximal exercise in these patients should be rapid and shallow compared with that during exercise. This study was performed to test these hypotheses. Seven patients with chronic obstructive pulmonary disease (COPD), 8 patients with interstitial lung disease (ILD), 7 patients with cardiac disease (CD) (mitral valve disease or left ventricular dysfunction) and 8 normal (NR) subjects each performed maximal incremental exercise on a cycle ergometer. Exercise breathing pattern was compared with that during recovery by calculating the mean difference in tidal volume (at the same levels of minute ventilation) between exercise and recovery for each subject. Recovery breathing pattern was similar to that during exercise for the COPD, ILD, and NR subjects. In contrast, breathing pattern during recovery was rapid and shallow compared with that during exercise for the CD patients; recovery tidal volume was less than that during exercise for the same level of minute ventilation. The fact that rapid shallow breathing does not develop during recovery from maximal exercise in patients with COPD or ILD suggests that inspiratory muscle fatigue does not limit their exercise tolerance. The relative rapid shallow breathing during recovery from maximal exercise in patients with CD is probably due to the development of pulmonary edema at maximal exercise, but further studies are needed to confirm this.(ABSTRACT TRUNCATED AT 250 WORDS)
Lung diseases cause morbidity, mortality, and economic burden. Susceptibility to pathogenesis of most lung diseases result from a complex interaction of a relevant challenge from the environment, genetic background, and the nature of the host responses. Cutting-edge research in lung disease now centers on understanding the lung as a genetically determined biological organ that functions to mediate gas exchange and defend against a hostile environment. A major challenge is to determine the hierarchy of gene expression that integrates the function of multiple cell types in this complex anatomy. Emerging therapies that will play a major role in the future treatment of lung disease include the use of recombinant proteins, including monoclonal antibodies, cell therapy (including stem cells), and gene therapy. Future advances will include the cure of the major hereditary lung disorders by gene therapy, new treatment for asthma, chronic obstructive pulmonary disease, and interstitial lung disease; development of vaccines to protect the lung from major lung pathogens; and pathogen-specific "designer" therapies to eradicate chronic lung infections.
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Lung biopsy remains an important investigation in the diagnosis of diffuse interstitial lung disease despite improved diagnostic yield of high resolution computed tomography scanning. We describe 19 pulmonary wedge biopsies (13 men and 6 women) performed using videothoracoscopic technique. The median age of the patients was 56 years (range 32-72 years). All our patients were suspected to have diffuse interstitial lung disease and were referred for lung biopsy to obtain a histological diagnosis. Thoracoscopic wedge excisions were accomplished under general anaesthesia using high frequency jet ventilation and a percutaneous stapling device. A tissue diagnosis was obtained in all patients: 8 had cryptogenic fibrosing alveolitis, 3 had interstitial pulmonary fibrosis, 2 had emphysema, 2 had extrinsic allergic alveolitis, 2 had sarcoidosis, 1 had non-specific chronic inflammation, and 1 had pulmonary haemosiderosis. There were no operative deaths. There was one failure resulting in conversion to an open procedure. There were three complications: two air leaks and one effusion. Median postoperative hospital stay was 2 days (range 2-7 days). We conclude that videothoracoscopic wedge biopsy is a safe and effective procedure and should be recommended in patients who require a histological diagnosis of diffuse interstitial lung disease.
Lung disease is a major cause of morbidity and is the leading cause of mortality in patients with systemic sclerosis, most commonly occurring as interstitial lung disease or as pulmonary hypertension. Cyclophosphamide has been used to treat the interstitial lung disease and a placebo-controlled trial is planned. Potent pulmonary vasodilators, many of which have been studied in primary pulmonary hypertension, are now undergoing study in patients with systemic sclerosis.
Lung biopsy tissue from eight infants with chronic lung disease was evaluated for the presence of Ureaplasma urealyticum. Specimens from four infants grew the organism. Pleural fluid cultures matched lung tissue but tracheal cultures were negative in two babies with positive lung tissue. There were no distinguishing pathologic findings in the four culture-positive infants which could be used to identify them vs. the culture-negative infants. Three culture-positive infants improved clinically after therapy directed at Ureaplasma even though two remained culture-positive. Ureaplasma grows in lung tissue of infants with chronic lung disease, it does not demonstrate any specific standard pathologic findings and tissue cultures do not match endotracheal cultures.
Lung cancer is one of the predominant causes of cancer death. The aim of this project is the development of a screening method in persons with high risk for developing lung cancer, based on the measurement of Tumor M2-pyruvate kinase (Tumor M2-PK). Tumor M2-PK is quantitatively detectable in ethylenediaminetetraacetic acid-plasma with a sensitive enzyme-linked immunosorbent assay. So far, 60 patients with newly diagnosed lung cancer were included. These were compared to 24 patients with acute inflammatory lung diseases, 56 patients with pneumoconiosis, 22 patients with obstructive airway diseases, and 28 healthy persons. Tumor patients and some individuals suffering from severe inflammatory lung diseases had significantly higher Tumor M2-PK concentrations in ethylenediaminetetraacetic acid-plasma than all the other groups. The histologic tumor type had no influence on the plasma levels of Tumor M2-PK. Tumor M2-PK concentrations correlate strongly with the tumor stage, showing significantly increasing concentrations with progressive tumor stages. The present data indicate that Tumor M2-PK could be a valuable tumor marker for the detection of lung cancer.
