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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #119: Diabetes and Sleep Apnea Part 9

Apr 3, 2018
 

OSA management

OSA should be treated promptly and the aim of treatment is to reduce the morbidity and mortality associated with this condition. Weight loss and positional treatment (i.e., avoiding the position in which most episodes occur, which is usually the supine position) are important aspects of treatment. As with all obesity-related disorders, weight loss (regardless of the means) can result in significant improvements in OSA. In a randomized controlled trial of intensive lifestyle intervention in 264 patients with OSA and T2DM (the Sleep AHEAD study), weight loss of 11 kg on average in the treatment group resulted in a reduction in the AHI of about 10 events per hour [157].

Similar results were found in a study of men with OSA, in which 10% weight loss resulted in improvements in the RDI by about 16 events per hour [158]. Weight loss after bariatric surgery has also been associated with significant improvements in OSA severity [159].

Mandibular advancement devices (MAD) are effective in treating patients with mild to moderate OSA. They work by pulling the tongue forward or by moving the mandible and soft palate anteriorly, enlarging the posterior airspace, which results in opening and increasing the airway size. MAD are considered as a second-line treatment for patients with mild to moderate OSA who cannot tolerate CPAP [160].

Surgery has a limited role in patients with OSA and produces variable results [160]. If the patient has upper airway obstruction (such as tonsils or tumors) then surgery is the most important aspect of the treatment, otherwise its role is limited and it is usually associated with significant side effects [160].

CPAP is the mainstay of treatment for patients with OSA. CPAP works by providing a “pneumatic splint” by delivering an intraluminal pressure that is positive with reference to the atmospheric pressure and by increasing lung volumes [161]. CPAP treatment has been shown to reduce AHI, reduce BP, improve sleepiness, improve quality of life, improve cognitive function, and reduce motor vehicle accidents [161]. Furthermore, evidence from an observational study suggests that CPAP treatment reduces the risk of cardiovascular events [150]. An in-depth review on CPAP, its technical aspects, evidence behind its use, and its complications can be found elsewhere in [161].

Impact of T2DM on OSA

Although the bulk of this chapter describes the impact of OSA on glucose metabolism and T2DM, this association could be directional and having IR or T2DM may have an impact on pre-existing OSA and result in the development of “new” OSA or CSA.

In a study of 3565 participants, who were followed up for a 6-year period, the presence of a history of witnessed apneas was an independent predictor of incident sleep apnea [162]. After adjustment for age, sex, and waist circumference, the standardized OR for incident sleep apnea for HOMA-IR was 1.31 (1.13–1.51). This suggests that not only can sleep apnea result in dysglycemia as shown by longitudinal studies, but that pre-existing dysglycemia also predicts the development of sleep apnea. This may be related in part to the loss of upper airway innervations or the autonomic dysfunction that can occur in patients with dysglycemia; autonomic neuropathy has been implicated in the central respiratory centre response to hypercapnic stimulus [163] and may result in changes in respiratory control resulting in CSA as seen in other conditions such as multisystem atrophy (Shy–Drager syndrome) [164].

CSA has indeed been shown to be common in patients with T2DM. In a subgroup analysis of the Sleep Heart Health Study, there were significant differences in RDI, sleep stages, central apnea index, and periodic breathing between patients with and without DM. However, most of these differences lost their statistical significance after adjusting for confounders with the exception of percent time in REM sleep and prevalence of periodic breathing [110]. Similarly, Sanders and colleagues found a greater prevalence of CSA in patients with DM compared to those without (3.8% vs. 1.8%, DM vs. non-DM patients, respectively, p=0.002) [165].

The natural history of OSA in patients with T2DM and the impact of T2DM on pre-existing OSA is currently unknown, but the ongoing Sleep AHEAD study will be able to answer this Question.

Summary and future directions

OSA is a very common medical disorder that is associated with significant morbidity and mortality. OSA is associated with obesity, hypertension, insulin resistance, and possibly impaired β-cell function. OSA is associated with several mechanisms that lead to insulin  resistance and β-cell dysfunction including intermittent hypoxia, inflammation, sympathetic activation, activation of the hypothalamic pituitary adrenal axis, reduction in adiponectin, increased leptin, and the development of nonalcoholic steatohepatitis. As a result, dysglycemia is very common in patients with OSA.

OSA is associated with worse glycemic control in patients with T2DM but CPAP treatment does not seem to improve glycemic control. The impact of CPAP treatment on other metabolic parameters in patients with T2DM including blood pressure and dyslipidemia are also needed. OSA is associated with increased oxidative and nitrosative stress and impaired microvascular and endothelial function in patients with diabetes, hence it is not surprising that OSA is associated with diabetes-related microvascular complications. However, prospective and interventional studies are required to confirm causality. In addition, T2DM is associated with CSA, and not only OSA, and this seems to be related to autonomic dysfunction.

The field of OSA in patients with T2DM is still in its infancy and most of the work in regard to OSA in patients with T2DM has focused on glycemic control, it is time to address the impact of OSA on other aspects of T2DM.

Declaration

Dr. Abd Tahrani is a clinician scientist supported by the UK National Institute for Health Research. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research, or the Department of Health.

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