Document Detail

Genetic factors in fetal growth restriction and miscarriage.
MedLine Citation:
PMID:  16052406     Owner:  NLM     Status:  MEDLINE    
Recently, several investigations concerning disadvantageous genetic factors in human reproduction have progressed. Inherited thrombophilia, such as factor V Leiden, prothrombin, and methylenetetrahydrofolate reductase mutations; gene polymorphisms of detoxification enzyme (CYP1A1); growth factors (insulin-like growth factor-I); and hormones such as angiotensinogen and CYP17 are involved in the pathogenesis of fetal growth restriction. The inherited thrombophilia, gene polymorphisms of coagulation and anticoagulation factor such as thrombomodulin, endothelial protein C receptor, plasminogen activator inhibitor 1, and factor XIII; human lymphocyte antigen (HLA-G); detoxification enzymes (glutathione- S-transferase M1); cytokines such as interleukin (IL) -1 and IL-6; hormones (CYP17); vasodilators (nitric oxide synthase 3); and vitamins (transcobalamin) are involved in the pathogenesis of sporadic and recurrent miscarriage. It is likely that a gene polymorphism or mutation susceptible to reproductive failure has a beneficial effect on the process of human reproduction with or without the environmental interaction. The factor V Leiden mutation has genetic advantages that are believed to be an improved implantation rate in in vitro fertilization and a reduction of maternal intrapartum blood loss. It has also been demonstrated that the CYP17 A2 allele has bidirectional effects on human reproduction, including increases in susceptibility to recurrent miscarriage and fetal growth enhancement.
Hideto Yamada; Fumihiro Sata; Yasuaki Saijo; Reiko Kishi; Hisanori Minakami
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Seminars in thrombosis and hemostasis     Volume:  31     ISSN:  0094-6176     ISO Abbreviation:  Semin. Thromb. Hemost.     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-07-29     Completed Date:  2005-10-18     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0431155     Medline TA:  Semin Thromb Hemost     Country:  United States    
Other Details:
Languages:  eng     Pagination:  334-45     Citation Subset:  IM    
Associate Professor, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
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MeSH Terms
Abortion, Spontaneous / etiology,  genetics*
Fetal Growth Retardation / etiology,  genetics*
Genetic Predisposition to Disease
Polymorphism, Genetic

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