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The study of gouty arthritis has provided a common meeting ground
for the research interests of both the basic scientist and the
clinician. The interest of the chemist in gout began 1776 with the
isolation of uric acid from a concretion of the urinary tract by
the Swedish chemist SCHEELE. The same substance was subsequently
extracted from a gouty tophus by the British chemist WOLLASTONE in
1797 and a half century later the cause of the deposits of sodium
urate in such tophi was traced to a hyperuricemia in the serum of
gouty patients by the British physician Alfred Baring GARROD who
had also received training in the chemical laboratory and was
therefore a fore-runner of many of today's clinician-investigators.
The recent surge of progress in understanding of some of the causes
of gout in terms of specific enzyme defects marks the entrance of
the biochemist into this field of investigation. The identification
of the first primary defect of purine metabolism associated with
over-production of uric acid, a severe or partial deficiency of the
enzyme hypoxanthine-guanine phospho ribosyltransferase was achieved
less than a decade ago. The knowledge of the mechanism of purine
over-production that it generated led shortly to the identification
of families carrying a dominantly (possibly X-linked) inherited
increase in the activity of the enzyme phosphoribosylpyrophosphate
synthetase as a cause of purine over-production. Yet this is only a
start as these two types of enzyme defects account for less than
five per cent of gouty patients."
The study of gouty arthritis has provided a common meeting ground
for the research interests of both the basic scientist and the
clinician. The interest of the chemist in gout began 1776 with the
isolation of uric acid from a concretion of the urinary tract by
the Swedish chemist SCHEELE. The same substance was subsequently
extracted from a gouty tophus by the British chemist WOLLASTONE in
1797 and a half century later the cause of the deposits of sodium
urate In such tophi was traced to a hyperuricemia in the serum of
gouty patients by the British physician Alfred Baring GARROD who
had also received training in the chemical laboratory and was
therefore a fore-runner of many of today's clinician-investigators.
The recent surge of progress in understanding of some of the causes
of gout in terms of specific enzyme defects marks the entrance of
the biochemist into this field of investigation. The identification
of the first primary defect of purine metabolism associated with
over-production of uric acid, a severe or partial deficiency of the
enzyme hypoxanthine-guanine phospho ribosyl transferase was
achieved less than a decade ago. The knowledge of the mechanism of
purine over-production that it generated led shortly to the
identification of families carrying a dominantly (possibly
X-linked) inherited increase in the activity of the enzyme
phosphoribosylpyrophosphate synthetase as a cause of purine
over-production. Yet this is only a start as these two types of
enzyme defects account for less than five per cent of gouty
patients."
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