Chest
Volume 96, Issue 1, July 1989, Pages 216-218
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Gold-Naproxen Pneumonitis: A Toxic Drug Interaction?

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A patient with rheumatoid arthritis developed restrictive lung disease and blood eosinophilia. Gold pneumonitis was suspected but the patient did not improve until naproxen was discontinued as well. Lymphocyte transformation studies suggested hypersensitivity to gold. We hypothesize that naproxen unmasked and perpetuated the manifestations of gold hypersensitivity in our patient.

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Case Report

A 62 year-old man developed seropositive RA in 1984 and was treated with various NSAIDs. Chrysotherapy was initiated in May 1986 and he received a total of 685 mg SATM over three months when the drug had to be discontinued because of mucodermatitis. Naproxen, 500 mg twice daily, had been started in July 1986. About this time, he began to complain of malaise, fatigue, anorexia, and a nocturnal cough. Over the next four weeks, his cough became continuous, he developed mild dyspnea and chest

In Vitro Studies

In an effort to determine the etiology of what appeared to be a hypersensitivity pneumonitis, in vitro studies thought to be relatively predictive of cell-mediated immunity to pharmacologic agents were performed.10, 11, 12, 13 Briefly, PBMC, harvested from Ficoll-Hypaque cushions were obtained from the patient and three healthy male volunteers. The PBMC from the patient were cultured in the presence of media alone (control), mitogen (1 percent PHA), and various concentrations of naproxen and

DISCUSSION

Previous investigators have demonstrated an inhibitory effect of various gold salts on the cell-mediated immune response in vitro,14, 15, 16, 17 compatible with its role as an immunosuppressive agent in RA patients. We have also demonstrated that SATM inhibits the in vitro proliferation of mitogen treated cells from healthy subjects, and have also shown that naproxen may have additional immunosuppressive effects when used in combination with SATM (Fig 1). In contrast, cells from our patient

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