Moonshine and lead Relationship to the Pathogenesis of Hyperuricemia in Gout

Thirty‐three patients with gouty arthritis were evaluated for clinical features of gout as well as for causes of hyperuricemia. None of the gout patients overexcreted urate and all exhibited a decrease in urate clearance. Fifty‐five percent of these patients had a history of significant illicit alcohol ingestion, while only 27% had evidence of excessive lead stores. There was no correlation between extent of depression in urate or creatinine clearance and amount of lead excreted following EDTA infusion. There was also no evidence of an increased prevalence of anemia, hypertension, or peripheral neuropathy in the gout patients with excessive versus those with normal lead stores. Nineteen patients with a comparable history of moonshine ingestion but no evidence of gouty arthritis were also studied. Eight patient volunteers with no history of moonshine ingestion or arthritis served as controls. None of the controls had evidence of excessive lead stores, while 42% of the non‐arthritis moonshine drinkers excreted over 500 m̈g of lead after EDTA administration. There was no evidence of decreased urate or creatinine clearance or increased prevalence of anemia, hypertension, or peripheral neuropathy in those patients with excessive lead stores. We conclude that factors other than lead nephropathy, such as obesity, ethanol consumption, hypertension, and hereditary factors, are responsible for the decreased urate clearance observed in over 70% of our gout patients, many of whom give a history of moonshine ingestion. The results in non‐gout patients indicate that increased lead excretion following EDTA administration cannot be equated with lead nephropathy or clinical lead toxicity. Thus it is uncertain whether gout patients with evidence of excessive lead stores necessarily have lead nephropathy as the reason for their reduction in urate clearance and consequent hyperuricemia.