Evidence map›Paper›PMID 34144382›Full record

ArticleSeminars in arthritis and rheumatism2021

The phenotype of myositis patients with anti-Ku autoantibodies.

Maria Casal-Dominguez, Iago Pinal-Fernandez, Assia Derfoul, Rose Graf, Harlan Michelle, Jemima Albayda, Eleni Tiniakou, Brittany Adler, Sonye K Danoff, Thomas E Lloyd and 3 more

Open access · greenAbstract read
In one paragraph

Article in Seminars in arthritis and rheumatism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Guideline
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  13. Systemic sclerosis associated myopathy: how to treat.Current treatment options in rheumatology · 2023
    Article
  14. Review
  15. Article
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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

13 authors at 4 institutions in 2 countries.

Maria Casal-DominguezMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD USA; Johns Hopkins University School of Medicine, Baltimore, Maryland USA. Electronic address: maria.casal-dominguez@nih.gov.
Iago Pinal-FernandezMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD USA; Johns Hopkins University School of Medicine, Baltimore, Maryland USA; Faculty of Health Sciences and Faculty of Computer Science, Multimedia and Telecommunications, Universitat Oberta de Catalunya, Barcelona, Spain.
Assia DerfoulMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD USA.
Rose GrafMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD USA.
Harlan MichelleJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Jemima AlbaydaJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Eleni TiniakouJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Brittany AdlerJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Sonye K DanoffJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Thomas E LloydJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Lisa Christoper-StineJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Julie J PaikJohns Hopkins University School of Medicine, Baltimore, Maryland USA.
Andrew L MammenMuscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD USA; Johns Hopkins University School of Medicine, Baltimore, Maryland USA. Electronic address: andrew.mammen@nih.gov.
Johns Hopkins Medicine · USJohns Hopkins University · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USNational Institutes of Health · US

Funding

Muscle Disease UnitZIAAR041203 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MAMMEN, ANDREW · 2015 to 2025
$19.7M
Sample Processing and Immunoassay Research CoreP30AR070254 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI Antony Rosen · 2016 to 2026
$8.9M
Skeletal Myopathy in Systemic Sclerosis: Devising a Classification Schema Predictive of OutcomesK23AR073927 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI PAIK, JULIE JISUN · 2020 to 2024
$787k
Intramural NIH HHS ZIA AR041203NIAMS NIH HHS K23 AR073927NIAMS NIH HHS P30 AR070254
6 · The paper itself

Abstract

objectivesTo define the clinical features of anti-Ku-positive myositis patients and to determine the reliability of the Euroline assay to detect anti-Ku autoantibodies.

methodsSerum samples were screened for anti-Ku autoantibodies by Euroline and positive samples were confirmed by ELISA. The prevalence and severity of clinical features at onset and during follow-up in patients with anti-Ku-positive myositis were compared to those with dermatomyositis, immune-mediated necrotizing myopathy (IMNM), the antisynthetase syndrome (AS), inclusion body myositis (IBM), anti-U1-RNP-positive myositis, and anti-PM/Scl-positive myositis.

results72 (2.9%) of 2475 samples were anti-Ku positive by Euroline using the manufacturer's recommended cutoff of >15. Just 17 (23.6%) of these were confirmed by ELISA and considered anti-Ku-positive for the analysis. Comparators included 169 IMNM, 168 AS, 387 IBM, 20 anti-U1-RNP-positive, and 47 anti-PM/Scl-positive patients. Muscle weakness was a presenting feature in 38% of anti-Ku-positive patients; 81% developed weakness during follow-up. Anti-Ku-positive patients had increased distal weakness compared to the non-IBM comparators. Interstitial lung disease (ILD) was present in 19% of anti-Ku-positive patients at the first visit and eventually developed in 56% of them. Throughout the course of disease, Gottron's papules and/or heliotrope rashes were less common in anti-Ku-positive patients (19%) compared to those with dermatomyositis (94%) or anti-PM/Scl-positive myositis (89%). Anti-Ku-positive patients never developed calcinosis.

conclusionsThe phenotype of anti-Ku positive myositis is distinguished by distal weakness, frequent ILD, infrequent rash, and no calcinosis. When used according to the current manufacturer's instructions, the Euroline assay has a high false-positive rate for anti-Ku autoantibodies.

Indexed as

DermatomyositisMyositisAutoantibodiesHumansPhenotypeReproducibility of ResultsAutoantibodiesanti-KuElisaEurolineMyositis

Identifiers

PMID34144382
PMCPMC8384675
OpenAlexW3158895154

What OpenQuestion holds

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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.