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Previous Volume 334:1602-1604 June 13, 1996 Number 24 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Since first described 32 years ago, Lesch–Nyhan disease has caught the imagination of clinicians and scientists,¹ largely because of the intriguing fact that a precise metabolic error produces a complex set of clinical manifestations. Particularly intriguing are the behavioral and neurologic manifestations of the disease, which are unaccompanied by anatomical abnormalities in the brain, indicating that their pathogenesis must be chemical. Some of the clinical features of the disease, which are also present in gout, are the direct consequences of hyperuricemia and can be readily understood from the nature of the metabolic abnormality. However, the pathogenesis of the abnormalities of . . . [Full Text of this Article]

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