Document Detail

Disease-modifying drugs for multiple sclerosis in pregnancy: a systematic review.
MedLine Citation:
PMID:  22933738     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To systematically review the literature regarding safety of disease-modifying drug (DMD) use during pregnancy on perinatal and developmental outcomes in offspring of patients with multiple sclerosis (MS).
METHODS: A PubMed and EMBASE search up to February 2012 was conducted with a manual search of references from relevant articles. Selected studies were evaluated using internationally accepted criteria.
RESULTS: Fifteen studies identified 761 interferon β-, 97 glatiramer acetate-, and 35 natalizumab-exposed pregnancies. Study quality ranged from poor to good; no study was rated excellent. Small sample sizes limited most studies. Compared with data for unexposed pregnancies, fair- to good-quality prospective cohort studies reported that interferon β exposure was associated with lower mean birth weight, shorter mean birth length, and preterm birth (<37 weeks), but not low birth weight (<2,500 g), cesarean delivery, congenital anomaly (including malformation), or spontaneous abortion. Fewer studies of fair quality were available for glatiramer acetate and natalizumab. Glatiramer acetate exposure was not associated with lower mean birth weight, congenital anomaly, preterm birth, or spontaneous abortion. Natalizumab exposure did not appear to be associated with shorter mean birth length, lower mean birth weight, or lower mean gestational age. No studies examined mitoxantrone or fingolimod exposure. One study of paternal DMD use during conception found no effect on gestational age or birth weight. Few studies examined longer-term developmental outcomes.
CONCLUSION: Further studies are needed to determine the potential risks associated with preconceptional and in utero DMD exposure in patients with MS. Discontinuation of DMDs before conception is still recommended.
Ellen Lu; Bing Wei Wang; Colleen Guimond; Anne Synnes; Dessa Sadovnick; Helen Tremlett
Related Documents :
25140488 - Effect of maternal coffee, smoking and drinking behavior on adult son's semen quality: ...
23314068 - Polycyclic aromatic hydrocarbons (pahs) as determinants of various anthropometric measu...
24143288 - Exposure to music and noise during pregnancy influences neurogenesis and thickness in m...
9512318 - Serum levels of human placental lactogen, pregnancy-associated plasma protein a and end...
1424328 - Viability of preimplantation embryos.
19393998 - Oocyte retrieval versus conversion to intrauterine insemination in patients with poor r...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2012-08-29
Journal Detail:
Title:  Neurology     Volume:  79     ISSN:  1526-632X     ISO Abbreviation:  Neurology     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-11     Completed Date:  2012-12-04     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  0401060     Medline TA:  Neurology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1130-5     Citation Subset:  AIM; IM    
Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antibodies, Monoclonal, Humanized / adverse effects*,  therapeutic use
Immunologic Factors / adverse effects*,  therapeutic use
Interferon-beta / adverse effects*,  therapeutic use
Multiple Sclerosis / drug therapy*
Peptides / adverse effects*,  therapeutic use
Pregnancy Complications / drug therapy*
Grant Support
//Canadian Institutes of Health Research
Reg. No./Substance:
0/Antibodies, Monoclonal, Humanized; 0/Immunologic Factors; 0/Peptides; 0/copolymer 1; 0/natalizumab; 77238-31-4/Interferon-beta

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Extreme delta brush: a unique EEG pattern in adults with anti-NMDA receptor encephalitis.
Next Document:  Genetic dysfunction of MT-ATP6 causes axonal Charcot-Marie-Tooth disease.