Relevant bibliographies by topics / Immune necrotizing myopathies

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Academic literature on the topic 'Immune necrotizing myopathies'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Immune necrotizing myopathies"

1

Mohammed, Abdel Gaffar A., Ayanda Gcelu, Farzana Moosajee, Stella Botha, and Asgar Ali Kalla. "Immune Mediated Necrotizing Myopathy: Where do we Stand?" Current Rheumatology Reviews 15, no. 1 (2018): 23–26. http://dx.doi.org/10.2174/1573397114666180406101850.

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Immune-mediated necrotizing myopathies (IMNMs) are a group of acquired autoimmune muscle disorders which are characterized by proximal muscle weakness, high levels of creatinine kinase, and myopathic findings on electromyogram (EMG). Muscle biopsy in IMNM differentiates it from the other subgroups of Idiopathic Inflammatory Myositis (IIM) by the presence of myofibre necrosis and prominent regeneration without substantial lymphocytic inflammatory infiltrates. Anti-signal recognition particle (SRP) and anti-3hydroxy-3 methylglutarylcoenzyme A reductase (HMGCR) autoantibodies were found in two-thirds of IMNM patients. In terms of treatment, IMNM is more resistant to conventional immunosuppressive treatment, therefore, other modalities of treatment such as Intravenous Immunoglobulin (IVIG) and rituximab are often required.
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2

Allenbach, Yves, and Olivier Benveniste. "Peculiar clinicopathological features of immune-mediated necrotizing myopathies." Current Opinion in Rheumatology 30, no. 6 (2018): 655–63. http://dx.doi.org/10.1097/bor.0000000000000547.

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3

Akbar, Shalla, Sandhya Dasaraju, and Osama Elkadi. "A Case of Immune-Mediated Necrotizing Myopathy With Associated Skeletal Muscle Involvement by Sarcoid Granulomata: A Rare Association." American Journal of Clinical Pathology 152, Supplement_1 (2019): S69. http://dx.doi.org/10.1093/ajcp/aqz113.078.

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Abstract Skeletal muscle involvement by noncaseating granulomata occurs in a variety of conditions, including sarcoidosis, infections, and rarely in association with primary inflammatory myopathies such as inclusion body myositis (IBM) and dermatomyositis (DM). Sarcoid myopathy is typically asymptomatic; however, a picture of acute myositis with proximal muscle weakness has been described. Immune-mediated necrotizing myopathy (IMNM) is a subgroup of inflammatory myopathies typically presenting with proximal muscle weakness and markedly elevated muscle enzymes, mostly occurring in the setting of statin treatment. IMNM is associated with positive autoantibodies, but a subset of cases is antibody negative. Here we describe a case of myopathy occurring in association with sarcoidosis with combined features of granulomatous and necrotizing myopathy. The patient was a 54-year-old African American male with medical history significant for statin use 3 years ago, which was discontinued due to myalgia and elevated muscle enzymes and biopsy-proven sarcoidosis diagnosed on a pulmonary lymph node biopsy. He presented with progressive worsening of bilateral proximal weakness involving the upper and lower extremities. Electromyogram showed features of active myopathy with no evidence of peripheral neuropathy. Myositis panel was negative for the following antibodies: anti-Jo1, Mi-2, anti-Ku, PL-7, PL-12, OJ, EJ, and SRP. However, there was elevation of aldolase, CRP, and CK-MB. Biopsy of thigh and deltoid muscle showed necrotic muscle fibers, myophagocytosis with associated minimal inflammation, and multiple well-formed nonnecrotizing granulomas with multinucleated giant cells. Myopathic features include increased internalized nuclei, round atrophic fibers, and scattered split fibers. Specific features of IBM or DM were not present. Conclusion Myopathies developing or worsening after discontinuation of statin are rare. The association of necrotizing myopathy with sarcoidosis is not well described in the literature. Additional studies are warranted to elucidate this association.
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4

Pinal-Fernandez, Iago, and Andrew L. Mammen. "Spectrum of immune-mediated necrotizing myopathies and their treatments." Current Opinion in Rheumatology 28, no. 6 (2016): 619–24. http://dx.doi.org/10.1097/bor.0000000000000335.

