STUDY OBJECTIVES: To measure surfactant protein-A (SP-A) in the BAL of patients with idiopathic pulmonary fibrosis (IPF). DESIGN: We examined SP-A in BAL and lung tissue of patients with IPF who met the stricter recommended criteria for IPF at the time of diagnosis and prior to the beginning of treatment. PATIENTS: Twenty-six patients with IPF confirmed at biopsy and 22 patients with hypersensitivity pneumonitis (HP) were compared with 9 normal volunteers. INTERVENTIONS: All patients were subjected to pulmonary function testing, BAL, and lung biopsy prior to the beginning of treatment. MEASUREMENTS AND RESULTS: We measured SP-A in BAL fluids and performed SP-A immunohistochemistry on lung specimens. Lung tissues of patients with IPF showed extensive type II cell hyperplasia, usually containing greatly increased levels of immunoreactive SP-A. By enzyme-linked immunosorbent assay, we found a twofold increase over normal values in BAL SP-A without changes in total phospholipids. These data were in agreement with semiquantitative assessments of SP-A by protein immunoblotting and by Western blotting of sodium dodecyl sulfate gels. Patients with HP exhibited a threefold increase of BAL SP-A. CONCLUSIONS: The reasons for the difference between our results and previously published reports describing decreased SP-A levels in IPF is not clear. It may relate to the stricter criteria for diagnosis, the absence of treatment prior to BAL, differences in the patient population, or to other methodologic differences.
STUDY OBJECTIVES: To measure surfactant protein-A (SP-A) in the BAL of patients with idiopathic pulmonary fibrosis (IPF). DESIGN: We examined SP-A in BAL and lung tissue of patients with IPF who met the stricter recommended criteria for IPF at the time of diagnosis and prior to the beginning of treatment. PATIENTS: Twenty-six patients with IPF confirmed at biopsy and 22 patients with hypersensitivitypneumonitis (HP) were compared with 9 normal volunteers. INTERVENTIONS: All patients were subjected to pulmonary function testing, BAL, and lung biopsy prior to the beginning of treatment. MEASUREMENTS AND RESULTS: We measured SP-A in BAL fluids and performed SP-A immunohistochemistry on lung specimens. Lung tissues of patients with IPF showed extensive type II cell hyperplasia, usually containing greatly increased levels of immunoreactive SP-A. By enzyme-linked immunosorbent assay, we found a twofold increase over normal values in BAL SP-A without changes in total phospholipids. These data were in agreement with semiquantitative assessments of SP-A by protein immunoblotting and by Western blotting of sodium dodecyl sulfate gels. Patients with HP exhibited a threefold increase of BAL SP-A. CONCLUSIONS: The reasons for the difference between our results and previously published reports describing decreased SP-A levels in IPF is not clear. It may relate to the stricter criteria for diagnosis, the absence of treatment prior to BAL, differences in the patient population, or to other methodologic differences.
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