Evidence map›Paper›PMID 24849934›Full record

ArticleJournal of human genetics2014

Severe exacerbation of Andersen-Tawil syndrome secondary to thyrotoxicosis.

Jordi Díaz-Manera, Luis Querol, Aída Alejaldre, Ricard Rojas-García, Alba Ramos-Fransi, Eduard Gallardo, Isabel Illa

Erratum issuedOpen access · bronzeAbstract readCase Reports
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 94% of its field
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, 3 citations in OpenAlex.

  1. Andersen-Tawil Syndrome With Novel Mutation inFrontiers in pediatrics · 2021
    Article
  2. Article
  3. Observational
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jordi Díaz-Manera1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Luis Querol1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Aída Alejaldre1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Ricard Rojas-García1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Alba Ramos-Fransi1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Eduard Gallardo1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Isabel Illa1] Neurology Department, Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Barcelona, Spain [2] Centro de Investigación Básica en Red en Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Universitat Autònoma de Barcelona · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism characterized by episodes of weakness. Although TPP has been described in patients all over the world, it is especially frequent in Asiatic patients. Recently, two genomewide association studies have found a susceptibility locus on chromosome 17q24.3 near the KCNJ2 gene, which is responsible for another cause of periodic paralysis, the Andersen-Tawil syndrome (ATS). We report the first patient diagnosed with ATS with a de novo c.G899C mutation in the KCNJ2 gene in 2010 who developed an autoimmune hyperthyroidism and TPP in 2013. At the time of the ATS diagnosis other causes of periodic paralysis, including thyroid dysfunction, were ruled out. The condition of the patient, who had mild episodes of proximal weakness at follow-up, deteriorated dramatically in 2013, presenting continuous episodes of severe generalized weakness associated with low levels of potassium requiring frequent admissions to the hospital. After a few months, he also presented signs of hyperthyroidism, and a diagnosis of Grave's disease was made. In our opinion, this case clearly demonstrates that a dysfunction of the Kir2.1 potassium channel encoded by the KCNJ2 gene is a risk factor to develop TPP, and can be a useful tool to identify patients at risk in daily clinics.

Indexed as

AdultAndersen SyndromeAutoimmune DiseasesChromosomes, Human, Pair 17Graves DiseaseHumansMaleMutationPotassium Channels, Inwardly RectifyingRisk FactorsThyrotoxicosisKCNJ2 protein, humanPotassium Channels, Inwardly Rectifying

Identifiers

PMID24849934
OpenAlexW1981197364

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.