Evidence map›Paper›PMID 40369875›Full record

ArticleHGG advances2025

The phenotypic spectrum of individuals with SLC16A2 variants in MCT8 deficiency.

Kirsty McWalter, Houda Zghal Elloumi, Richard Sidlow, Ben Willis, Andrew J Bauer

Abstract read
In one paragraph

Article in HGG advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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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

2 citing papers in PubMed.

  1. Thyrotoxicosis in MCT8 deficiency.The Journal of clinical endocrinology and metabolism · 2026
    Review
  2. Review
4 · The record

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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

5 authors.

Kirsty McWalterGeneDx LLC, Gaithersburg, MD, USA. Electronic address: kmcwalter@genedx.com.
Houda Zghal ElloumiGeneDx LLC, Gaithersburg, MD, USA.
Richard SidlowValley Children's Hospital, Madera, CA, USA.
Ben WillisEgetis Therapeutics, Stockholm, Sweden.
Andrew J BauerChildren's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocarboxylate transporter 8 (MCT8) deficiency is a rare, X-linked condition caused by pathogenic variants in the SLC16A2 gene, resulting in dysfunctional thyroid hormone transport throughout the body. Human Phenotype Ontology (HPO) terms provide a standardized clinical vocabulary of symptomology in human disease. Here, we contribute a cohort of individuals with fully categorized SLC16A2 variants and associated HPO terms to the phenotypic spectrum of MCT8 deficiency. We queried de-identified genetic data for SLC16A2 variants mostly determined through exome sequencing. Clinical abstraction of medical records was performed to generate HPO terms. In a cohort of 122 individuals with SLC16A2 variants, we identified 68 cases with likely pathogenic/pathogenic (L/PATH) variants and 54 individuals with variants of uncertain significance (VUSs). A total of 611 different HPO terms were retrieved for 108 individuals with characterized SLC16A2 variants. Common HPO terms included global developmental delay (79/108, 73.1%), generalized hypotonia (40/108, 37.0%), and delayed speech and language development (29/108, 26.9%). Some HPO terms associated with a severe MCT8 deficiency phenotype, such as failure to thrive, feeding difficulties, and delayed myelination, were more common in individuals with L/PATH variants than in those with VUSs. HPO terms related to thyroid function and/or hormone levels were not commonly reported, with hypothyroidism the most frequently reported term, seen in six individuals. This study highlights the utility of comprehensive genetic testing and standardized clinical vocabulary in diagnosing rare genetic conditions. In MCT8 deficiency, this approach can help characterize genotype-phenotype correlations, expedite concurrent thyroid hormone testing, and improve affected individual and caregiver support.

Indexed as

Monocarboxylic Acid TransportersMuscular AtrophyMutationX-Linked Intellectual DisabilityAdolescentAdultChildChild, PreschoolFemaleHumansInfantMaleMuscle HypotoniaPhenotypeSymportersMonocarboxylic Acid TransportersSLC16A2 protein, humanSymportersAHDSAllan–Herndon–Dudley syndromeclinical geneticsexome sequencinggenotype-phenotypeHPOHuman Phenotype OntologyMCT8 deficiencyrare diseasethyroid hormone

Identifiers

PMID40369875
PMCPMC12182792

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LicenceCC BY-NC-ND
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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.