Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The obstructive sleep apnea syndrome (OSAS) is characterized by collapse of the upper airway during sleep, recurring apneas, intermittent hypoxemia and daytime somnolence. OSAS is often associated with obesity, and its prevalence is expected to rise due to the obesity epidemics worldwide. OSAS is associated with increased cardiovascular risk which appears to be normalized by treatment with nasal continuous positive airway pressure (nCPAP) during sleep, suggesting an independent role of OSAS in accelerating atherosclerosis. Insulin resistance (IR) and the metabolic syndrome (MetS) are often found in OSAS patients, but the relative role played by OSAS and obesity is still unclear. Both OSAS and MetS may exert negative synergistic effects on the cardiovascular system through multiple mechanisms (hypoxemia, sleep disruption, activation of the sympathetic nervous system, inflammatory activation). Besides nCPAP treatment, pharmacologic interventions to treat obesity and the MetS could improve cardiovascular prevention in OSAS.
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PMID:Metabolic effects of the obstructive sleep apnea syndrome and cardiovascular risk. 1872 87

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a complex disease with multifactorial etiology. It is marked by the occurrence of apnea and hypopnea events caused by repeated obstructions of the upper airways. OSAHS is strongly associated with obesity, and the prevalence of this disease in morbidly obese patients is very high. Nevertheless, not all patients with OSAHS are obese, and for this reason, there may be other anatomical predispositions to airway collapse. In obese patients, fatty deposition in the parapharyngeal region results in airway reduction and predisposes to airway collapse, worsened by neurologic loss of the normal dilator muscle tone of the neck. However, in nonobese patients, specific craniofacial characteristics such as posterior air pharyngeal space, tongue length, hyoid position, and maxillomandibular deficiencies may predispose some people to develop OSAHS. Treatment strategies for OSAHS patients vary from clinical treatment with continuous positive airway pressure, oral appliances, or medications for mild and moderate OSAHS patients, bariatric surgery for severe obese OSAHS patients to maxillomandibular advancement for obese or nonobese OSAHS patients.
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PMID:Obstructive sleep apnea-hypopnea syndrome--the role of bariatric and maxillofacial surgeries. 1912 88

Obstructive sleep apnoea syndrome (OSAS), due to the collapse of the upper airways, is a common but still underestimated condition. The 'dose-response' type relationship between OSAS and hypertension (HT) has now been clearly proven. There are multiple mechanisms explaining this relationship, the main one being an increase in sympathetic activity during the apnoeas. HT associated with OSAS has several characteristics: high prevalence, diastolic and nocturnal predominance, and frequent non-dipper status. Furthermore, as OSAS is found in the majority of subjects with refractory HT, it should be systematically investigated in this situation. HT associated with OSAS should be tested for by means of a clinical blood pressure (BP) measurement, to which 24-h ambulatory BP monitoring (ABPM) is often added due to the fact that BP anomalies are frequently present at night. HT during OSAS is frequently associated with metabolic anomalies (for example, obesity, dyslipidaemia and insulin resistance), therefore explaining the high prevalence of metabolic syndrome in this population. The reference treatment for OSAS-nasal continuous positive airway pressure (nCPAP)-seems to be able to lower the BP of hypertensive patients, especially if the HT is severe, untreated or refractory. Moreover, the BP response to nCPAP depends on the severity of the OSAS, in particular the scale of the nocturnal desaturations, and on patient tolerance of the treatment. Optimal treatment for HT associated with OSAS has not been evidenced. Antihypertensive drugs do not change the respiratory parameters during OSAS.
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PMID:Hypertension and obstructive sleep apnoea syndrome: current perspectives. 1912 54

