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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the possible relationship between sleep apnea syndrome (SAS) and diabetes mellitus, we first examined the prevalence of SAS among 12,787 general patients (6554 males and 6233 females) who visited Katsumata Hospital at Nagoya, Japan. Among them, thirty-five males and five females were diagnosed as having SAS. The male patients were statistically analysed by the corrected Mantel-Haenszel chi-square test taking the body type into account, and it was found that the prevalence of SAS was significantly high both in a diabetic population and in a hypertensive one. Among 40 SAS patients of both sexes, 34 were given a glucose tolerance test (GTT) with oral administration of 75 g glucose. Thirteen showed a diabetic pattern, 12 a borderline pattern and only 9 had a normal pattern. All 13 diabetic patients had non-insulin-dependent type diabetes (NIDDM). The present results showed that SAS has a close relationship not only to hypertension but also to NIDDM.
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PMID:High incidence of sleep apnea syndrome in a male diabetic population. 177 13

The frequent association of sleep apnea syndrome and essential hypertension led to think of sleep apnea as an etiology of hypertension, especially as a good correlation has been found between the severity of both diseases. Moreover, treating the apnea syndrome results in a decrease of blood pressure. The aim of our study is to depict the outlines of a severe hypertensive individual with sleep apnea by comparing 9 men primarily referred to the hypertension clinic with refractory hypertension and finally found to have sleep apnea (study group) to 23 men whose diagnosis of sleep apnea was made in the pulmonary unit (controls). Fifteen of these were hypertensives. Mean age of the study group was 47 +/- 7 years vs 60 +/- 11. Controls were less overweighted: BMI = 33 +/- 6 kg/m3 vs 39 +/- 5. Mean blood pressure was 171 +/- 16/107 +/- 4 mmHg in the study group vs 157 +/- 19/92 +/- 12 mmHg in controls. Prevalence of glucose metabolism disorders was significantly greater in the study group: 6 patients with maturity onset diabetes and 3 with proven glucose intolerance, vs respectively 4 and 6 controls. Triglycerides were elevated in both groups whereas mean cholesterol was slightly above normal values. Six patients of the study group could have an echocardiogram which showed left ventricular hypertrophy (mean left ventricular mass index = 206 +/- 31 g/m2 after the Penn convention).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Should arterial hypertension in sleep apnea syndrome be stressed?]. 183 55

A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.
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PMID:The sleep apnoea syndrome in obesity: risk of sudden death. 186 65

Cerebral edema occurs in fatal cases of acute mountain sickness. Dexamethasone, commonly used to treat cerebral edema due to other causes, also reduces the symptoms of acute mountain sickness when given prophylactically. However, the efficacy of dexamethasone in the treatment of established acute mountain sickness remains uncertain. To investigate this question, we exposed six men in a hypobaric chamber to a simulated altitude of 3700 m (barometric pressure, 64 kPa [481 mm Hg]) for 48 hours on two occasions. Acute mountain sickness was diagnosed with use of a symptoms questionnaire, and dexamethasone (4 mg every six hours) or placebo was then given in a randomized, double-blind, crossover fashion. Dexamethasone reduced the symptoms of acute mountain sickness by 63 percent (P less than 0.05), whereas placebo had a minimal effect (reduction by 23 percent; P not significant). In spite of this response, one subject had mild cerebral edema on brain CT after both placebo and dexamethasone. Dexamethasone had no effect on fluid shifts, oxygenation, sleep apnea, urinary catecholamine levels, the appearance of chest radiographs or perfusion scans, serum electrolyte levels, hematologic profiles, or the results of psychometric tests. Dexamethasone treatment was complicated by mild hyperglycemia in all subjects (mean [+/- SE] glucose level, 7.3 +/- 1.3 mmol per liter [132 +/- 23 mg per deciliter]). We conclude that dexamethasone effectively reduces the symptoms of acute mountain sickness. However, it did not improve objective physiologic abnormalities related to exposure to high altitudes. We therefore recommend that dexamethasone be used only when descent is impossible, or to facilitate cooperation in evacuation efforts.
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PMID:Dexamethasone in the treatment of acute mountain sickness. 1168 Apr 63

