Abstract
Myasthaenia gravis (MG) is an autoimmune neuromuscular disorder which is twice as common among women, often presenting in the second and third decades of life. Typically, the first trimester of pregnancy and first month postpartum are considered high-risk periods for MG exacerbations. During pregnancy, treatment for MG is usually individualised, thus improving its management. Plasma exchange and immunoglobulin therapies can be safely used to treat severe manifestations of the disease or myasthaenic crises. However, thymectomies are not recommended because of the delayed beneficial effects and possible risks associated with the surgery. Assisted vaginal delivery-either vacuum-assisted or with forceps-may be required during labour, although a Caesarean section under epidural anaesthesia should be reserved only for standard obstetric indications. Myasthaenic women should not be discouraged from attempting to conceive, provided that they seek comprehensive counselling and ensure that the disease is under good control before the start of the pregnancy.
Highlights
Myasthaenia gravis (MG) is an autoimmune neuromuscular disorder which is twice as common among women, often presenting in the second and third decades of life
Myasthaenia gravis is an acquired organ-specific autoimmune disease in which autoantibodies are directed against the post-synaptic nicotinic acetylcholine receptor (AChR) on the neuromuscular endplate of skeletal muscles, leading to fatigable weakness of the diaphragm and the ocular, oropharyngeal and/or limb muscles.[1,2,3]
The majority of myasthaenic patients are seropositive for AChR antibodies, while seronegative patients may have antibodies to other targets at the neuromuscular junction (NMJ), such as muscle-specific kinase (MuSK).[3]
Summary
Abstract: Myasthaenia gravis (MG) is an autoimmune neuromuscular disorder which is twice as common among women, often presenting in the second and third decades of life. Myasthaenia gravis (mg) is an acquired organ-specific autoimmune disease in which autoantibodies are directed against the post-synaptic nicotinic acetylcholine receptor (AChR) on the neuromuscular endplate of skeletal muscles, leading to fatigable weakness of the diaphragm and the ocular, oropharyngeal and/or limb muscles.[1,2,3] In Western countries, the prevalence of MG is 50–125 cases per million individuals and can present at any age.[1] the incidence is twice as common among women (ratio: 3:2) and typically occurs during the second and third decades of life; in contrast, the disease most commonly presents in males during the sixth and seventh decades of life.[2] The majority of myasthaenic patients are seropositive for AChR antibodies, while seronegative patients may have antibodies to other targets at the neuromuscular junction (NMJ), such as muscle-specific kinase (MuSK).[3]
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