Sleep-induced apnea and disordered breathing refers to intermittent, cyclical cessations or reductions of airflow, with or without obstructions of the upper airway (OSA). In the presence of an anatomically compromised, collapsible airway, the sleep-induced loss of compensatory tonic input to the upper airway dilator muscle motor neurons leads to collapse of the pharyngeal airway. In turn, the ability of the sleeping subject to compensate for this airway obstruction will determine the degree of cycling of these events. Several of the classic neurotransmitters and a growing list of neuromodulators have now been identified that contribute to neurochemical regulation of pharyngeal motor neuron activity and airway patency. Limited progress has been made in developing pharmacotherapies with acceptable specificity for the treatment of sleep-induced airway obstruction. We review three types of major long-term sequelae to severe OSA that have been assessed in humans through use of continuous positive airway pressure (CPAP) treatment and in animal models via long-term intermittent hypoxemia (IH): 1) cardiovascular. The evidence is strongest to support daytime systemic hypertension as a consequence of severe OSA, with less conclusive effects on pulmonary hypertension, stroke, coronary artery disease, and cardiac arrhythmias. The underlying mechanisms mediating hypertension include enhanced chemoreceptor sensitivity causing excessive daytime sympathetic vasoconstrictor activity, combined with overproduction of superoxide ion and inflammatory effects on resistance vessels. 2) Insulin sensitivity and homeostasis of glucose regulation are negatively impacted by both intermittent hypoxemia and sleep disruption, but whether these influences of OSA are sufficient, independent of obesity, to contribute significantly to the "metabolic syndrome" remains unsettled. 3) Neurocognitive effects include daytime sleepiness and impaired memory and concentration. These effects reflect hypoxic-induced "neural injury." We discuss future research into understanding the pathophysiology of sleep apnea as a basis for uncovering newer forms of treatment of both the ventilatory disorder and its multiple sequelae.
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PMID:Pathophysiology of sleep apnea. 2008 74

Objective. Obesity is a significant contributor to oxygen demand and dynamic airway obstruction. The objective of the current study is to determine the long-term success of conservative measures directed toward weight reduction on airway management without respect to specific airway disease etiology. Methods. Patients with chronic airway obstruction secondary anatomic lesions or obstructive sleep apnea were recruited and followed prospectively. Demographics, initial and final weights, diagnosis, and followup information were recorded. Patients were referred to a registered dietician, provided counseling, and started on a weight-loss regimen. Outcome measures were change in body mass index (BMI) and rate of decannulation from weight loss alone. Results. Of fourteen patients, ten remained tracheostomy-dependent and four had high-grade lesions with the potential for improvement in oxygen demand and dynamic airway collapse with weight loss. The mean follow up period was 25 months. The mean change in BMI was an increase of 1.4 kg/m(2) per patient. Conclusions. Conservative measures alone were not effective in achieving weight reduction in the population studied. This may be due to comorbid disease and poor compliance. The promise of decannulation was an insufficient independent motivator for weight loss in this study. Although the theoretical benefits of weight loss support its continued recommendation, the long-term success rate of conservative measures is low. More aggressive facilitated interventions including pharmacotherapy or bariatric surgery should be considered early in the course of treating airway disease complicated by obesity.
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PMID:Efficacy of a conservative weight loss program in the long-term management of chronic upper airway obstruction. 2010 69

Obstructive sleep apnea (OSA) is an increasingly common disorder. It is characterized by frequent episodes of airway obstruction associated with a reduced caliber of the upper airway and is vulnerable to further narrowing and collapse. Acute and repetitive effects of apnea and hypopnea include oxygen desaturation, reduction in intrathoracic pressure, excessive daytime sleepiness, impaired executive function and central nervous system arousals. The apnea-hypopnea index and respiratory distress index help quantify the severity of the condition. The condition is associated with several clinical symptoms of which daytime sleepiness is considered the cardinal symptom. Obesity is one of the major predisposing factors. Three types of apneas have been recognized -obstructive, central and mixed; OSA is the commonest. This review will cover aspects of their radiologic features, diagnosis and management.
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PMID:Obstructive sleep apnea: clinical and diagnostic features. 2013 77

