Literature DB >> 8976110

[Inherited disorders of uric acid metabolism--classification, enzymatic- and DNA-diagnosis].

H Iwahana1, M Itakura.   

Abstract

Uric acid is the end product of purine metabolism in human. Then, the enzymatic abnormalities, concerning purine metabolism, cause disorders of uric acid metabolism including hyperuricemia and hypouricemia. The superactivity of 5-phosphoribosyl-pyrophosphate (PRPP) synthetase and deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) caused hyperuricemia. In glycogen storage diseases of type I, III, V, and VII, decreased energy supply induces hyperuricemia by accelerating ATP degradation. Deficiencies of xanthine oxidase (XO), purine nucleoside phosphorylase (PNP), and PRPP were reported causing hypouricemia. Many methods for DNA-diagnosis were developed including Southern blot, Northern blot, PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism), PCR-RFLP (restriction fragment length polymorphism), and allele specific oligonucleotide hybridization etc.

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Year:  1996        PMID: 8976110

Source DB:  PubMed          Journal:  Nihon Rinsho        ISSN: 0047-1852


  2 in total

1.  Upfront Enzyme Replacement via Erythrocyte Transfusions for PNP Deficiency.

Authors:  Anna Eichinger; Horst von Bernuth; Michael H Albert; Fabian Hauck; Cinzia Dedieu; Sebastian A Schroeder; Giancarlo la Marca
Journal:  J Clin Immunol       Date:  2021-02-27       Impact factor: 8.317

2.  Contribution of SLC22A12 on hypouricemia and its clinical significance for screening purposes.

Authors:  Do Hyeon Cha; Heon Yung Gee; Raul Cachau; Jong Mun Choi; Daeui Park; Sun Ha Jee; Seungho Ryu; Kyeong Kyu Kim; Hong-Hee Won; Sophie Limou; Woojae Myung; Cheryl A Winkler; Sung Kweon Cho
Journal:  Sci Rep       Date:  2019-10-07       Impact factor: 4.379

  2 in total

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