1997 Fiscal Year Final Research Report Summary
Pathogenesis and Prevention of intrauterine growth retardation and fetal distress by antiphospholipid antibody
| Project/Area Number |
07671824
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Teikyo University |
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Principal Investigator |
YAMAMOTO Tatsuo Dept.Obstet.& Gynecol, Associate Professor Teikyo University School of Medicine, 医学部, 助教授 (40167721)
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| Co-Investigator(Kenkyū-buntansha) |
SASAMORI Yukifumi Teikyo University School of Medicine, Research fellow, 医学部, 助手 (50276721)
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| Project Period (FY) |
1995 – 1997
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| Keywords | antiphospholipid antibody / intrauterine growth retardation / fetal distress / pregnancy / endothelin / cytokine |
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| Research Abstract |
1.We demonstrated the presence of anticardiolipin antibody (ACA) in preeclampsia and the binding ability for placental villi by ACA.In ACA positive cases, high incidence of intrauterine growth retardation (IUGR) was found. 2.Using the ELISA using beta_2-GPI,high incidence of placental insufficiency and IUGR were detected in positive ACA cases. 3.To investigate the pathogenetic mechanism by beta2-GPI dependent ACA,the effects on beta2-GPI dependent ACA for endothelial cell were evaluated. ACA tended to decrease the PGF1_<alpha> production. However, ACA increased the production of Endothelin 1 (ET-1) which is strong vasoactive substance from endothelial cell. After isolation of IgG from ACA positives sera, we demonstrated that the effect of sera was originated from IgG.Moreover, the effects on cytokine production by beta2-GPI dependent ACA was evaluated. The IL8 production tended to increase without the changes of IL1 alpha and IL6.4.When the effect on the productions of PGF1 alpha and ET-1 by beta2-GPI itself was evaluated, beta_2-GPI suppressed those productions. When the effects on the cytokine productions by beta_2-GPI itself were evaluated, the IL1 production tended to increase without the changes of IL6 and IL8. There is a possibility that beta_2-GPI dependent ACA prevents to suppress the production of ET-1.
We suggest that ACA may bind to placental villi and endothelium during pregnancy and that the vascular constriction by increased ET-1 production may produce IUGR.
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