Obstructive Sleep Apnea and Diabetic Neuropathy

Tahrani, Abd A; Ali, Asad; Raymond, Neil T.; Begum, Safia; Dubb, Kiran; Mughal, Shanaz; Jose, Biju; Piya, Milan K.; Barnett, Anthony; Stevens, Martin J.

doi:10.1164/rccm.201112-2135oc

Cited by 155 publications

(63 citation statements)

References 47 publications

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“…In addition, DPN and CAN commonly co-exist and we have shown previously that CAN predicts the eGFR decline in patients with Type 2 Diabetes [7, 9]. We have also previously shown an association between OSA and foot insensitivity, and that OSA predicts eGFR decline in patients with Type 2 diabetes [8, 10]. Hence, the observed relationships between DPN and eGFR in our study could be mediated, at least in part, by the relationships between DPN and OSA and CAN.…”

Section: Discussionmentioning

confidence: 99%

“…The study was approved by the Warwickshire Research Ethics Committee (REC number 08/H1211/145) and funded by the National Institute for Health Research (NIHR) in the UK. Previous publications related to this study population can be found in [7, 8, 10, 11]. …”

Section: Methodsmentioning

confidence: 99%

“…Clinically evident DPN is common in patients with CAN and in patients with OSA [9, 10] and as diabetic peripheral neuropathy (DPN) shares many aspects of its pathogenesis with CKD, we hypothesised that foot insensitivity may predict changes in renal function in patients with Type 2 diabetes.…”

Section: Introductionmentioning

confidence: 99%

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Foot insensitivity is associated with renal function decline in patients with type 2 diabetes: a cohort study

et al. 2016

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BackgroundIdentifying patients with diabetes at increased risk of chronic kidney disease (CKD) is essential to prevent/slow the progression to end-stage renal disease (ESRD). CKD and diabetic peripheral neuropathy (DPN) share common mechanisms. Hence, we aimed to examine the relationship between foot insensitivity and CKD in patients with Type 2 diabetes.MethodsA prospective observational cohort study in adults with Type 2 diabetes. Patients with ESRD were excluded. Foot insensitivity was assessed using the 10-g monofilament test. Renal function was assessed using estimated glomerular filtration rate (eGFR) based on the MDRD equation. Albuminuria was defined as the presence of urinary albumin/creatinine ratio (ACR) >3.4 mg/mmol.ResultsTwo hundred and twenty eight patients were recruited and followed-up for 2.5 years. One hundred and ninety patients (83.4%) had eGFR ≥ 60 ml/min/1.73 m2. Seventy six (33.3%) patients had foot insensitivity (i.e. abnormal monofilament test). Patients with foot insensitivity had lower eGFR and higher prevalence of albuminuria compared to patients with normal monofilament test. After adjustment for age, gender, ethnicity, diabetes duration, HbA1c, body mass index, insulin treatment, number of anti-hypertensives, history of peripheral vascular disease, and baseline eGFR (R2 0.87), baseline foot insensitivity was associated with study-end eGFR (B = −3.551, p = 0.036).ConclusionsPatients with Type 2 diabetes and foot insensitivity are at increased risk of eGFR decline. Identifying these patients offers an opportunity to intensify metabolic and blood pressure control to prevent/retard the development of CKD. Future studies of larger sample size and longer follow up from multiple centres are needed to assess the diagnostic performance of our findings in predicting CKD development, and to compare the performance of the monofilament test with albuminuria.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Foot insensitivity is associated with renal function decline in patients with type 2 diabetes: a cohort study

et al. 2016

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“…It is unknown to what extent chronic intermittent hypoxemia in OSAS causes damage to the motor and sensory peripheral nerve, but muscle action potential and sensory nerve action potential amplitudes are significantly reduced in the nerves outside UA in patients with OSAS suggesting that axonal damage exists in patients with OSAS to a greater extent than previously thought [24]. On the other hand, association between OSAS and sensory neuropathy, and nerve damage outside the UA [18,[25][26][27], type 2 or type 1A diabetic neuropathy, and axonal subtypes of Charcot-Marie-Tooth disease [28][29][30][31] has been also demonstrated. Of particular interest is the epidemiological association between OSAS and anterior ischemic optic neuropathy [32] although a concluding rapport cannot be established [33].…”

Section: The Neurological Theory Of Osas and The Upper Airways Remodementioning

confidence: 91%

Nerve and Muscle Changes in the Upper Airways of Subjects with Obstructive Sleep Apnea: Structural Basis for the Neurogenic Theory

Cobo¹,

Macías²,

Alvarez³

et al. 2017

Sleep Apnea - Recent Updates

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Obstructive sleep apnea syndrome (OSAS) is a widely diffused disease associated with specific genetics, age, gender, craniofacial and upper airways anatomy, obesity, and endocrine conditions, but not with ethnicity profiles. The so-called neurogenic neurogenic theory of OSAS postulates that the collapse of the upper airways that characterize this disease is due to peripheral nerve degeneration that leads to muscle atrophy and collapse. This review attempts to summarize the structural and functional changes in both the sensory and motor innervation of the walls of the upper air ways in patients suffering from OSAS.

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“…In contrast, the Sleep AHEAD study found no association between glycemic control and AHI [95]. Finally, adults with T2DM and severe OSA are at greater risk of developing diabetes complications vs. those without OSA [96, 97]. Taken together, these studies demonstrate the importance of screening adults with T2DM for OSA and encouraging compliance with OSA treatment, which may improve glycemic control and reduce the risk of comorbidities.…”

Section: Introductionmentioning

confidence: 99%

Metabolic and Glycemic Sequelae of Sleep Disturbances in Children and Adults

2014

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The prevalence of obesity in adults and children has increased greatly in the past three decades, as have metabolic sequelae, such as insulin resistance and type 2 diabetes mellitus (T2DM). Sleep disturbances are increasingly recognized as contributors to this widespread epidemic in adults, and data are emerging in children as well. The categories of sleep disturbances that contribute to obesity and its glycemic co-morbidities include the following: (1) alterations of sleep duration, chronic sleep restriction and excessive sleep; (2) alterations in sleep architecture; (3) sleep fragmentation; (4) circadian rhythm disorders and disruption (i.e., shift work); and (5) obstructive sleep apnea. This article reviews current evidence supporting the contributions that these sleep disorders play in the development of obesity, insulin resistance, and T2DM as well as possibly influences on glycemic control in type 1 diabetes, with a special focus on data in pediatric populations.

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Obstructive Sleep Apnea and Diabetic Neuropathy

Cited by 155 publications

References 47 publications

Foot insensitivity is associated with renal function decline in patients with type 2 diabetes: a cohort study

Foot insensitivity is associated with renal function decline in patients with type 2 diabetes: a cohort study

Nerve and Muscle Changes in the Upper Airways of Subjects with Obstructive Sleep Apnea: Structural Basis for the Neurogenic Theory

Metabolic and Glycemic Sequelae of Sleep Disturbances in Children and Adults

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