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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid deficiency states are now a well recognized cause of the sleep apnea syndrome. The spectrum of disease ranges from mild, asymptomatic hypothyroidism to severe myxedema, and the disorder is associated with both obstructive and central types of sleep apnea. A variety of factors may be involved, including upper airway obstruction with or without obesity, and alterations in ventilatory drive. The definitive therapy is thyroid hormone replacement, which has been shown to diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency. The incidence of thyroid deficiency states in patients with sleep apnea syndrome is not known, but it seems reasonable to evaluate thyroid function in all patients. Thyroid replacement therapy seems logical for the treatment of sleep apnea in patients with previously unrecognized subclinical hypothyroidism. Much remains to be learned about the diagnosis and treatment of sleep apnea syndromes associated with thyroid hormone deficiency, and further studies are needed.
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PMID:Sleep apnea and hypothyroidism. 305 27

In a double-blind placebo controlled randomised study, the effects of almitrine bismesylate on the sleep induced Hb desaturations, associated or not with disorders of breathing, were tested. Patients (37-75 yrs, 8M and 2F) were affected by chronic bronchitis (out of any exacerbation) and obesity (weight excess at least 20%). They were known to have at least one nocturnal episode of hypoxemia (SaO2 fall higher or equal to 10%) with respect to the wakefulness level. Patients received either placebo or almitrine (1.5 mg/Kg/day) for 18 days and nocturnal polysomnography was performed both before and the last day of treatment. Almitrine induced an increase in PaO2 during wakefulness (p less than .05), an increase in mean SaO2 during sleep (p less than .01) and a decrease in the quantity of desaturation (Qd) during sleep, defined as the product of the mean desaturation by the duration of the episodes of desaturation (p less than .025). No clear effect could be observed either on the mean duration of the sleep disordered breathing (SDB) events or on their frequency whereas the desaturations due to them had a decrease.
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PMID:Effects of almitrine bismesylate on nocturnal hypoxemia in patients with chronic bronchitis and obesity. 309 64

To assess the relative contributions of age, gender, obesity, pulmonary function, and the severity of sleep-induced respiratory abnormalities to the development of alveolar hypoventilation in patients with occlusive sleep apnea syndrome, prospective data from III patients with occlusive sleep apnea were analyzed by stepwise logistic and multiple regression techniques. The significant variables in a logistic regression model predicting the presence of hypercapnia were daytime arterial oxygen pressure (PaO2; p less than 0.0001) and gender (p less than 0.04), the latter reflecting the higher number of hypercapnic women in our patient population. Multiple regression analysis performed in the hypercapnic group to study the determinants of the severity of elevation of arterial carbon dioxide tension (PaCO2) revealed significant contribution from the PaO2, the apnea-plus-hypopnea index (AHI), and the percent predicted forced vital capacity (r2 = 0.56; p less than 0.0001), whereas in the normocapnic patients, PaCO2 related to PaO2 only. These results suggest that daytime hypoxemia, mechanical impairment of the respiratory system due to obesity or obstructive airway disease (or both), and the severity of sleep-induced respiratory abnormalities as assessed by AHI contribute to the severity of carbon dioxide retention in patients with occlusive sleep apnea in a multifactorial fashion.
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PMID:Determinants of hypercapnia in occlusive sleep apnea syndrome. 311 99

Sleep apnea syndrome (SAS) is a rare disorder which is being diagnosed more often with increasing knowledge among physicians and patients. SAS presents with daytime hypersomnolence, intellectual deterioration and personality changes, chiefly in obese men, and is caused by intermittent upper airway obstruction during sleep at the level of the mesopharynx. Consecutive repetitive apneas of more than 10 seconds' duration are immediately abolished by pneumatic splinting with continuous positive pressure of 5 to 15 cm H2O with a nasal mask (nCPAP). A case report on a 31-year-old man with obesity and hypercapnia demonstrates that, although nCPAP by itself does not lead to weight reduction, it is more acceptable than surgical therapy (tracheostomy or uvulopalatopharyngoplasty).
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PMID:[Continuous nasal positive pressure respiration (nCPAP) as a therapeutic possibility in the sleep apnea syndrome]. 327 74

