Between January 1988 and December 1992, 68 patients admitted to our Department of Internal Medicine with haematological malignancies or solid tumours showed colonization of the respiratory tract with Stenotrophomonas maltophilia. To characterize the significance of respiratory tract colonization by S. maltophilia, we retrospectively reviewed the medical records of the 68 patients colonized with this organism. Twenty-nine of these 68 patients developed pneumonia, with S. maltophilia being implicated in 10 cases. The majority of these 10 patients showed lobular infiltration on chest X-ray. Pleural effusion was observed in two (20%) of the 10 patients. All 68 strains of S. maltophilia were resistant to imipenem. Latamoxef was effective against 98 center dot 5% of strains, while minocycline was effective against 100% of strains. This report describes the clinical features of nosocomial S. maltophilia pneumonia in immunocompromised patients.

It has been suggested that cytokeratin 19 is expressed in regenerated bronchoepithelial cells in patients with pulmonary fibrosis, and serum cytokeratin 19 fragment is elevated in patients with pulmonary fibrosis. We hypothesized that serum antibodies to cytokeratin 19 may be formed in patients with pulmonary fibrosis. To prove the existence of anti-cytokeratin 19 antibodies in patients' sera, human recombinant cytokeratin 19 was stained with patients' sera by a Western immunoblot. Then, we tried to establish an enzyme-linked immunosorbent assay to quantitate anti-cytokeratin 19 antibody in the sera of patients with idiopathic pulmonary fibrosis (IPF) and pulmonary fibrosis associated with collagen vascular disorders (PF-CVD). We demonstrated the anti-cytokeratin 19 antibody in patient' sera by a Western immunoblot. In patients with IPF and PF-CVD, significantly high anti-cytokeratin 19 antibody was demonstrated compared with normal volunteers, patients with chronic bronchitis, and patients with pneumonia. These results suggest that anti-cytokeratin 19 antibody may have played a role in the process of lung injury in pulmonary fibrosis.

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