myasthenia gravis/tyrosine

OBJECTIVE Important concepts regarding the pathogenesis, clinical features, diagnosis and treatment of muscle-specific tyrosine kinase (MuSK) antibody positive myasthenia gravis will be reviewed. Special attention will be paid to clinical phenotypes and treatment, particularly encouraging responses

Antibodies to muscle-specific receptor tyrosine kinase (MuSK-Ab) are detected in approximately 40% of generalized acetylcholine receptor (AChR) antibody-negative myasthenia gravis (MG). Based on a growing number of clinical series, a MuSK-Ab-positive phenotype is emerging. While these clinical

Muscle-specific tyrosine-kinase-antibody-positive myasthenia gravis (MuSK-MG) has emerged as a distinct entity since 2001. This disease has been reported worldwide, but with varying rates among patients with generalized acetylcholine-receptor-antibody-negative MG. MuSK-MG was detected in

Autoimmune myasthenia gravis is usually characterized by the presence of autoantibodies against the acetylcholine receptor (~80-90% of patients) or muscle-specific tyrosine kinase (MuSK) (~5% of patients). In the remaining patients, no such antibodies (Abs) are detectable, but this could be due

BACKGROUND Childhood onset myasthenia gravis associated with anti-muscle-specific tyrosine kinase antibodies is very rare and atypical in presentation. METHODS As a baby, the pre- sented patient was choking and sleeping with open eyes. She had weak cry and breathing difficulties. In childhood, there

Anti-muscle specific tyrosine kinase antibody-associated myasthenia gravis (MuSK-MG) is a rare subtype of MG characterized by more frequent relapses and a clinical course that is refractory to standard treatments. Rituximab, a monoclonal antibody targeting CD20+ B cells, has been used effectively in

Myasthenia gravis (MG) and its murine model experimental autoimmune myasthenia gravis (EAMG) are T cell-dependent, antibody-mediated autoimmune diseases. Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) is a cytosolic tyrosine phosphatase that is involved in regulating the T

Myasthenia gravis (MG) with muscle-specific tyrosine kinase (MuSK) antibody (MuSK-MG) is often associated with prominent facial and bulbar muscle atrophy. It remains unclear whether the muscle atrophy is a consequence of long-term corticosteroid treatment, or of the disease process per se. Herein,

Background: The onset of myasthenia (MG) gravis with anti-muscle-specific tyrosine kinase (MuSK) antibodies most commonly peaks in the fourth decade of life, and MG with MuSK antibodies (MuSK-MG) rarely coexists with a malignant tumor. To

A 31-year-old woman presented with a nasal voice, dysarthria, and upper limb weakness during her first pregnancy. Soon after delivery of her first baby, her symptoms disappeared. At the age of 34 years, during her second pregnancy, her nasal voice re-appeared. After delivery of the second baby, her

OBJECTIVE Myasthenia gravis (MG) is an autoimmune disease but certain genetic factors predispose its development. Since susceptibility to different forms of MG is linked to a number of allelic variants, the aim of this study was to explore the human leukocyte antigen (HLA) profile of our patients

The use of cyclophosphamide and rituximab for patients with refractory myasthenia gravis has shown promising results. We report on a 31-year-old Chinese woman with acetylcholine receptor antibody-negative and muscle-specific tyrosine kinase antibody-positive generalised myasthenia gravis who had

Muscle-specific tyrosine kinase (MuSK) antibodies are detected in a proportion of myasthenia gravis (MG) patients who are negative for acetylcholine receptor (AChR) antibodies and have prominent bulbar weakness and crises. In the MuSK ectodomains, the immunoglobulin-like 1 and 2 domains (Ig1/2)

Myasthenia gravis with antibodies to muscle-specific tyrosine kinase (MuSK-MG) is generally considered a severe disease because of the associated weakness distribution with prevalent involvement of bulbar muscles and a rapidly progressive course and early respiratory crises. Its treatment can be