Diagnosis of obstructive sleep apnoea in primary care.

BACKGROUND: Obstructive sleep apnoea (OSA) is a highly prevalent condition associated with significant adverse health consequences affecting multiple organ systems. As the first point of contact for most patients with OSA, general practitioners (GPs) have an important role in the diagnosis of this common sleep disorder. OBJECTIVE: The aim of this paper is to improve awareness of common risk factors for and clinical presentation of OSA in primary care to improve patient health outcomes. We seek to understand how screening tools, such as the OSA50 questionnaire and the Epworth Sleepiness Scale, can help GPs identify patients who are at high risk for OSA with significant daytime sleepiness. DISCUSSION: Patients at high risk of symptomatic moderate-severe OSA should proceed to further investigation with sleep study testing. Referral to a sleep physician should be considered for patients with complex presentations or other suspected sleep disorders, commercial drivers, and those who fail to comply with or respond to initial OSA treatments.

Management of obstructive sleep apnoea in primary care.

BACKGROUND: Obstructive sleep apnoea (OSA) is common in the community and is increasing in prevalence. Primary care plays a pivotal role in the diagnosis and management of OSA. OBJECTIVE: This article focuses on the management options for a patient with an established diagnosis of OSA and provides a guide for driving licensing requirements. Indications for continuous positive airway pressure (CPAP) are discussed and tips provided to consider when conducting a review appointment, including trouble shooting. DISCUSSION: There are several treatment options available for patients with an established diagnosis of OSA. Selecting the optimal therapy involves aligning the symptoms and severity of OSA with the presence of comorbidities. CPAP is a highly effective therapy for symptomatic adults with moderate-to-severe OSA and for some symptomatic patients with mild OSA. Early trouble shooting of side effects and using supportive interventions increases the probability of long-term adherence, which is key to symptomatic improvement.

Sleep health primary care clinical resource.

BACKGROUND: Obstructive sleep apnoea (OSA) and insomnia are the two most common sleep disorders and are frequent reasons for presentation in Australian general practice. OBJECTIVE: This article describes the development, content and suggested uses of the online sleep health primary care clinical resource, which provides general practitioners and other primary healthcare professionals with evidence-based information on the aetiology, assessment, management, referral and ongoing care for OSA and chronic insomnia. DISCUSSION: The Royal Australian College of General Practitioners-accepted clinical resource for the management of OSA and chronic insomnia in primary care was developed by the Australian National Centre for Sleep Health Services Research. The resource is designed to be used during consultations (eg following the steps in assessment and management and the use of online questionnaires for the assessment of OSA [Epworth Sleepiness Scale/OSA50/STOP-Bang] and insomnia [Sleep Condition Indicator/and Insomnia Severity Index]) and as an education/training tool (eg evidence on the role of continuous positive airway pressure/mandibular advancement splints for management of OSA and brief behavioural therapy for insomnia/cognitive behavioural therapy for insomnia for the management of insomnia).

Obstructive Sleep Apnea Effects on Chronic Airway Disease Exacerbations-Missed Opportunities for Improving Outcomes in Chronic Obstructive Pulmonary Disease and Asthma.

In patients with chronic obstructive pulmonary disease (COPD) and asthma, exacerbations determine the natural history of both diseases. Patients with both respiratory diseases who suffer from obstructive sleep apnea (OSA) as a comorbidity (overlap syndromes) have a higher risk of exacerbations and hospitalization. In cases of OSA/COPD and OSA/asthma, continuous positive airway pressure treatment is indicated. Adequate adherence to therapy appears to reduce exacerbations and their severity, especially in OSA/COPD overlap. However, there is a lack of randomized trials that definitively demonstrate this evidence.

Contribution of Obstructive Sleep Apnea to Asthmatic Airway Inflammation and Impact of Its Treatment on the Course of Asthma.