Obstructive sleep apnea syndrome (OSAS) is an often underestimated sleep disorder that has been associated with cardiovascular disease. OSAS is characterized by cycles of apnea and/or hypopnea during sleep caused by the collapse of the upper airways. Intermittent hypoxia deriving from the cycles of apnea/arousals (to retrieve the ventilation) plays a pivotal role in the pathogenesis of the disease. Obesity is the most frequent predisposing condition of OSAS. Recent evidence suggests that OSAS could be considered as a pro-atherosclerotic disease, independently of visceral fat amount. Oxidative stress, cardiovascular inflammation, endothelial dysfunction, and metabolic abnormalities in OSAS could accelerate atherogenesis. The present review is focused on the possible pathophysiological mediators which could favor atherosclerosis in OSAS.
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PMID:Inflammation accelerates atherosclerotic processes in obstructive sleep apnea syndrome (OSAS). 2019 12

Obstructive sleep apnoea (OSA) is increasingly being recognized as an important health issue in the last two to three decades. It is characterized by frequent episodes of upper airway collapse during sleep, causing recurrent arousals, intermittent hypoxaemia, sleep fragmentation and poor sleep quality. There is accumulating evidence that OSA is being considered as an independent risk factor for hypertension, glucose intolerance / diabetes mellitus, cardiovascular diseases and stroke, leading to increased cardiometabolic morbidity and mortality. The prevalence rates of OSA have been estimated in the range of 2 to 10 per cent worldwide, and the risk factors for obstructive sleep apnoea include advanced age, male sex, obesity, family history, craniofacial abnormalities, smoking and alcohol consumption. The common clinical presenting symptoms are heavy snoring, witnessed apnoeas and daytime hypersomnolence, which would help to identify the affected individuals. With increasing awareness of this disease entity and associated complications in our society, there have been increased referrals to sleep physicians or expertise for further investigations and diagnostic evaluation. Early recognition and treatment of obstructive sleep apnoea may prevent from adverse health consequences. Some of the epidemiological aspects of obstructive sleep apnoea in adults are reviewed.
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PMID:Obstructive sleep apnoea: definitions, epidemiology & natural history. 2030 41

Obstructive sleep apnoea (OSA) is a highly prevalent condition with proven neurocognitive and cardiovascular consequences. OSA patients experience repetitive narrowing or collapse of the pharyngeal airway during sleep. Multiple factors likely underlie the pathophysiology of this condition with considerable inter-individual variation. Important risk factors for OSA include obesity, male gender, and ageing. However, the mechanisms underlying these major risk factors are not well understood. We briefly review the state-of-the-art knowledge regarding OSA pathogenesis in adults and highlight the potential role of genetics in influencing key OSA pathophysiological traits.
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PMID:Pathophysiology & genetics of obstructive sleep apnoea. 2030 43

Sleep is an essential part of our daily living, and sleep disturbances may intervene with the biological and physiological processes in human body leading to the development of metabolic dysfunction. Short sleep duration and poor sleep quality have adverse effects on metabolism and hormonal processes, contributing to increased cardiovascular risk. Obstructive sleep apnoea is a chronic condition characterized by repetitive upper airway collapse during sleep, causing intermittent hypoxaemia, recurrent arousals and sleep fragmentation. Sleep disturbances can increase sympathetic activity, provoke systemic inflammation and oxidative stress, and impair vascular endothelial function. Obstructive sleep apnoea is increasingly recognized to be an independent cardiovascular risk factor. There is intense research interest in the association between obstructive sleep apnoea and the metabolic syndrome - the constellation of inter-related metabolic derangements including central obesity, hypertension, insulin resistance and dyslipidaemia, which appears to directly promote the development of atherosclerosis. The underlying pathophysiologic pathways or mechanistic links between obstructive sleep apnoea and metabolic syndrome have not been well delineated. This article reviews the current knowledge of the relationship between sleep disturbances, sleep-disordered breathing and the metabolic syndrome in adults.
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PMID:Sleep & the metabolic syndrome. 2030 46


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