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5

Lee, Jong-Mok. "Immune-Mediated Necrotizing Myopathy: A Review for Clinicians." Journal of Electrodiagnosis and Neuromuscular Diseases 24, no. 3 (2022): 57–61. http://dx.doi.org/10.18214/jend.2022.00087.

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Immune-mediated necrotizing myopathy (IMNM) is a group of inflammatory myopathies showing necrotic and regenerating fibers without noteworthy inflammatory cell infiltration on pathology. The pathologic findings are different from those of dermatomyositis or sporadic inclusion body myositis. Furthermore, the discovery of myositis-specific antibodies in patients with IMNM, such as anti-signal recognition particle or anti-3-hydroxy-3-methylglutaryl-CoA reductase antibodies, has enabled us to expand our knowledge of IMNM. However, the phenotype and pathological findings of IMNM are unremarkable; therefore, it is difficult to diagnose, and IMNM has been relatively unrecognized. In this review, we introduce the clinical features, diagnosis, pathomechanism, and treatment of IMNM for clinicians.
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6

Knauss, Samuel, Corinna Preusse, Yves Allenbach, et al. "PD1 pathway in immune-mediated myopathies." Neurology - Neuroimmunology Neuroinflammation 6, no. 3 (2019): e558. http://dx.doi.org/10.1212/nxi.0000000000000558.

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ObjectiveTo investigate the relevance of dysfunctional T cells in immune-mediated myopathies. We analyzed T-cell exhaustion and senescence, in the context of programmed cell death protein 1 (PD1)-related immunity in skeletal muscle biopsies from patients with immune-mediated necrotizing myopathy (IMNM), sporadic inclusion body myositis (sIBM), and myositis induced by immune checkpoint inhibitors (irMyositis).MethodsSkeletal muscle biopsies from 12 patients with IMNM, 7 patients with sIBM, and 8 patients with irMyositis were analyzed by immunostaining and immunofluorescence as well as by quantitative PCR. Eight biopsies from nondisease participants served as controls.ResultsCD3+CD8+ T cells in biopsies from IMNM, sIBM, and irMyositis were largely PD1-positive, while CD68+ macrophages were sparsely positive to the ligand of programmed cell death protein 1 (PD-L1). The sarcolemma of myofibers was PD-L2+ and was colocalized with major histocompatibility complex (MHC) class I. CD68+ macrophages were colocalized with PD-L2. Senescent T cells were strongly enriched in skeletal muscle of sIBM, revealing a distinct immunologic signature. Biopsies from patients with irMyositis showed mild signs of senescence and exhaustion.ConclusionPersistent exposure to antigens in IMNMs and sIBM may lead to T-cell exhaustion, a process controlled by the PD1 receptor and its cognate ligands PD-L1/PD-L2. To our knowledge, these data are the first evidence of presence of dysfunctional T cells and relevance of the PD1 pathway in IMNM, sIBM, and irMyositis. These findings may guide the way to a novel understanding of the immune pathogenesis of immune-mediated myopathies.
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7

Swafford, Collin, and E. Steve Roach. "Juvenile Dermatomyositis and the Inflammatory Myopathies." Seminars in Neurology 40, no. 03 (2020): 342–48. http://dx.doi.org/10.1055/s-0040-1705120.

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AbstractThe inflammatory myopathies comprise disorders of immune-mediated muscle injury. The histopathology and clinical features help distinguish them. Juvenile dermatomyositis (JDM) is the most common form of myositis in children and adolescents. Children with JDM present with proximal muscle weakness and characteristic rashes. The presentation is similar in children and adults, but JDM is a primary disorder and the adult form often is concerning for a paraneoplastic syndrome. Proximal muscle weakness occurs with dermatomyositis, polymyositis, and immune-mediated necrotizing myopathy, but the latter two conditions have no dermatologic findings or distinct tissue changes which set them apart from dermatomyositis. Inclusion body myositis, also included in the inflammatory myopathies, presents with more distal involvement, and microscopically exhibits identifiable rimmed vacuoles. We review key features of these disorders, focusing in more detail on JDM because it is more often encountered by the child neurologist.
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8

