Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight obese patients (4 male, 4 female; mean age = 35.9 years) before [mean body mass index (BMI) = 37.1] and after (mean BMI = 31.4) weight loss by means of a mixed hypocaloric diet were compared with 8 lean subjects (4 male, 4 female; mean age = 37.1 years, mean BMI = 22.3) in a study of their nocturnal sleep patterns and sleep-related growth hormone (GH) secretions. Although no sleep disorders (in particular, sleep apnea and hypersomnia) were observed, GH secretion was markedly altered in obese patients that showed no sleep-related GH peaks. After weight loss, the sleep architecture in obese subjects was unchanged. On the contrary, GH peak appeared to be only partially restored and delayed until after stage III-IV of non-REM sleep. Our study on obese subjects suggests that the altered nocturnal GH secretion, probably related to a hypothalamic dysfunction, may be the result of the obesity per se.
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PMID:Sleep-related growth hormone secretion in human obesity: effect of dietary treatment. 175 83

To evaluate the effect of human growth hormone (hGH) on the growth of children with achondroplasia, three patients with achondroplasia and one patient with hypochondroplasia were treated with 0.5 IU/kg/W of pituitary-extracted hGH for 6-12 months. Mean height velocity was significantly increased from 4.0 +/- 0.4 to 7.5 +/- 0.7 cm/year (P less than 0.05) by hGH. The tibial index, defined as the length/width ratio of left tibia, did not change during the treatment, indicating that hGH promotes growth without exaggeration of tubular bone deformity. Case 2, who had atlantoaxial dislocation, developed sleep apnea and neurological deficits during the second hGH treatment, but these were cured by operation. Thus, hGH therapy is effective in promoting growth in patients with achondroplasia, but the complication of atlantoaxial dislocation should be explored and corrected before the treatment.
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PMID:Growth-promoting effect of human growth hormone on patients with achondroplasia. 178 32

Daytime somnolence and fatigue are frequently ignored symptoms in acromegaly. To examine whether sleep apnea or other abnormalities in the sleep structure is the underlying cause, 9 young patients with active untreated acromegaly for 2-7 years were studied with all night polysomnography. It revealed a decrease in REM sleep time in all the acromegalics compared to age- and sex-matched normal subjects (p less than 0.001) and also a reduction in delta sleep (p less than 0.05). None had obstructive sleep apnea. At reexamination 12-15 months posttreatment the daytime sleepiness had disappeared in all patients. REM sleep time increased in all patients (p less than 0.001) to normal level; delta sleep time increased moderately (p less than 0.05). Thus sleepiness in patients with high fasting level of growth hormone (GH) is not related to sleep apnea but more likely to a reduced amount of REM sleep time. By normalizing the GH concentration, REM sleep time became normal and the daytime sleepiness disappeared in all patients.
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PMID:Sleep in acromegaly before and after treatment with adenomectomy. 204 66

A patient with longstanding acromegaly complicated by sleep apnea was treated with bromocriptine prior to surgery. In addition to a significant reduction of the plasma growth hormone concentration and measurable decrease in acral overgrowth, a dramatic improvement of the sleep apnea was observed. After three months of therapy, the amount of sleep time occupied by apneic episodes fell from 48 to 12%. The response indicates: (a) that the sequelae sleep apnea in acromegaly can be improved even when ablative therapy of the pituitary is impossible and (b) bromocriptine may prevent perioperative complications caused by clinically significant airway obstruction in patients with acromegaly.
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PMID:Relief of sleep apnea in acromegaly by bromocriptine. 333 38

