Myasthenia gravis

Müllges, Wolfgang; Stoll, Guido

doi:10.1007/s00115-019-00798-8

Cited by 11 publications

(8 citation statements)

References 45 publications

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“…Myasthenia gravis (MG) is a neuromuscular disorder with antibodies directed against the skeletal muscle nicotinic acetylcholine receptor (AChR), the muscle specific kinase (MuSK) [ 12 ]. Considerable progress has been made in exploring the onset and therapeutic improvement.…”

Section: Discussionmentioning

confidence: 99%

Integrated proteomics and metabolomics analysis reveals hubs protein and network alterations in myasthenia gravis

Tong

Zhang

et al. 2022

Aging

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Background: Thymoma-associated myasthenia gravis (TAMG) is a well-described subtype of Myasthenia gravis (MG). Nevertheless, the detailed proteins and bioprocess differentiating TAMG from TAMG (−) thymoma have remained unclear. Methods: The proteomics and metabolomics were carried out on serum samples from thymoma group ( n = 60, TNMG), TAMG (+) thymoma group ( n = 70, TAMG (+)), and TAMG (−) thymomas group ( n = 62, TAMG (−)), and controls ( n = 159). groups. Proteomics and metabolomics analyses, including weighted gene co-expression network analysis (WGCNA), was conducted to detect the hub proteins and metabolomics processes that could differentiate TAMG (+) from TAMG (−) thymomas. MetaboAnalyst was used to examine the integration of proteomic and metabolomic analysis to differentiate TAMG (+) from TAMG (−) thymomas. Results: The of module–trait correlation of WGCNA analysis identified KRT1, GSN, COL6A1, KRT10, FOLR2, KRT9, KRT2, TPI1, ARF3, LYZ, ADIPOQ, SEMA4B, IGKV1-27, MASP2, IGF2R was associated with TAMG (+) thymomas. In addition, organismal systems-immune system and metabolism-biosynthesis of other secondary metabolites were closely related to the mechanism of TAMG (+) pathogenesis. Conclusion: Our integrated proteomics and metabolomics analysis supply a systems-level view of proteome changes in TAMG (+), TAMG (−) thymomas and exposes disease-associated protein network alterations involved in.

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Section: Discussionmentioning

confidence: 99%

Integrated proteomics and metabolomics analysis reveals hubs protein and network alterations in myasthenia gravis

Tong

Zhang

et al. 2022

Aging

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“…Myasthenia gravis (MG) is the typical autoimmune manifestation of thymoma. 62 About 35% of thymoma patients have myasthenia gravis. 63 MG is frequently caused by autoantibodies against the components of nicotinic acetylcholine receptor (AChR) on the postsynaptic membrane of the neuromuscular junction and is characterized by fatigue and muscle weakness.…”

Section: Thymoma-related Myasthenia Gravismentioning

confidence: 99%

Therapeutic Plasma Exchange: For Cancer Patients

Yang

Shao

et al. 2022

CMAR

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Therapeutic plasma exchange is used as a trial method for the treatment of cancer patients. Therapeutic plasma exchange uses in vitro technology to remove pathogenic factors in the plasma, returning the replacement and remaining components to the patient to facilitate cure. In the effort to explore new methods of cancer treatment, the introduction of therapeutic plasma exchange brings new hope for cancer treatment; however, the current evidence supporting therapeutic plasma exchange is controversial, and most of the evidence comes from observational studies, lacking large prospective randomized trials. Therefore, this review attempts to focus on the main indications of therapeutic plasma exchange for the treatment of tumors and their complications, including hematological tumors (multiple myeloma cast nephropathy and hyperviscosity syndrome), nervous system tumors (myasthenia gravis associated with thymoma, paraneoplastic neurological syndrome, Lambert-Eaton myasthenia syndrome, and anti-N-methyl-D-aspartate receptor encephalitis), overdose of chemotherapy drugs. In addition, the issues of side-effects and safety in the use of therapeutic plasma exchange are also discussed. However, well-designed prospective trials are needed to better define the role of therapeutic plasma exchange in cancer.

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“…Verantwortliche Antikörper lassen sich bei etwa 90 % der generalisierten MG-Fälle nachweisen [18]. Am häufigsten finden sich Antikörper gegen den AChR, bei etwa 5 % gegen eine postsynaptisch gelegene Muskelserinkinase (MuSK) und noch seltener andere Antikörper gegen Rezeptorbestandteile, was für die Akutbehandlung aber keine Rolle spielt (Übersicht bei [19]). Antikörper blockieren nicht nur die neuromuskuläre Transmission, sondern wirken mit an einer zunehmenden Zerstörung der Synapsen durch Komplementaktivierung [20], was die schwer rehabilitierbaren Muskelatrophien bei länger währender MG erklärt.…”

Section: Myasthene Kriseunclassified

“…In jeder Phase myasthener Schwächeaußer bei tiefer Sedierungist symptomatisch die Gabe von ACh-Esterasehemmern indiziert [19]. Diese hemmen den Abbau von ACh, sodass dies für die neuromuskuläre Aktivierung vermehrt verfügbar wird.…”

Section: Spezielle Therapieunclassified

“…Die Standarddosis beträgt 3 × 50 bis 2 × 100 mg/d, um die langfristig angestrebte Lymphozytenzahl von 600-1000/µl bzw. Leukozytenzahl von 3500-5000/µl ohne und 6000-8000/µl mit Glukokortikoid zu erreichen.Falls Azathioprin nicht vertragen wird oder nicht effektiv isterkennbar an einer refraktären oder wiederholten Krise mit langer Beatmungsdauer und wiederholten PE/ IVIG-Sitzungen -, können andere Immunsuppressiva wie Ciclosporin A, Mycophenolatmofetil, Cyclophosphamid oder auch Rituximab zur B-Zell-Hemmung eingesetzt werden, alle mit individuellen Vor-und Nachteilen (Details bei[19]). In welcher Reihenfolge diese Medikamente indiziert werden sollten, ist nicht durch Studien belegt[29].…”

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