History of Fetal Growth Restriction Is More Strongly Associated With Severe Rather Than Milder Pregnancy-Induced Hypertension

Medical Birth Registry of Norway, Locus of Registry Based Epidemiology, Institute of Community Medicine and Primary Health Care, University of Bergen and Norwegian Institute of Public Health, Bergen, Norway.
Hypertension (Impact Factor: 6.48). 04/2008; 51(4):1231-8. DOI: 10.1161/HYPERTENSIONAHA.107.096248
Source: PubMed


We assessed whether fetal growth restriction without pregnancy-induced hypertension (PIH) is associated with the different clinical subgroups of PIH in the subsequent pregnancy. We also assessed the maternal and paternal contributions to this effect. Pairs of first and second, second and third, third and fourth, and fourth and fifth births were identified among all of the births in Norway: 137 375 pairs with same mother and father, 18 376 pairs with same mother and different fathers, and 18 916 pairs with same father and different mothers. Second births in each pair were restricted to those that occurred in 1998-2005. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension in the second birth from birth weight <1500 g in the first compared with 3500 to 3999 g were 13.8, 7.1, 3.5, and 2.2, respectively. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension from birth weight below the 2.5th percentile compared with percentiles 10.0 to 89.9 were 4.2, 2.5, 2.1, and 1.7, respectively. Men who fathered a child with low birth weight in 1 woman were not more likely to later father a PIH pregnancy in another woman. The results indicate that placental dysfunction and PIH share a genetic factor that can be expressed as fetal growth restriction in 1 pregnancy and PIH in a subsequent pregnancy. Future genetic study is needed to confirm whether the association is caused by delayed genetic expression of endothelial dysfunction and whether the clinical subgroups of PIH have different genetic backgrounds.

Download full-text


Available from: Lorentz M Irgens, Sep 30, 2014
15 Reads
  • Source
    Hypertension 05/2008; 51(4):989-90. DOI:10.1161/HYPERTENSIONAHA.107.100248 · 6.48 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Altered levels of pregnancy hormones have been suggested to initiate testicular cancer prenatally in the male fetus. The placenta is the main source of pregnancy hormones, and pregnancy hypertension and preeclampsia are associated with placental malfunction, including altered levels of hormones such as estrogen and human chorionic gonadotropin. We therefore evaluated fetal exposure to pregnancy hypertension and preeclampsia in relation to risk of testicular cancer in adolescent and adult life. We identified 293 cases of germ cell testicular cancer in the Swedish Cancer Register, and 861 controls in the Swedish Medical Birth Register. The standardized antenatal and delivery charts of the cases and controls were traced in the archives of the delivery units, and information about maternal and pregnancy characteristics such as gestational hypertension, proteinuria, anemia, and glucosuria were extracted. Odds ratios (OR) with 95% confidence intervals (CI) were calculated using conditional logistic regression. We found a strongly decreased risk of testicular cancer among subjects exposed to severe gestational hypertension (OR, 0.29; 95% CI, 0.12-0.74, compared with no hypertension), whereas the risk was increased among those exposed to mild gestational hypertension (OR, 1.62; 95% CI, 0.98-2.69) during the fetal period. The mechanism behind the association between pregnancy hypertension and testicular cancer is unclear, but our findings may reflect a potentially protective effect of the altered pregnancy hormones such as human chorionic gonadotropin that occur in severe gestational hypertension and preeclampsia.
    Cancer Research 12/2008; 68(21):8832-6. DOI:10.1158/0008-5472.CAN-08-2309 · 9.33 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 1. Events in utero appear to have a significant role in the development of cardiovascular dysfunction in adulthood. In the present study, we evaluated the effects of prenatal exposure to zymosan, a non-infectious and non-bacterial agent capable of inducing inflammation, on mean systolic arterial pressure (MSAP) in rat offspring at 6-66 weeks of age. 2. Pregnant rats were divided into three groups: (i) a control group, administered 0.5 mL, i.p., saline on gestation Days 8, 10 and 12; (ii) a zymosan-treated group, given 2.37 mg/kg, i.p., zymosan on gestation Days 8, 10 and 12; and (iii) a pyrrolidine dithiocarbamate (PDTC) + zymosan-treated group, which was given 100 mg/kg, i.p., PDTC 1 h before zymosan. At 6, 16, 26, 36, 56 and 66 weeks of age, MSAP was determined in rat offspring from all three groups. Serum levels of tumour necrosis factor (TNF)-alpha were determined in dams, as well as in offspring at 24 and 56 weeks of age. In addition, protein levels of nuclear factor (NF)-kappaB (p65) in the myocardium and kidney of offspring were determined at 24 weeks of age. 3. The results showed that MSAP and NF-kappaB (p65) levels in the myocardium and kidney of offspring from the zymosan-treated group were increased significantly compared with control. This increase was inhibited by concomitant treatment with PDTC. Serum TNF-alpha levels in dams exposed to zymosan and in their offspring at 56 weeks of age (but not at 24 weeks of age) were significantly increased compared with levels in the control group. Following lipopolysaccharide treatment (1 mg/kg, i.p.) of adult rat offspring at 24 weeks of age, there was a further increase in serum TNF-alpha levels in offspring in the zymosan-treated group compared with the other two groups. 4. The findings of the present study suggest that non-bacterial inflammation during gestation can lead to hypertension in offspring and that NF-kappaB signalling may play a critical role in this process.
    Clinical and Experimental Pharmacology and Physiology 01/2009; 35(12):1413-8. DOI:10.1111/j.1440-1681.2008.05062.x · 2.37 Impact Factor
Show more