Urinary cortisol to cortisone metabolites in hypertensive obese children

Childhood obesity is accompanied by a variety of cardiovascular risk factors (hypertension, insulin resistance, dyslipidaemia) which tend to aggregate (syndrome X), 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) is supposed to play a role in the pathogenesis of hypertension and the development of syndrome X. There are two isoforms of 11 beta-HSD. 11 beta-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 allo-tetrahydrocortisol (5 alpha-THF)/tetrahydrocortisone (THE) is elevated, 11 beta-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 11 beta-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+5 alpha THF/THE had a significant correlation with systolic blood pressure. On the basis of our study the ratio of THF+5 alpha-THF/THE reflecting on altered enzyme activity seems to be an independent factor influencing especially systolic blood pressure in hypertensive obese children. (C) 2000, Editrice Kurtis.