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Morbid obesity is not infrequently associated with severe respiratory impairment. In our experience approximately 10 per cent of morbidly obese patients who underwent gastric surgery had severe respiratory impairment. Respiratory insufficiency of obesity can be divided into two primary breathing disorders: the obstructive sleep apnea syndrome (SAS) and the obesity hypoventilation syndrome (OHS). In its most severe form, when both SAS and OHS are present, it is called the Pickwickian syndrome. In our series 59 morbidly obese patients with respiratory insufficiency secondary to obesity underwent gastric surgery for weight reduction. Fourteen had OHS, 19 had SAS and 26 had both. Of these, two patients died of postoperative complications and one died at five weeks with an inconclusive autopsy, totalling an operative mortality rate of 3.4 per cent and a total mortality of 5.1 per cent. In our overall experience morbidly obese patients lost 67 per cent of excess weight after gastric procedures. In conclusion, surgically induced weight loss will markedly improve or correct respiratory insufficiency secondary to obesity. It will improve arterial oxygenation, minimize CO2 retention, expand lung volumes, correct polycythemia, and reduce apnea frequency. The magnitude of changes in these variables is clinically significant. Therefore, respiratory insufficiency of obesity should be considered a major indication for an aggressive approach to weight reduction. The jejunoileal bypass and unbanded gastroplasty operations have an unacceptable incidence of complications or failure, respectively. There is a high degree of recidivism following dietary programs. Sweets eaters will not do well with a gastroplasty procedure. Gastric bypass for individuals addicted to sweets or the vertical banded gastroplasty for "gorgers" are currently our procedures of choice and are associated with the average loss of two thirds of excess weight and correction of breathing problems associated with morbid obesity.
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PMID:Pulmonary function in morbid obesity. 331 3

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Morbid obesity is often associated with severe respiratory insufficiency, commonly known as the pickwickian syndrome. This can be divided into the following two primary breathing disorders which can affect patients alone or in combination: the obstructive sleep apnea syndrome (SAS); and the obesity-hypoventilation syndrome (OHS). Thirty-eight (14 percent) of 263 morbidly obese patients with respiratory insufficiency of obesity underwent gastric surgery for weight reduction. Ten had OHS, nine has SAS, and 19 had both. Of these patients, one died of postoperative complications, one died at five weeks with an inconclusive autopsy, one was lost to follow-up, and the time since surgery was too short (less than three months) in three. A total of 30 patients lost 45 +/- 25 percent (p less than 0.0001) of excess body weight within 3 to 12 months following surgery, when repeat pulmonary studies were done. Most patients continued to lose additional weight until two years, when they had lost 62 +/- 26 percent of excess weight. Nine patients failed initial surgery (gastroplasty); seven of these were successfully converted to gastric bypass. Weight loss was associated with a significant decrease in the percentage of sleep apnea from 44 +/- 15 to 8 +/- 11 (p less than 0.0001). In patients with OHS, the arterial oxygen pressure (PaO2) increased from 53 +/- 9 to 68 +/- 11 mm Hg (p less than 0.0001), and the arterial carbon dioxide tension decreased from 51 +/- 7 to 41 +/- 4 mm Hg (p less than 0.0001). Pulmonary function tests in the patients with OHS revealed significant increases, as a percentage of predicted normal, in the forced vital capacity, forced expiratory volume in one second, expiratory reserve volume, functional residual capacity, and total lung capacity. Secondary polycythemia, defined as a hemoglobin level greater than 16 g/dl associated with a PaO2 less than 60 mm Hg, was noted in 13 of 29 patients with OHS. This fell from 16.9 +/- 1.1 to 14.9 +/- 1.7 g/dl (p less than 0.001) after weight loss and improved pulmonary function.
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PMID:Gastric surgery for respiratory insufficiency of obesity. 372 Mar 90


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