To determine the efficacy of oral
gold in
asthma, 20 patients with
steroid-dependent
asthma received
auranofin at a dose of 3 mg by mouth, twice daily, in a 24-week open clinical trial. Prospective evaluation of bronchial responsiveness to
methacholine was determined before and 8 and 16 weeks after initiation of
auranofin therapy. Serial spirometry (FEV1 and FVC), lung volumes, and diffusing capacities (single breath
carbon monoxide diffusing capacity of the lungs) were measured before and
at 10 and 20 weeks
after treatment. All subjects were required to record concomitant medications, symptom scores, and morning and evening peak expiratory flow rates. In vitro immunologic studies performed before and after 8 and 20 weeks of
auranofin therapy included leukocyte histamine release in response to antihuman
IgE, lymphocyte blast transformation in response to
concanavalin A and
phytohemagglutinin, and
leukocyte inhibitory factor activity in response to Candida albicans and
tetanus toxoid antigens. In 18 patients evaluated, there were no significant differences between baseline and posttreatment spirometry, single breath
carbon monoxide diffusing capacity of the lungs, and lung volumes. At week 16 of treatment, the
steroid cumulative dose or the total
prednisone dose administered from 7 days before through 10 days after each
methacholine test day decreased from a mean of 293 +/- 125 mg at baseline to 192 +/- 115 mg. At week 16, nine of 18 patients (50%) exhibited decreased
methacholine responsiveness as defined by a more than one-half log10 increase in the concentration of
methacholine causing a 20% decrease in FEV1. A significant correlation (r = 0.60) was observed between the increase in the concentration of
methacholine causing a 20% decrease in FEV1 and the decrease in
steroid cumulative dose after 16 weeks of treatment. Leukocyte histamine release to
anti-IgE exhibited significant reductions from baseline at week 20 to 10(-2) (p less than 0.002) and
at 10(-3) (p less than 0.005) dilutions. At week 20,
leukocyte inhibitory factor activity in response to Candida increased from baseline at the 0.1 mg per well (p = 0.025) and 1 mg per well (p = 0.05) concentrations; similarly, the responses to
tetanus toxoid increased at the 1 mg per well (p less than 0.05) and 0.1 mg per well (p less than 0.01) concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)