Abstract |
Intrauterine growth restriction (IUGR) depends on the placental capacity to transfer oxygen and nutrients from the maternal to the fetal circulation. Placental insufficiency may be caused by impairment of the maternal or fetal circulation by a thrombotic event, possibly associated with thrombophilic disorders. The goals of our study were to define the role of maternal/fetal gain-of-function factor V Leiden and prothrombin G20210A mutations in the development of IUGR and to evaluate whether maternal pregnancy-induced hypertensive diseases would modify any such association. This is a case-control study: controls were 259 normal pregnancies, cases were 77 IUGR, 28 with and 49 without preeclampsia (PE) or pregnancy-induced hypertension (PIH). An association was found between IUGR and fetal thrombophilia (OR 2.09 CI 95% 1-4.5). The association was stronger in IUGR without PE and PIH (OR 2.9 CI 95% 1.3-6.6). This suggests a role for the fetal genotype in the development of IUGR.
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Authors | Paola Pileri, Franca Franchi, Irene Cetin, Chiara Mandò, Patrizio Antonazzo, Buthaina Ibrahim, Federica Rossi, Eugenia Biguzzi |
Journal | Reproductive sciences (Thousand Oaks, Calif.)
(Reprod Sci)
Vol. 17
Issue 9
Pg. 844-8
(Sep 2010)
ISSN: 1933-7205 [Electronic] United States |
PMID | 20601540
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- factor V Leiden
- Factor V
- Prothrombin
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Topics |
- Blood Pressure
- Case-Control Studies
- Chi-Square Distribution
- Factor V
(genetics)
- Female
- Fetal Diseases
(genetics)
- Fetal Growth Retardation
(etiology, genetics, physiopathology)
- Genotype
- Humans
- Hypertension, Pregnancy-Induced
(physiopathology)
- Italy
- Logistic Models
- Mutation
- Odds Ratio
- Phenotype
- Placental Circulation
- Pre-Eclampsia
(physiopathology)
- Pregnancy
- Pregnancy Complications, Hematologic
(genetics)
- Prothrombin
(genetics)
- Risk Assessment
- Risk Factors
- Thrombophilia
(genetics)
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