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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty seven workers employed for at least three years in oil impregnation of cables during 1963-83 were followed up in 1990 to study the development of pulmonary fibrosis and consequences for lung function. They had been exposed to concentrations of mineral oil vapours of 50-100 mg/m3, and concentrations of oil mist of 0.5-1.5 mg/m3. All 29 living persons were traced. For each person one control matched for age, height, and smoking habits was selected. Among 25 workers followed up with radiographic studies, 10 cases of pulmonary fibrosis were found, by contrast with one case in the control group (p less than 0.01). Chest radiographs from 1979-80 and 1989-90 were reviewed. The profusion of small opacities increased in seven of 16 persons during 10 years without exposure. Seventeen workers had lung function tests. The bellows function (VC, FEV1, MVV) and lung volumes (TLC, RV) did not differ from those in the matched controls (p greater than 0.05), but the carbon monoxide transfer factor (TLCO) was decreased. The largest reduction of TLCO (1.5 mmol/kPa/min) was found among workers exposed for 10 years or more (p less than 0.05). Arterial blood gases were not affected at rest, but during maximum tread mill exercise, PO2 and HbO2 were reduced in exposed workers compared with controls, particularly among those exposed for at least 10 years (p less than 0.05). Exposure to low viscosity oil mist and vapour is the most plausible cause of the fibrosis. Unaffected bellows function, reduced TLCO, and decreased arterial blood oxygen during exercise is compatible with peribronchiolar fibrosis.
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PMID:Lung function and radiographic signs of pulmonary fibrosis in oil exposed workers in a cable manufacturing company: a follow up study. 159 68

From a conceptual standpoint, the tests of pulmonary function can be divided into those that assess the ventilatory function of the lungs and those concerned with gas exchange. Tests of ventilatory function reflect alterations of the elastic resistance and flow resistance of the respiratory apparatus. The elastic properties of the lungs are assessed by determining the position and shape of the curve representing the relationship between the pressure across the lungs and absolute lung volume. When there is reduced distensibility of either the lungs or the chest wall, the volume-pressure curve is shifted down and to the right. The slope of the curve is reduced in the patient with pulmonary fibrosis, while it is normal in the patient with obesity. In asthma (or chronic bronchitis) and emphysema, the volume-pressure curve is shifted up and to the left. In emphysema, the slope of the curve is increased, while it is normal in patients with asthma or bronchitis. In practice, lung volume is used as an index of alterations of the volume-pressure characteristics of the lungs and/or chest wall. The vital capacity is often used as a surrogate for the TLC but it is lower than expected in both restrictive and obstructive disorders. The FEV1.0 reflects the degree of expiratory flow limitation. In a restrictive disorder, lung volume and the FEV1.0 are reduced, but the FEV1.0/FVC ratio is normal. In airflow limitation, lung volume, the FEV1.0, and the FEV1.0/FVC ratio are lower than expected. In airflow limitation, the reversibility with inhaled bronchodilator should be determined. Tests of airway responsiveness are indicated when evaluating patients with unexplained chronic cough, chest tightness, or wheezing, particularly if other lung function tests are normal. The adequacy of gas exchange is assessed by determining the arterial blood gas tensions--PaO2 and PaCO2--and the alveoloarterial pO2 gradient--P(A-a)O2. A lower-than-expected PaO2 can result from several different physiologic disturbances. When alveolar hypoventilation is the sole disturbance, the oxygen in the alveoli and in the blood perfusing them virtually comes into equilibrium, so that the P(A-a)O2 is normal. An elevated P(A-a)O2 is caused by either mismatching of ventilation and perfusion, true venous admixture, a diffusion abnormality, or a combination of these disturbances. Because dyspnea on exertion is a cardinal symptom of respiratory disease, exercise tolerance should be assessed. A reduced exercise tolerance may result from ventilatory limitation, impaired gas exchange, cardiac impairment, impaired delivery of the oxygen to the working muscles, or an inability to use the energy.
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PMID:Evaluation of respiratory function in health and disease. 160 91

The first Danish experience of treatment of the respiratory distress syndrome (RDS) in preterm infants with exogenous surfactant is described. Fifteen infants with birthweights of 645-1,865 g and gestational ages of 25-32 weeks, all receiving artificial ventilation with at least 60% oxygen for severe RDS, were treated with purified porcine surfactant (Curosurf) within the first 28 hours of life. Pulmonary function improved immediately in all of the infants. Four infants (27%) died, four (27%) developed bronchopulmonary dysplasia (pulmonary fibrosis) and two (13%) had late neurological sequelae. These preliminary results are considered to be promising and they are in complete agreement with the results of randomised, controlled investigations from abroad. Systematic registration is, however, still necessary.
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PMID:[Treatment of severe respiratory distress syndrome with surfactant]. 163 99