Mecoli, Christopher A., Arash H. Lahouti, Robert A. Brodsky, Andrew L. Mammen, and Lisa Christopher-Stine. "High-dose cyclophosphamide without stem cell rescue in immune-mediated necrotizing myopathies." Neurology - Neuroimmunology Neuroinflammation 4, no. 5 (2017): e381. http://dx.doi.org/10.1212/nxi.0000000000000381.

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Objective:To describe the experience managing treatment-refractory immune-mediated necrotizing myopathies (IMNM) with high-dose cyclophosphamide (HiCy) therapy.Methods:Five patients with severe refractory IMNM who were treated with HiCy without stem cell rescue were identified. Their medical records were reviewed to assess demographic, clinical, and histologic characteristics as well as response to therapy.Results:Three patients with anti–signal recognition particle (SRP) and 2 patients with anti-HMG-CoA reductase autoantibodies were included. The mean follow-up time after HiCy therapy was 37 ± 28 months. Two patients demonstrated substantial response, evidenced by improved muscle strength and decreased muscle enzymes after HiCy therapy; both of these patients were anti-SRP positive. Four patients experienced febrile neutropenia after HiCy therapy, one of which required a prolonged intensive care unit stay for infectious complications, from which they eventually recovered.Conclusions:These data suggest that HiCy therapy without stem cell rescue may be considered as an alternative for the treatment of refractory IMNM.
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9

Chiapparoli, Ilaria, Claudio Galluzzo, Carlo Salvarani, and Nicolò Pipitone. "A glance into the future of myositis therapy." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2211002. http://dx.doi.org/10.1177/1759720x221100299.

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The idiopathic inflammatory myopathies are chronic diseases of the skeletal muscle that comprise various conditions, including dermatomyositis, polymyositis, immune-mediated necrotizing myopathy, and the antisynthetase syndrome. Although there are a number of distinguishing features, all these disorders are characterized by an immune and inflammatory response mainly directed against the muscle. Hence, therapy is geared toward curbing the autoimmune and inflammatory response. A quite wide range of medications are currently available to treat these disorders, but despite all therapeutic progress still a number of patients are unable to maintain a sustained remission. In this review article, we have marshaled a variety of potential therapeutic agents that may hold promise for the future treatment of the idiopathic inflammatory myopathies. It is to be expected that by increasing the therapeutic armamentarium with agents that have different mechanisms of action even challenging cases could be successfully managed, thus reducing disease burden and disability.
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10

Park, Sunha, Dae-Hyun Jang, Jae-Min Kim, and Nara Yoon. "Prominent Asymmetric Muscle Weakness and Atrophy in Seronegative Immune-Mediated Necrotizing Myopathy." Diagnostics 11, no. 11 (2021): 2064. http://dx.doi.org/10.3390/diagnostics11112064.

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Immune-mediated necrotizing myopathy, a new subgroup of inflammatory myopathies, usually begins with subacute onset of symmetrical proximal muscle weakness. A 35-year-old male presented with severe asymmetric iliopsoas atrophy and low back pain with a previous history of left lower extremity weakness. Although his first left lower extremity weakness occurred 12 years ago, he did not receive a clear diagnosis. Magnetic resonance imaging of both thigh muscles showed muscle edema and contrast enhancement in patch patterns, and the left buttock and thigh muscles were more atrophied compared to the right side. Serum creatine kinase levels were elevated, and serologic testings were all negative. Genetic testing using a targeted gene-sequencing panel for neuromuscular disease including myopathy identified no pathogenic variants. Muscle biopsy on the right vastus lateralis showed scattered myofiber necrosis with phagocytosis and an absence of prominent inflammatory cells, consistent with seronegative necrotizing myopathy. Thus, unusual asymmetric muscle weakness and atrophy can be a manifestation of inflammatory myopathy.
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