Evidence map›Paper›PMID 33381924›Full record

ArticleESC heart failure2021

Plasma growth differentiation factor 15: a novel tool to detect early changes of hereditary transthyretin amyloidosis.

Masamitsu Okada, Yohei Misumi, Teruaki Masuda, Seiji Takashio, Masayoshi Tasaki, Hiroaki Matsushita, Akihiko Ueda, Yasuteru Inoue, Toshiya Nomura, Makoto Nakajima and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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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

16 authors at 2 institutions in 1 country.

Masamitsu OkadaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Yohei MisumiDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Teruaki MasudaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Seiji TakashioDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Masayoshi TasakiDepartment of Morphological and Physiological Sciences, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hiroaki MatsushitaDepartment of Amyloidosis Research, Nagasaki International University, Nagasaki, Japan.
Akihiko UedaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Yasuteru InoueDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Toshiya NomuraDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Makoto NakajimaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Taro YamashitaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Satoru ShinrikiDepartment of Molecular Laboratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hirotaka MatsuiDepartment of Molecular Laboratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kenichi TsujitaDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Yukio AndoDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.
Mitsuharu UedaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-0811, Japan.ORCID 0000-0002-6814-0582
Kumamoto University · JPNagasaki International University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHereditary transthyretin (ATTRv) amyloidosis is the most frequent and representative form of autosomal dominant hereditary systemic amyloidosis. Disease-modifying treatments of the disease are more effective during the early stages, and we require biomarkers to detect early pathological changes for prompt diagnosis. This study aimed to investigate whether plasma growth differentiation factor 15 (GDF-15) levels could aid detection of early pathological changes in ATTRv amyloidosis. METHODS AND

resultsWe retrospectively studied 32 patients with ATTRv amyloidosis, eight asymptomatic TTR mutation carriers, and eight healthy volunteers. We evaluated plasma GDF-15 levels in these subjects as related to levels of brain natriuretic peptide and high-sensitivity troponin T, echocardiographic features,

conclusionsGrowth differentiation factor 15 may reflect early pathological changes of ATTRv amyloidosis.

Indexed as

Growth Differentiation Factor 15Amyloid Neuropathies, FamilialContrast MediaGadoliniumHumansRetrospective StudiesContrast MediaGadoliniumGrowth Differentiation Factor 15AmyloidosisAsymptomatic mutation carrierGrowth differentiation factor 15Hereditary transthyretin amyloidosis

Identifiers

PMID33381924
PMCPMC8006664
OpenAlexW3117010954

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.