Abstract
The pathogenesis of myasthenia gravis (MG) involves a T cell-directed antibody-mediated autoimmune attack on the nicotinic acetylcholine receptor (AChR) or, occasionally, on other postsynaptic antigens. The antibodies induce their effects through complement-mediated destruction of the post-synaptic endplate membrane with resultant reduction in endplate AChR, and to a lesser degree by increased turnover of endplate AChR or blockade of AChR function. Considerable progress in the treatment of MG has accrued from so-called symptomatic treatments, including improved critical care of seriously ill patients and medications (e.g., cholinesterase inhibitors) increasing the concentration of acetylcholine at the remaining endplate AChRs. Information from other autoimmune diseases and from the response of the normal immune system to invading pathogens supports the view that the course of MG is characterized by exacerbations and remissions. Therefore, the goal in MG treatment is to induce and maintain a remission. This usually involves combinations of short-term and long-term immunosuppressive agents. Selection of the particular combinations of agents in a given patient is guided by the goal of minimizing the cost/benefit ratio of the regimen in an individual patient. In general, the plan involves an initial forceful attack followed by a slow and measured withdrawal.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 457-472 |
| Number of pages | 16 |
| Journal | Annals of the New York Academy of Sciences |
| Volume | 998 |
| DOIs | |
| State | Published - 2003 |
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Keywords
- Acetylcholine receptor
- Acetylcholinesterase
- Autoimmune
- Immunosuppression
- Intravenous immunoglobulln
- Myasthenia gravis
- Neuromuscular junction
- Plasma exchange
- Treatment
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Treatment principles in the management of autoimmune myasthenia gravis. / Richman, David P; Agius, Mark A.
In: Annals of the New York Academy of Sciences, Vol. 998, 2003, p. 457-472.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Treatment principles in the management of autoimmune myasthenia gravis
AU - Richman, David P
AU - Agius, Mark A.
PY - 2003
Y1 - 2003
N2 - The pathogenesis of myasthenia gravis (MG) involves a T cell-directed antibody-mediated autoimmune attack on the nicotinic acetylcholine receptor (AChR) or, occasionally, on other postsynaptic antigens. The antibodies induce their effects through complement-mediated destruction of the post-synaptic endplate membrane with resultant reduction in endplate AChR, and to a lesser degree by increased turnover of endplate AChR or blockade of AChR function. Considerable progress in the treatment of MG has accrued from so-called symptomatic treatments, including improved critical care of seriously ill patients and medications (e.g., cholinesterase inhibitors) increasing the concentration of acetylcholine at the remaining endplate AChRs. Information from other autoimmune diseases and from the response of the normal immune system to invading pathogens supports the view that the course of MG is characterized by exacerbations and remissions. Therefore, the goal in MG treatment is to induce and maintain a remission. This usually involves combinations of short-term and long-term immunosuppressive agents. Selection of the particular combinations of agents in a given patient is guided by the goal of minimizing the cost/benefit ratio of the regimen in an individual patient. In general, the plan involves an initial forceful attack followed by a slow and measured withdrawal.
AB - The pathogenesis of myasthenia gravis (MG) involves a T cell-directed antibody-mediated autoimmune attack on the nicotinic acetylcholine receptor (AChR) or, occasionally, on other postsynaptic antigens. The antibodies induce their effects through complement-mediated destruction of the post-synaptic endplate membrane with resultant reduction in endplate AChR, and to a lesser degree by increased turnover of endplate AChR or blockade of AChR function. Considerable progress in the treatment of MG has accrued from so-called symptomatic treatments, including improved critical care of seriously ill patients and medications (e.g., cholinesterase inhibitors) increasing the concentration of acetylcholine at the remaining endplate AChRs. Information from other autoimmune diseases and from the response of the normal immune system to invading pathogens supports the view that the course of MG is characterized by exacerbations and remissions. Therefore, the goal in MG treatment is to induce and maintain a remission. This usually involves combinations of short-term and long-term immunosuppressive agents. Selection of the particular combinations of agents in a given patient is guided by the goal of minimizing the cost/benefit ratio of the regimen in an individual patient. In general, the plan involves an initial forceful attack followed by a slow and measured withdrawal.
KW - Acetylcholine receptor
KW - Acetylcholinesterase
KW - Autoimmune
KW - Immunosuppression
KW - Intravenous immunoglobulln
KW - Myasthenia gravis
KW - Neuromuscular junction
KW - Plasma exchange
KW - Treatment
UR - http://www.scopus.com/inward/record.url?scp=0141838992&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0141838992&partnerID=8YFLogxK
U2 - 10.1196/annals.1254.060
DO - 10.1196/annals.1254.060
M3 - Article
C2 - 14592915
AN - SCOPUS:0141838992
VL - 998
SP - 457
EP - 472
JO - Annals of the New York Academy of Sciences
JF - Annals of the New York Academy of Sciences
SN - 0077-8923
ER -