The authors suggest the hypothesis that the obesity often associated with sleep apnea syndromes is related to changes in HG secretion. Indeed, as HG secretion is sleep related any disturbances due to apnea during may alter the GH secretion. In order to test their hypothesis the authors studied, during the course of 24-hour polygraphic recordings, the levels of HG, blood glucose and free fatty acids, in 16 subjects, 14 of whom were obese and 9 of whom had the sleep apnea syndrome. The results obtained confirmed the relationship between the number of apnea and the stability of sleep. They also demonstrated a relationship between GH secretion and both the stability of sleep and obesity. These results, therefore, suggest that apnea plays a role in obesity development.
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PMID:[Nycterohemeral variations in plasma growth hormone (GH) levels and sleep apnea syndromes: their relationship with obesity (author's transl)]. 730 33

This report concerns the relative contributions of body weight and sleep apnea to the following cardiovascular risk factors: blood pressure, fasting insulin and fasting glucose. We cross-sectionally examined the relationship of various levels of apneic activity [apnea-hypopnea index (AHI)] and a measure of obesity [body mass index (BMI)] to mean morning blood pressure and fasting serum insulin and fasting blood glucose concentrations sampled the morning after polysomnography. Subjects were 261 males (age 47 +/- 13 years, mean +/- SD), who were referred to a sleep laboratory for symptoms of sleep-disordered breathing. The dependent variables, mean morning blood pressure, insulin and fasting blood glucose (FBG) levels, were significantly related to both AHI (eta'2 = 0.10) and BMI (eta'2 = 0.18). AHI and BMI combined to account for approximately 30% of the variability in the best linear combination of these three factors. Further analysis indicated that mean morning blood pressure and fasting insulin levels each correlated positively with BMI and AHI, whereas FBG correlated only with BMI. We conclude that, although these data do not prove a causal relationship, there is evidence for an independent association between sleep apnea and not only blood pressure, but also fasting insulin levels.
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PMID:Insulin levels, blood pressure and sleep apnea. 784 59

The present study was to investigate the effect of four different antihypertensive medications [atenolol, hydrochlorothiazide (HCTZ), isradipine and spirapril] on the blood pressure and metabolic state of 18 patients with obstructive sleep apnoea. All patients received each of the drugs for a period of 8 weeks according to a randomized crossover design. Although all of the medications decreased systolic blood pressure (SBP), only spirapril decreased SBP significantly (17 +/- 15 mmHg; p < 0.001). All of the medications decreased diastolic blood pressure (DBP) significantly, but spirapril produced the greatest reduction (5-8 vs 10 mmHg, respectively). Both HCTZ and isradipine increased fasting serum total cholesterol concentration (0.3 +/- 0.5 and 0.3 +/- 0.4 mmol/l, respectively; p < 0.05). Atenolol decreased fasting serum high-density lipoprotein (HDL)-cholesterol concentration significantly (0.12 +/- 0.15 mmol/l; p < 0.01). Both HCTZ and isradipine increased fasting serum glucose concentration significantly (0.7 +/- 0.8 mmol/l and 0.6 +/- 0.7 mmol/l, respectively; p < 0.01). No significant effect on serum lipid and glucose levels was observed with spirapril. On the basis of these results, spirapril was the best medication for hypertensive patients with obstructive sleep apnoea.
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PMID:Effects of antihypertensive medication on hypertension in patients with sleep apnoea. 806 54