Multiple reactive oxygen species-induced epithelial injury by glucose, glucose oxidase, and lactoperoxidase instillation in the lung results in a progressive interstitial fibrosis. To test the hypothesis that multiple pulmonary inflammatory responses alone would not result in fibrosis, three sequential inflammatory reactions were produced at weekly intervals in hamster lungs via intratracheal instillation of human recombinant C5a. Numbers of neutrophils and total inflammatory cells in bronchoalveolar lavage (BALF) increased significantly at 24 h after each C5a treatment compared with saline controls. Neutrophils increased by 3-, 33-, and 34-fold compared with the corresponding controls at 24 h after the first, second, and third doses, respectively, but returned to control levels by six days postinstillation. LTB4 levels increased by 24% and 20% compared with the corresponding controls at 24 h after the first and second doses but were not different from controls at other times. Hydroxyproline levels in treated animals did not differ significantly from control levels throughout the study. Protein levels were significantly increased at 24 h after the second and third doses and six days after the third dose compared with the corresponding controls. Occasional foci of neutrophils in alveolar spaces were observed at 24 h after each dose, but they decreased in frequency after six days. No foci of neutrophils were observed six days after the final dose, although some epithelial degeneration was observed by transmission electron microscopy. Our results indicate that pulmonary inflammation resulting from repeated influx of neutrophils in response to multiple instillations of C5a in the lung does not cause sufficient injury to result in pulmonary fibrosis.
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PMID:Repeated episodes of C5a-induced neutrophil influx do not result in pulmonary fibrosis. 165 81

Exposure of phagocytic cells to asbestos in vitro results in an augmented production of reactive oxygen metabolites and increased peroxidation of lipids. The aim of this investigation was to assess the extent of lipid peroxidation both in cells and fluid obtained from bronchoalveolar lavage (BAL), and in lungs of rats exposed to crocidolite asbestos or titanium dioxide (TiO2), a nonfibrous particulate control. In comparison to sham and TiO2-exposed rats, the BAL fluid and cells of crocidolite-exposed animals contained significantly elevated levels of malondialdehyde (MDA), a breakdown product of lipid peroxidation detected using high-pressure liquid chromatography (HPLC). In contrast, no significant differences in MDA were detected in lavaged lung tissue from these animals. Inhalation of crocidolite caused an early inflammatory response characterized by elevated numbers of polymorphonuclear leukocytes and lymphocytes, as well as enhanced total protein in BAL. Pulmonary fibrosis and increased lung hydroxyproline also were observed after 20 days of exposure. Exposure to TiO2 did not cause inflammation, pulmonary fibrosis, or elevated amounts of hydroxyproline in the lung. Our results show that exposure to the fibrogenic and inflammatory mineral, crocidolite, results in an enhanced lipid peroxidation in BAL cells and fluid not observed after inhalation of the particulate TiO2. These novel observations suggest that MDA in BAL may be useful as a biomarker of exposure to inhaled asbestos or other oxidants.
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PMID:Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos. 166 39

Bleomycins are a family of compounds produced by Streptomyces verticillis. They have potent tumour killing properties which have given them an important place in cancer chemotherapy. They cause little marrow suppression, but pulmonary toxicity is a major adverse effect. The mechanisms of cell toxicity are well described based on in vitro experiments on DNA. The bleomycin molecule has two main structural components: a bithiazole component which partially intercalates into the DNA helix, parting the strands, as well as pyrimidine and imidazole structures, which bind iron and oxygen forming an activated complex capable of releasing damaging oxidants in close proximity to the polynucleotide chains of DNA. This may lead to chain scission or structural modifications leading to release of free bases or their propenal derivatives. The mechanisms are well described based on in vitro experiments on DNA, but how they relate to intact cells in whole animals is more tenuous. Bleomycin is able to cause cell damage independent from its effect on DNA by induction lipid peroxidation. This may be particularly important in the lung and in part account for its ability to cause alveolar cell damage and subsequent pulmonary inflammation. The lung injury seen following bleomycin comprises an interstitial oedema with an influx of inflammatory and immune cells. This may lead to the development of pulmonary fibrosis, characterized by enhanced production and deposition of collagen and other matrix components. Several polypeptide mediators capable of stimulating fibroblasts replication or excessive collagen deposition have been implicated in this, but the precise role of these in bleomycin-induced fibrosis is yet to be demonstrated. Current therapy for bleomycin-induced lung damage is inadequate, with corticosteroids most often used. Given the mechanism of action described above, antioxidants and iron chelators might be beneficial. Although, studies to date are equivocal and there is insufficient evidence to promote their use clinically. Novel drugs are currently being developed and it is hoped these may be more useful.
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PMID:Mechanisms of bleomycin-induced lung damage. 171 38

