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Alteration of the Activity of the 11ß-Hydroxysteroid Dehydrogenase in Pregnancy: Relevance for the Development of Pregnancy-Induced Hypertension?

Departments of Internal Medicine I (Endocrinology and Metabolism) (P.H., E.B., R.Z.) and Gynecology and Obstetrics (J.W.), University of Heidelberg, D-69115 Heidelberg, Germany

Address all correspondence and requests for reprints to: Dr. Peter Heilmann, Department of Internal Medicine I (Endocrinology and Metabolism), Luisenstrasse 5, Gebäude 8, D-69115 Heidelberg, Germany. E-mail: Peter_Heilmann{at}med.uni-heidelberg.de

Abstract

In this study we evaluated the activity of renal 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD₂) in patients with pregnancy-induced hypertension (PIH). A reduction of the activity of 11ß-HSD₂ leads to pseudohyperaldosteronism due to insufficient interconversion of cortisol to its inactive 11-oxo-metabolite cortisone in the renal tubulus cell. We measured urinary free cortisol and cortisone in patients with and without PIH and calculated the urinary free cortisol to free cortisone ratio, which is well accepted as a correlate of the activity of renal 11ß-HSD₂. One hundred twenty-six pregnant women were included. Fifty-nine patients had PIH (mean age 31.5 ± 4.4 yr, blood pressure 158.7 ± 16.0/100.8 ± 9.5 mm Hg), and 67 were normotensive (mean age 29.4 ± 4.6, blood pressure 112.6 ± 8.9/68.8 ± 8.6 mm Hg). The excretion rate of cortisol was increased in the PIH group (138.8 ± 93.0 vs. 106.5 ± 65.4 nmol/d, P = 0.027), whereas excretion rate of cortisone was similar (362.9 ± 254.1 vs. 366.5 ± 221.7 nmol/d, P = 0.933). The free cortisol to free cortisone ratio was significantly higher in the PIH group (0.47 ± 0.25 vs. 0.31 ± 0.12, P < 0.00002). Within this group, the patients with blood pressure in the uppermost quartile had a significantly higher free cortisol to free cortisone ratio than those in the lowest quartile [0.61 ± 0.31 vs. 0.38 ± 0.15 (P = 0.019) for diastolic, 0.60 ± 0.29 vs. 0.35 ± 0.13 (P = 0.012) for systolic, and 0.62 ± 0.32 vs. 0.39 ± 0.16 (P = 0.023) for mean blood pressure, respectively]. We conclude that a reduction of the activity of the 11ß-HSD₂ is a relevant factor for the development of PIH. Whether the ratio of urinary free cortisol to free cortisone is a useful risk factor for the development of PIH must be investigated in further prospective studies.

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