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Lack of Previous Exposure to Paternal Antigens Does not Predispose to Hypertensive Pregnancy Complications
Objective: To test the hypothesis that previous exposure to paternal antigens should protect against preeclampsia and pregnancy-induced hypertension, we compared the occurrence of these complications and intrauterine growth retardation in pregnancies in women who conceived using sperm from a donor (...
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Published in: | Hypertension in pregnancy 1998, Vol.17 (3), p.291-295 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Objective: To test the hypothesis that previous exposure to paternal antigens should protect against preeclampsia and pregnancy-induced hypertension, we compared the occurrence of these complications and intrauterine growth retardation in pregnancies in women who conceived using sperm from a donor (no previous exposure to fertilizing sperm) or from the husband (maximal previous exposure to fertilizing sperm).
Subjects and Design: Follow-up study of 123 pregnancies in 123 primigravid women who conceived either by donor sperm (donor insemination or in vitro fertilization) (n = 73) or by husbands' sperm (spontaneous, insemination, or in vitro fertilization) (n = 50) after 2-10 years of infertility.
Main Outcome Measures: Occurrence of preeclampsia (elevation in blood pressure and proteinuria), pregnancy-induced hypertension (elevation in blood pressure, no proteinuria), and intrauterine growth retardation (birth weight < mean - 2 SD).
Results: The multiple pregnancy rate was 14% in both study groups. Preeclampsia developed in one woman in the donor group (1.4%) as compared with seven women in the control group (14.0%) [odds ratio = 0.09, 95% confidence interval (CI) = 0.01-0.72]. Two women in the donor group (2.7%) and three women in the control group (6.0%) had pregnancy-induced hypertension. The risk of either preeclampsia or pregnancy-induced hypertension was reduced in the donor group (odds ratio = 0.17, CI = 0.04-0.65). The rate of intrauterine growth retardation in singleton pregnancies in the donor group (3.2%) did not differ from that in die control group (4.6%).
Conclusions: Lack of previous exposure to paternal antigens does not enhance the risk of preeclampsia and/or pregnancy-induced hypertension. Our data raise doubts about previous suggestions that exposure to paternal antigens should protect against hypertensive pregnancy complications. |
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ISSN: | 1064-1955 1525-6065 |
DOI: | 10.3109/10641959809009602 |