Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea

1987 ◽  
Vol 116 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Steven J. Goldstein ◽  
Richard H. K. Wu ◽  
Michael J. Thorpy ◽  
Robert J. Shprintzen ◽  
Robert E. Marion ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Obstructive Sleep

Abstract. Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (> 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

ERRATA Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea

1987 ◽  
Vol 116 (4) ◽  
pp. 568
Author(s):  
Steven J. Goldstein ◽  
Richard H. K. Wu ◽  
Michael J. Thorpy ◽  
Robert J. Shprintzen ◽  
Robert E. Marion ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Obstructive Sleep

scholarly journals Correction of obstructive sleep apnea and sleep en-gained growth hormone release by tracheostomy in achondroplasia

1984 ◽  
Vol 18 (11) ◽  
pp. 1215-1215
Author(s):  
S Goldstein ◽  
R H K Wu ◽  
M Thorpy ◽  
R Shprintzen ◽  
S Hahm ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Obstructive Sleep

nCPAP Treatment of Obstructive Sleep Apnea Increases Slow Wave Sleep in Prefrontal EEG

2007 ◽  
Vol 38 (3) ◽  
pp. 148-154 ◽  
Author(s):  
Veera Eskelinen ◽  
Toomas Uibu ◽  
Sari-Leena Himanen
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Treatment Period ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Eeg ◽  
Sleep Stages ◽  
Obstructive Sleep ◽  
Sleep Stage Scoring

According to standard sleep stage scoring, sleep EEG is studied from the central area of parietal lobes. However, slow wave sleep (SWS) has been found to be more powerful in frontal areas in healthy subjects. Obstructive sleep apnea syndrome (OSAS) patients often suffer from functional disturbances in prefrontal lobes. We studied the effects of nasal Continuous Positive Airway Pressure (nCPAP) treatment on sleep EEG, and especially on SWS, in left prefrontal and central locations in 12 mild to moderate OSAS patients. Sleep EEG was recorded by polysomnography before treatment and after a 3 month nCPAP treatment period. Recordings were classified into sleep stages. No difference was found in SWS by central sleep stage scoring after the nCPAP treatment period, but in the prefrontal lobe all night S3 sleep stage increased during treatment. Furthermore, prefrontal SWS increased in the second and decreased in the fourth NREM period. There was more SWS in prefrontal areas both before and after nCPAP treatment, and SWS increased significantly more in prefrontal than central areas during treatment. Regarding only central sleep stage scoring, nCPAP treatment did not increase SWS significantly. Frontopolar recording of sleep EEG is useful in addition to central recordings in order to better evaluate the results of nCPAP treatment.

Effect of epoxyeicosatrienoic acids on growth hormone release from somatotrophs

1989 ◽  
Vol 256 (2) ◽  
pp. E221-E226 ◽  
Author(s):  
G. D. Snyder ◽  
P. Yadagiri ◽  
J. R. Falck
Keyword(s):  
Growth Hormone ◽  
Arachidonic Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Epoxyeicosatrienoic Acids ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Epoxyeicosatrienoic Acid ◽  
Releasing Hormone

Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids. 5,6-Epoxyeicosatrienoic and 14,15-epoxyeicosatrienoic acid stimulated growth hormone release from an enriched population of somatotrophs (approximately 85%) by twofold. Inhibition of arachidonic acid metabolism by indomethacin did not affect growth hormone-releasing hormone stimulation of growth hormone release. In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release. 14,15-Epoxyeicosatrienoic acid stimulated a concentration-dependent increase (twofold) in the cytoplasmic concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the somatotrophs. 14,15-Epoxyeicosatrienoic acid also rapidly increased the intracellular free calcium concentration in somatotrophs from resting levels (approximately 80 nM) to greater than 250 nM. Growth hormone-releasing hormone increased the free intracellular calcium to 160-180 nM. Preincubation of somatotrophs with somatostatin inhibited growth hormone-releasing hormone-stimulated growth hormone secretion, cAMP accumulation, and 14,15-epoxyeicosatrienoic acid stimulated cAMP accumulation. These data are suggestive that the epoxyeicosatrienoic acids may have a role in the secretion of growth hormone.

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