Clinical characterization of tremor in patients with phenylketonuria.


Journal

Molecular genetics and metabolism
ISSN: 1096-7206
Titre abrégé: Mol Genet Metab
Pays: United States
ID NLM: 9805456

Informations de publication

Date de publication:
Historique:
received: 13 03 2019
revised: 30 05 2019
accepted: 31 05 2019
pubmed: 19 6 2019
medline: 1 5 2020
entrez: 19 6 2019
Statut: ppublish

Résumé

Phenylketonuria (PKU) is due to the deficit of the enzyme phenylalanine hydroxylase, the first step of dopamine synthesis. If not early treated the disease results in severe neurological impairment. Minor neurological signs have been reported in early treated PKU (ETPKU) subjects. Prolactin level is affected by (and reflects) brain dopamine availability. Object of the study was to assess the occurrence, age at onset, distribution, associated neurological signs, and possible pathogenetic biomarkers of tremor in ETPKU. Fifty-nine ETPKU and 43 control subjects (age range 7-54) underwent individual and familiar tremor history, clinical assessment of tremor by means of the Fahn-Tolosa-Marin Tremor Rating Scale, and IQ evaluation. Historical and concomitant biochemical data (blood levels of Phe) and serum prolactin were included in the analysis. Thirty-two percent of ETPKU patients were affected by postural and kinetic tremor. We found a significant correlation between severity of tremor and: prolactin level at the day of examination (part A: r The main clinical features of tremor in ETPKU evoke those of essential tremor, although with a higher prevalence and an earlier onset than in general population. The severity of tremor was related to concomitant prolactin rather than Phe levels. This pattern suggests that metabolic alterations associated with PKU may result in an anticipation of the tremor onset in subjects who are possibly prone to this disorder.

Sections du résumé

BACKGROUND
Phenylketonuria (PKU) is due to the deficit of the enzyme phenylalanine hydroxylase, the first step of dopamine synthesis. If not early treated the disease results in severe neurological impairment. Minor neurological signs have been reported in early treated PKU (ETPKU) subjects. Prolactin level is affected by (and reflects) brain dopamine availability. Object of the study was to assess the occurrence, age at onset, distribution, associated neurological signs, and possible pathogenetic biomarkers of tremor in ETPKU.
METHODS
Fifty-nine ETPKU and 43 control subjects (age range 7-54) underwent individual and familiar tremor history, clinical assessment of tremor by means of the Fahn-Tolosa-Marin Tremor Rating Scale, and IQ evaluation. Historical and concomitant biochemical data (blood levels of Phe) and serum prolactin were included in the analysis.
RESULTS
Thirty-two percent of ETPKU patients were affected by postural and kinetic tremor. We found a significant correlation between severity of tremor and: prolactin level at the day of examination (part A: r
CONCLUSIONS
The main clinical features of tremor in ETPKU evoke those of essential tremor, although with a higher prevalence and an earlier onset than in general population. The severity of tremor was related to concomitant prolactin rather than Phe levels. This pattern suggests that metabolic alterations associated with PKU may result in an anticipation of the tremor onset in subjects who are possibly prone to this disorder.

Identifiants

pubmed: 31208951
pii: S1096-7192(19)30214-8
doi: 10.1016/j.ymgme.2019.05.017
pii:
doi:

Substances chimiques

Biomarkers 0
Prolactin 9002-62-4
Phenylalanine Hydroxylase EC 1.14.16.1

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

53-56

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Francesca Nardecchia (F)

Department of Human Neuroscience, Sapienza University of Rome, Italy.

Filippo Manti (F)

Department of Human Neuroscience, Sapienza University of Rome, Italy.

Sabrina De Leo (S)

Department of Internal Medicine and Clinical Nutrition, Sapienza University of Rome, Italy.

Claudia Carducci (C)

Department of Experimental Medicine, Sapienza University of Rome, Italy.

Vincenzo Leuzzi (V)

Department of Human Neuroscience, Sapienza University of Rome, Italy. Electronic address: Vincenzo.leuzzi@uniroma1.it.

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Classifications MeSH