Search

Purpose: We aimed to determine the impact of insulin resistance and hyperandrogenemia on polysomnographic variables in obese adolescents with polycystic ovarian syndrome (PCOS), as studies in adults with PCOS suggest that parameters of glucose metabolism and serum androgens are related to respiratory polysomnographic variables (RPV), and the symptoms of PCOS usually begin around menarche. Methods: We divided our study group of obese adolescents with PCOS according to HOMA-index and in a second analysis according to free androgen index (FAI). Study group A consisted of 14 girls with HOMA-index <4, study group B of 17 girls with HOMA-index >4. Study group C consisted of 19 girls with FAI <10, and study group D of 18 girls with FAI >10. The control group for both analyses consisted of 19 healthy obese adolescents without PCOS. All girls underwent overnight 12-channel polysomnography. Results: In both analyses, we found no differences between the groups concerning the RPV. Study group B demonstrated a significantly lower percentage of REM-sleep than the control group ( p = 0.02). Study group D demonstrated a significantly lower percentage sleep stages 3 and 4 of non-REM-sleep than study group C and the controls ( p = 0.008). Study group D demonstrated significantly lower sleep efficiency than the controls ( p = 0.03). Conclusions: Insulin resistance and hyperandrogenemia do not seem to have a significant impact on RPV in obese adolescents with PCOS. Differences in sleep architecture found between patients with PCOS and controls, however, are possibly influenced by insulin resistance and/or serum androgens. [ABSTRACT FROM AUTHOR]

The purpose of this paper is to confirm a hypothesis claiming that in clinically healthy term infants sleep-wake cycle development and maturation of breathing control – as objectivated in polysomnography – proceed in parallel. Irregular breathing movements as equivalent of Active (REM-)Sleep and paradoxical patterns of thoracic and abdominal breathing movements decrease in the first year of life whereas regular breathing movements – the equivalent of Quiet Sleep – and coordinated patterns of thoracic and abdominal breathing movements increase. With growing maturation, periodic breathing and the different kinds of respiratory pauses decrease. Deviations from normal respiratory phenomena were seen as well in sick and in preterm infants as in infants belonging to epidemiologically defined groups at high risk of Sudden Infant Death. Thus, breathing patterns were impaired by prematurity, after intrauterine exposure to nicotine and drugs, and during upper airway infections. At last, in prospective studies of infants,who subsequently died of sudden infant death, peculiar breathing behavior was described. [ABSTRACT FROM AUTHOR]