Abnormal serum uric acid levels in children

Wilcox, W.D.

doi:10.1016/s0022-3476(96)70322-0

Cited by 84 publications

(69 citation statements)

References 98 publications

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“…Uric acid (UA) is the product of purine metabolism, and the serum UA level is determined by its production in the liver, renal excretion or both [7]. Elevated serum UA levels are associated with hypertension, metabolic syndrome, coronary disease, cerebrovascular disease, vascular dementia and kidney disease [8].…”

Section: Introductionmentioning

confidence: 99%

“…Even higher normal levels of UA seem to be associated with cardiovascular disease, although it remains a matter of controversy whether elevation in UA is actually a risk factor for cardiovascular disease. In children, hyperuricemia is known to be associated with malignant diseases, Rye syndrome, genetic disorders with impaired purine metabolism, renal failure and drugs [7]. During childhood and adolescence, an elevated UA level is also associated with obesity, metabolic syndrome and hypertension [8,9].…”

Section: Introductionmentioning

confidence: 99%

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Association of Uric Acid with Obesity and Endothelial Dysfunction in Children and Early Adolescents

Ishiro

Takaya²,

Mori³

et al. 2013

Ann Nutr Metab

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Background: Hyperuricemia in adults is known to be associated with hypertension, the metabolic syndrome and cardiovascular disease. The purpose of this study was to elucidate the factors associated with hyperuricemia in obese children and early adolescents and to investigate the threshold serum level of uric acid (UA) for the metabolic syndrome in children. Methods: We assessed anthropometric measurements, blood pressure, body composition and biochemical data in 1,559 obese children. To assess endothelial dysfunction, flow-mediated dilatation (FMD) was measured in 92 children. The correlations between serum UA levels and various parameters were examined. The threshold serum UA level for the metabolic syndrome was calculated by receiver-operating characteristic (ROC) curve analysis. Results: Serum UA levels were positively correlated with lipids in both boys and girls, and they were inversely correlated with FMD in the boys but not the girls. The threshold serum UA level for the metabolic syndrome was 5.25 mg/dl in boys and 5.05 mg/dl in girls. However, the specificity and sensitivity of ROC curve analysis are not so striking. Conclusion: The correlation between UA and FMD showed gender differences and might be affected by the hormonal status. The cutoff level of serum UA as a marker of the metabolic syndrome in obese children was affected by both age and gender.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association of Uric Acid with Obesity and Endothelial Dysfunction in Children and Early Adolescents

Ishiro

Takaya²,

Mori³

et al. 2013

Ann Nutr Metab

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“…The most common causes of hyperuricemia are diet, alcohol consumption, and physical activity excesses, and obesity is a strongly associated factor. Hyperuricemic therapy consists of recommendations for a diet low in purines, hydration, alkalinization of urine, and the use of drugs that increase excretion or decrease uric acid production 7 . During clinical follow-up of these patients, little emphasis has been given to nonpharmacologic control of hyperuricemia, compared with other risk factors for cardiovascular diseases.…”

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confidence: 99%

Diet and medication in the treatment of hyperuricemia in hypertensive patients

Peixoto¹,

Monego²,

Jardim³

et al. 2001

Arq. Bras. Cardiol.

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“…This entails measurement of purine metabolites in body fluids as well as enzyme assays in lysed and intact cells. [2][3][4][5][6][7][8][9][10][11][12] In addition, clinicians should be aware of the pitfalls involved when assessing uric acid status and the fact that in acute renal failure attributable to uric acid nephropathy in HPRT deficiency, only the plasma, not the urine uric acid, may be grossly elevated. 2,3,11 Second, the family history was particularly relevant in that 2 maternal uncles had a similar history suggesting an X-linked disorder.…”

Section: Discussionmentioning

confidence: 99%

Partial Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency as the Unsuspected Cause of Renal Disease Spanning Three Generations: A Cautionary Tale

Augoustides‐Savvopoulou

Papachristou

Fairbanks

et al. 2002

Pediatrics

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ABSTRACT. Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is an X-linked defect of purine metabolism. Clinical manifestations are usually related to the degree of enzyme deficiency: complete HPRT deficiency (Lesch-Nyhan syndrome) presenting with severe neurologic or renal symptoms, or partial HPRT deficiency (Kelley-Seegmiller syndrome) manifesting as a gout-urolithiasis syndrome. A 3-generation kindred is described in which the recognition of partial HPRT deficiency in 2 adolescent male siblings presenting with uric acid lithiasis led to the diagnosis in 2 maternal uncles already in renal failure of unknown cause. This report highlights the importance of clinical awareness leading to early diagnosis, appropriate diagnostic methodology, and therapy of a treatable inherited disorder of purine metabolism for the prevention of renal failure. Pediatrics 2002;109(1). URL: http://www. pediatrics.org/cgi/content/full/109/1/e17; hypoxanthineguanine phosphoribosyltransferase deficiency, renal failure.ABBREVIATIONS. HPRT, hypoxanthine-guanine phosphoribosyltransferase; LND, Lesch-Nyhan disease.H ypoxanthine-guanine phosphoribosyltransferase (HPRT, EC 2.4.3.8) is an ubiquitous, cytoplasmic, housekeeping enzyme with highest activity in the brain and testes. HPRT catalyzes the transfer of the phosphoribosyl moiety of PP-ribose-P to hypoxanthine and guanine, forming inosine monophosphate and guanosine monophosphate, respectively. Inability to recycle hypoxanthine and guanine produces a lack of feedback control of synthesis accompanied by rapid catabolism of these bases to uric acid (Fig 1). 1-3 HPRT deficiency (McKusick #308000) is an X-linked defect (Xq26-q27.2) of purine metabolism with considerable genetic and clinical heterogeneity, the biochemical hallmark being increased levels of uric acid in blood and urine. [1][2][3][4][5][6] Clinical manifestations are related to the degree of enzyme deficiency, complete HPRT deficiency (Lesch-Nyhan disease; LND) presenting with severe neurologic (compulsive self-injury biting, choreoathetosis), gout, and renal symptoms (kidney stones, renal failure). 1-4 Partial HPRT deficiency (Kelley-Seegmiller syndrome) has a broad spectrum of presentation ranging from gout and urolithiasis only, to intermediate forms characterized according to the severity of neurologic involvement. [1][2][3][4][5][6] Prognosis in terms of renal complications in the partial defect depends on early diagnosis. Prenatal diagnosis is possible in LND by direct enzyme assay in a chorionic villous sample, or by molecular analysis where the mutation is well-defined. [1][2][3][4] From the University A' ‡Pediatric Department, *Biochemistry Laboratory, University Second Internal Medicine Department, Hippocration General Hospital, Thessaloniki, Greece; and §Purine Research Unit, Guy's Hospital, London, United Kingdom. We describe a 3-generation kindred in which the diagnosis of partial HPRT deficiency in 2 adolescent male siblings presenting with urolithiasis led to the diagnosis in a maternal brother and...

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Abnormal serum uric acid levels in children

Cited by 84 publications

References 98 publications

Association of Uric Acid with Obesity and Endothelial Dysfunction in Children and Early Adolescents

Association of Uric Acid with Obesity and Endothelial Dysfunction in Children and Early Adolescents

Diet and medication in the treatment of hyperuricemia in hypertensive patients

Partial Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency as the Unsuspected Cause of Renal Disease Spanning Three Generations: A Cautionary Tale

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