Evidence map›Paper›PMID 41215497›Full record

GuidelineJournal of inherited metabolic disease2025

Consensus Guideline for the Diagnosis and Treatment of Tyrosine Hydroxylase (TH) Deficiency.

Mariya Sigatullina Bondarenko, Oya Kuseyri Hübschmann, Jan Kulhánek, Roser Pons, Toni S Pearson, Kathrin Jeltsch, Ivana Badnjarevic, Tessa Wassenberg, Gabriella Horvath, Galina Stevanovic and 10 more

Abstract readPractice Guideline
In one paragraph

Guideline in Journal of inherited metabolic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Mariya Sigatullina BondarenkoNeurometabolic Unit and Synaptic Metabolism Lab, Neurology Department, Institut Pediàtric de Recerca, Hospital Sant Joan de Déu, Barcelona, Spain.
Oya Kuseyri HübschmannHeidelberg University, Medical Faculty Heidelberg, Center for Paediatric and Adolescent Medicine Department I, Division of Pediatric Neurology and Metabolic Medicine, Heidelberg, Germany.
Jan KulhánekDepartment of Pediatrics and Inherited Metabolic Disorders, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Roser PonsFirst Department of Paediatrics, Agia Sofia Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Toni S PearsonDivision of Neurology, Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, Ohio, USA.
Kathrin JeltschHeidelberg University, Medical Faculty Heidelberg, Center for Paediatric and Adolescent Medicine Department I, Division of Pediatric Neurology and Metabolic Medicine, Heidelberg, Germany.
Ivana BadnjarevicLil' Brave One (Hrabrisa)-Patient Organization for Rare Neurotransmitter Diseases, Novi Sad, Serbia.
Tessa WassenbergDepartment of Pediatrics, Pediatric Neurology and Metabolic Unit, Research Group Vitality, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Gabriella HorvathDivision of Biochemical Genetics, Vancouver General Hospital & BC Children's Hospital, Vancouver, British Columbia, Canada.ORCID 0000-0003-2573-2489
Galina StevanovicClinic for Neurology and Psychiatry for Children and Youth, Belgrade, Serbia.
Manju A KurianDevelopmental Neurosciences, Zayed Centre for Research, UCL GOS-ICH; Department of Neurology, Great Ormond Street Hospital, London, UK.
Elisenda Cortès-SaladelafontPediatric Department, Son Llàtzer University Hospital, Palma (Mallorca), Spain.ORCID 0000-0002-8604-2230
Agathe RoubertieNeuropediatric Service, CHU Montpellier, Montpellier, France.
Vincenzo LeuzziDepartment of Human Neuroscience, Child Neurology and Psychiatry, Sapienza University, Rome, Italy.ORCID 0000-0002-2314-6139
Mariarita BertoldiDepartment of Neuroscience, Biomedicine and Movement Sciences, Verona University, Verona, Italy.
Mario MastrangeloChild Neurology and Psychiatry Unit, Department of Neuroscience/Mental Health, Policlinico Umberto I, Rome, Italy.ORCID 0000-0001-7664-5807
Birgit AssmannHeidelberg University, Medical Faculty Heidelberg, Center for Paediatric and Adolescent Medicine Department I, Division of Pediatric Neurology and Metabolic Medicine, Heidelberg, Germany.
THD Guidelines Working Group
Angeles Garcia-CazorlaNeurometabolic Unit and Synaptic Metabolism Lab, Neurology Department, Institut Pediàtric de Recerca, Hospital Sant Joan de Déu, Barcelona, Spain.
Thomas OpladenHeidelberg University, Medical Faculty Heidelberg, Center for Paediatric and Adolescent Medicine Department I, Division of Pediatric Neurology and Metabolic Medicine, Heidelberg, Germany.ORCID 0000-0003-4349-7662

Funding

Chan Zuckerberg Initiative Foundation 2024-347839Fondo Europeo de Desarrollo RegionalInstituto de Salud Carlos III PI21/00073Instituto de Salud Carlos III PI24/00469La Fundació La Marató de TV3 1026(NIFG61209706)Lil' Brave One (Hrabrisa) 109840069Lil' Brave One (Hrabrisa) 28218303SSIEM Guidelines Development Support
6 · The paper itself

Abstract

Tyrosine hydroxylase (TH) catalyses the rate-limiting step in dopamine biosynthesis. Autosomal recessive tyrosine hydroxylase deficiency (THD) leads to clinical phenotypes reflecting the deficiency of dopamine, norepinephrine, or epinephrine in the central nervous system (CNS), presenting along a continuous spectrum from mild to severe forms of the disease. The diagnosis is suggested by the detection of low CSF homovanillic acid (HVA) and confirmed by identifying biallelic pathogenic variants in the TH gene. L-dopa/decarboxylase inhibitor (DCI) supplementation is often the first-line treatment, and most patients have a good therapeutic response. However, initiation of therapy can be challenging in patients with severe disease forms who develop L-dopa/DCI-induced dyskinesia. Therefore, alternative treatment options, such as monoamine oxidase (MAO) inhibitors, must be evaluated to optimize motor symptom control. Clinical experience suggests that early diagnosis and treatment initiation may improve the outcome. Additionally, a multidisciplinary treatment approach should be utilized to monitor neurocognitive development and other comorbidities that may occur in THD. In this consensus guideline, representatives of the International Working Group on Neurotransmitter related Disorders (iNTD) and patient advocates evaluated all the evidence available in the literature on the diagnosis and management of THD and developed recommendations using the SIGN and GRADE methodologies. Based on the limited evidence, practical recommendations have been developed to support clinical diagnosis, laboratory testing, neuroimaging, medical treatment, and non-medical interventions. Research topics for further development were identified. This guideline aims to improve the care of patients with THD worldwide and raise general awareness of this rare disease.

Indexed as

Dystonic DisordersTyrosine 3-MonooxygenaseConsensusHumansLevodopaMonoamine Oxidase InhibitorsSystematic Reviews as TopicLevodopaMonoamine Oxidase InhibitorsTyrosine 3-Monooxygenasedopa‐responsive dystoniainternational working group on neurotransmitter related disordersneurotransmittertyrosine hydroxylase deficiency

Identifiers

PMID41215497
PMCPMC12603479

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.