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Autoimmune Myasthenia Gravis (autoimmune + myasthenia_gravis)

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Medical Sciences	100%

Selected Abstracts

Autoimmune myasthenia gravis: place of thymectomy and preferred technique

INTERNAL MEDICINE JOURNAL, Issue 8 2002
E. Byrne
No abstract is available for this article. [source]

Mycophenolate mofetil substitution for cyclosporine-dependent myasthenia gravis and nephrotoxicity

INTERNAL MEDICINE JOURNAL, Issue 1 2007
A. K. H. Lim
Abstract Severe autoimmune myasthenia gravis is difficult to manage and may require immunosuppression with cyclosporine. However, cyclosporine dependency is associated with the risk of nephrotoxicity. Mycophenolate mofetil is a non-nephrotoxic alternative which should be considered to rescue cyclosporine-dependent, severe myasthenia gravis sufferers with renal impairment from progression to end-stage renal failure. However, the evidence is limited and studies have not assessed the outcome of a direct substitution in these cyclosporine-dependent patients. We study three such patients who successfully converted to mycophenolate mofetil, and briefly examine the evidence behind this option. We believe that total cyclosporine withdrawal is feasible, but strongly recommend overlapping mycophenolate mofetil treatment with cyclosporine. [source]

Lack of association between acetylcholine receptor , polymorphisms and early-onset myasthenia gravis

MUSCLE AND NERVE, Issue 3 2004
Domenico Marco Bonifati MD
Abstract A patient with mutations in the acetylcholine receptor (AChR) , subunit, who subsequently developed autoimmune myasthenia gravis (MG), led us to search for , AChR mutations and polymorphisms in 167 patients with early-onset MG. No ,-subunit mutations or increased incidence of exonic ,-subunit polymorphisms were found. The allelic frequency of the intron polymorphism IVS11+ 20del20 was more prevalent in non,United Kingdom subjects, both patients and healthy individuals, than in United Kingdom subjects (15.8 vs. 6.2%, P = 0.0008) but not between MG patients and healthy individuals. These data provide no evidence that heteroallelic mutations or polymorphisms in the AChR , subunit are involved in the development of autoimmune early-onset MG but raise issues for future studies. Muscle Nerve 29: 436,439, 2004 [source]

Specific immunotherapy of experimental myasthenia gravis by a novel mechanism

ANNALS OF NEUROLOGY, Issue 4 2010
Jie Luo PhD
Objective Myasthenia gravis (MG) and its animal model, experimental autoimmune myasthenia gravis (EAMG), are antibody (Ab)-mediated autoimmune diseases, in which autoantibodies bind to and cause loss of muscle nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction. To develop a specific immunotherapy of MG, we treated rats with ongoing EAMG by intraperitoneal injection of bacterially-expressed human muscle AChR constructs. Methods Rats with ongoing EAMG received intraperitoneal treatment with the constructs weekly for 5 weeks beginning after the acute phase. Autoantibody concentration, subclassification, and specificity were analyzed to address the underlying therapeutic mechanism. Results EAMG was specifically suppressed by diverting autoantibody production away from pathologically relevant specificities directed at epitopes on the extracellular surface of muscle AChRs toward pathologically irrelevant epitopes on the cytoplasmic domain. A mixture of subunit cytoplasmic domains was more effective than a mixture containing both extracellular and cytoplasmic domains or than only the extracellular domain of ,1 subunits. Interpretation Therapy using only cytoplasmic domains, which lack pathologically relevant epitopes, avoids the potential liability of boosting the pathological response. Use of a mixture of bacterially-expressed human muscle AChR cytoplasmic domains for antigen-specific immunosuppression of myasthenia gravis has the potential to be specific, robust, and safe. ANN NEUROL 2010;67:441,451 [source]

Monozygous twins with neuromuscular transmission defects at opposite sides of the motor endplate

ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009
A. R. Punga
Disorders affecting the postsynaptic side of the neuromuscular junction include autoimmune myasthenia gravis (MG) as well as some of the congenital myasthenic syndromes (CMS). Lambert-Eaton myasthenic syndrome (LEMS) is an acquired autoimmune neuromuscular disorder in which autoantibodies are directed against the presynaptic calcium channels. Here we describe two monozygous twin brothers: case 1 was diagnosed with an indeterminate form of acquired postsynaptic neuromuscular junction defect at age 32 and case 2 with LEMS at age 47. Case 1 presented clinically with mild generalized myasthenic weakness, neurophysiological examination revealed disturbed neuromuscular transmission along with probable myositis and serum analysis regarding antibodies against the acetylcholine receptor and muscle-specific tyrosine kinase was negative. Case 2 presented with proximal muscle fatigue accompanied by areflexia at rest and antibodies against the P/Q-type voltage-gated calcium channels were present. Neurophysiologically, case 2 had reduced baseline compound motor action potential amplitudes on neurography, decrement on low-frequency repetitive nerve stimulation (RNS) and pathological increment on high frequency RNS. To our knowledge this is the first case report of its kind and adds an intriguing contrast to the more common diagnosis of CMS in monozygous twins. [source]

Interferon- , -modified dendritic cells suppress B cell function and ameliorate the development of experimental autoimmune myasthenia gravis

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2004
S. B. ADIKARI
SUMMARY This study was designed to investigate the therapeutic effects of interferon (IFN)- , -modulated dendritic cells (DC) in experimental autoimmune myasthenia gravis (EAMG). We induced EAMG in Lewis rats by immunization with Torpedo nicotinic acetylcholine receptor (nAChR) and adjuvant. On day 33 post-immunization (p.i.), splenic DC were prepared, exposed to IFN- , alone (IFN- , -DC) or to IFN- , in combination with 1-methyl-DL-tryptophan (1-MT), the specific inhibitor of indoleamine 2,3-dioxygenase (IDO) (IFN- , + 1-MT-DC), and injected subcutaneously into rats with incipient EAMG on day 5 p.i. A control group of EAMG rats received naive DC on day 5 p.i., while another group received 1-MT every other day, intraperitoneally (p.i.), from days 5 to 41 p.i. The severity of clinical signs of EAMG was reduced dramatically in IFN- , -DC-treated rats compared to rats receiving naive DC, IFN- , + 1-MT-DC or 1-MT alone. The number of plasma cells secreting nAChR antibodies was reduced and the expression of B cell activation factor (BAFF) on splenic and lymph node mononuclear cells (MNC) was down-regulated in rats treated with IFN- , -DC. In vitro co-culture of MNC derived from EAMG rats with IFN- , -DC produced relatively few cells secreting nAChR antibodies. Addition of 1-MT to the co-culture significantly increased the number of cells secreting nAChR antibodies. We conclude that IFN- , -DC reduced the number of plasma cells secreting nAChR antibodies in an IDO-dependent manner and ameliorated the development of EAMG in Lewis rats. [source]