PRIMARY AND SECONDARY GOUT

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Abstract
The clinical syndrome of gout appears to comprise several distinct anomalies of purine metabolism. The usual form of the disease reflects an inborn error of purine metabolism and may be regarded as primary gout. Secondary gout may develop occasionally in the course of disease involving the hematopoietic system, and in related disorders. The major pathways of purine metabolism are reviewed. The metabolic pathways for direct biosynthesis of purines appear to be chiefly involved in primary gout; those concerned with the biosynthesis and degradation of "endogenous" nucleic acids seem to be largely responsible for secondary gout; the processes involved in degradation of ingested preformed nucleoproteins may affect the course of both primary and secondary gout. The role of the kidney in gout is descr. There is no convincing evidence for an intrinsic renal defect characteristic of either primary or secondary gout. Nevertheless, retention of urate by the impaired kidney may have a deleterious effect on the course of both forms of gout. The principles of management of acute and chronic manifestations of gout are reviewed. The therapeutic response to the usual measures is essentially the same in both primary and secondary gout.
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