Willingness to pay and accept risks to cure chronic disease.

Measurements of disease burden focus most often on economic outputs--neglecting effects on quality of life. More comprehensive quantification is based on what people would pay or risk to avoid illness. Many, however, find it difficult to respond thoughtfully to hypothetical questions about what they would pay or risk. With response rates frequently under 50 per cent, the practicality of these methods has been of concern. In this study, specially trained interviewers asked 247 subjects with rheumatoid arthritis how much of their income they would pay and how large a mortal risk they would accept to achieve a hypothetical cure. Ninety-eight per cent of the subjects estimated their maximum acceptable risk (MAR) at an average 27 per cent chance of immediate death. Eighty-four per cent gave plausible responses to the willingness-to-pay (WTP) questions, with a mean WTP of 22 per cent of household income. The aspect of disease most strongly associated with WTP was impairment in activities of daily living; measured pain was most associated with MAR. The response rates achieved indicate the overall feasibility of these methods; the associations of WTP and MAR with other variables suggest systematic consideration of personal circumstances.

Auranofin and D-penicillamine: a one year comparative study of safety and efficacy in patients with rheumatoid arthritis followed by a two year open assessment of auranofin.

Forty-six patients with classical or definite rheumatoid arthritis participated in a prospective clinical trial comparing auranofin 6 mg/day (26 patients) with D-penicillamine 500 mg/day (20 patients) during one year. NSAIDs were also given throughout the study period. After the first year, patients receiving auranofin with a satisfactory response continued for a further two years with a reduced dose of 3 mg/day. However the 6 mg dose could be reinstituted in patients showing deterioration after dose reduction. This paper only discusses the long-term treatment with auranofin. Seven out of 26 patients did not complete the one year treatment period; three because they did not return to follow-up, one because of inefficacy, and 3 because of untoward events. During the second year 5 more patients discontinued treatment, one because he was lost to follow-up, two because of inefficacy, one because of untoward events and another one because of a surgical procedure of the left knee. Two more patients discontinued auranofin treatment during the third year, one because of a flare up of his disease activity, and one because of a rash. Statistically significant improvements in the number of tender joints, activity and articular indices, duration of morning stiffness, pain score and ESR were observed at each time analysed. Statistically significant reductions in the number of swollen joints were seen throughout the first two years of treatment. Increases in grip strength were statistically significant at 6, 24 and 30 months. A statistically significant reduction was seen after 6 months of treatment in serum IgA and IgM concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of immune response during chrysotherapy. Comparison of gold sodium thiomalate vs. auranofin.

Auranofin (AF) differs significantly from gold sodium thiomalate (GST) in formulation, i.e., aurous gold is stabilized by dual sulfur and phosphorus ligands, has hydrophobic rather than hydrophilic characteristics, and lacks ionic charge. These attributes facilitate: oral absorption of AF, plasma membrane penetration, increase in intracellular lymphocyte gold concentration and perhaps thereby influence lymphocyte function. AF therapy was observed to affect primarily T rather than B lymphocyte function in 16 RA subjects receiving 6 mg of AF per day for an average of 45 weeks (range 20-74 weeks) compared with GST-treated RA subjects. Lymphocytes from AF-treated subjects manifested prompt and sharp declines in mitogen-induced lymphoproliferative response (LPR); suppressed response to skin testing with dinitrochlorobenzene (DNCB); and blebbing of lymphocyte membranes as shown by scanning electron microscopy. Suppression of LPR with AF was approximately 60% after the first week and 80% after 20 weeks of therapy, contrasting with 0% and 30% for the respective intervals in GST-treated subjects. DNCB skin testing of AF patients, indicated 11 of 14, failed to respond, whereas all GST patients responded. Local or systemic fungal, bacterial and/or opportunistic infections were not encountered. The effect of AF on B cell effector function, e.g., suppression of immunoglobulins and rheumatoid factor titer, was less marked when contrasted with GST therapy in RA subjects, as previously reported.