Articles: interstitial-lung-diseases.
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Pneumonitis is a rare but potentially life threatening side effect of methotrexate treatment for rheumatoid arthritis which needs to be distinguished from interstitial lung disease due to rheumatoid arthritis. ⋯ Methotrexate pneumonitis was associated with lymphocytic alveolitis with a preferential increase in CD4+ cells. This pattern differs from that in interstitial lung disease due to rheumatoid arthritis and may therefore assist in making an early diagnosis of methotrexate pneumonitis.
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Am. J. Respir. Crit. Care Med. · Mar 1997
ReviewGold-induced pulmonary disease: clinical features, outcome, and differentiation from rheumatoid lung disease.
Gold-induced pulmonary disease is difficult to diagnose, especially, in the case in which interstitial pneumonia appears in the course of gold therapy for rheumatoid arthritis. We analyzed the literature to define the clinical features and prognosis of gold-induced pulmonary disease, and to identify those features that distinguish gold-induced pulmonary disease from pulmonary disease secondary to the underlying disease process of rheumatoid arthritis. Relevant articles from the medical literature were identified using a Mediline search, and the bibliographies of the articles were retrieved. ⋯ Features that distinguish gold-induced pulmonary disease from rheumatoid lung disease include female predominance, presence of fever or skin rash, absence of subcutaneous nodules or finger clubbing, low titers of rheumatoid factor at onset of lung disease, lymphocytosis in bronchoalveolar lavage fluid (BALF), and alveolar opacities along the bronchovascular bundles on chest CT scan. Gold-induced lung disease is a distinct entity that can be distinguished from rheumatoid lung disease. It usually improves with cessation of therapy or treatment with corticosteriods.
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J Invest Allerg Clin · Mar 1997
Interstitial pneumonitis induced in guinea pigs by the antigens of Rhizopus nigricans.
Rhizopus nigricans (Rn) is one of the most common members of the Mucorales that produces opportunistic infections and hypersensitivity states. Data concerning experimental induction in guinea pigs of hypersensitivity pneumonitis with a glycoprotein antigen are presented. This antigen was obtained from the mycelial and metabolic products of the cultures and was aerosolized during 12 weeks. ⋯ Single non-necrotizing granulomas were characteristic from the tenth week to the end of the experiment. The results from this animal model suggest that hypersensitivity pneumonitis is a typical delayed-type reaction due to chronic contact with the heterologous glycoprotein of Rn. The relation of Rn antigen and the development of occupational diseases of the lung such as malt-worker's lung and wood-trimmer's disease is proposed and discussed.
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Am. J. Respir. Cell Mol. Biol. · Feb 1997
Pulmonary lymphoid cell activation and cytokine expression in murine AIDS-associated interstitial pneumonitis.
Limited information is available about the pathogenesis of acquired immune deficiency syndrome (AIDS)-associated idiopathic interstitial pneumonitis, a common noninfectious complication of human immunodeficiency virus (HIV) infection. Infection of C57B1/6 mice with LP-BM5 retrovirus, a murine model of AIDS, leads to development of a diffuse interstitial pneumonitis that displays many features of human AIDS-associated interstitial pneumonitis. To further characterize the cellular and molecular features of this lung disease, the temporal development of cellular infiltration, cytokine expression, and virus replication were evaluated in lung tissue of virus-infected mice. ⋯ Similarly, expression by interstitial lung lymphoid cells of mRNA for the proinflammatory cytokine IL-1 and the fibrogenic cytokine transforming growth factor-beta (TGF-beta) was also increased following infection. These results indicate that retrovirus-induced immunodeficiency in mice is associated with infiltration and chronic activation of lymphoid cells in the lungs. Furthermore, simultaneous expression of IL-10, IFN-gamma, and TGF-beta suggests that cytokine-expressing cells in infected lungs may be unresponsive to inhibitory and antiinflammatory effects of IL-10 and/or TGF-beta, thus contributing to chronicity of inflammation in this disorder.
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Monaldi Arch Chest Dis · Feb 1997
ReviewInterstitial lung disease: basic mechanisms and genetic predisposition.
Diffuse (interstitial) lung disease comprises a wide variety of relatively uncommon conditions, which present with characteristic clusters of clinical features and often with aberrant lung function. These diseases cause major morbidity and mortality due to lung injury and fibrosis. ⋯ However, since not all individuals exposed to a common environment develop interstitial diseases, we can hypothesize that there is a genetic predisposition to their development. Therefore, if we can identify individuals who are genetically predisposed to develop diseases characterized by lung injury and fibrosis, then management strategies can be designed which will attempt to identify early disease and, in the longer term, to develop targeted genetic interventional approaches to treatment.