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Myasthenia gravis (MG) may be a rare condition, but it’s been recognized for a long time—in fact, it was first described in 1672! But it’s only within the last 100 years that scientists and doctors began to understand that MG is an autoimmune condition and have developed approaches for helping manage the disease. Some, like acetylcholinesterase inhibitors and thymectomy, were among the first treatments available. Others, such as complement inhibitors and FcRn inhibitors, reflect more recent scientific discoveries.
MG is associated with recurrent and fluctuating muscle weakness that can appear in the form of MG symptoms. Whether you’re newly diagnosed or have been on an MG therapy for years, ongoing symptom management is an important goal to consider.
Management strategies are consistently evolving. Remember, everyone is different; what works for one person may not be right for someone else. It's important to discuss with your doctor what management option(s) may be right for you. Some strategies include:
Target acetylcholinesterase, an enzyme that breaks down acetylcholine, an important chemical that transmits signals between the nerves and muscles.
HOW THEY WORK
Inhibit the breakdown of acetylcholine at the neuromuscular junction, increasing the amount of acetylcholine to help with nerve-muscle function.
HOW THEY ARE GIVEN
Intravenous infusion
Intramuscular injection
Oral
Target the complement system, a part of the immune system, that, in MG, mistakenly damages muscle cells.
HOW THEY WORK
They block C5, a key complement protein that can cause muscle damage and weakness that may lead to MG symptoms. The exact way complement inhibitors work as a treatment for MG is unknown.
By blocking C5, complement inhibitors also affect bacteria helpful for preventing meningitis. Due to an increased risk of meningitis, patients taking complement inhibitors must complete meningococcal vaccines before starting treatment.
HOW THEY ARE GIVEN
Intravenous infusion
Subcutaneous injection
They can have a variety of targets, including T cells, DNA/RNA replication, calcineurin, and folic acid, depending on the medication.
HOW THEY WORK
Limit the immune system’s ability to make harmful antibodies by interfering with cell production, replication, and multiplication.
HOW THEY ARE GIVEN
Intravenous infusion
Subcutaneous injection
Oral
Target the neonatal Fc receptor (FcRn), a protein that helps keep immunoglobulin G (IgG) antibodies, including autoantibodies that mistakenly cause MG, circulating in the bloodstream.
HOW THEY WORK
They block FcRn, preventing it from recycling IgG antibodies and decreasing their numbers in the bloodstream. This can lead to the removal of both harmful and normal antibodies from the body.
HOW THEY ARE GIVEN
Intravenous infusion
Subcutaneous injection
Target harmful antibodies in severe cases of MG.
HOW THEY WORK
PLEX involves using an intravenous (IV) machine to remove harmful antibodies from the blood. IVIg does something different: it adds healthy antibodies from many different donors to counter the harmful antibodies caused by MG. Both PLEX and IVIg are considered short-term treatment options, and they are usually effective for a few weeks or months.
HOW THEY ARE GIVEN
Plasmapheresis machine
Intravenous injection
Surgery to remove the thymus gland, which may be associated with MG.
HOW THEY WORK
10% to 15% of people with MG are found to have a thymoma (tumor of the thymus gland). And 30% of people with a thymoma will develop MG. People who have a thymectomy have been shown to have improved muscle weakness and to lower their dependence on medications. In about 50% of cases, thymectomy may lead to long-lasting, complete remission.
HOW THEY ARE GIVEN
Thymus surgery
*These treatments are commonly used in clinical practice to treat symptoms of MG but are not FDA-approved specifically for this indication.
There’s a dedicated Patient Education Manager (PEM) in your area ready to meet with you to help you navigate life with MG.