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Paternal Age and Preeclampsia

Harlap, Susan1; Paltiel, Ora2; Deutsch, Lisa2; Knaanie, Ariella2; Masalha, Sausan2; Tiram, Efrat2; Caplan, Lee S.3; Malaspina, Dolores4; Friedlander, Yechiel2

Original Articles

Background.  Paternal aging is associated with premeiotic damage to spermatogonia, a mechanism by which new point mutations are introduced into the gene pool. We hypothesized that paternal age might contribute to preeclampsia.

Methods.  We studied the incidence of preeclampsia in 81,213 deliveries surveyed in 1964–1976 in the Jerusalem Perinatal Study. We controlled for maternal age, parity and other risk factors using logistic regression.

Results.  Preeclampsia was reported in 1303 deliveries (1.6%). Compared with fathers age 25–34 years, the odds ratios (ORs) for preeclampsia were 1.24 (95% confidence interval = 1.05–1.46) for age 35–44 and 1.80 (1.40–2.31) for age 45+. For fathers age <25, the OR was 1.25 (1.04–1.51). Although weaker than maternal age effects, paternal effects were consistent within subgroups of other variables.

Conclusions.  These findings support the hypothesis that a modest proportion of preeclampsia might be explained by new mutations acquired from fathers and add to a growing body of evidence for paternal age effects in birth defects, neuropsychiatric disease and neoplasia.

From the 1Department of Obstetrics and Gynecology and Kaplan Cancer Center, New York University School of Medicine, New York, NY;

2Department of Social Medicine, Hebrew University-Hadassah School of Public Health, Jerusalem, Israel;

3Morehouse School of Medicine Prevention Research Center, Atlanta, GA; and

4Department of Psychiatry, College of Physicians and Surgeons, Columbia University, and New York State Psychiatric Institute, New York, NY.

Address correspondence to: Susan Harlap, Department of OBGYN, Room NB-9E2, New York University School of Medicine, 550 First Avenue, New York, NY 10016;

Supported by National Cancer Institute/NIH Grant R01-CA80197 and National Center for Research Resources/NIH Grant M01-RR00096.

Submitted 11 December 2001; final version accepted 17 July 2002.

© 2002 Lippincott Williams & Wilkins, Inc.