Successful treatment of progressive rheumatoid interstitial lung disease with cyclosporine: a case report.

Treatment of interstitial lung disease (ILD) in rheumatoid arthritis (RA) has been controversial. Although there have been several anecdotal reports on the efficacies of corticosteroids or cytotoxic agents such as methotrexate, cyclophosphamide, azathioprine, and D-penicillamine for the treatment of ILD associated with RA, no controlled studies have been performed. To date, corticosteroids have been a central agent for the treatment of this disease, but their effects are partial and temporary in most cases. In addition, the adverse effects of these agents are considerable. On the other hand, limited information is available on the cyclosporine use in ILD associated with RA. We describe a 49-yr old female patient with RA and ILD that had initially responded to high dose prednisolone and cyclophosphamide intravenous pulse therapy, and the lung disease was aggravated with the tapering of prednisolone. After 10 months of follow-up loss, the patient was successfully treated with low dose cyclosporine without high dose corticosteroids.

Inhaled nitric oxide attenuates acute lung injury via inhibition of nuclear factor-kappa B and inflammation.

The effect of inhaled nitric oxide (NO) on inflammatory process in acute lung injury (ALI) is unclear. The aims of this study were to 1) examine whether inhaled NO affects the biochemical lung injury parameters and cellular inflammatory responses and 2) determine the effect of inhaled NO on the activation of nuclear factor-kappa B (NF-kappa B) in lipopolysaccharide (LPS)-induced ALI. Compared with saline controls, rabbits treated intravenously with LPS showed increases in total protein and lactate dehydrogenase in the bronchoalveolar lavage (BAL) fluid, indicating ALI. LPS-treated animals with NO inhalation (LPS-NO) showed significant decreases in these parameters. Neutrophil numbers in the BAL fluid, the activity of reactive oxygen species in BAL cells, and the levels of interleukin (IL)-1 beta and IL-8 in alveolar macrophages were increased in LPS-treated animals. In contrast, neutrophil numbers and these cellular activities were substantially decreased in LPS-NO animals, compared with LPS-treated animals. NF-kappa B activation in alveolar macrophages from LPS-treated animals was also markedly increased, whereas this activity was effectively blocked in LPS-NO animals. These results suggest that inhaled NO attenuates LPS-induced ALI and pulmonary inflammation. This attenuation may be associated with the inhibition of NF-kappa B activation.