PMID- 30133097 OWN - NLM STAT- MEDLINE DCOM- 20190513 LR - 20190513 IS - 1468-1331 (Electronic) IS - 1351-5101 (Linking) VI - 25 IP - 12 DP - 2018 Dec TI - Maternal myasthenia gravis represents a risk for the child through autoantibody transfer, immunosuppressive therapy and genetic influence. PG - 1402-1409 LID - 10.1111/ene.13788 [doi] AB - 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 keywords 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 the 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. Methotrexate, mycophenolate mofetil and cyclophosphamide are teratogenic. Mother's MG implies at least a 10-fold increased risk for MG and other autoimmune diseases 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. CI - (c) 2018 EAN. FAU - Gilhus, N E AU - Gilhus NE AUID- ORCID: 0000-0001-6522-5102 AD - Department of Clinical Medicine, University of Bergen, Bergen, Norway. AD - Department of Neurology, Haukeland University Hospital, Bergen, Norway. FAU - Hong, Y AU - Hong Y AD - Department of Clinical Medicine, University of Bergen, Bergen, Norway. LA - eng PT - Journal Article PT - Review DEP - 20180914 PL - England TA - Eur J Neurol JT - European journal of neurology JID - 9506311 RN - 0 (Autoantibodies) RN - 0 (Immunoglobulins, Intravenous) RN - 0 (Immunosuppressive Agents) RN - 0 (Receptors, Cholinergic) RN - EC 2.7.10.1 (MUSK protein, human) RN - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases) RN - KVI301NA53 (Pyridostigmine Bromide) SB - IM MH - Adult MH - *Autoantibodies MH - Family MH - Female MH - Humans MH - Immunoglobulins, Intravenous/*adverse effects MH - Immunosuppressive Agents/*adverse effects/therapeutic use MH - Infant, Newborn MH - Myasthenia Gravis/drug therapy/*immunology MH - Neuromuscular Diseases MH - Pregnancy MH - Prenatal Exposure Delayed Effects/*immunology MH - Pyridostigmine Bromide/adverse effects/therapeutic use MH - Receptor Protein-Tyrosine Kinases/immunology MH - Receptors, Cholinergic/immunology OTO - NOTNLM OT - arthrogryposis OT - autoantibodies OT - breastfeeding OT - genetics OT - immunosuppressive therapy OT - myasthenia gravis OT - neonatal myasthenia OT - pregnancy EDAT- 2018/08/23 06:00 MHDA- 2019/05/14 06:00 CRDT- 2018/08/23 06:00 PHST- 2018/05/15 00:00 [received] PHST- 2018/08/17 00:00 [accepted] PHST- 2018/08/23 06:00 [pubmed] PHST- 2019/05/14 06:00 [medline] PHST- 2018/08/23 06:00 [entrez] AID - 10.1111/ene.13788 [doi] PST - ppublish SO - Eur J Neurol. 2018 Dec;25(12):1402-1409. doi: 10.1111/ene.13788. Epub 2018 Sep 14.