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Juvenile Gouty Arthritis-Reply

Juvenile Gouty Arthritis-Reply This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Diseases of Children American Medical Association

Juvenile Gouty Arthritis-Reply

Abstract

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract 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...
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Publisher
American Medical Association
Copyright
Copyright © 1985 American Medical Association. All Rights Reserved.
ISSN
0002-922X
DOI
10.1001/archpedi.1985.02140080017020
Publisher site
See Article on Publisher Site

Abstract

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract 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

Journal

American Journal of Diseases of ChildrenAmerican Medical Association

Published: Jun 1, 1985

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