The United States is experiencing an epidemic of obesity among both adults and children. Approximately 35 percent of women and 31 percent of men age 20 and older are considered obese, as are about one-quarter of children and adolescents. While government health goals for the year 2000 call for no more than 20 percent of adults and 15 percent of adolescents to be obese, the prevalence of this often disabling disease is increasing rather than decreasing. Obesity, of course, is not increasing because people are consciously trying to gain weight. In fact, tens of millions of people in this country are dieting at any one time; they and many others are struggling to manage their weight to improve their appearance, feel better, and be healthier. Many programs and services exist to help individuals achieve weight control. But the limited studies paint a grim picture: those who complete weight-loss programs lose approximately 10 percent of their body weight, only to regain two-thirds of it back within 1 year and almost all of it back within 5 years. These figures point to the fact that obesity is one of the most pervasive public health problems in this country, a complex, multifactorial disease of appetite regulation and energy metabolism involving genetics, physiology, biochemistry, and the neurosciences, as well as environmental, psychosocial, and cultural factors. Unfortunately, the lay public and health-care providers, as well as insurance companies, often view it simply as a problem of willful misconduct--eating too much and exercising too little. Obesity is a remarkable disease in terms of the effort required by an individual for its management and the extent of discrimination its victims suffer. While people often wish to lose weight for the sake of their appearance, public health concerns about obesity relate to this disease's link to numerous chronic diseases that can lead to premature illness and death. The scientific evidence summarized in Chapter 2 suggests strongly that obese individuals who lose even relatively small amounts of weight are likely to decrease their blood pressure (and thereby the risk of hypertension), reduce abnormally high levels of blood glucose (associated with diabetes), bring blood concentrations of cholesterol and triglycerides (associated with cardiovascular disease) down to more desirable levels, reduce sleep apnea, decrease their risk of osteoarthritis of the weight-bearing joints and depression, and increase self-esteem. In many cases, the obese person who loses weight finds that an accompanying comorbidity is improved, its progression is slowed, or the symptoms disappear. Healthy weights are generally associated with a body mass index (BMI; a measure of whether weight is appropriate for height, measured in kg/m2) of 19-25 in those 19-34 years of age and 21-27 in those 35 years of age and older. Beyond these ranges, health risks increase as BMI increases. Health risks also increase with excess abdominal/visceral fat (as estimated by a waist-hip ratio [WHR] > 1.0 for males and > 0.8 for females), high blood pressure (> 140/90), dyslipidemias (total cholesterol and triglyceride concentrations of > 200 and > 225 mg/dl, respectively), non-insulin-dependent diabetes mellitus, and a family history of premature death due to cardiovascular disease (e.g., parent, grandparent, sibling, uncle, or aunt dying before age 50). Weight loss usually improves the management of obesity-related comorbidities or decreases the risks of their development. The high prevalence of obesity in the United States together with its link to numerous chronic diseases leads to the conclusion that this disease is responsible for a substantial proportion of total health-care costs. We estimate that today's health-care costs of obesity exceed $70 billion per year.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Weighing the options: criteria for evaluating weight-management programs. The Committee to Develop Criteria for Evaluating the Outcomes of Approaches to Prevent and Treat Obesity. 865 36

Fifty healthy, normotensive individuals (34 women) with a mean age of 44.3 +/- 13.2 yr and a mean body mass index of 27.1 +/- 5.4 kg/m2 were tested for the presence or absence of insulin resistance and sleep-disordered breathing. The hypothesis of this investigation was that insulin resistance is associated with sleep-disordered breathing. In vivo insulin action with determination of steady-state plasma glucose (SSPG) and insulin was measured using simultaneous intravenous infusion of somatostatin, glucose, and insulin via a Harvard pump. Determination of sleep-disordered breathing was performed through clinical assessment and portable nocturnal monitoring using a validated sleep apnea recorder. Individuals with > or = 10 hypoxic respiratory events per hour of sleep were significantly more insulin-resistant than subjects without sleep-breathing disorders. After adjusting the relationship between insulin resistance and sleep-disordered breathing for potential confounding variables, it was found that this relationship was entirely dependent on body mass.
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PMID:Insulin resistance and sleep-disordered breathing in healthy humans. 868 Jun 75

There exist real and potential links between the risk factors for and co-morbidity associated with diabetes and sleep apnea. The common occurrence of obesity, hypertension, and disorders of metabolism in each disease is but one example. While the occurrence of sleep apnea with glucose intolerance or insulin resistance could present sampling bias or intersection of common human diseases, an alternative hypothesis is that the events in obstructive sleep apnea (OSA) trigger different, perhaps unique, adaptations in metabolic processes involving insulin action and glucose regulation. Further, clinical studies can be designed to define the extent and potential mechanisms for alterations in insulin and glucose levels in OSA and to determine the sample size and power for a longitudinal study that would follow the relative rates of progression of obesity (including neck size as a body characteristic), breathing abnormalities during sleep, insulin sensitivity, and subsequent risk for non-insulin-dependent diabetes mellitus (NIDDM) and/or symptomatic OSA.
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PMID:Diabetes and sleep apnea. 908 17


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