Evidence map›Paper›PMID 32999234›Full record

ArticleInternal medicine (Tokyo, Japan)2021

Late-onset Hereditary ATTR Amyloidosis with a Novel p.P63S (P43S) Transthyretin Variant.

Yuya Aono, Yasuhiro Hamatani, Nagaaki Katoh, Mayuko Nakagawa, Katsuya Nakamura, Masahide Yazaki, Fuyuki Kametani, Moritake Iguchi, Ikuko Murakami, Hisashi Ogawa and 3 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Internal medicine (Tokyo, Japan), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 91% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

13 authors at 3 institutions in 1 country.

Yuya AonoDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Yasuhiro HamataniDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Nagaaki KatohDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Japan.
Mayuko NakagawaClinical Laboratory Science Division, Shinshu University Graduate School of Medicine, Japan.
Katsuya NakamuraDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Japan.
Masahide YazakiClinical Laboratory Science Division, Shinshu University Graduate School of Medicine, Japan.
Fuyuki KametaniDepartment of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Japan.
Moritake IguchiDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Ikuko MurakamiClinical Laboratory, National Hospital Organization Kyoto Medical Center, Japan.
Hisashi OgawaDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Mitsuru AbeDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Masaharu AkaoDepartment of Cardiology, National Hospital Organization Kyoto Medical Center, Japan.
Yoshiki SekijimaDepartment of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Japan.
Kyoto Medical Center · JPShinshu University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The patient was an 82-year-old Japanese man with no family history suggestive of amyloidosis. He developed bilateral leg edema and shortness of breath and was referred to our hospital. An electrocardiogram showed atrial fibrillation with right bundle branch block. Echocardiography showed concentric LV hypertrophy. An endomyocardial biopsy showed severe ATTR amyloid deposits. A genetic analysis of the transthyretin (TTR) gene revealed a heterozygous c.187C>T missense variant resulting in p.P63S (P43S). In silico analyses predicted that this variant only modestly altered the structure and function of the TTR protein. The p.P63S variant might be associated with an elderly-onset cardiac-dominant ATTRv phenotype.

Indexed as

Amyloid Neuropathies, FamilialPrealbuminAgedAged, 80 and overEchocardiographyGenetic TestingHumansMalePhenotypePrealbumincardiomyopathyhereditary ATTR amyloidosistransthyretin

Identifiers

PMID32999234
PMCPMC7946494
OpenAlexW3089636004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.