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Myasthenia gravis — autoantibody characteristics and their implications for therapy
- Source :
- Nature Reviews Neurology. 12:259-268
- Publication Year :
- 2016
- Publisher :
- Springer Science and Business Media LLC, 2016.
-
Abstract
- Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies that target the neuromuscular junction, leading to muscle weakness and fatigability. Currently available treatments for the disease include symptomatic pharmacological treatment, immunomodulatory drugs, plasma exchange, thymectomy and supportive therapies. Different autoantibody patterns and clinical manifestations characterize different subgroups of the disease: early-onset MG, late-onset MG, thymoma MG, muscle-specific kinase MG, low-density lipoprotein receptor-related protein 4 MG, seronegative MG, and ocular MG. These subtypes differ in terms of clinical characteristics, disease pathogenesis, prognosis and response to therapies. Patients would, therefore, benefit from treatment that is tailored to their disease subgroup, as well as other possible disease biomarkers, such as antibodies against cytoplasmic muscle proteins. Here, we discuss the different MG subtypes, the sensitivity and specificity of the various antibodies involved in MG for distinguishing between these subtypes, and the value of antibody assays in guiding optimal therapy. An understanding of these elements should be useful in determining how to adapt existing therapies to the requirements of each patient.
- Subjects :
- 0301 basic medicine
Thymoma
Neuromuscular disease
medicine.medical_treatment
Neuromuscular Junction
Disease
03 medical and health sciences
Cellular and Molecular Neuroscience
0302 clinical medicine
Myasthenia Gravis
Humans
Medicine
Autoantibodies
biology
business.industry
Autoantibody
Muscle weakness
medicine.disease
Myasthenia gravis
Thymectomy
030104 developmental biology
Immunology
biology.protein
Neurology (clinical)
medicine.symptom
Antibody
business
Biomarkers
030217 neurology & neurosurgery
Subjects
Details
- ISSN :
- 17594766 and 17594758
- Volume :
- 12
- Database :
- OpenAIRE
- Journal :
- Nature Reviews Neurology
- Accession number :
- edsair.doi.dedup.....5bc12d72aed8421422456157049d6178