Previous case reports have shown an association between acromegaly and the sleep apnea syndrome (SAS). Some of the patients described had central SAS, raising the possibility that an elevation of the growth hormone (GH) level may cause a defect in respiratory drive. We determined the prevalence of SAS in 21 patients with a history of acromegaly. We separated them into two groups based on serum GH concentrations. Ten patients had active acromegaly (mean GH concentration, 62.2 ng/mL; range, 12.6 to 148 ng/mL), while 11 patients had inactive acromegaly (mean GH, 3.2 ng/mL; range, 0.7 to 6.4 ng/mL). Four of the ten patients with active acromegaly had SAS; none of the 11 patients with inactive acromegaly had SAS. Three patients with SAS had the purely obstructive type, and one had the mixed central and obstructive type. The hypercapnic ventilatory response was normal in all patients tested and was not influenced by the GH level. We conclude that SAS is associated with active acromegaly and that the GH level does not affect the hypercapnic ventilatory response. The absence of SAS in successfully treated patients suggests that it may resolve after a normal GH level is restored.
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PMID:Sleep apnea in active acromegaly. 399 62

Sleep-disturbed breathing, which includes apneas, hypopneas, and oxygen desaturations, occurs in asymptomatic individuals and increases with age. Obstructive apnea is the most frequent type of respiratory disturbance documented by polysomonography, the gold standard test for assessing sleep-disturbed breathing. Many of the prevalence studies done to date have had one or more methodological weaknesses, including selection biases, varying definitions of obstructive sleep apnea, failure to distinguish types of apneas, failure to control for confounding variables, and small sample size. Although there is consensus on the definitions of sleep-disturbed breathing, the appropriate number of apneas and hypopneas for diagnosing clinically significant obstructive sleep apnea is uncertain. While the cutoff of five or more apneas and hypopneas per hour is historically considered abnormal, the origins of this number are vague, and the longevity of those who have this value on polysomnography is not necessarily reduced. This is particularly true among those without symptoms of obstructive sleep apnea syndrome, which include excessive daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Investigators should be careful to distinguish symptomatic study subjects from asymptomatic subjects, and to exclude central apneas in calculating their estimates. In addition, various studies have used different definitions of sleep apnea syndrome, making comparisons of point estimates difficult. It would be more appropriate for researchers to estimate morbidity and mortality indices with confidence intervals, using several different cutoff points. Subject selection in all studies should follow a two-stage sampling procedure. All subjects with symptoms compatible with obstructive sleep apnea syndrome and a subsample of asymptomatic individuals should be studied with all-night polysomnography. If portable monitoring is used, the validity and reproducibility of this diagnostic method should be assessed. Subjects with significant comorbidity should be excluded from prevalence studies. Factors that clearly increase the risk of sleep-disturbed breathing and obstructive sleep apnea and its related symptoms include age, structural abnormalities of the upper airway, sedatives and alcohol, and probably family history. Although endocrine changes such as growth hormone, thyroid hormone, and progesterone deficiency also have been suggested as risk factors for exacerbating obstructive sleep apnea syndrome, there is minimal epidemiologic evidence to support this. Case-control studies are recommended to assess the relation of endocrine factors to obstructive sleep apnea syndrome in a rigorous fashion. A limited number of mortality studies have suggested decreased survival in persons with the obstructive sleep apnea syndrome, possibly primarily due to vascular-related disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of obstructive sleep apnea. 771 77

The authors examined 19 nonselected patients with acromegaly (8 women and 11 men), incl. 16 where the disease was hormonally active, 3 had normal growth hormone values, 11 patients had a surgical operation of the pituitary. The examination was made by the MESAM 4 method (all-night recording of the heart rate, respiratory sounds, body position and arterial oxygen blood saturation). The sleep apnoea syndrome was diagnosed in 10 patients (52.6%). In patients where the sleep apnoea syndrome was not confirmed by MESAM 4, so-called intermittent snoring was found, an indirect sign of impaired ventilation during sleep.
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PMID:[The sleep apnea syndrome in patients with acromegaly]. 771 94

