Correlation of muscle ultrasound with clinical and pathological findings in idiopathic inflammatory myopathies.


Journal

Muscle & nerve
ISSN: 1097-4598
Titre abrégé: Muscle Nerve
Pays: United States
ID NLM: 7803146

Informations de publication

Date de publication:
07 2023
Historique:
revised: 04 04 2023
received: 31 10 2022
accepted: 09 04 2023
medline: 15 6 2023
pubmed: 29 4 2023
entrez: 29 4 2023
Statut: ppublish

Résumé

In idiopathic inflammatory myopathies (IIMs), the change in muscle echogenicity and its histopathological basis are not well understood. We quantitatively measured muscle echogenicity in patients with IIMs and evaluated its correlation with disease activity and histopathological findings. This study involved patients with IIMs who underwent both ultrasonography (US) and muscle biopsy, as well as age- and sex-matched rheumatoid arthritis patients as inflammatory disease controls. On US, axial images of the right biceps brachii and vastus medialis were obtained. Standardized histopathological scoring was used to quantitatively measure each pathological domain. Forty-two patients (17 with inclusion body myositis [IBM] and 25 with IIMs other than IBM) and 25 controls were included. The muscle echo intensity (EI) of patients with IIMs was significantly higher than that of controls. Muscle EI showed significant correlations with creatine kinase (r = 0.66, p < .001) and muscle strength (r = -0.73, p < .0001) in patients with non-IBM IIMs. In patients with IBM, moderate correlation was found between muscle EI and quadriceps muscle strength (r = -0.53, p = .028). Histopathologically, the number of infiltrating CD3+ inflammatory cells correlated with muscle EI in the non-IBM group (r = 0.56, p = .017), but not in the IBM group. Muscle EI may be useful as a surrogate marker of muscle inflammation in non-IBM IIM. Increased muscle EI may be difficult to interpret in patients with long-standing IBM, which has advanced and complex histopathology.

Identifiants

pubmed: 37118940
doi: 10.1002/mus.27833
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

39-47

Informations de copyright

© 2023 Wiley Periodicals LLC.

Références

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Auteurs

Takeshi Yoshida (T)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.
Department of Rheumatology, Chikamori Hospital, Kochi, Japan.

Hiroki Yamazaki (H)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.

Yukako Nishimori (Y)

Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan.
Department of Clinical Genome Analysis, Medical Genome Center (MGC), NCNP, Tokyo, Japan.

Naoko Takamatsu (N)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.

Koji Fukushima (K)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.

Yusuke Osaki (Y)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.

Yoshinori Taniguchi (Y)

Department of Endocrinology, Metabolism, Nephrology and Rheumatology, Kochi Medical School Hospital, Nankoku, Japan.

Taiki Nozaki (T)

Department of Radiology, St. Luke's International Hospital, Tokyo, Japan.

Yoshitaka Kumon (Y)

Department of Rheumatology, Chikamori Hospital, Kochi, Japan.

Jemima Albayda (J)

School of Medicine, Division of Rheumatology, Johns Hopkins University, Baltimore, Maryland, USA.

Ichizo Nishino (I)

Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), Tokyo, Japan.
Department of Clinical Genome Analysis, Medical Genome Center (MGC), NCNP, Tokyo, Japan.

Yuishin Izumi (Y)

Department of Neurology, Tokushima University School of Medicine, Tokushima, Japan.

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