It has been assumed that low birth weight and high placenta weight were key factors for predicting hypertension in human adulthood. Adeficiency in placental 11β-HSD-II enzyme activity was supposed to be the underlying cause. To possibly establish 11β-HSD-II as a leading factor, we determined 11β-HSD-II activities in 133 healthy pregnancies, 21 proteinuric pregnancies complicated by pregnancy-induced hypertension (PIH), 26 non proteinuric PIH pregnancies and 15 pregnancies complicated by fetal growth restriction (32nd–41st gestational week). We could not identify differences in 11β-HSD-II activity between pregnancies with the rare combination of small babies with big placentas and others (p 5 0,59; Kruskal-Wallis test). And although there was no correlation between 11β-HSD-II activity and birth weight, in the control gestational age correlated with 11β-HSD-II activity (r = 0,22; p < 0.05; Spearman).
11β-HSD-II activity in the proteinuric PIH group was significantly higher than in the controls (11,7 pmol/min/mg prot.; range 10–13,2 vs. 7,9; range 7,0–9,1; p < 0,05). The lowest, but not significant, enzyme activities were in the IUGR group (5,8 pmol/min/mg prot.; range 4,0–9,2). In this group, analysis of variance detected a correlation between enzyme activity and placental weight.
In conclusion, we could not confirm that placental 11β-HSD-II deficiencies act as an indicator for the risk of adult hypertension in small fetuses with large placentas. However, in growth restriction 11β-HSD-II activity might play a role. To clarify the influence in this group, further research is needed.
Increased 11β-HSD-II activities with gestational age in the control may serve to sustain fetal adrenal steroid genesis and to prepare the fetus for autonomic life.
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