A patient with rheumatoid arthritis developed severe exacerbation of symptoms 18 hours after an injection of gold thiomalate (sodium aurothiomalate). Immune complexes were present in his serum and synovial fluid; in the synovial fluid they were associated with intense complement activation. The effect of gold salts on splenic reticuloendothelial function was determined by measuring the clearanc...

As part of our studies of the interaction of gold(I) with thiols and other sulphur-containing molecules we have managed to isolate and characterize by X-my crystallography, the first gold(I)-thiomalate complex. We shall describe this work and speculate on its significance to the nature of the gold drug myochrysine, and its mode of biochemical action.

Gold sodium thiomalate, a drug used widely in the therapy of rheumatoid arthritis, was found to be an activator of latent human polymorphonuclear leukocyte collagenase. The activation was demonstrated by two distinct and independent collagenase assays: by recording with a spectrophotometer at 227 nm the enzyme-induced increase in ultraviolet difference absorbance of native type I collagen conne...

We review the crystal structures, electrospray ionization mass spectra (ESI-MS) data and chiral HPLC data for the racemic and optically pure mononuclear AuL2 complexes, and for racemic [AuLI]n and optically pure [AgLII]n polymers (LI = thiomalate, LII = D-penicillamine). We postulate an equilibrium between polymeric, mononuclear and free ligand species for [AuLII]n (gold sodium thiomalate or GS...

to determine the complications of gold sodium thiomalate therapy in rheumatoid arthritis (ra), 32 patients with active ra (27 female, 5 male) treated for a mean period of 28 ? 14 weeks were studied. from these patients, 62.5 (46-79) percent showed at least one drug reaction. pruritus was the most common complication occurred in 59 (42-76) percents, and was accompanied by skin rush in 37 (15-57)...

Treatment of a newly prepared digold(i) complex, [Au2(dppe)(H2msa)2] ([H41]; dppe = 1,2-bis(diphenylphosphino)ethane, msa = thiomalate), with Ni(2+) gave two interconvertible multinuclear complexes, [Ni{Au2(dppe)(msa)2}](2-) ([2](2-)) and [Ni3{Au2(dppe)(Hmsa)2}{Au2(dppe)(msa)2}(MeOH)3] ([3]), dependent on solution acidities.

Treatment of adult mice with gold sodium thiomalate made the normally non-lethal Semliki Forest virus and Sindbis virus infections lethal and increased the virulence of Langat and West Nile viruses. These changes were associated with an enhanced virus invasion of the brain. Depression of the humoral antibody response was not observed.

Separation of smooth membrane vesicles from whole mouse brain by isopycnic centrifugation in discontinuous sucrose density gradients show an increased membrane proliferation in gold sodium thiomalate (GSTM) treated mice. Induction of membrane proliferation by GSTM seems to be an important factor in converting the avirulent Semliki Forest virus infection into a lethal one.