Cell adhesion & migration · 2008
Cardiac progenitor migration and specification: The dual function of Wnts.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Salvatoni A, Veronelli E, Nosetti L, Berini J, de Simone S, Iughetti L, Bosio L, Chiumello G, Grugni G, Delù G, Castelnuovo P, Trifirò G, Nespoli L
Аннотация
AIMS: The aim of this study was to establish whether short-term GH treatment causes obstructive apnea in patients with Prader-Willi syndrome and normal upper airway patency.
SUBJECTS AND METHODS: We performed an observational longitudinal 6-week GH treatment study. Thirty-four non-severely obese Prader-Willi syndrome patients (20 boys, age range 0.94-11.8 yr, median 2.24 yr) entered an observational longitudinal 6-week study. Sixteen boys received recombinant human GH (rhGH) treatment; the remaining 18 represented the control group and received no treatment. Polysomnography monitoring and othorhinolaringoiatric video endoscopy were performed one night before and after 6 weeks of rhGH treatment (0.03 mg/kg body weight/day). All patients underwent auxologic assessment, fasting blood glucose, insulin and IGF-I evaluation. The main polysomnographic parameter considered was total apnea hypopnea index, consisting of two components: central apnea hypopnea index and obstructive apnea hypopnea index. All patients were free of severe or moderate upper airway obstruction when rhGH treatment began.
RESULTS: After 6 weeks of rhGH therapy, obstructive apnea hypopnea index increased in 8/16 (50%), decreased in 5/16 (31%), and did not change in 3/16 (19%) patients. The changes were not statistically significant. The rhGH-treated group did not differ from the control group for the apnea hypopnea index both before and after 6 weeks of treatment. Adenoids and tonsils showed a slight increase in 1 and 2 patients on rhGH treatment, respectively, and did not change in the untreated patients.
CONCLUSIONS: Our data show that short-term rhGH treatment does not cause restrictions of the upper airways in patients with Prader-Willi syndrome and normal upper airway patency.
SUBJECTS AND METHODS: We performed an observational longitudinal 6-week GH treatment study. Thirty-four non-severely obese Prader-Willi syndrome patients (20 boys, age range 0.94-11.8 yr, median 2.24 yr) entered an observational longitudinal 6-week study. Sixteen boys received recombinant human GH (rhGH) treatment; the remaining 18 represented the control group and received no treatment. Polysomnography monitoring and othorhinolaringoiatric video endoscopy were performed one night before and after 6 weeks of rhGH treatment (0.03 mg/kg body weight/day). All patients underwent auxologic assessment, fasting blood glucose, insulin and IGF-I evaluation. The main polysomnographic parameter considered was total apnea hypopnea index, consisting of two components: central apnea hypopnea index and obstructive apnea hypopnea index. All patients were free of severe or moderate upper airway obstruction when rhGH treatment began.
RESULTS: After 6 weeks of rhGH therapy, obstructive apnea hypopnea index increased in 8/16 (50%), decreased in 5/16 (31%), and did not change in 3/16 (19%) patients. The changes were not statistically significant. The rhGH-treated group did not differ from the control group for the apnea hypopnea index both before and after 6 weeks of treatment. Adenoids and tonsils showed a slight increase in 1 and 2 patients on rhGH treatment, respectively, and did not change in the untreated patients.
CONCLUSIONS: Our data show that short-term rhGH treatment does not cause restrictions of the upper airways in patients with Prader-Willi syndrome and normal upper airway patency.