It has long been known, that irregular, heavy snoring and daytime sleepiness are common features of acromegaly. Only recently has the high incidence (30-60%) and clinical relevance of the sleep apnoea underlying these symptoms been recognized. Both diseases have a group of common symptoms and prognostic features: Increased cardiovascular and respiratory mortality, elevated incidence of hypertension, daytime sleepiness, decreased vitality, headaches and depression. These are very prominent in sleep apnoea and often reversible under treatment. In acromegaly their etiology has been widely unexplained and they commonly persist even when human growth hormone (hGH) levels remain normal after operative treatment. We report on 2 patients presenting with excessive daytime sleepiness and severe obstructive sleep apnoea caused by acromegaly. Both had macroglossia and hypertrophy of hypopharyngeal tissues regressive after surgical therapy. The average hGH-levels were 20 and 31 ng/ml before and 3 and 1.7 ng/ml several months after operation respectively. Apnoea indices and minimal oxygen saturations (SO2) were 59/h and 55/h, and 60% and 58% initially and improved postoperatively to 40/h and 50/h, and 72% and 70%. Polysomnographic parameters were normalized by NCPAP-therapy pre- and postoperatively and daytime sleepiness improved dramatically. In one patient the NCPAP-pressure could be decreased postoperatively. Since patients with sleep apnoea have an increased perioperative risk of hypoxia and because transsphenoidal operation and postoperative nasal tamponade were performed, both patients were tracheostomized perioperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnoea in acromegaly--prevalence, pathogenesis and therapy. Report on two cases. 783 Dec 13

Obstructive sleep apnea syndrome is a complex disorder that has been associated with a variety of abnormalities of the upper airway, including tonsil and adenoid hypertrophy, nasal obstruction, retrognathia, and macroglossia. The cause of the airway obstruction in acromegaly is believed to be related to osseous and soft-tissue changes surrounding the upper airway, which lead to narrowing and subsequent collapse during sleep. We describe the results of treatment in seven patients with both sleep apnea and acromegaly. Four patients were treated by transsphenoidal hypophysectomy alone with a resolution of sleep apnea syndrome. One underwent hypophysectomy followed by postoperative radiation therapy, which reduced his apnea. Three patients underwent unsuccessful uvulopalatopharyngoplasty. Successful treatment of the primary disorder, in this case acromegaly, resulted in improved breathing during sleep in five patients. This series would suggest that acromegalic patients with sleep apnea should be treated for their pituitary tumor to reduce growth hormone before consideration of surgery to enlarge or bypass the upper airway.
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PMID:Obstructive sleep apnea syndrome and acromegaly. 802 37

Although obstructive sleep apnea (OSA) occurs commonly in acromegaly, we have recently reported an unexpectedly high prevalence of central sleep apnea (CSA) in these patients. Acromegalic patients with CSA have increased growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels compared with their counterparts with OSA. Studies in animals, normal humans, and patients with sleep apnea have suggested that CSA is associated with increased gain of the respiratory control system. To examine the relationship between sleep apnea, respiratory control, and hormonal activity in acromegaly, we performed sleep studies and examined ventilatory responses to hypoxia at resting CO2 (HVR) and 8 mm Hg above resting CO2 (HHVR) and hypercapnia (HCVR) in 54 patients with acromegaly who also underwent detailed endocrine evaluation. Patients with CSA (n = 11) had higher HCVR (3.47 +/- 0.57 L/min/mm Hg) than did patients with obstructive sleep apnea (OSA) (1.86 +/- 0.19, n = 33) and patients without sleep apnea (1.77 +/- 0.21, n = 10). Measures of ventilatory control were all correlated with the mean of 12 hourly GH concentrations, but only HCVR was correlated with IGF-1 levels. Multiple linear regression analysis revealed that HCVR, HHVR, and IGF-1 could explain 39% of the variability in the degree of CSA in acromegalic patients with sleep apnea. We conclude that increased ventilatory responsiveness and elevated hormonal parameters of disease activity both contribute to the pathogenesis of central sleep apnea in acromegaly.
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PMID:Central sleep apnea is associated with increased ventilatory response to carbon dioxide and hypersecretion of growth hormone in patients with acromegaly. 804 36


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