Sleep apnoea syndrome in 2011: current concepts and future directions

Lévy, Patrick; Tamisier, Renaud; Minville, Caroline; Launois, Sandrine; Pépin, Jean‐Louis

doi:10.1183/09059180.00003111

Cited by 61 publications

(46 citation statements)

References 190 publications

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“…Although significant evidence links OSA to proatherogenic factors, such as the metabolic syndrome [9][10][11][12], systemic inflammation [13][14][15] and oxidative stress [16,17], little is known about the role of genetic factors for increasing atherosclerotic risk in OSA. In particular, no data are available on potential links between OSArelated dyslipidaemia and susceptibility genes for dyslipidaemia in such patients.…”

Section: Introductionmentioning

confidence: 99%

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Tisko

Sopkova

Habalová

et al. 2013

European Respiratory Journal

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There is increasing evidence that intermittent hypoxia resulting from obstructive sleep apnoea (OSA) is independently associated with dyslipidaemia. Currently, no data exist on potential links between OSA-related dyslipidaemia and susceptibility genes for dyslipidaemia in such patients. Our aim was to study the effects of the apolipoprotein E (APOE) genotype and sleep apnoea severity on atherogenic dyslipidaemia in patients with OSA.519 clinically stable subjects prospectively recruited at a tertiary referral teaching hospital underwent full polysomnography. APOE gene polymorphisms were assessed using real-time PCR.In all APOE genotype groups, serum triglycerides increased while high-density lipoprotein (HDL) cholesterol was reduced with increasing severity of OSA in each APOE genotype group, whereas the deleterious effects of OSA on serum apolipoprotein (Apo)B levels were observed in e2 carriers and the e3/e3 genotype only. Nevertheless, the e4 allele carriers had ApoB levels within the risk range, irrespective of nocturnal hypoxia. In addition, among patients with the high-risk e4 genotype, those with the most severe nocturnal hypoxia had significantly higher triglyceride and lower HDL cholesterol levels compared with nonhypoxic e4 subjects. APOE genotype and the oxygen desaturation index were both independent predictors of serum triglyceride levels (p50.009 and p,0.001, respectively; R 2 50.148) and ApoB levels (p50.001 and p50.003, respectively; R 2 50.104). Our findings suggest that OSA has adverse effects on several lipid parameters over and above the effects carried by APOE genotype. Further st1udies are needed to analyse the effects of high-risk genotypes on metabolic and cardiovascular outcomes in patients with OSA. @ERSpublications OSA has adverse effects on several lipid parameters in addition to the effects carried by the APOE genotype

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Section: Introductionmentioning

confidence: 99%

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Tisko

Sopkova

Habalová

et al. 2013

European Respiratory Journal

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“…In inherited metabolic diseases and suspected OSAS the assessments based upon clinical history alone are generally inadequate [105,123,124]. Overnight polysomnography is the first-line procedure in MPS and suspected upper airways involvement [104].…”

Section: Approach To Diagnosis and Treatment Of Respiratory Manifestamentioning

confidence: 99%

Respiratory manifestations in patients with inherited metabolic diseases

Santamaria

Montella

Mirra

et al. 2013

European Respiratory Review

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Growing evidence indicates that inherited metabolic diseases are increasingly being recognised. Life expectancy for many patients is progressively improving because new therapeutic strategies are available. Because most inherited metabolic diseases are systemic disorders, virtually all organs may be involved. Respiratory disease complicates the management of several inherited metabolic diseases, either at presentation or as late-onset features. This review will describe the most exemplary respiratory manifestations of inherited metabolic diseases in childhood and adulthood. Since airways disease worsens the morbidity of many inherited metabolic disorders, leading to increased hospitalisations, mortality and overall healthcare costs, respiratory manifestations of inherited metabolic diseases need to be carefully recognised and treated. All patients with inherited metabolic disease and suspected airway disease should undergo a detailed diagnostic work-up. Current treatments for several inherited metabolic diseases (including enzyme replacement therapy, substrate reduction, bone marrow transplantation, or even more innovative strategies such as pharmacological chaperone or gene therapies) may provide significant benefits for associated respiratory disease. The integration of several specialists dedicated to airway disease management in a multidisciplinary team is essential to provide the most appropriate care to children and adults with inherited metabolic disease. @ERSpublications Proper management of respiratory disease is mandatory for reducing morbidity and mortality of inherited metabolic disease

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“…OSAS may trigger a cascade of intermediate mechanisms that are potentially harmful to the cardiovascular and metabolic system, and include sympathetic activation activity, oxidative stress, and systemic inflammation [2]. All these intermediate mechanisms may help to explain the contribution of OSAS to several diseases, including hypertension, stroke, diabetes, and cardiac arrhythmias and the increased mortality associated with the disease [3][4][5][6].…”

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confidence: 99%

Bone mineral density in patients with obstructive sleep apnea syndrome

2012

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In the past two decades, obstructive sleep apnea syndrome (OSAS) has been identified as a common clinical condition with high prevalence in middle-aged adults [1]. OSAS may trigger a cascade of intermediate mechanisms that are potentially harmful to the cardiovascular and metabolic system, and include sympathetic activation activity, oxidative stress, and systemic inflammation [2]. All these intermediate mechanisms may help to explain the contribution of OSAS to several diseases, including hypertension, stroke, diabetes, and cardiac arrhythmias and the increased mortality associated with the disease [3][4][5][6]. Cardiovascular morbidity and mortality associated with sleep apnea have been extensively studied in the last decade [4,7,8]. Furthermore, several former and recent studies have indicated strong association between cardiovascular diseases and osteoporosis [9-13], with the above intermediate mechanisms of OSAS to have a critical role in the common pathophysiological pathway of both diseases. Therefore, this association leads us to hypothesize that OSAS may also be responsible for the development of osteoporosis.In this issue of Sleep and Breathing, Hulya Uzkeser, and colleagues of the Ataturk University, Turkey, in their paper "Bone mineral density in patients with obstructive sleep apnea syndrome" tried to investigate the relationship between OSAS and osteoporosis by examining both the bone metabolic abnormalities and bone mineral density (BMD) in OSAS patients compared to individuals without OSAS. The authors found a significant difference between OSAS patients and the control group in relation to lumbar L1-L4 BMD, femoral neck BMD, and lumbar L1-L4 t score values, evaluating the underlying assumption of the relationship between OSAS and osteoporosis. Taking into account that there have been no previous reports about the correlation between OSAS and osteoporosis, assessed by bone mineral density, we appreciate this type of work. Furthermore, the study certainly has clinical importance as the issue of osteoporosis is very important, underestimated, and with rising prevalence. Many well-designed epidemiologic studies worldwide have demonstrated that this disease and its consequences represent a high burden on health systems due to the high costs and the resources needed for the care of patients suffering from it [14].What can these results be attributed to? There are at least three mechanisms that may potentially affect abnormal bone metabolism in OSAS: hypoxia, increased oxidative stress, and inflammation [15]. As the authors hypothesize, the balance between osteoclasts and osteoblasts is disrupted in favor of osteoclasts in the presence of hypoxia. However, the fact that they did not find any significant differences in serum Ca, P, ALP, and urinary Dpd levels in OSAS patients compared to controls is still not clear.In the literature, the first clinical indication of the adverse effects of OSAS on bone metabolism was by Tomiyama et al. [15]. The authors investigated the association between the severity o...

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Sleep apnoea syndrome in 2011: current concepts and future directions

Cited by 61 publications

References 190 publications

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea

Respiratory manifestations in patients with inherited metabolic diseases

Bone mineral density in patients with obstructive sleep apnea syndrome

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