Obstructive Sleep-Related Breathing Disorders in Patients Evaluated for Bariatric Surgery

Frey, William C.; Pilcher, John

doi:10.1381/096089203322509228

Cited by 366 publications

(176 citation statements)

References 15 publications

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“…We demonstrated a greater than 80% prevalence of OSA in severe obesity, which is consistent with previous reports (10,11,36). Thus, in severe obesity metabolic dysfunction can be related not only to adiposity per se but also to concomitant OSA.…”

Section: Osa Systemic Inflammation and Metabolic Dysfunction In Sevsupporting

confidence: 93%

“…Both insulin resistance and systemic inflammation may contribute to the increased cardiovascular risk in patients with OSA (7)(8)(9). Insulin resistance, systemic inflammation, and OSA are particularly prevalent in patients with severe obesity defined as a body mass index (BMI) exceeding 40 kg/m 2 (2,(10)(11)(12). While obesity causes systemic inflammation, insulin resistance, and sleep apnea (12)(13)(14)(15), sleep apnea may further exacerbate the inflammatory and metabolic disturbances (2,3,6).…”

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confidence: 99%

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Obstructive Sleep Apnea, Insulin Resistance, and Steatohepatitis in Severe Obesity

Polotsky

Patil

Savransky

et al. 2009

Am J Respir Crit Care Med

191

139

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Rationale: Obstructive sleep apnea is associated with insulin resistance and liver injury. It is unknown whether apnea contributes to insulin resistance and steatohepatitis in severe obesity. Objectives: To examine whether sleep apnea and nocturnal hypoxemia predict the severity of insulin resistance, systemic inflammation, and steatohepatitis in severely obese individuals presenting for bariatric surgery. Methods: We performed sleep studies and measured fasting blood glucose, serum insulin, C-reactive protein, and liver enzymes in 90 consecutive severely obese individuals, 75 women and 15 men, without concomitant diabetes mellitus or preexistent diagnosis of sleep apnea or liver disease. Liver biopsies (n 5 20) were obtained during bariatric surgery. Measurements and Main Results: Obstructive sleep apnea with a respiratory disturbance index greater than 5 events/hour was diagnosed in 81.1% of patients. The median respiratory disturbance index was 15 6 29 events/hour and the median oxygen desaturation during apneic events was 4.6 6 1.8%. All patients exhibited high serum levels of C-reactive protein, regardless of the severity of apnea, whereas liver enzymes were normal. Oxygen desaturation greater than 4.6% was associated with a 1.5-fold increase in insulin resistance, according to the homeostasis model assessment index. Histopathology data suggested that significant nocturnal desaturation might predispose to hepatic inflammation, hepatocyte ballooning, and liver fibrosis. Fasting blood glucose levels and steatosis scores were not affected by nocturnal hypoxia. There was no relationship between the respiratory disturbance index and insulin resistance or liver histopathology. Conclusions: Hypoxic stress of sleep apnea may be implicated in the development of insulin resistance and steatohepatitis in severe obesity.Keywords: hypoxemia; fatty liver disease; metabolic syndrome; sleepdisordered breathing; liver injury Obstructive sleep apnea (OSA) is a complex disorder consisting of upper airway obstruction, chronic intermittent hypoxia (CIH), and sleep fragmentation (1). Epidemiologic studies have demonstrated that OSA is associated with insulin resistance and glucose intolerance, independent of obesity (2-4). Clinical investigations have also shown that OSA results in low-grade systemic inflammation (5, 6). Both insulin resistance and systemic inflammation may contribute to the increased cardiovascular risk in patients with OSA (7-9). Insulin resistance, systemic inflammation, and OSA are particularly prevalent in patients with severe obesity defined as a body mass index (BMI) exceeding 40 kg/m 2 (2, 10-12). While obesity causes systemic inflammation, insulin resistance, and sleep apnea (12-15), sleep apnea may further exacerbate the inflammatory and metabolic disturbances (2, 3, 6). Nevertheless, it is not known whether concomitant OSA is implicated in metabolic dysregulation and systemic inflammation in severe obesity.One of the consequences of obesity and insulin resistance is nonalcoholic fatty liver disease (N...

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Section: Osa Systemic Inflammation and Metabolic Dysfunction In Sevsupporting

confidence: 93%

mentioning

confidence: 99%

Obstructive Sleep Apnea, Insulin Resistance, and Steatohepatitis in Severe Obesity

Polotsky

Patil

Savransky

et al. 2009

Am J Respir Crit Care Med

191

139

View full text Add to dashboard Cite

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“…However, our data are much lower than those found in previous studies, in which obese patients were submitted to polysomnography and was found a prevalence of OSAHS in 83.7% and 71% of the patients (12,22) . Other study identified mild sleep disturbance in 21.9% of obese patients, moderate in 28.8% and severe in 49.3% (23) .…”

Section: Discussioncontrasting

confidence: 91%

Prevalence of sleep disorders in obese before bariatric surgery.

Carlos¹,

Oliver²,

Cruz³

et al. 2020

mtprehabjournal

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Introduction:The prevalence of sleep disorders (SD) has increased significantly in recent decades in parallel to the worldwide obesity epidemic. The presence of SD provides an increased risk of postoperative complications, requiring greater care in these patients. The gold standard for evaluation and diagnosis of SD is polysomnography, but it is an expensive and highly complex exam, making the questionnaires and scales more accessible for diagnosis and screening. Objectives: To evaluate the presence of SD and to analyze the influence of anthropometric measures on the scores of the Epworth Sleepiness Scale (ESS), snoring (ERS) and Stanford Sleepiness Scale (SSS) in obese patients. Method: An observational, cross-sectional study performed from August 2015 to August 2016. The patients in the preoperative group of bariatric surgery of the University Hospital were submitted to anthropometric evaluation and application of the ESS, ERS and SSS during the preoperative physiotherapy evaluation. Results: Were evaluated 100 obese (78 women), mean age of 41.4±10.7 years and BMI of 46.1±7.8kg/m 2 . SD were identified in 25% by ESS and 21% by SSS of obese. There were no differences between genders for the scales scores. The score of the ERS correlated itself with waist (r=0.20, p=0.04) and neck (r=0.33, p=0.001) circumferences. Conclusion: The use of scales for diagnosis of SD is useful in the follow-up of the preoperative of bariatric surgery and our study found that 25% of patients present daytime somnolence. We also observed the influence of waist and neck circumferences on increasing snoring scale.

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“…In severe obesity (BMI . 40 kg/m 2 ), the prevalence of sleep apnea was estimated to vary between 40 and 90% (17)(18)(19)(20)(21)(22)(23)(24), and the severity of sleep apnea was generally greater than that found in leaner clinical populations (17,25,26). In addition, Peppard and colleagues have provided further evidence for a link between sleep apnea and obesity by demonstrating that a 10% change in body weight was associated with a parallel change of approximately 30% in the apnea-hypopnea index (AHI), the major index of sleep apnea severity (16).…”

Section: Sleep Apnea Risk Factors: Roles Of Obesity Sex Fat Distribmentioning

confidence: 99%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

584

395

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Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

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Obstructive Sleep-Related Breathing Disorders in Patients Evaluated for Bariatric Surgery

Cited by 366 publications

References 15 publications

Obstructive Sleep Apnea, Insulin Resistance, and Steatohepatitis in Severe Obesity

Obstructive Sleep Apnea, Insulin Resistance, and Steatohepatitis in Severe Obesity

Prevalence of sleep disorders in obese before bariatric surgery.

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

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