Sodium aurothiosulfate

Gold has a long medical history. Gold compounds were first investigated for RA treatment because of the reported relief of joint pain in tubercular patients being treated unsuccessfully with sodium aurothiosulfate. Use of gold therapy and its mechanism of therapeutic benefit have long been controversial. However, clinical studies reported in 1960 confirmed its antiarthritic value. 

FIGU RE 10.1 Chemical structures of gold thiolates used in the treatment of rheumatoid arthritis (a) aurothioglucose, (b) sodium aurothiosulfate, (c) sodium aurothiomalate, and (d) sodium aurothiopropanol sulfonate. 

Sodium aurothiomalate is water-soluble and is given intramuscularly as an aqueous solution. Aurothioglucose is water-soluble and is given intramuscularly in either an aqueous solution or an oily suspension. Sodium aurothio-propanol sulfonate, aurotioprol, and aurothiosulfate have similar actions and uses to those of sodium aurothiomalate. They are given by intramuscular injection. 

In rheumatoid arthritis the most commonly used gold salts are sodium aurothiomalate and aurothioglucose (3). There is some reason to believe that adverse effects are less frequent with the suspensions (of aurothioglucose or aurothiosulfate) than with the more rapidly absorbed solution (of sodium gold thiomalate) (SEDA-16, 233) (4). 

Tissue damage present in RA is attributed in part to action of lytic lysosomal enzymes released by phagocytic cells in inflammed tissue. Auranofin inhibits the release of lysosomal enzymes from phagocytizing leukocytes at micromolar concentrations (1-10 uM) (44> 45). It did not produce leukocyte cytotoxicity nor inhibition of cell free lysosomal enzyme activity at these effective concentrations. Sodium aurothiomalate, aurothioglucose and odium aurothiosulfate did not exhibit this potent activity. 

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