Evidence map›Paper›PMID 40178989›Full record

ArticleRheumatology (Oxford, England)2025

Clinicopathological features of anti-HMGCR and anti-SRP myopathies that do not satisfy the EULAR/ACR criteria of inflammatory myopathies.

Shogo Komaki, Akatsuki Kubota, Asuka Kitamura, Meiko Maeda, Masato Kadoya, Keiichi Hokkoku, Shunsuke Kobayashi, Taro Bannai, Yasushi Shiio, Naohiro Uchio and 18 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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

28 authors.

Shogo KomakiDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Akatsuki KubotaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-5623-3602
Asuka KitamuraDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Meiko MaedaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masato KadoyaDepartment of Neurology, National Hospital Organization Shimoshizu National Hospital, Chiba, Japan.
Keiichi HokkokuDepartment of Neurology, Teikyo University Hospital, Tokyo, Japan.
Shunsuke KobayashiDepartment of Neurology, Teikyo University Hospital, Tokyo, Japan.
Taro BannaiDepartment of Neurology, Tokyo Teishin Hospital, Tokyo, Japan.
Yasushi ShiioDepartment of Neurology, Tokyo Teishin Hospital, Tokyo, Japan.
Naohiro UchioDepartment of Neurology, Mitsui Memorial Hospital, Tokyo, Japan.
Yoshikazu UesakaDepartment of Neurology, Toranomon Hospital, Tokyo, Japan.
Junko KikuchiDepartment of Neurology, Toranomon Hospital Kajigaya, Kanagawa, Japan.
Izumi SugimotoDepartment of Neurology, Toranomon Hospital Kajigaya, Kanagawa, Japan.
Takashi MikataDepartment of Neurology, National Hospital Organization Shimoshizu National Hospital, Chiba, Japan.
Rena OkuderaDivision of Neurology, Internal Medicine, National Defense Medical College, Saitama, Japan.
Kazushi SuzukiDivision of Neurology, Internal Medicine, National Defense Medical College, Saitama, Japan.
Noritoshi AraiDepartment of Neurology, National Center for Global Health and Medicine, Tokyo, Japan.
Yoshio SakiyamaDepartment of Neurology, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Shin-Ichi TokushigeDepartment of Neurology, Kyorin University School of Medicine, Tokyo, Japan.
Yaeko IchikawaDepartment of Neurology, Kyorin University School of Medicine, Tokyo, Japan.
Nobuyuki YajimaDivision of Rheumatology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.ORCID 0000-0002-8292-3962
Ran NakashimaDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0001-6247-0647
Tsuneyo MimoriDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Jun ShimizuDepartment of Physical Therapy, Tokyo University of Technology, Tokyo, Japan.ORCID 0000-0002-9828-6494
Toshihiko KomaiDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Haruka TsuchiyaDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keishi FujioDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tatsushi TodaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Funding

Intramural Research GrantNational Center of Neurology and PsychiatryNeurological and Psychiatric Disorders
6 · The paper itself

Abstract

objectivesThe clinicopathological features of immune-mediated necrotizing myopathy (IMNM) sometimes mimic muscular dystrophy, complicating accurate diagnosis. The European League Against Rheumatism (EULAR)/American College of Rheumatology (ACR) classification criteria of idiopathic inflammatory myopathies (IIMs) are superior in terms of sensitivity and specificity; however, the sensitivity is reported to be relatively low in IMNM. We examined the clinicopathological characteristics and the prognoses of anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibody-positive and anti-signal recognition particle (SRP) antibody-positive cases that do not satisfy the EULAR/ACR classification criteria.

methodsSeventy-one anti-HMGCR antibody-positive cases and 94 anti-SRP antibody-positive cases were included. We compared the clinicopathological characteristics of the groups that were not classified as IIMs (<possible group) with those classified as IIMs (definite-possible group) on the basis of the EULAR/ACR classification criteria. For the <possible group whose follow-up data were available, their clinical features were assessed up to 24 months.

resultsNineteen anti-HMGCR antibody-positive cases (26%) and 19 anti-SRP antibody-positive cases (20%) were classified as the <possible group. The <possible group had milder weakness, less frequent dysphagia, lower serum creatine kinase and aldolase levels and fewer necrotic fibres and granular p62-positive fibres than the definite-possible group. Of the 26 cases in the <possible group that could be followed up, only three cases were classified as the definite-possible group, and the other cases remained in the <possible group during the follow-up period.

conclusionsSome IMNM cases showing a clinicopathologically mild phenotype and a benign course cannot be classified as IIMs by the EULAR/ACR classification criteria, and antibody testing is crucial for accurate diagnosis.

Indexed as

AutoantibodiesHydroxymethylglutaryl CoA ReductasesMyositisSignal Recognition ParticleAdultAgedDiagnosis, DifferentialFemaleHumansMaleMiddle AgedMuscle, SkeletalNecrosisPrognosisAutoantibodiesHMGCR protein, humanHydroxymethylglutaryl CoA ReductasesSignal Recognition ParticleEULAR/ACR classification criteriaimmune-mediated necrotizing myopathyinflammatory myopathy

Identifiers

PMID40178989
PMCPMC12316373

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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.