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Urinary cortisol to cortisone metabolites in hypertensive obese children

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Abstract

Childhood obesity is accompanied by a variety of cardiovascular risk factors (hypertension, insulin resistance, dyslipidaemia) which tend to aggregate (syndrome X). 11ß-hydroxysteroid dehydrogenase (11ß-HSD) is supposed to play a role in the pathogenesis of hypertension and the development of syndrome X. There are two isoforms of 11ß-HSD. 11ß-HSD-2 is responsible for the inactivation of cortisol to inactive cortisone. In the case of impaired enzyme activity the ratio of urinary tetrahydrocortisol (THF)+ its isomer allotetrahydrocortisol (5α-THF)/tetrahydrocortisone (THE) is elevated. 11ß-HSD-1 is an oxo-reductase, which type catalyses the conversion of cortisone to cortisol. The aim of the present study was to investigate if there was any alteration in the urinary cortisol metabolites reflecting 11ß-HSD activity in hypertensive obese children (no.=15) as compared to normotensive obese (no.=11) and normotensive non-obese children (no.=15). We found an increased excretion of cortisol metabolites in hypertensive obese children compared to obese and normal — weight children having normal blood pressure. The ratio of THF+5αTHF/THE had a significant correlation with systolic blood pressure. On the basis of our study the ratio of THF+5α-THF/THE reflecting on altered enzyme activity seems to be an independent factor influencing especially systolic blood pressure in hypertensive obese children.

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Authors and Affiliations

  1. Department of Pediatrics, University Medical School of Pécs, 7623 Pécs, József A. u.7., Hungary

    Györgyi Csábi MD & D. Molnár

  2. Central Research Laboratory, University Medical School of Pécs, Hungary

    S. Juricskay

Authors
  1. Györgyi Csábi MD
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  2. S. Juricskay
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  3. D. Molnár
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Csábi, G., Juricskay, S. & Molnár, D. Urinary cortisol to cortisone metabolites in hypertensive obese children. J Endocrinol Invest 23, 435–439 (2000). https://doi.org/10.1007/BF03343752

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