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

The reality of metabolic syndrome (MS) as a specific entity is debatable. However, the simple measure of waist circumference (>94 cm in men and >80 cm in women) is useful: (1) to check for insulin resistance by measuring serum levels of fasted glucose and insuline, cholesterol, triglycerides; (2) to look for diseases associated with MS such as hypertension, non alcohoolic steatohepatitis, sleep apnea, polycystic ovary disease, hypogonadism and to measure serum levels of ferritine, ALAT, ASAT, urate acid, CRP hs, testosterone and (3) to make obese people aware of their risk of becoming diabetic and to motivate them to change their life style. The utility of exercise and of various diets is discussed as well as the efficiency of drugs acting on different components of MS such as rimonabant, orlistat, metformin, glitazones, telmisartan and testosterone. The importance of political measures to fight the obesity epidemic is underlined.
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PMID:[Metabolic syndrome: jumble syndrome of obesity or specific entity? Which treatment: diet or polypill?]. 1838 74

Obesity is known to be a major aetiological factor in the development of hypertension. It also leads to dyslipidaemia and raised blood glucose. All of these are components of the metabolic syndrome. Thus, hypertension, as part of the syndrome, is often found together with these other abnormalities. Obesity raises blood pressure by a number of mechanisms, including activation of the sympathetic nervous system and the renin- angiotensin system. Apart from cardiovascular disease and diabetes, the metabolic syndrome is also associated with fatty liver disease, sleep apnoea and some malignancies. Measures to reduce obesity through lifestyle changes are therefore highly desirable, not because of reductions in blood pressure alone.
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PMID:Hypertension as part of the metabolic syndrome. 1854 89

Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Large-scale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed.
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PMID:Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components. 1859 41

Sleep-disordered breathing is highly prevalent in childhood obesity. Two recent cross-sectional studies have demonstrated an independent association between the severity of sleep-disordered breathing and the metabolic syndrome. A limited number of studies have also addressed the correlation between sleep-disordered breathing and insulin resistance, the core factor of the metabolic syndrome. Cross-sectional reports in modestly obese children are in favor of an association between sleep apnea and insulin resistance. However, these findings were not confirmed in studies of normal-weight children and of morbidly obese children. Only one out of three treatment studies before and after adenotonsillectomy confirmed the association between sleep apnea and insulin resistance, but only in obese children. Although statistical power issues and differences in patient characteristics might partially explain these contradicting results, the evidence to date is far from establishing a causal link between sleep-disordered breathing and insulin resistance. Longitudinal studies and randomized control trials are therefore warranted to investigate a possible causal link between sleep-disordered breathing and insulin resistance.
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PMID:Is sleep-disordered breathing an additional risk factor for the metabolic syndrome in obese children and adolescents? 1877 26

Obesity has reached epidemic proportions in much of the industrialized world, and is also increasing in prevalence in the developing world. In the later decades of the 20th century until present, there have been numerous epidemiological studies reporting the relationship between excess weight and total, or all-cause, mortality. Obesity is associated with a wide variety of comorbidities such as type 2 diabetes, systemic hypertension, cardiovascular disease, certain cancers and sleep apnea, most of which may lead to disability or death. In general, the risk of developing comorbidities such as diabetes and cardiovascular disease rises as body mass index (BMI) increases. Using BMI, an indicator of relative weight for height (kg/m(2)) and a frequently used surrogate for assessing excess body fat, epidemiological studies have found linear, U- or J-shaped relationships between total mortality and BMI. However, obesity is remarkably heterogeneous. Obese patients considered to be 'at risk' are mostly characterized by features associated with the metabolic syndrome. The aim of the present paper is to review the cardiovascular consequences of obesity and to review some of the literature emphasizing why the cardiologist should measure other indices of adiposity in order to refine clinical assessment of obese individuals.
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PMID:Targeting abdominal obesity in cardiology: can we be effective? 1878 31

Sleep-disordered breathing and sleep apnoea are conditions frequently associated with comorbidity, including obesity, diabetes, hypertension, insulin resistance (metabolic syndrome) and cardiovascular disease. The diabetic state (type 1 and type 2 diabetes) may be associated to diminished lung function and, in particular, decreased vital capacity, and the association between chronic obstructive pulmonary disease (COPD) and type 2 diabetes may be due to a shared inflammatory process. Also, the alteration in circulating endothelial progenitor cells found in respiratory disease, the metabolic syndrome and cardiovascular disease reflect a common condition of endothelial dysfunction.
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PMID:The metabolic syndrome, diabetes and lung dysfunction. 1882 64

Metabolic syndrome is a disorder characterized by abdominal obesity, hypertension, increased triglycerides, decreased HDL cholesterol and increased blood glucose. Accumulating evidence strongly indicates that insulin resistance and an increased amount of abdominal fat are the pathogenic factors for the characteristics of metabolic syndrome. The metabolic syndrome is characterized by an increased risk for the development of cardiovascular disease and type 2 diabetes mellitus. Studies indicate that sleep apnea may be a manifestation of the metabolic syndrome. It has also been suggested that the metabolic syndrome or "syndrome X" should also comprise obstructive sleep apnea and should then be called syndrome "Z". It appears that obstructive sleep apnea and the metabolic syndrome are characterized by the same pathophysiologic environment, which increases the risk for the development of cardiovascular disease. The increased amount of visceral fat and the accompanying insulin resistance seem to be the main characteristics responsible for the development of obstructive sleep apnea and the metabolic syndrome.
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PMID:Metabolic syndrome and sleep apnea. 1892 60

