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Query: UMLS:C0028754 (obesity)
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Four male obese patients with obstructive sleep apnea were evaluated by polysomnography, both prior and 3-4 months following gastroplasty. The surgery was performed as an alternative weight loss treatment. These patients were selected for gastroplasty because they had severe obesity, obstructive sleep apnea with cardiopulmonary impairment and noncompliance on a weight loss diet. Tracheostomy was performed concomitantly in three cases. Preoperative recording demonstrated 21.2 to 100.3 apneas per hour of sleep; stage 3 was decreased in three and absent in one case; stage 4 was absent in every patient; stage REM was decreased in three cases; arterial oxygen saturation (SaO2) was below 80% in every case during apneas. Follow-up recordings with occluded tracheostomy were obtained 3-4 months after surgery. The weight reduction varied from 16.3 to 41.4% of the initial weight. The recording documented normal sleep apnea indices in three cases and partial recovery in the remainder; increase in stages 3, 4 and REM; normal SaO2 in three out of 4 cases. These findings suggest that gastroplasty may be used as an alternative treatment for weight reduction in selected OSA patients.
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PMID:[The role of gastroplasty in the treatment of obstructive sleep apnea]. 374 Nov 81

The presence of obesity, defined as weight 20 per cent or more above ideal body weight or increased body fat content, significantly increases risk of pulmonary, cardiovascular, metabolic, and gastrointestinal problems. Obesity is a major cause of shortened life expectancy. While obesity is not essential for the development of the obstructive sleep apnea syndrome, a significant percentage of patients with obstructive sleep apnea are obese. When evaluating these patients who have obstructive sleep apnea, it is important to search diligently for medical problems that are commonly found among the obese. While there is an increased incidence of obese patients among those who have obstructive sleep apnea, the exact reason for this is uncertain. The study of endorphins and enkephalins may expand our understanding of obesity, ventilatory regulation, and obstructive sleep apnea. This may, in fact, enable us to understand better the interrelationship between obesity and obstructive sleep apnea. The role that thyroid hormone, testosterone, and progesterone play in obstructive sleep apnea has also been reviewed. Patients who have obstructive sleep apnea should not be treated with testosterone. All patients given testosterone should be observed quite closely for the possible signs and symptoms of obstructive sleep apnea. Progesterone seems to be of some help in patients who have obesity hypoventilation syndrome. Its effectiveness in patients with obstructive sleep apnea is less clear. The obesity hypoventilation syndrome as described by Burwell is relatively uncommon. Many of the manifestations of the obesity hypoventilation syndrome, however, are found in patients with obstructive sleep apnea. The recognition that the symptoms stem from underlying obstructive sleep apnea offers great potential for therapy. Weight reduction is valuable therapy for patients with obesity and pulmonary dysfunction, obesity and obstructive sleep apnea, and obesity hypoventilation syndrome. Weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome. Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up.
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PMID:Obesity and hormonal factors in sleep and sleep apnea. 390 3

Patients with severe obesity and obstructive sleep apnea (OSA) have been shown to have abnormalities in respiratory muscle function and respiratory control. The present study was done to evaluate diaphragmatic function and the diaphragm fiber-length-compensating reflex in morbidly obese patients with OSA (1). Twelve normal subjects and 13 morbidly obese patients with OSA were studied in recumbent and upright positions. In the normal subjects, the diaphragm fiber-length-compensating reflex operated normally causing the diaphragm's inspiratory EMG to increase when the diaphragm's fibers shortened with assumption of the upright position. However, 8 of the 13 obese patients with OSA showed a decrease rather than an increase in the inspiratory diaphragmatic EMG on assuming the upright posture. Further data indicate greater diaphragmatic efficiency in the upright than in the supine position in a majority of the obese patients, a reversal of the normal response. Two possible explanations of these observations are: an abnormality of central respiratory control in obese patients with OSA and overstretching of the diaphragm in the recumbent obese patient. The observation of reduced maximal transdiaphragmatic pressures in the recumbent position in some of the obese patients with OSA supports the second explanation. Diaphragmatic overstretching may be an important mechanism in the development of hypoventilation in the morbidly obese.
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PMID:Diaphragmatic responses to body position changes in obese patients with obstructive sleep apnea. 394 77

The clinical course and characteristics of severe obstructive sleep apnea are described for 50 adults whose condition warranted recommendation for tracheostomy. All patients had a history of snoring, excessive daytime sleepiness and sleep attacks, nocturnal snorting and gasping sounds and observer-noted nocturnal breath cessations. Generally, these symptoms became manifest before age 40, their appearance tended to cluster together within only a few years and, invariably, they were chronic. Aside from snoring, excessive daytime sleepiness was on average often the first symptom and began at a mean age of 36 years. However, in half of the patients either hypertension or overweight preceded excessive daytime sleepiness by at least 1 year. Physicians in the office setting should suspect severe obstructive sleep apnea in patients who have loud snoring and either excessive daytime sleepiness, hypertension, or obesity. Further evidence of apnea can be obtained by determining the presence of the additional signs of loud nocturnal snorting and gasping sounds and nocturnal breath cessations.
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PMID:Severe obstructive sleep apnea--I: Onset, clinical course, and characteristics. 399 56