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OBJECTIVE: The association between previous lung diseases (PLD) and lung cancer risk has not been studied extensively. We conducted a registry-based case-control study to examine the relation between previous lung diseases and lung cancer among women in Missouri. METHODS: Incident cases (n = 676) were identified through the Missouri Cancer Registry for the period 1 January 1993 to 31 January 1994. Controls (n = 700) were selected through drivers' license files and Medicare files. RESULTS: Whether analyzing all respondents or in-person interviews only, elevated effect estimates were noted for several types of PLD. Elevated relative risk estimates were shown for chronic bronchitis (odds ratio [OR] = 1.7; 95% confidence interval [CI] = 1.2-2.3), emphysema (OR = 2.7; 95% CI = 1.8-4.2), pneumonia (OR = 1.6; 95% CI = 1.2-2.0), and for all PLDs combined (OR = 1.5; 95% CI = 1.2-1.9). Analysis of only direct interviews did not show a substantial or consistent pattern of change in relative risk estimates. Because PLDs identified close to the time of cancer diagnosis could conceivably be misdiagnosed, resulting from early lung cancer symptoms, we evaluated the effects on risk estimates of a "latency exclusion" of up to three years. When these exclusions were taken into account, ORs remained statistically significantly elevated only for emphysema. CONCLUSION: When earlier epidemiologic findings and underlying biological and genetic factors are taken into account, an association between PLD and lung cancer is plausible.
Lung volumes and breathing patterns used during speech differ from those of quiet respiration and may be expected to vary with different types of lung disease. To test this possibility, 41 patients with asthma, emphysema, or sarcoidosis and 16 healthy subjects completed a speech protocol. Volumes, times, and flow rates were recorded during conversation and during a counting task. A total of 16 measured variables were derived for each breath and analyzed statistically. Alterations in speech breathing were disease and task specific. Discriminant function analysis applied to data from either speech task could correctly classify subjects with more than 50% accuracy, showing that different patterns were significantly disease specific. Compared with healthy subjects during conversation, all patients averaged a more rapid respiratory rate and increased the proportion of time spent on inspiration (Ti/Ttot). During counting, patient groups showed a variety of patterns, most commonly subordinating metabolic need to communication drive and sounding more breathless to observers. Regression analysis was used to determine how strongly changes in measured speech variables related to degree of physiologic impairment. The effect of severity of disease on speech production is distinguishable from the effect of the diagnostic category.
Preexisting lung disease was examined as a risk factor for lung cancer in a population-based, case-control study of nonsmoking women in Missouri conducted between June 1, 1986, and April 1, 1991. A history of lung disease was reported by approximately 41% of 618 cases and 35% of 1,402 controls (odds ratio (OR) = 1.2; 95% confidence interval (Cl) 1.0-1.5. The risk was more pronounced when next-of-kin interviews were excluded (OR = 1.5). Previous lung disease was significantly related both to adenocarcinoma (OR = 1.4), which accounted for 62% of the cancers, and to all other cell types of lung cancer combined (OR = 1.8). Despite having discontinued smoking for more than 15 years, long-term ex-smokers were at a 2.2-fold risk of lung cancer compared with lifetime nonsmokers. Among lifetime nonsmokers, significant risks were noted for asthma (OR = 2.7) and pneumonia (OR = 1.5). Emphysema (OR = 2.6) and tuberculosis (OR = 2.0) were also significantly related to lung cancer, but only among former smokers. Chronic bronchitis was linked to elevated risks of nonadenocarcinomas only (OR = 2.3). Pleurisy was not reported more frequently by cases than by controls. Approximately 16% of all lung cancers among nonsmoking women could be attributed to previous lung diseases, most notably asthma, pneumonia, emphysema, and tuberculosis.
Lung volumes were measured at rest and during exercise by an open-circuit N2-washout technique in patients with interstitial lung disease (ILD). Exercise tidal flow-volume (F-V) curves were also compared with maximal F-V curves to investigate whether these patients demonstrated flow limitation. Seven patients underwent 4 min of constant work rate bicycle ergometer exercise at 40, 70, and 90% of their previously determined maximal work rates. End-expiratory lung volume and total lung capacity were measured at rest and near the end of each period of exercise. There was no significant change in end-expiratory lung volume or total lung capacity when resting measurements were compared with measurements at 40, 70, and 90% work rates. During exercise, expiratory flow limitation was evident in four patients who reported stopping exercise because of dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evident. In all patients, the mean ratio of maximal minute ventilation to maximal ventilatory capacity (calculated from maximal F-V curves) was 67%. We conclude that lung volumes during exercise do not significantly differ from those at rest in this population and that patients with ILD may demonstrate expiratory flow limitation during exercise. Furthermore, because most patients with ILD are not breathing near their maximal ventilatory capacity at the end of exercise, we suggest that respiratory mechanics are not the primary cause of their exercise limitation.
Lung function studies using 13Nitrogen have been used to determine regional and total lung function in 16 children suspected of having localized lung disease amenable to surgery. This method is simple, requires no active co-operation on the part of the child and gives a radiation dosage of about one-third of that for a bronchogram. The studies provided information about the severity and localization of the disease, and in addition, information about the remaining lung areas.