“…The prevalence of OSA in the obese population is about 50% [26], and body mass index (BMI) is linearly related with OSA severity. However, a recent metanalysis on the effect of surgical weight loss on OSA [27] showed that there is no relationship between the amount of weight loss and AHI reduction in these patients likely because other factors are at play in determining the AHI even when the anatomical defect has been reduced. According to this metanalysis, despite frequent complications, bariatric surgery showed an average 28% weight reduction, with a consequent reduction in AHI by 68% in severe OSA patients [27].…”
Section: Upper Airway Anatomymentioning
confidence: 99%
“…However, a recent metanalysis on the effect of surgical weight loss on OSA [27] showed that there is no relationship between the amount of weight loss and AHI reduction in these patients likely because other factors are at play in determining the AHI even when the anatomical defect has been reduced. According to this metanalysis, despite frequent complications, bariatric surgery showed an average 28% weight reduction, with a consequent reduction in AHI by 68% in severe OSA patients [27]. Another recent metanalysis showed that weight loss programs including lifestyle changes (without medications or surgery) can lead to ~13% of weight loss in about 12 months with an average reduction in AHI by 48% in moderate OSA patients [28,29].…”
Obstructive sleep apnea (OSA) is a highly prevalent condition with few therapeutic options. To date there is no approved pharmacotherapy for this disorder, but several attempts have been made in the past and are currently ongoing to find one. The recent identification of multiple endotypes underlying this disorder has oriented the pharmacological research towards tailored therapies targeting specific pathophysiological traits that contribute differently to cause OSA in each patient. In this review we retrospectively analyze the literature on OSA pharmacotherapy dividing the medications tested on the basis of the four main endotypes: anatomy, upper airway muscle activity, arousal threshold and ventilatory instability (loop gain). We show how recently introduced drugs for weight loss that modify upper airway anatomy may play an important role in the management of OSA in the near future, and promising results have been obtained with drugs that increase upper airway muscle activity during sleep and reduce loop gain. The lack of a medication that can effectively increase the arousal threshold makes this strategy less encouraging, although recent studies have shown that the use of certain sedatives do not worsen OSA severity and could actually improve patients’ sleep quality.
“…The prevalence of OSA in the obese population is about 50% [26], and body mass index (BMI) is linearly related with OSA severity. However, a recent metanalysis on the effect of surgical weight loss on OSA [27] showed that there is no relationship between the amount of weight loss and AHI reduction in these patients likely because other factors are at play in determining the AHI even when the anatomical defect has been reduced. According to this metanalysis, despite frequent complications, bariatric surgery showed an average 28% weight reduction, with a consequent reduction in AHI by 68% in severe OSA patients [27].…”
Section: Upper Airway Anatomymentioning
confidence: 99%
“…However, a recent metanalysis on the effect of surgical weight loss on OSA [27] showed that there is no relationship between the amount of weight loss and AHI reduction in these patients likely because other factors are at play in determining the AHI even when the anatomical defect has been reduced. According to this metanalysis, despite frequent complications, bariatric surgery showed an average 28% weight reduction, with a consequent reduction in AHI by 68% in severe OSA patients [27]. Another recent metanalysis showed that weight loss programs including lifestyle changes (without medications or surgery) can lead to ~13% of weight loss in about 12 months with an average reduction in AHI by 48% in moderate OSA patients [28,29].…”
Obstructive sleep apnea (OSA) is a highly prevalent condition with few therapeutic options. To date there is no approved pharmacotherapy for this disorder, but several attempts have been made in the past and are currently ongoing to find one. The recent identification of multiple endotypes underlying this disorder has oriented the pharmacological research towards tailored therapies targeting specific pathophysiological traits that contribute differently to cause OSA in each patient. In this review we retrospectively analyze the literature on OSA pharmacotherapy dividing the medications tested on the basis of the four main endotypes: anatomy, upper airway muscle activity, arousal threshold and ventilatory instability (loop gain). We show how recently introduced drugs for weight loss that modify upper airway anatomy may play an important role in the management of OSA in the near future, and promising results have been obtained with drugs that increase upper airway muscle activity during sleep and reduce loop gain. The lack of a medication that can effectively increase the arousal threshold makes this strategy less encouraging, although recent studies have shown that the use of certain sedatives do not worsen OSA severity and could actually improve patients’ sleep quality.
