Abstract
PurposeThe diminished function of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) was found in placentae from preeclamptic pregnancies. Here, we examine the overall maternal glucocorticoid balance in pregnancy-related hypertension. We aim to answer the question if the functions of primary enzymes involved in cortisol metabolism: 11β-HSD1 and 11β-HSD2 and 5-reductases (both 5α- and 5β) are altered in the course of hypertensive pregnancy.MethodsWe determined plasma and urinary cortisol and cortisone as well as their urinary tetrahydro- and allo-tetrahydrometabolites, both in free and conjugated forms in samples obtained from 181 Polish women in the third trimester of pregnancy. We compared steroid profiles in women with preeclampsia (PE), gestational hypertension (GH), chronic hypertension (CH) and in normotensives (controls).ResultsWe found significant differences in glucocorticoid balance in pregnancy-related hypertension. Plasma cortisol to cortisone was significantly lower in PE than in controls (3.00 vs. 4.79; p < 0.001). Increased function of renal 11β-HSD2 in PE and GH was manifested by significantly lower urinary free cortisol to cortisone ratio (0.169 and 0.206 vs. 0.277 in controls; p < 0.005). Markedly enhanced metabolism of cortisol was observed in pregnancy-related hypertension, with no significant alterations in CH, and the changes were more clearly expressed in PE than in GH.ConclusionsThe glucocorticoid balance in PE and GH is shifted towards decreasing cortisol concentration either due to intensified conversion to cortisone or enhanced production of tetrahydro and allo-tetrahydrometabolites.
Highlights
Pathogenesis of preeclampsia (PE) is not fully explained
The Endocrine (2018) 61:125–133 placenta is an important source of CRH, which further stimulates the release of maternal ACTH
The aim of this study was to evaluate the overall maternal GC balance in pregnancy-related hypertension and to verify if the functions of primary enzymes involved in F metabolism: 11β-HSD1, 11β-HSD2, 5α and 5β-reductase are altered in hypertensive pregnancy
Summary
Pathogenesis of preeclampsia (PE) is not fully explained. It is believed to be initiated by the placental ischemia. In PE, the invasion of the trophoblast is aberrant; the spiral arteries remodeling is impaired. In normal pregnancy CBG levels rise with advancing gestation, with a corresponding increase of total plasma F, with a decline from 36 weeks onwards; this decline results in the rise of free F in maternal plasma [5]. The Endocrine (2018) 61:125–133 placenta is an important source of CRH, which further stimulates the release of maternal ACTH. It leads to the elevation of F levels in the course of pregnancy [4, 5]. Maternal CRH, ACTH and F levels increase in maternal plasma and drop at 4 days postpartum [4]
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