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Auteur Stenzel W |
Documents disponibles écrits par cet auteur (41)



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Immune-mediated necrotizing myopathy: clinical features and pathogenesis
Allenbach Y, Benveniste O, Stenzel W, et al.
Nature reviews. Rheumatology, 2020
Revue : Nature reviews. Rheumatology Titre : Immune-mediated necrotizing myopathy: clinical features and pathogenesis Type de document : Article Auteurs : Allenbach Y ; Benveniste O ; Stenzel W ; Boyer O Editeur : United States Année de publication : 22/10/2020 Langues : Anglais (eng) Pubmed / DOI : Pubmed : 33093664 / DOI : 10.1038/s41584-020-00515-9
N° Profil MNM : 2020102 En ligne : http://www.ncbi.nlm.nih.gov/pubmed/33093664 Avis des lecteurs Aucun avis, ajoutez le vôtre !
(mauvais) 15 (excellent)
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Where are we moving in the classification of idiopathic inflammatory myopathies?
Tanboon J, Uruha A, Stenzel W, et al.
Current opinion in neurology, 2020, 33, 5, p 590
Revue : Current opinion in neurology, 33, 5 Titre : Where are we moving in the classification of idiopathic inflammatory myopathies? Type de document : Article Auteurs : Tanboon J ; Uruha A ; Stenzel W ; Nishino I Editeur : England Année de publication : 04/2020 Pages : p 590 Langues : Anglais (eng) Pubmed / DOI : Pubmed : 32852298 / DOI : 10.1097/WCO.0000000000000855
N° Profil MNM : 2020091 En ligne : http://www.ncbi.nlm.nih.gov/pubmed/32852298 Avis des lecteurs Aucun avis, ajoutez le vôtre !
(mauvais) 15 (excellent)
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A spontaneous missense mutation in the chromodomain helicase DNA binding protein 8 (CHD8) gene: a novel association with congenital myasthenic syndrome
Lee CY, Petkova M, Morales-Gonzalez S, et al.
Neuropathology and applied neurobiology, 2020
Revue : Neuropathology and applied neurobiology Titre : A spontaneous missense mutation in the chromodomain helicase DNA binding protein 8 (CHD8) gene: a novel association with congenital myasthenic syndrome Type de document : Article Auteurs : Lee CY, Auteur ; Petkova M ; Morales-Gonzalez S ; Gimber N ; Schmoranzer J ; Meisel A ; BÃ hmerle W ; Stenzel W ; Schuelke M ; Schwarz JM Editeur : England Année de publication : 04/2020 Langues : Anglais (eng) Pubmed / DOI : Pubmed : 32267004 / DOI : 10.1111/nan.12617
N° Profil MNM : 2020041 En ligne : http://www.ncbi.nlm.nih.gov/pubmed/32267004 Avis des lecteurs Aucun avis, ajoutez le vôtre !
(mauvais) 15 (excellent)
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Complement deposition at the neuromuscular junction in seronegative myasthenia gravis
Hoffmann S, Harms L, Schuelke M, et al.
Acta neuropathologica, 2020
Revue : Acta neuropathologica Titre : Complement deposition at the neuromuscular junction in seronegative myasthenia gravis Type de document : Article Auteurs : Hoffmann S, Auteur ; Harms L ; Schuelke M ; Ruckert JC ; Goebel HH ; Stenzel W ; Meisel A Editeur : Germany Année de publication : 03/2020 Langues : Anglais (eng) Résumé : The involvement of the complement system in the pathogenesis of myasthenia gravis (MG) depends on the IgG subtype. The serum anti-acetylcholine receptor antibody (AChR-ab, present in about 80% of all MG patients) essentially belongs to the IgG1 subtype and can, therefore, activate the classical complement pathway. In contrast, serum antibodies against the muscle-specific tyrosine kinase (MuSK-ab, present in about 3% of all MG patients) are mostly from the IgG4 subtype that do not activate the complement system [6, 12]. Other previously identified antibodies are directed against the lipoprotein-related protein 4 (LRP4-ab, present in 2% of all MG patients) [2]. Approximately, 15% of MG patients are termed “seronegative” (SNMG), meaning that no known serum antibodies can be detected. Clinicoserological diagnosis alone carries the risk of under-diagnosis, which may exclude SNMG patients from modern therapies: targeted complement inhibition (eculizumab) has recently been introduced in the treatment of AChR-ab-positive generalized MG patients who do not respond to standard treatment [5]. The aim of this study was to identify a reliable biomarker to justify complement-targeting therapies in SNMG.
