Gout is one of the better understood of the rheumatic diseases, and certainly one of the most satisfactory to treat. It is characterized by chronic hyperuricaemia, recurrent attacks of acute arthritis provoked by the release of monosodium urate crystals into synovial cavities, and development in some patients of gross urate deposits (tophi). It chiefly affects middle-aged and elderly men, and occurs in three overlapping stages: a long phase of asymptomatic hyperuricaemia, a period of recurrent acute gouty attacks separated by asymptomatic intervals (intercritical gout), followed in about 10% of patients by chronic tophaceous gouty arthritis (Becker, 1988). When gout is diagnosed, the patient is usually committed to some form of long-term therapy. It is important, therefore, to establish a firm diagnosis at the outset. This can be secured by the demonstration of intracellular or extracellular urate crystals in joint effusions, or aspirates from tophaceous deposits (Fam, 1986). However, this may not be possible in all patients because of factors such as the absence of a detectable joint effusion or visible tophi, inaccessible joints, small number of crystals, lack of experience with joint aspiration or evaluation of effusions for crystals, and excessive delay in the examination of synovial fluid following aspiration (Wade and Liang, 1988; Kerolus et al, 1989). Under these circumstances, the diagnosis of gout can be made on the basis of a typical clinical history (middle-aged or elderly male, self-limited attacks of acute monoarticular or oligoarticular arthritis in lower extremities, especially the big toes, with severe local pain, tenderness, swelling and redness, followed by a return to normal joint function), in association with documented hyperuricaemia. Hyperuricaemia--elevated serum urate over 450 txmol/1 (7.0mg/dl) in men and 350 ixmol/1 ((6.0 mg/dl) in women--is the biochemical hallmark of gout. However, it is improper to equate the finding of hyperuricaemia with gout; many people who have lifelong hyperuricaemia do not develop gouty arthritis (asymptomatic hyperuricaemia), and serum urate levels may initially be normal in some patients with gout (Becker, 1988; Wade and Liang, 1988). Gouty arthritis nearly always occurs in the setting of chronic hyperuricaemia. The management of a patient with gout, therefore, requires that two objectives be considered independently: immediate control of the acute Bailli~re's Clinical Rheumatology