The etiology of the obesity-hypoventilation syndrome (OHS) is unknown. Recent reports that treatment of obstructive sleep apnea with nasal continuous positive-airway pressure eliminates the manifestations of OHS suggests that obstructive sleep apnea may contribute to OHS. The purpose of this study was to determine whether hypoxemia during sleep was more severe in patients with OHS than in those without OHS. In our sleep laboratory, we studied 32 subjects with a ratio of the forced expiratory volume in one second over the forced vital capacity (FEV1/FVC) greater than 0.73 and no neuromuscular disease. Seven subjects had OHS characterized by obesity and daytime hypercapnia, and 25 subjects did not. The seven patients with OHS all had sleep apnea. Of the 25 without OHS, 23 had sleep apnea. Subjects with OHS had significantly greater oxyhemoglobin desaturation during sleep than subjects without OHS, even when subjects with and without OHS were matched for sex and weight. These findings are consistent with the hypothesis that severe sleep apnea is a contributing cause of OHS.
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PMID:Oxyhemoglobin saturation during sleep in subjects with and without the obesity-hypoventilation syndrome. 400 62

Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.
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PMID:Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea. 406 66

Twenty-seven cases of adult sleep apnea are reported. The patients were studied with all-night polysomnography. Seven (26%) had predominately obstructive sleep apnea, while another seven (26%) had predominantly central sleep apnea. Thirteen patients (48%) were found to have a mixed pattern. Obesity was not a reliable guideline for predicting differential etiology. We conclude that sleep studies with specific monitoring are essential in the evaluation of the adult with sleep apnea prior to therapeutic intervention.
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PMID:Evaluation of the adult with sleep apnea. 662 51

Thirty-five patients diagnosed with obstructive sleep apnea syndrome (OSAS) underwent palatopharyngoplasty (PPP) after an objective evaluation. They were all monitored polygraphically after surgery. The group's postsurgical results were positive, with significant improvement in the apnea-hypopnea index (A + H index) and oxygen desaturation. However, patients with hypopharyngeal or mandibular problems or massive obesity had poor postsurgical results. As no subject has been followed for longer than two years, the long-term prognosis for this surgical approach is unknown.
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PMID:Palatopharyngoplasty and obstructive sleep apnea syndrome. 665 66

Although flow-volume curves are valuable in detecting extrathoracic airway obstruction, their role in testing patients with sleep-disordered breathing is undefined. To determine whether patients with sleep-disordered breathing have abnormal flow-volume curves consistent with variable extrathoracic obstruction, 60 subjects referred with suspected sleep disorders prospectively underwent spirometry and assessment of flow-volume curves. These tests were interpreted independent of the outcome of polysomnography. Fourteen of 35 subjects (40%) with sleep-disordered breathing had abnormal flow-volume curves consistent with variable extrathoracic airway obstruction, and 2 of 25 (8%) with no breathing disorder had extrathoracic obstruction (p less than 0.02). The presence of extrathoracic airway obstruction in subjects with mixed or obstructive sleep apnea did not correlate with age, the presence of snoring, excessive daytime hypersomnolence, obesity, or the severity of sleep apnea. Abnormal flow-volume curves were found more frequently in women who had no obvious structural upper airway abnormality. Because of the high specificity (92%) of the flow-volume curve, the finding of extrathoracic obstruction in patients with a history consistent with sleep-disordered breathing substantially increases the likelihood that sleep apnea is present.
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PMID:Abnormal inspiratory flow-volume curves in patients with sleep-disordered breathing. 730 12

Obstructive sleep apnea (OSA) occurs in about 10% of the middle-aged population but in about 30% of the hypertensive population of the same age. About 20% of the middle-aged population has hypertension but about 50% of patients with OSA have hypertension. Despite this close relationship between these two entities, previous attempts to determine whether the respiratory abnormalities in OSA were responsible for the hypertension were inconclusive, particularly because of the confounding effect of obesity which is common to both conditions. Data from recent observational and intervention studies, however, have succeeded in avoiding many of the pitfalls of earlier studies and it is now becoming evident that OSA may be a major cause of hypertension--responsible for about 30% of all cases. Successful treatment of OSA by any means has been shown in most studies to cause significant reductions in blood pressure throughout the 24 h period, while at the same time alleviating the vast array of symptoms and clinical abnormalities associated with this common and serious condition. Despite the encouraging results of these recent data, more studies are urgently required which should include larger numbers of patients and controls in order to clarify further the relationship between OSA and hypertension.
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PMID:Is obstructive sleep apnea a common cause of essential hypertension? 755 81


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