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Effects of food, fast and alcohol on serum uric acid and acute attacks of gout

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      Abstract

      The interrelationship of the effects of brief periods of fasting and of alcohol on uric acid metabolism has been investigated in nine gouty patients and in two normouricemic subjects. There were appreciable elevations in serum urate concentration after one and two day fasts, which were accompanied by increases in both serum beta-hydroxybutyrate and blood acetoacetate. The rise in serum urate could be accounted for in most cases by a diminution in the urinary output of uric acid, which was presumably the result of inhibition, by the elevated ketone levels, of urate excretion by the tubules.
      The administration of from 68 to 100 gm. of ethyl alcohol together with a low purine diet produced only minor changes in serum urate levels and urinary excretion of uric acid. Larger doses of alcohol (112 to 135 gm.) given with food led to significant increases in blood lactate concentration, diminution in urinary uric acid output and hyperuricemia.
      When the same (smaller) amounts of alcohol which had been found to be without effect on serum urate levels were taken during brief periods of fasting, there was an elevation in serum urate levels which was slightly greater than that observed after fasting alone. This was accompanied by greater increases in blood lactate than observed after the administration of alcohol with food, and greater increases in serum beta-hydroxybutyrate than observed after an equivalent period of fasting alone. It appears that the combination of fasting and ethyl alcohol may be additive or mutually potentiating with respect to the effects of each of these factors on uric acid metabolism.
      Eight of the nine patients experienced one or more acute attacks of gout during the course of these studies. In the majority of cases the onset of the attack appeared to be related to rapid fluctuations in serum urate levels induced by fasting or by fasting together with alcohol ingestion. Serum urate levels tended to remain stable during and immediately after these attacks, giving little or no indication of the changes which had preceded the onset of acute gouty-arthritis.
      Although treatment with probenecid in two cases produced the expected uricosuria, it did not prevent the increase in serum urate induced by fasting and alcohol.
      The patient with gout should be cautioned to avoid prolonged fasting and other situations which produce rapid changes in serum urate concentration. However, our gouty patients do not go out to fast, but to drink. Unfortunately the alcoholic bout often continues in the absence of food, thus resulting in a combination of metabolic changes which often lead to an acute attack.
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