Idiopathic pulmonary fibrosis (IPF) is a chronic lung disorder characterized by an increased density of inflammatory cells, fibroblasts, and collagen within the lung parenchyma. To gain insights into the mechanisms leading to the increased density of fibroblasts and altered collagen metabolism in the IPF lung, bronchoalveolar lavage fluid from normal subjects and patients with IPF or sarcoidosis was analyzed for (1) the presence of antigenic material related to the aminoterminal propeptide domain of type III procollagen, and (2) fibroblast growth-promoting activity in the extracellular milieu of the lower respiratory tract. Whereas bronchoalveolar lavage fluid (BALF) type III procollagen aminoterminal peptide-related antigen levels in 59 patients with sarcoidosis were similar to the levels of control subjects (p greater than 0.10), 31 patients with IPF had markedly increased levels (12-fold over controls; p less than 0.025, IPF versus controls; p less than 0.01, IPF versus sarcoidosis). Type III procollagen aminoterminal peptide-related antigen levels correlated with an increase in the ability of BALF to stimulate fibroblast proliferation (p less than 0.05). Furthermore, BALF from patients with IPF markedly stimulated human lung fibroblast proliferation in vitro (199% increase, p less than 0.01), whereas lavage fluid from patients with sarcoidosis and from control subjects did not. The enhanced fibroblast proliferation induced by IPF BALF occurred in the absence of serum and exogenous growth factors, suggesting that both competence- and progression-type growth factors were present in the lavage fluid.(ABSTRACT TRUNCATED AT 250 WORDS)
To analyze the clinical features of asbestos-induced alveolitis and stage its activity, we evaluated 217 asbestos workers by the usual clinical, radiological, and functional parameters and computerized gallium 67(Ga) lung scan; we obtained bronchoalveolar lavage (BAL) in 33 and lung biopsy in 6. In addition, we scored the profusion of lung rales and correlated it with other parameters of severity of asbestosis. In the 55 workers without asbestosis and normal 67Ga scan, BAL analyses were comparable to those of controls. Of the 56 without asbestosis but increased 67Ga lung uptake, BAL analyses in 8 documented a predominantly macrophagic alveolitis (confirmed on lung biopsy in 3), with the highest levels of BAL fibronectin. In the 106 workers with asbestosis, 67Ga lung uptake was increased in 75; BAL in 17 demonstrated a macrophagic and neutrophilic alveolitis with elevated fibronectin levels. Lung biopsy in 3 of the latter workers documented peribronchiolar fibrosing alveolitis. Rale scores in all workers or in those without asbestosis did not correlate with 67Ga scores; they correlated fairly well with profusion of parenchymal opacities (Rs = 0.42) and rigidity of the lung pressure-volume curve (Rs = 0.39). Thus, 67Ga lung uptake is an early indicator of chronic macrophagic alveolitis in asbestos workers, which usually progresses to asbestosis. In the disease, profusion of lung rales constitutes a simple clinical mode of assessment of disease severity that correlates better with radiological and functional parameters than with parameters of alveolitis.
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