Clinical and scientific aspects of acetylcholine receptor myasthenia gravis

Keijzers, Marlies; Nogales‐Gadea, Gisela; Baets, Marc De

doi:10.1097/wco.0000000000000125

Cited by 10 publications

(14 citation statements)

References 48 publications

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“…In the present study, the patient's teratoma was mature and may have contained myoid cells with antigenicity for AchR, as has been established in the thymus (14). The existence of this tumor could have led to the continuous stimulation of anti-AchR antibody and unsatisfactory therapeutic efficacy with hormones.…”

Section: Discussionmentioning

confidence: 87%

Retroperitoneal teratoma causing ptosis: A case report

Zhao

Zhang

et al. 2015

Oncology Letters

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Abstract. The present study reports the case of a patient who had undergone unsuccessful hormone therapy for ocular myasthenia gravis 14-years prior to the current presentation. The diagnosis of ocular myasthenia gravis was once again confirmed by a neostigmine test and repeat nerve stimulation study. Computed tomography scans in an external institution revealed a retroperitoneal cystic tumor with calcification above the left adrenal gland. The tumor was removed via a transperitoneal laparoscopic resection and was diagnosed as a mature cystic teratoma upon pathological examination. A teratoma is a common form of germ cell tumor, but primary teratomas of the retroperitoneum are quite rare in the adult population. Post-operative observation of the patient showed resolution of the ptosis and improved movement of the eyeballs. The potential mechanism was unclear, but the patient's teratoma was mature and may have contained myoid cells with antigenicity for anti-acetylcholine receptor (anti-AchR), as has been established in the thymus. Therefore, the anti-AchR antibody may have been involved.

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Section: Discussionmentioning

confidence: 87%

Retroperitoneal teratoma causing ptosis: A case report

Zhao

Zhang

et al. 2015

Oncology Letters

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“…MG subgroups with autoantibodies against them have been found to be with relatively distinct clinical features (2)(3)(4). Functional blocking antibodies and tissue-damaging antibodies of different subclass (IgG1, IgG3 or IgG4) against various epitopes of the autoantigens have been reported (2,3). Severity of MG was found to be correlated with antibody levels with conflicting evidence, partially due to the intrinsic mechanism of different antibodies, difference in methods of antibody testing, and the measurement of severity.…”

Section: Introductionmentioning

confidence: 95%

“…These antigens are proteins at the neuromuscular junction (NMJ), which maintain the structure of motor synapse and facilitate neuromuscular conduction of motor impulses. MG subgroups with autoantibodies against them have been found to be with relatively distinct clinical features (2)(3)(4). Functional blocking antibodies and tissue-damaging antibodies of different subclass (IgG1, IgG3 or IgG4) against various epitopes of the autoantigens have been reported (2,3).…”

Section: Introductionmentioning

confidence: 99%

Precision medicine in myasthenia graves: begin from the data precision

Hong

Xie

et al. 2016

Ann. Transl. Med.

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Myasthenia gravis (MG) is a prototypic autoimmune disease with overt clinical and immunological heterogeneity. The data of MG is far from individually precise now, partially due to the rarity and heterogeneity of this disease. In this review, we provide the basic insights of MG data precision, including onset age, presenting symptoms, generalization, thymus status, pathogenic autoantibodies, muscle involvement, severity and response to treatment based on references and our previous studies. Subgroups and quantitative traits of MG are discussed in the sense of data precision. The role of disease registries and scientific bases of precise analysis are also discussed to ensure better collection and analysis of MG data.

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“…In the majority of MG patients, autoantibodies targeting acetylcholine receptor mediate tissue injury, through multiple possible mechanisms, including: (1) block acetylcholine binding to its receptor; (2) induce acetylcholine receptor endocytosis and degradation; (3) activate complement cascade, resulting in the damage of the postsynaptic membrane [15]. A subset of patients with autoimmune encephalitis develop autoantibodies targeting anti- N -methyl- d -aspartate receptor and these autoantibodies can potentially cause neuronal dysfunction and tissue injury [16].…”

Section: Role Of B Cells In Autoimmune Neurological Diseasesmentioning

confidence: 99%

Inebilizumab, a B Cell-Depleting Anti-CD19 Antibody for the Treatment of Autoimmune Neurological Diseases: Insights from Preclinical Studies

Chen

Gallagher²,

Monson

et al. 2016

JCM

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Exaggerated or inappropriate responses by B cells are an important feature in many types of autoimmune neurological diseases. The recent success of B-cell depletion in the treatment of multiple sclerosis (MS) has stimulated the development of novel B-cell-targeting therapies with the potential for improved efficacy. CD19 has emerged as a promising target for the depletion of B cells as well as CD19-positive plasmablasts and plasma cells. Inebilizumab (MEDI-551), an anti-CD19 antibody with enhanced antibody-dependent cell-mediated cytotoxicity against B cells, is currently being evaluated in MS and neuromyelitis optica. This review discusses the role of B cells in autoimmune neurological disorders, summarizes the development of inebilizumab, and analyzes the recent results for inebilizumab treatment in an autoimmune encephalitis mouse model. The novel insights obtained from these preclinical studies can potentially guide future investigation of inebilizumab in patients.

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Clinical and scientific aspects of acetylcholine receptor myasthenia gravis

Cited by 10 publications

References 48 publications

Retroperitoneal teratoma causing ptosis: A case report

Retroperitoneal teratoma causing ptosis: A case report

Precision medicine in myasthenia graves: begin from the data precision

Inebilizumab, a B Cell-Depleting Anti-CD19 Antibody for the Treatment of Autoimmune Neurological Diseases: Insights from Preclinical Studies

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