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Lung Fibrosis in Hypersensitivity Pneumonitis (1)

Lung Fibrosis in Hypersensitivity Pneumonitis (1)Hypersensitivitv pneumonitis (HP) occurs after exposure to a variety of environmental antigens. An acute phase of HP is assumed to be triggered by the massive inhalation of the relevant antigens leading to the development of immune complex disease followed by T-cell-mediated hypersensitivity reactions. There are reports that chronic HP develops into lung fibrosis after a prolonged period of repeated insults and persistent inflammation, although repeated exposure does not always result in fibrosis. The development of pulmonary fibrosis appears to depend on the immune responses of individual patients and/ or the biologic characteristics of the causative antigen.
Bronchoalveolar lavage (BAL) has revealed many characteristic aspects of cellular and humoral components of HP It is widely accepted that predominant CD8+ T lymphocyte alveolitis is a feature of HP at an acute phase. However, in several cases, especially at a chronic phase, pulmonary fibrosis may be another feature of radiologic findings of HP, and CD8 + T-cell dominance in BAL fluids may disappear.
The radiologic features of HP have been investigated extensively on plain chest radiographs, although the distinction between the linear or linear-nodular shadows of acute interstitial pneumonia and actual pulmonary fibrosis was difficult. Recently, high-resolu-tion computed tomography (CT) has been proved to be useful for differentiating interstitial fibrotic changes from the cellular inflammation.
In this study, we attempted (1) an assessment of pulmonary fibrosis of HP by CT in reference to the histologic findings of transbronchial biopsy materials and (2) a characterization of HP accompanied by pulmonary fibrosis based on analyses of cellular components of BAL fluids, pulmonary function test results, and clinical course.

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