The mechanisms of action of conventional chrysotherapy.
The discovery of chrysotherapy occurred 90 years ago. Gold salts (GS) as an antibacterial agent were used initially for tuberculosis (TB), but an infectious etiology was also suspected for rheumatoid arthritis (RA). Patients who received GS for TB and who also had RA noted improvement of their arthritis. The injectable GS regimen now commonly used evolved from the empirical use of GS for RA from 1920-1960. Originally, clinical experience perpetuated the use of injectable GS to modify RA and its progression. However, scientific data obtained in the last 2 decades have supported the efficacy of chrysotherapy. Studies of protein binding, blood and serum concentrations, tissue distribution, and the toxicity of GS all provided suggestions for its mode of action. As chemical and cellular mediators of inflammation were uncovered, the possible actions of gold have been refined. Because the immune system seems to perpetuate rheumatoid inflammation, the interactions with GS continue to be studied. The in vitro and in vivo actions of GS with the immune system so far have provided conflicting data for its immunological effect. Studies by models of mucosal immunity may lead to new insights in the mode of action for gold.
D001168:Arthritis / Q000188:drug therapy; D001172:Arthritis, Rheumatoid / Q000473:pathology; D006051:Aurothioglucose / Q000008:administration & dosage / Q000627:therapeutic use; D001696:Biomechanical Phenomena; D002477:Cells / Q000187:drug effects; D006046:Gold / Q000627:therapeutic use*; D006052:Gold Sodium Thiomalate / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects; D007273:Injections, Intramuscular
D006052:Gold Sodium Thiomalate; D006051:Aurothioglucose; D006046:Gold