Distribution and Reactivity of Myocrisin

For many years gold compounds have been used reluctantly by clinicians treating aggressive rheumatoid arthritis [1]. The reluctance stems from the fact that the compounds are effective only in some patients and from the potential toxicity of gold in vivo. Various alternatives have been suggested over the past 20 years and none have proved sufficiently good to completely replace gold as a major contributor in the therapy of rheumatoid arthritis. However, the in vivo chemistry of gold is extremely complex and it may be possible to improve the therapeutic effectiveness of gold compounds through an understanding of the chemistry. The discovery of an effective orally active gold compound auranofin -led to comparative studies with the injectable drug myocrisin. One clear conclusion to be reached was that the distribution and in vivo reactivity of the two compounds was very different, suggesting that the optimum therapeutic-to-toxic ratio could be significantly improved by a better targetted compound. The purpose of the present article is to review work on the distribution and reactivity in vivo of gold following injection with myocrisin. Some current investigations into possible modes of toxic and therapeutic action are described.