To investigate the role of the complement system in SNMG, we performed a cross-sectional study in 11 patients with treatment-refractory SNMG who prospectively underwent external intercostal muscle biopsy. Furthermore, we retrospectively analyzed previously performed biopsies of deltoid muscles from two patients with SNMG. Diagnosis of SNMG was established as follows: (i) typical clinical presentation with fatigable muscle weakness that improves with rest and (ii) absence of detectable autoantibodies against AChR, MuSK (measured by enzyme-linked immunosorbent assay, ELISA) and LRP4 (measured by indirect immunofluorescence test, IIFT) in patients’ sera and (iii) abnormal results in repetitive nerve stimulation and/or single-fiber electromyography and/or (iv) clinical response to intravenous or oral acetylcholinesterase inhibitors. Generalized, treatment-refractory disease course was defined as follows: (i) Myasthenia Gravis Foundation of America (MGFA) classification ≥ II despite (ii) standard therapy consisting of acetylcholinesterase inhibitors, steroids, and long-term immunosuppressants and/or (iii) repeated need for intravenous immunoglobulins and/or plasmapheresis/immunoadsorption. Muscle specimens were analyzed by conventional and immunostaining, immunofluorescence and electron microscopy. The results were compared to ‘disease controls’ (i.e. patients with AChR-ab-positive MG) and ‘non-disease controls’ (i.e. patients with non-specific muscle complaints who had no morphological or serological abnormalities). In all patients, stains were done under standardized conditions using the same batches of antibodies. Endplates could be identified in all patients by staining with non-specific esterase (NSE), acetylcholine esterase (AChE) and CD56 (a neural cell adhesion molecule on the pre- and postsynaptic membrane). All patients gave written informed consent. All procedures were approved by the official institutional ethics review committee (EA2/163/17) at the Charité—University Hospital Berlin...Lien associé : Texte complet disponible sur le site de la revue Pubmed / DOI : Pubmed : 32157386 / DOI : 10.1007/s00401-020-02147-5
N° Profil MNM : 2020031 En ligne : http://www.ncbi.nlm.nih.gov/pubmed/32157386 Avis des lecteurs Aucun avis, ajoutez le vôtre !
(mauvais) 15 (excellent)
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Systematic retrospective study on 64 patients anti-Mi2 dermatomyositis: a classic skin rash with a necrotizing myositis and high risk of malignancy
Monseau G, Landon-Cardinal O, Stenzel W, et al.
Journal of the American Academy of Dermatology, 2020
Voir aussiAvis des lecteurs Aucun avis, ajoutez le vôtre !
(mauvais) 15 (excellent)
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Accumulation of autophagosome cargo protein p62 is common in idiopathic inflammatory myopathies
Milisenda JC, Pinal-Fernández I, Lloyd TE, et al.
Clinical and experimental rheumatology, 2020
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239th ENMC International Workshop: Classification of dermatomyositis, Amsterdam, the Netherlands, 14-16 December 2018
Mammen AL, Allenbach Y, Stenzel W, et al.
Neuromuscular disorders : NMD, 2019
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Sequestosome-1 (p62) expression reveals chaperone-assisted selective autophagy in immune-mediated necrotizing myopathies
Fischer N, Preusse C, Radke J, et al.
