Acute gout and the accident and emergency department.

The classical description of Gout (za lrobayplKa-f7robaypa 'the foot-pain'-Aristotle, 350 BC; Hippocrates, 430 BC) suggests that the earliest references were to the characteristic crystal synovitis of the first metatarsophalangeal joint. Antoni van Leuwenhoek published a beautiful drawing of urate crystals from a tophus in 1679. Since that time the term 'gout' has been applied to an increasingly vague and ill-defined collection of inflammatory diseases reaching a peak of confusion in the eighteenth century. By that time it had become almost entirely non-specific. There are innumerable articles on 'gout' and urate metabolism and a few about 'pseudo-gout' among them, but there are three or four which stand out as light-houses to the bewildered explorer: Professor George Nuki's review article of purine metabolism and crystal disease of connective tissue is interesting on its own account and has 135 references to the literature (Nuki, 1971). Alexander Gutman's review of the whole field of gout is masterly and equates 'gout' with a state of hyperuricaemia, however caused (Gutman, 1973). This assumption is almost universal. Edward W. Holmes's contribution however concedes that not all cases of acute gout present with a raised serum uric acid but goes on to say that 'hyperuricaemia is manifested at sometime in 98% of individuals with gout' (1977). Finally, a review article in the British Medical Journal describes contemporary work on the role of leucocytes in the pathogenesis of the acute attack of crystal synovitis (1973). 'Gout' is in essence a disorder of purine metabolism leading to deposits of urate crystal in the synovium, or peri-articular connective tissues. 'Pseudo-gout' or pyrophosphate arthropathy describes the acute synovitis due to deposition of calcium pyrophosphate in a joint. This article limits itself