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In Reply.—I have carefully read Dr Howell's letter and think that the issue raised by him was, at least partially, addressed in our article. As mentioned in the introduction, secondary gout in children has been encountered with glycogen storage disease type I, severe uremia, and myeloproliferative disorders. Other disorders, such as methylmelonic acidemia, cirrhosis, psoriasis, and sickle cell anemia have also been associated with hyperuricemia, but there are no reports of definite gout in children having these disorders. Our clinical and laboratory data did not suggest that our patients had any of the aforementioned diseases. It is true that we did not analyze enzymes affecting purine metabolism, specifically phosphoribosylpyrophosphate synthetase or hypoxanthine guanine phosphoribosyl transferase. However, we have looked at 24-hour uric acid excretion and uric acid–creatinine ratios and both were low. As we mentioned in the discussion, this finding strongly suggests that the patients were not overproducers of
YAROM A, LEVINSON JE. Juvenile Gouty Arthritis-Reply. Am J Dis Child. 1985;139(6):547. doi:10.1001/archpedi.1985.02140080017020
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