The history of saturnine gout is almost as old as civilization itself. Studies carried out in recent decades explain the development of hyperuricaemia and gout, with the inhibiting effect of lead on the tubular urate transport causing decreased urate excretion. In the case of lead intoxication these effects are often associated with renal failure but may occur without clinical features of lead toxicity and renal damage. The clinical features of saturnine gout are essentially similar to those of primary gout; however, acute attacks tend to occur in the knee more frequently than the first metatarsophalangeal joint. Acute attacks in saturnine gout are frequently polyarticular and tophi rarely develop. The diagnosis of saturnine gout rests on the history of exposure to lead, clinical features of lead toxicity, biochemical confirmation of high serum lead levels and other biochemical abnormalities, and the exclusion of other forms of gout. Treatment consists of excluding the patient from further exposure to lead, the use of chelating agents to remove lead, and control of acute gouty arthritis and hyperuricaemia.
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