Articles: pulmonary-fibrosis-etiology.
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A number of disorders for which an association with hepatitis C virus infection exist. These disorders include essential mixed cryoglobulinemia, membranoproliferative glomerulonephritis, and idiopathic pulmonary fibrosis. This study was initiated to investigate the cellular content and lymphocyte subpopulations of bronchoalveolar lavage fluid obtained from individuals with chronic hepatitis C and to compare the results to those of controls. ⋯ No difference in the percentage, median or range of individual T cell subsets or B cell numbers in the bronchoalveolar lavage fluid existed between the groups. It is concluded that hepatitis C virus infection may be associated with an occult pulmonary inflammatory reaction manifested by an increased number of polymorphonuclear neutrophils in bronchoalveolar lavage fluid. This finding may contribute to the process that leads to idiopathic pulmonary fibrosis seen in a minority of cases of chronic hepatitis C.
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Comparative Study
Interstitial lung disease in patients with rheumatoid arthritis: a comparison with cryptogenic fibrosing alveolitis.
There is a lack of information on the natural history of patients with rheumatoid arthritis (RA) and associated interstitial lung disease (ILD). However, cryptogenic fibrosing alveolitis (CFA) is known to have a poor long-term prognosis. As part of a longitudinal prospective study, we compared baseline characteristics in 18 patients with RA-ILD and 18 patients with CFA matched for age, sex and symptoms. We wished to establish whether there were significant baseline differences in clinical, physiological or radiological parameters. ⋯ Clubbing is more common in patients with CFA, while RA-ILD patients have a higher prevalence of rheumatoid factor. Together with the differences in baseline HRCT, these variables in two groups of patients with similar physiological impairment at baseline may be important predictors of outcome in the longer term.
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Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. ⋯ Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.
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The involvement of the apical pleura is infrequent in diffuse pleural thickening secondary to asbestos exposure. Most often diffuse pleural thickening is accompanied by an obliteration of the costophrenic angle and the posterior and paraspinous pleural surfaces of the pleura are involved to the greatest extent. ⋯ Apical pleural thickening with upper lobe changes in asbestos-exposed persons should be regarded as due to the asbestos exposure, after exclusion of other causes like tuberculosis and the apex tumors. Usually the evolution of the lesions is slowly progressive over several years or even decade, and results in mild restrictive defect.