The systemic forms of scleroderma are disabling entities included in the group of "collagen diseases" but, unlike others in the group, are unresponsive to steroids. The absence of a useful therapeutic agent in the treatment of scleroderma is a serious clinical handicap, especially since the incidence of scleroderma is probably greater than that of systemic lupus erythematosus, dermatomyositis, or periarteritis nodosa. In a recent report, a new chelating agent, edathamil disodium (Disodium Versenate), was shown to have markedly beneficial effects in a case of advanced scleroderma with extensive calcinosis.1 The intravenous administration of this drug in protracted courses led to definite clinical improvement, with dissolution of large quantities of pathologic calcification. In the past year, other reports attesting to the ameliorative effect of edathamil in scleroderma have appeared.2-4 In this project our purpose has been to explore the effects of this new agent