“…Treatment of obesity and comorbid OSA with bariatric surgery has been demonstrated to improve OSA-specific outcomes, in addition to other metabolic outcomes and obesityrelated mortality [15]. A recent meta-analysis of outcomes for sleep apnea following bariatric surgery demonstrated a significant improvement in weight loss and associated improvement in the severity of OSA post-operatively [16]. However, there is limited data to support a protective effect of bariatric surgery on developing OSA in patients without a pre-operative diagnosis.…”
Background
Obstructive sleep apnea (OSA) is an increasingly common disorder associated with increased cardiovascular disease, mortality, reduced productivity, and an increased risk of road traffic accidents. A significant proportion of patients with OSA in the UK are undiagnosed. This study aims to identify risk factors for OSA in an obese cohort.
Method
A population-based study was conducted of obese patients (BMI ≥ 30 kg/m2) from the Clinical Practice Research Datalink (CPRD). A logistic regression model was used to calculate odds ratios (ORs) for developing OSA according to other clinicopathological characteristics. Multivariate analysis was conducted of individual factors that affect the propensity to develop OSA. Statistical significance was defined as p < 0.050.
Results
From 276,600 obese patients identified during a data extraction of the CPRD in July 2017, the prevalence of OSA was 5.4%. The following risk factors were found to be independently associated with increased likelihood of OSA: male sex (OR = 3.273; p < 0.001), BMI class II (OR = 1.640; p < 0.001), BMI class III (OR = 3.768; p < 0.001), smoking (OR = 1.179; p < 0.001), COPD (OR = 1.722; p < 0.001), GERD (OR = 1.557; p < 0.001), hypothyroidism (OR = 1.311; p < 0.001), acromegaly (OR = 3.543; p < 0.001), and benzodiazepine use (OR = 1.492; p < 0.001). Bariatric surgery was associated with reduced risk of OSA amongst this obese population (OR = 0.260; p < 0.001).
Conclusions
In obese patients, there are numerous comorbidities that are associated with increased likelihood of OSA. These factors can help prompt clinicians to identify undiagnosed OSA. Bariatric surgery appears to be protective against developing OSA.
“…A meta-analysis confirmed the positive impact of bariatric surgery on OSA severity, by showing a significant reduction of AHI post surgery (by 38.2 events/h, 95% CI: 31.9-44.4) (20). A more recent systematic review and meta-analysis by Wong et al showed that bariatric surgery was associated with a reduction in the AHI (WMD −25.1 events/h (95% CI −29.9, −20.2)); with the pooled mean pre-and post-surgery AHI of 39.3 ± 15.1 and 12.5 ± 5.6 events/h respectively; however, OSA persisted in most patients and there was high between-studies heterogeneity mostly due to baseline AHIO and duration of follow-up (21). Hence, RCTs remain needed to address the impact of bariatric surgery on OSA, although these might be challenging to conduct.…”
Section: The Impact Of Weight Change On Osamentioning
confidence: 98%
“…One possibility is that OSA could lead to worsening obesity via multiple mechanisms such as increased excessive daytime tumour necrosis factor-alpha; IL6, interleukin-6; CNS, central nervous system; EDS, excessive daytime sleepiness; CPAP, continuous positive airway pressure. Obesity can lead to increased UA collapsibility via increased parapharyngeal fat deposition, UA narrowing, intramuscular fatty deposits leading to reduced UA muscles activity and increased UA muscle fatigability and reduced lung volume resulting in reduced tracheal caudal traction (19,20,21,22,23,24,25,26,27). In addition, the low lung volume in obesity can lead to hypoxaemia and ventilatory instability in the presence of increased whole body oxygen demand due to obesity (high loop gain) (28).…”
Obstructive sleep apnoea (OSA) is a common disorder that is associated with serious comorbidities with a negative impact on quality of life, life expectancy and health costs. As OSA is related to obesity and is associated with sleep disruption, increased inflammation and oxidative stress, it is not surprising that OSA has an impact on the secretion of multiple hormones and is implicated in the development of many endocrine conditions. On the other hand, many endocrine conditions that can affect obesity and/or upper airways anatomy and stability have been implicated in the development or worsening of OSA. This bidirectional relationship between OSA and the endocrine system has been increasingly recognised in experimental and epidemiological studies and there are an increasing number of studies examining the effects of OSA treatment on endocrine conditions and vice versa. In this review article, we will critically appraise and describe the impact of OSA on the endocrine system including obesity, dysglycaemia, the pituitary, the thyroid, the adrenals, the reproductive system and the bones. In each section, we will assess whether a bidirectional relationship exists, and we will describe the potential underlying mechanisms. We have focused more on recent studies and randomised controlled trials where available and attempted to provide the information within clinical context and relevance.
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