Interstitial pulmonary fibrosis induced by bleomycin (BL) involves the production of reactive oxygen species and the impairment of repair of damaged epithelial cells. We have shown previously that taurine or niacin treatment partially attenuates BL-induced lung fibrosis in hamsters and that the two agents probably act through different mechanisms. In the present investigation, we have demonstrated that taurine and niacin in combination provide nearly complete protection against BL-induced pulmonary fibrosis. Based on the findings of this investigation, it is suggested that combined treatment with taurine and niacin offers the potential for a novel pharmacological approach in the prevention of lung fibrosis in humans.
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PMID:Amelioration of bleomycin-induced pulmonary fibrosis in hamsters by combined treatment with taurine and niacin. 171 34

A 42-year-old woman with a known history of paraquat ingestion was admitted to our hospital on the 10th day after ingestion complaining of dyspnea and general fatigue. Steroid therapy and low dose oxygen therapy were administered. She recovered and was discharged on the 190th day after paraquat ingestion. A chest X-ray film on admission disclosed a bilateral ground-glass shadow. As time passed, a reticular shadow with a loss of lung volume leaving a peripherally clear zone appeared on chest X-rays and shrank gradually toward the peri-hilar area during the course. CT of the lung clearly demonstrated progress of the pulmonary fibrosing process. In the early phase of paraquat poisoning, CT revealed diffuse high density areas dominant in the posterior part of the lungs with a subpleural intact area. The high density area was sharply demarcated from the subpleural intact area. As time passed, the high density area shrank toward the central zone, causing bullous changes in the subpleural area. The dominant fibrotic change in the intermediate and central zones seems to be one of the characteristic findings in paraquat induced pulmonary fibrosis.
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PMID:[Observations of the fibrosing process in paraquat lung injury by chest X-ray and CT]. 188 7

Nitrofurantoin is a widely utilized urinary antimicrobial drug which has been associated with pulmonary fibrosis, neuropathy, and hepatitis as well as hemolytic anemia in glucose-6-phosphate dehydrogenase-deficient individuals. Incubation of freshly isolated rat hepatocytes with nitrofurantoin caused oxygen activation as a result of futile redox cycling. Glutathione disulfide (GSSG) was formed and rapidly exported from the cell resulting in complete glutathione (GSH) depletion followed by cell death. However, fructose prevented the export of GSSG from the cell and GSH levels recovered rapidly without cytotoxicity occurring. Fructose did not affect nitrofurantoin metabolism but rapidly depleted cellular ATP levels by approximately 80% which remained depressed during the incubation period. Fructose, however, did not protect hepatocytes from nitrofurantoin-induced cytotoxicity if GSH was depleted beforehand. Protection by fructose only occurred at concentrations which caused ATP depletion. These results suggest that fructose prevents nitrofurantoin-induced toxicity by depleting ATP and thereby preventing the ATP-dependent GSSG efflux. GSSG is retained enabling NADPH and glutathione-reductase to reduce the GSSG back to GSH, thereby protecting the cell from nitrofurantoin-induced oxidative stress.
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PMID:Prevention of nitrofurantoin-induced cytotoxicity in isolated hepatocytes by fructose. 189 74

We recently described a technique for bilateral sequential lung transplantation that replaces the en bloc double-lung operation, a procedure that was accompanied by frequent problems with airway healing. Twenty-seven patients have undergone 28 bilateral sequential lung transplantations over the past 14 months. Eighteen patients had transplantation because of end-stage emphysema; 6, cystic fibrosis; and 1 each, obliterative bronchiolitis, usual interstitial pneumonitis with pulmonary fibrosis, and bronchiectasis. Cardiopulmonary bypass was used electively in the first 5 patients until it was recognized that the procedure could be done safely without it, and in only 3 additional recipients has it been employed. Mean ischemic time for the first lung was 276 +/- 43 minutes and for the second lung, 410 +/- 64 minutes. There have been five deaths, three in the postoperative period (11% operative mortality) and two late. The other patients are alive and well and do not require oxygen 2 to 15 months after transplantation. Mean forced expiratory volume in 1 second rose from 16% +/- 8% of predicted to 84% +/- 17% at 12 weeks. Six-minute walk values increased from a mean of 251 +/- 91 m to 666 +/- 42 m at 24 weeks. The excellent exposure afforded to both hemithoraces by the thoracosternotomy incision and the rare need of cardiopulmonary bypass have allowed us to offer the option of transplantation to patients who formerly would have been turned down because of previous pulmonary resection or pleurectomy. On four occasions, ventilator-dependent patients underwent successful transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bilateral sequential lung transplantation: the procedure of choice for double-lung replacement. 189 30


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