Despite the early recognition of the strong association between obstructive sleep apnoea (OSA) and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a "local abnormality" of the respiratory track rather than as a "systemic illness". In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. In subsequent studies, it was shown that IL-6, TNFalpha, and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat was the primary parameter linked with sleep apnoea. Further studies showed that women with the polycystic ovary syndrome (PCOS) were much more likely than controls to have sleep-disordered breathing (SDB) and daytime sleepiness, suggesting a pathogenetic role of insulin resistance in OSA. Additional accumulated evidence that supports the role of obesity and the associated metabolic aberrations in the pathogenesis of sleep apnoea and related symptoms include: obesity without sleep apnoea is associated with daytime sleepiness; the protective role of gonadal hormones as suggested by the increased prevalence of sleep apnoea in post-menopausal women and the significantly reduced risk for OSA in women on hormonal therapy; partial effects of continuous positive airway pressure (CPAP) in obese patients with apnoea on hypercytokinemia, insulin resistance indices, and visceral fat; and that the prevalence of the metabolic syndrome in the U.S. population from the Third National Health and Nutrition Examination Survey (1988-1994) parallels the prevalence of symptomatic sleep apnoea in general random samples. Furthermore, the beneficial effect of a cytokine antagonist on EDS and apnoea in obese, male apnoeics and that of exercise and weight loss on SDB and EDS in general random or clinical samples, supports the hypothesis that cytokines and insulin resistance are mediators of EDS and sleep apnoea in humans. Finally, our recent finding that in obese, hypothalamic CRH neuron is hypoactive, provides additional evidence on the potential central neural mechanisms for depressed ventilation and consequent development of sleep apnoea in obese individuals. In conclusion, accumulating evidence provides support to our thesis that obesity via inflammation, insulin resistance, visceral adiposity, and central neural mechanisms, e.g. hypofunctioning hypothalamic CRH, play a major role in the pathogenesis of sleep apnoea, sleepiness, and the associated cardiovascular co-morbidities.
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PMID:Does obesity play a major role in the pathogenesis of sleep apnoea and its associated manifestations via inflammation, visceral adiposity, and insulin resistance? 1894 82

The clinical relevance of the term "metabolic syndrome", the definition criteria, and predictive power are being disputed. Inclusion of sleep-disordered breathing and sleep apnoea into a definition of metabolic syndrome is also controversial once children and/or adolescents are affected. Nevertheless, along with the increasing prevalence of childhood obesity, the prevalence of the metabolic syndrome in obese children is reported at 30%, irrespective of the definition applied. Moreover, childhood obesity is associated with sleep-disordered breathing. Adipocytokines, cytokines secreted from adipose tissue, are thought to play a major role in the pathophysiology of metabolic syndrome. Leptin was initially suggested as a promising "anti-obesity" hormone. New concepts indicate that in humans leptin and its soluble receptor may be more important in states of energy deficiency rather than a predictor of the metabolic syndrome. Adiponectin, on the other hand, is not only related to obesity and insulin resistance, but appears to be the strongest predictor for metabolic syndrome, even in children. In newborns and infants, both adipocytokines occur in high concentrations, even though this cannot completely explain the increased risk for ensuing metabolic disease later in life. Finally, low-grade systemic inflammation may underlie the clustering of metabolic risk factors. Overall factors from the adipose tissue may constitute not only markers but also mediators of metabolic sequelae of obesity.
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PMID:Metabolic syndrome in children and adolescents--risk for sleep-disordered breathing and obstructive sleep-apnoea syndrome? 1894 84

Obstructive sleep apnea (OSA), a highly prevalent breathing disorder in sleep, characterized by intermittent and recurrent pauses in respiration, has emerged as an independent risk factor for cardiovascular morbidity and mortality. Accumulated evidence implicates Leukocyte-endothelial cell activation and adhesion as critical components that induce inflammation and injury to the vasculature resulting in the development of cardiovascular complications. Similar cellular interactions were described in conditions of ischemia/reperfusion, and various components of the metabolic syndrome as hypercholesterolemia and hypertension. The hallmark of sleep apnea--the multiple cycles of hypoxia/reoxygenation--promote oxidative stress and inflammation. These facilitate increased interactions of blood cells with endothelial cells, resulting in endothelial cell injury and dysfunction. Such events can promote atherosclerosis and the development of cardiovascular morbidities in OSA. However, inter-individual differences in response to intermittent hypoxia and activation of anti-inflammatory cytokine profiles in T lymphocytes can serve as protective mechanisms.
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PMID:Biology of peripheral blood cells in obstructive sleep apnea--the tip of the iceberg. 1894 85


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