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Previous Volume 348:1408 April 3, 2003 Number 14 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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To the Editor: In alkaptonuria, discussed by Phornphutkul et al. (Dec. 26 issue),¹ tissue injury is induced by a product of the oxidation of homogentisic acid (HGA) — namely, benzoquinone acetic acid (BQA). The oxidation of HGA to BQA is catalyzed by polyphenol oxidase.² Accordingly, therapy for alkaptonuria should be aimed at reducing BQA levels through the inhibition of 4-hydroxyphenyl-pyruvate dioxygenase (i.e., with the use of nitisinone). Nitisinone can reduce HGA production while increasing levels of plasma tyrosine and phenylalanine.¹ Thus, measuring the BQA level during a trial with nitisinone would be helpful. As described by Wolff et al.,² the . . . [Full Text of this Article]

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