Urinary sulphatoxymelatonin as a biomarker of serotonin status in biogenic amine-deficient patients
Melatonin is synthesized from serotonin and it is excreted as sulphatoxymelatonin in urine. We aim to evaluate urinary sulphatoxymelatonin as a biomarker of brain serotonin status in a cohort of patients with mutations in genes related to serotonin biosynthesis. We analized urinary sulphatoxymelaton...
Gespeichert in:
| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
07 November 2017
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| In: |
Scientific reports
Year: 2017, Jahrgang: 7 |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-017-15063-8 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1038/s41598-017-15063-8 Verlag, kostenfrei, Volltext: https://www.nature.com/articles/s41598-017-15063-8 |
| Verfasserangaben: | Marta Batllori, Marta Molero-Luis, Luisa Arrabal, Javier de las Heras, Joaquín-Alejandro Fernandez-Ramos, Luis González Gutiérrez-Solana, Salvador Ibáñez-Micó, Rosario Domingo, Jaume Campistol, Aida Ormazabal, Frederic Sedel, Thomas Opladen, Basiliki Zouvelou, Roser Pons, Angels Garcia-Cazorla, Eduardo Lopez-Laso, & Rafael Artuch |
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| 520 | |a Melatonin is synthesized from serotonin and it is excreted as sulphatoxymelatonin in urine. We aim to evaluate urinary sulphatoxymelatonin as a biomarker of brain serotonin status in a cohort of patients with mutations in genes related to serotonin biosynthesis. We analized urinary sulphatoxymelatonin from 65 healthy subjects and from 28 patients with genetic defects. A total of 18 patients were studied: 14 with autosomal dominant and recessive guanosine triphosphate cyclohydrolase-I deficiency; 3 with sepiapterin reductase deficiency; and 1 with aromatic L-amino acid decarboxylase deficiency. Further 11 patients were studied after receiving serotoninergic treatment (serotonin precursors, monoamine oxidase inhibitors, selective serotonin re-uptake inhibitors): 5 with aromatic L-amino acid decarboxylase deficiency; 1 with sepiapterin reductase deficiency; 3 with dihydropteridine reductase deficiency; and 2 with 6-pyruvoyltetrahydropterin synthase deficiency. Among the patients without therapy, 6 presented low urinary sulphatoxymelatonin values, while most of the patients with guanosine triphosphate cyclohydrolase-I deficiency showed normal values. 5 of 11 patients under treatment presented low urine sulphatoxymelatonin values. Thus, decreased excretion of sulphatoxymelatonin is frequently observed in cases with severe genetic disorders affecting serotonin biosynthesis. In conclusion, sulphatoxymelatonin can be a good biomarker to estimate serotonin status in the brain, especially for treatment monitoring purposes. | ||
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