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Maternal myasthenia gravis represents a risk for the child through autoantibody transfer, immunosuppressive therapy and genetic influence.
Gilhus NE1,2, Hong Y1.
Eur J Neurol. 2018 Aug 22. doi: 10.1111/ene.13788. [Epub ahead of print]
Females with myasthenia gravis (MG) worry about their disease having negative consequences for their children. Autoimmune disease mechanisms, treatment and heredity could all have an impact on the child.
This is a subject review where Web of Science was searched for relevant key words and combinations. Controlled and prospective studies were included, and also results from selected and unselected patient cohorts, guidelines, consensus papers, and reviews.
Neonatal MG with temporary muscle weakness occurs in 10% of newborn babies where mother has MG, due to transplacental transfer of antibodies against acetylcholine receptor (AChR), muscle-specific kinase (MuSK) or lipoprotein receptor-related protein 4 (LRP4). Arthrogryposis and fetal AChR inactivation syndrome with contractures and permanent myopathy are rare events caused by mother's antibodies against fetal type AChR. The MG drugs pyridostigmine, prednisolone and azathioprine are regarded as safe during pregnancy and breastfeeding. Methotreaxate, mycophenolate mofetil and cyclophosphamide are teratogenic. Mother's MG implies at least a ten-fold increased risk for MG and other autoimmune disease in the child.
MG females should receive specific information about pregnancy and giving birth. First-line MG treatments should usually be continued during pregnancy. Intravenous immunoglobulin and plasma exchange represent safe treatments for exacerbations. Neonatal MG risk means that MG women should give birth at hospitals experienced in neonatal intensive care. Neonatal MG needs supportive care, rarely also acetylcholine esterase inhibition or intravenous immunoglobulin. Women with MG should be supported in their wish to have children. This article is protected by copyright. All rights reserved
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