ArticleJournal of inherited metabolic disease2014
Inborn errors of purine metabolism: clinical update and therapies.
Article in Journal of inherited metabolic disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06092346 (Prospective Study of the Clinical, Genomic, Pharmacological, Laboratory, and Dietary Determinates of Pyrimidine and Purine Metabolism Disorders), which is not on this map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Prospective Study of the Clinical, Genomic, Pharmacological, Laboratory, and Dietary Determinates of Pyrimidine and Purine Metabolism Disorders
Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- Dynamic control of nucleotide metabolism in physiology and disease.Nature cell biology · 2026Review
- Genome-wide association studies of missing metabolite measures from two population-based studies.Genome biology · 2026Article
- Article
- Multiple Reaction Monitoring (MRM)-Based Targeted Kidney Metabolite Profiling of a Mouse Model of Hyperuricemia.Metabolites · 2026Article
- Article
- Pediatric hyperuricemia: genetic basis, metabolic mechanisms, and clinical implications.Frontiers in endocrinology · 2026Review
- Enzyme Assemblies in Nucleotide Metabolism: Structure, Regulation, and Disease Implications.Advances in experimental medicine and biology · 2026Review
- NUDT5 regulates purine metabolism and thiopurine sensitivity by interacting with PPAT.Science (New York, N.Y.) · 2025Article
- Adenylosuccinate synthetase deficiency and purine nucleotide cycle disruption impair neuromuscular function in Caenorhabditis elegans.Molecular genetics and metabolism · 2025Article
- Development of Cell-Permeable Adenylosuccinate Lyase Inhibitor.Methods and protocols · 2025Article
- Purine Metabolism and Dystonia: Perspectives of a Long-Promised Relationship.Annals of neurology · 2025Review
- IMPDH2 filaments protect from neurodegeneration in AMPD2 deficiency.EMBO reports · 2024Article
- Article
- Inborn Errors of Purine Salvage and Catabolism.Metabolites · 2023Review
- Extending inherited metabolic disorder diagnostics with biomarker interaction visualizations.Orphanet journal of rare diseases · 2023Article
- De novo purine nucleotide biosynthesis mediated by MoAde4 is required for conidiation, host colonization and pathogenicity in Magnaporthe oryzae.Applied microbiology and biotechnology · 2022Article
- Article
- Review
- Combined Targeted and Untargeted Profiling of HeLa Cells Deficient in Purine De Novo Synthesis.Metabolites · 2022Article
- Quantitation of Purine in Urine by Ultra-Performance Liquid Chromatography-Tandem Mass Spectrometry.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inborn errors of purine metabolism exhibit broad neurological, immunological, haematological and renal manifestations. Limited awareness of the phenotypic spectrum, the recent descriptions of newer disorders and considerable genetic heterogeneity, have contributed to long diagnostic odysseys for affected individuals. These enzymes are widely but not ubiquitously distributed in human tissues and are crucial for synthesis of essential nucleotides, such as ATP, which form the basis of DNA and RNA, oxidative phosphorylation, signal transduction and a range of molecular synthetic processes. Depletion of nucleotides or accumulation of toxic intermediates contributes to the pathogenesis of these disorders. Maintenance of cellular nucleotides depends on the three aspects of metabolism of purines (and related pyrimidines): de novo synthesis, catabolism and recycling of these metabolites. At present, treatments for the clinically significant defects of the purine pathway are restricted: purine 5'-nucleotidase deficiency with uridine; familial juvenile hyperuricaemic nephropathy (FJHN), adenine phosphoribosyl transferase (APRT) deficiency, hypoxanthine phosphoribosyl transferase (HPRT) deficiency and phosphoribosyl-pyrophosphate synthetase superactivity (PRPS) with allopurinol; adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) deficiencies have been treated by bone marrow transplantation (BMT), and ADA deficiency with enzyme replacement with polyethylene glycol (PEG)-ADA, or erythrocyte-encapsulated ADA; myeloadenylate deaminase (MADA) and adenylosuccinate lyase (ADSL) deficiencies have had trials of oral ribose; PRPS, HPRT and adenosine kinase (ADK) deficiencies with S-adenosylmethionine; and molybdenum cofactor deficiency of complementation group A (MOCODA) with cyclic pyranopterin monophosphate (cPMP). In this review we describe the known inborn errors of purine metabolism, their phenotypic presentations, established diagnostic methodology and recognised treatment options.
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