Brain pathology (Zurich, Switzerland), 2019
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Idiopathic inflammatory myopathy: Interrater variability in muscle biopsy reading
Olivier PA, de Paepe B, Aronica E, et al.
Neurology, 2019, 93, 9
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Inflammation-induced fibrosis in skeletal muscle of female carriers of Duchenne muscular dystrophy
Preube C, von Moers A, Kolbel H, et al.
Neuromuscular disorders : NMD, 2019, 29, 7, p 487
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Biomarkers in Inflammatory Myopathies-An Expanded Definition.
Benveniste O, Goebel HH, Stenzel W
Frontiers in neurology, 2019, 10, p 554
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1st ENMC European meeting: The EURO-NMD pathology working group Recommended Standards for Muscle Pathology : Amsterdam, The Netherlands, 7 December 2018
Udd B, Stenzel W, Oldfors A, et al.
Neuromuscular disorders : NMD, 2019, 29, 6, p 483
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Proteomic Profiling Unravels a Key Role of Specific Macrophage Subtypes in Sporadic Inclusion Body Myositis.
Roos A, Preusse C, Hathazi D, et al.
Frontiers in immunology, 2019, 10, p 1040
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Immunoglobulin (Ig)G-4 related myositis - A new entity?
Casteleyn V, Casteleyn V, Radbruch H, et al.
Neuromuscular disorders : NMD, 2019, 29, 1, p 70
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Immune checkpoint inhibitor-related myositis and myocarditis in patients with cancer
Touat M, Touat M, Maisonobe T, et al.
Neurology, 2018, 91, 10, e985
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Immune Checkpoint Inhibitor-Associated Myositis.
Anquetil C, Salem JE, Lebrun-Vignes B, et al.
Circulation, 2018, p. 743
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JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis
Ladislau L, Suarez-Calvet X, Toquet S, et al.
Brain : a journal of neurology, 2018, 141, 6, p 1609
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Necrosis in anti-SRP+ and anti-HMGCR+ myopathies: Role of autoantibodies and complement
Allenbach Y, Arouche-Delaperche L, Preusse C, et al.
Neurology, 2018, 90, 6, p 507
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Clinico-sero-pathological classification of immune-mediated necrotizing myopathies : 224th ENMC International Workshop: Zandvoort, The Netherlands, 14-16 October 2016
Allenbach Y, Mammen AL, Stenzel W, et al.
Neuromuscular disorders : NMD, 2018, 28, 1, p 87
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Pathogenic role of anti-signal recognition protein and anti-3-Hydroxy-3-methylglutaryl-CoA reductase antibodies in necrotizing myopathies: Myofiber atrophy and impairment of muscle regeneration in necrotizing autoimmune myopathies
Arouche-Delaperche L, Allenbach Y, Amelin D, et al.
Annals of neurology, 2017, 81, 4, p 538
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A recessive mutation in beta-IV-spectrin (SPTBN4) associates with congenital myopathy, neuropathy, and central deafness
Knierim E, Gill E, Seifert F, et al.
Human genetics, 2017, 136, 7, p 903
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Review: Integrated classification of inflammatory myopathies
Allenbach Y, Benveniste O, Goebel HH, et al.
Neuropathology and applied neurobiology, 2017, 43, 1, p 62
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Inherited and Acquired Muscle Weakness: A Moving Target for Diagnostic Muscle Biopsy
Stenzel W, Schoser B
Neuropediatrics, 2017, 48, 4, p 226
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MORC2 mutation causes severe spinal muscular atrophy-phenotype, cerebellar atrophy, and diaphragmatic paralysis
Schottmann G, Wagner C, Seifert F, et al.
Brain : a journal of neurology, 2016, 139
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Kyphoscoliosis peptidase (KY) mutation causes a novel congenital myopathy with core targetoid defects
Straussberg R, Schottmann G, Sadeh M, et al.
Acta neuropathologica, 2016, 132, 3, p 475
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