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...

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Hauptverfasser: Batllori, Marta (VerfasserIn) , Opladen, Thomas (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 07 November 2017
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
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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

MARC

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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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