Failure of low molecular weight dextran infusions in scleroderma.

Of the many treatments used in scleroderma (progressive systemic sclerosis), none has so far been shown to alter the fundamental course of the disease (see review Bywaters and Scott, 1965). Although corticosteroids may give symptomatic benefit in the early stages (Rodnan, Black, Bollet, and Bunim, 1956), prolonged therapy is unrewarding (Zion, Goldberg, and Suzman, 1955). Several other promising treatments such as relaxin (Jefferis and Dixon, 1962) and epsilon-aminocaproic acid (Hall and Scott, 1966) have not stood the test of a controlled study. Since their introduction in the late 1940s, dextrans have come to occupy an important place in clinical medicine. Low molecular weight dextran increases peripheral circulation by reducing both blood viscosity and intravascular red cell aggregation (Gelin and Zederfeldt, 1960) and an extensive literature has accumulated on its use in peripheral vascular disorders (Powley, 1964). Digital ischaemia is a prominent feature of scleroderma, yet scanty information is available on the use of low molecular weight dextran in this disease. Holti (1965) convincingly demonstrated that intermittent infusions temporarily improved digital ischaemic phenomena in ten out of twelve patients with scleroderma and noted that "these patients claimed to be remarkably better in themselves with an increased exercise tolerance and softening of their indurated facial skin". Using Holti's technique, Denis (1967) found a similar circulatory improvement in five of seven patients. In addition joint stiffness improved in some patients, dysphagia lessened in one, and facial telangiectasis in another. Kantor (1966) treated five scleroderma patients with single dextran infusions; in one the skin texture "improved about 50 per cent.", and in the remainder "a decided softening of the acral skin" was noted. Scleroderma is not primarily a vascular disease. Although dextran may temporarily improve the digital circulation, the important question of whether the course of progressive systemic sclerosis itself is inttluenced needed to be resolved in a carefully controlled clinical evaluation.