AbstractBackground and aims
It is known that obstructive sleep apnea (OSA) has been closely linked to hypertension and is considered an important stressor. The hypothalamic-pituitary-adrenal axis (HPA) is major component involved in stress response. However, response of HPA axis to OSA effects may be variable. Thus, the aim of this study is to estimate HPA axis hormonal profile in OSA and non-OSA adolescents with essential hypertension (EH).Methods
We examined 38 adolescents with EH (18 OSA patients – the 1-rst group, 20 non-OSA patients – the 2-nd group) aged 14–17 years, all male. OSA was verified by overnight polysomnography in the sleep laboratory applying system GRASS-TELEFACTOR Twin PSG (Comet, USA) if apnea-hypopnea index was>5/hr. EH was diagnosed with 24 hour ambulatory blood pressure (BP) monitoring using monitor Oscar 2 for OXFORD Medilog Prima. Demographic and anthropometric data were routinely collected. Three overweight patients were excluded from this study. Hormonal status, including TSH, PRL and cortisol, were routinely collected using an automatic analyzer Immunotest-800 (Russia) and test-system Dias (Russia). All differences were considered significant at p<0.05.Results
OSA hypertensive boys did not significantly differ from non-OSA participants in age and body mass index. There were statistically significant differences in morning serum cortisol and TSH levels of OSA adolescents (745,8±6,4 nmol/L versus 493,2±3,2 nmol/L in non-OSA participants, and 1,95±0,9 mkME/ml versus 1,5±0,2 mkME/ml, respectively, p<0,05 ). Morning serum PRL level in the both groups no statistically significant differences, but there is a trend towards its increasing in OSA adolescents with EH (482,8±4,2 mME/L in the 1-rst group and 442,2±4,1 mME/L in the 2-nd group).Conclusions
The results of this study indicate for chronic stress if OSA in adolescents with EH is present. This is due to the influence of sleep fragmentation and intermittent hypoxia on HPA axis with compensatory stress-related hormones release. Such intra systemic changes suggest the prevalence of sanogenetic above pathogenetic mechanisms for OSA in adolescents.