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Authors = Betty Soliven

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23 pages, 1210 KiB  
Review
Current Treatment of Myasthenia Gravis
by Mohammed K. Alhaidar, Sumayyah Abumurad, Betty Soliven and Kourosh Rezania
J. Clin. Med. 2022, 11(6), 1597; https://doi.org/10.3390/jcm11061597 - 14 Mar 2022
Cited by 80 | Viewed by 34173
Abstract
Myasthenia gravis (MG) is the most extensively studied antibody-mediated disease in humans. Substantial progress has been made in the treatment of MG in the last century, resulting in a change of its natural course from a disease with poor prognosis with a high [...] Read more.
Myasthenia gravis (MG) is the most extensively studied antibody-mediated disease in humans. Substantial progress has been made in the treatment of MG in the last century, resulting in a change of its natural course from a disease with poor prognosis with a high mortality rate in the early 20th century to a treatable condition with a large proportion of patients attaining very good disease control. This review summarizes the current treatment options for MG, including non-immunosuppressive and immunosuppressive treatments, as well as thymectomy and targeted immunomodulatory drugs. Full article
(This article belongs to the Special Issue Myasthenia Gravis: Clinical Manifestations, Epidemiology, Pathophysiology, Diagnosis, Current and Future Therapies)
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17 pages, 1383 KiB  
Review
Myasthenia Gravis: Epidemiology, Pathophysiology and Clinical Manifestations
by Laura Dresser, Richard Wlodarski, Kourosh Rezania and Betty Soliven
J. Clin. Med. 2021, 10(11), 2235; https://doi.org/10.3390/jcm10112235 - 21 May 2021
Cited by 239 | Viewed by 58147
Abstract
Myasthenia gravis (MG) is an autoimmune neurological disorder characterized by defective transmission at the neuromuscular junction. The incidence of the disease is 4.1 to 30 cases per million person-years, and the prevalence rate ranges from 150 to 200 cases per million. MG is [...] Read more.
Myasthenia gravis (MG) is an autoimmune neurological disorder characterized by defective transmission at the neuromuscular junction. The incidence of the disease is 4.1 to 30 cases per million person-years, and the prevalence rate ranges from 150 to 200 cases per million. MG is considered a classic example of antibody-mediated autoimmune disease. Most patients with MG have autoantibodies against the acetylcholine receptors (AChRs). Less commonly identified autoantibodies include those targeted to muscle-specific kinase (MuSK), low-density lipoprotein receptor-related protein 4 (Lrp4), and agrin. These autoantibodies disrupt cholinergic transmission between nerve terminals and muscle fibers by causing downregulation, destruction, functional blocking of AChRs, or disrupting the clustering of AChRs in the postsynaptic membrane. The core clinical manifestation of MG is fatigable muscle weakness, which may affect ocular, bulbar, respiratory and limb muscles. Clinical manifestations vary according to the type of autoantibody, and whether a thymoma is present. Full article
(This article belongs to the Special Issue Myasthenia Gravis: Clinical Manifestations, Epidemiology, Pathophysiology, Diagnosis, Current and Future Therapies)
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20 pages, 1255 KiB  
Review
Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update
by Shuja Sheikh, Usman Alvi, Betty Soliven and Kourosh Rezania
J. Clin. Med. 2021, 10(7), 1537; https://doi.org/10.3390/jcm10071537 - 6 Apr 2021
Cited by 80 | Viewed by 25822
Abstract
Myasthenia gravis (MG) is an autoimmune neuromuscular disorder which is characterized by presence of antibodies against acetylcholine receptors (AChRs) or other proteins of the postsynaptic membrane resulting in damage to postsynaptic membrane, decreased number of AChRs or blocking of the receptors by autoantibodies. [...] Read more.
Myasthenia gravis (MG) is an autoimmune neuromuscular disorder which is characterized by presence of antibodies against acetylcholine receptors (AChRs) or other proteins of the postsynaptic membrane resulting in damage to postsynaptic membrane, decreased number of AChRs or blocking of the receptors by autoantibodies. A number of drugs such as immune checkpoint inhibitors, penicillamine, tyrosine kinase inhibitors and interferons may induce de novo MG by altering the immune homeostasis mechanisms which prevent emergence of autoimmune diseases such as MG. Other drugs, especially certain antibiotics, antiarrhythmics, anesthetics and neuromuscular blockers, have deleterious effects on neuromuscular transmission, resulting in increased weakness in MG or MG-like symptoms in patients who do not have MG, with the latter usually being under medical circumstances such as kidney failure. This review summarizes the drugs which can cause de novo MG, MG exacerbation or MG-like symptoms in nonmyasthenic patients. Full article
(This article belongs to the Special Issue Myasthenia Gravis: Clinical Manifestations, Epidemiology, Pathophysiology, Diagnosis, Current and Future Therapies)
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