Asthma and obstructive sleep apnea (OSA) are very common respiratory disorders in the general population. Beyond their high prevalence, shared risk factors, and genetic linkages, bidirectional relationships between asthma and OSA exist, each disorder affecting the other's presence and severity. The author reviews here some of the salient links between constituents of the alternative overlap syndrome, that is, OSA comorbid with asthma, with an emphasis on the effects of OSA or its treatment on inflammation in asthma. In the directional relationship from OSA toward asthma, beyond direct influences, multiple factors and comorbidities seem to contribute.

Exosomes regulate SIRT3-related autophagy by delivering miR-421 to regulate macrophage polarization and participate in OSA-related NAFLD.

PURPOSE: To analyze the role of and mechanism underlying obstructive sleep apnea (OSA)-derived exosomes in inducing non-alcoholic fatty liver (NAFLD). METHODS: The role of OSA-derived exosomes was analyzed in inducing hepatocyte fat accumulation in mice models both in vivo and in vitro. RESULTS: OSA-derived exosomes caused fat accumulation and macrophage activation in the liver tissue. These exosomes promoted fat accumulation; steatosis was more noticeable in the presence of macrophages. Macrophages could internalize OSA-derived exosomes, which promoted macrophage polarization to the M1 type. Moreover, it inhibited sirtuin-3 (SIRT3)/AMP-activated protein kinase (AMPK) and autophagy and promoted the activation of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasomes. The use of 3-methyladenine (3-MA) to inhibit autophagy blocked NLRP3 inflammasome activation and inhibited the M1 polarization of macrophages. miR-421 targeting inhibited SIRT3 protein expression in the macrophages. miR-421 was significantly increased in OSA-derived exosomes. Additionally, miR-421 levels were increased in OSA + NAFLD mice- and patient-derived exosomes. In the liver tissues of OSA and OSA + NAFLD mice, miR-421 displayed similar co-localization with the macrophages. Intermittent hypoxia-induced hepatocytes deliver miR-421 to the macrophages via exosomes to inhibit SIRT3, thereby participating in macrophage M1 polarization. After OSA and NAFLD modeling in miR-421-/- mice, liver steatosis and M1 polarization were significantly reduced. Additionally, in the case of miR-421 knockout, the inhibitory effects of OSA-derived exosomes on SIRT3 and autophagy were significantly alleviated. Furthermore, their effects on liver steatosis and macrophage M1 polarization were significantly reduced. CONCLUSIONS: OSA promotes the delivery of miR-421 from the hepatocytes to macrophages. Additionally, it promotes M1 polarization by regulating the SIRT3/AMPK-autophagy pathway, thereby causing NAFLD.

SENP1 regulates intermittent hypoxia-induced microglia mediated inflammation and cognitive dysfunction via wnt/ß-catenin pathway.

Obstructive sleep apnea syndrome (OSAS), characterized by repeated narrow or collapse of the upper airway during sleep, resulting in periodic reductions or cessations in ventilation, consequent hypoxia, hypercapnia, increased sympathetic activity and sleep fragmentation, places a serious burden on society and health care. Intermittent hypoxia (IH), which cause central nervous system (CNS) inflammation, and ultimately lead to neuropathy, is thought to be a crucial contributor to cognitive impairment in OSAS. Wnt signaling pathway exerts an important role in the regulation of CNS disorders. Particularly, it may be involved in the regulation of neuroinflammation and cognitive dysfunction. However, its underlying mechanism remains poorly understood. Accumulating evidence demonstrated that Wnt signaling pathway may inhibited in a variety of neurological disorders. Recently studies revealed that SUMOylation was participated in the regulation of neuroinflammation. Members of Wnt/ß-catenin pathway may be targets of SUMOylation. In vitro and in vivo molecular biology experiments explored the regulatory mechanism of SUMOylation on Wnt/ß-catenin in IH-induced neuroinflammation and neuronal injury, which demonstrated that IH induced the SUMOylation of ß-catenin, microglia mediated inflammation and neuronal damage. Moreover, SENP1 regulated the de-SUMOylation of ß-catenin, triggered Wnt/ß-catenin pathway, and alleviated neuroinflammation and neuronal injury, thus improving IH-related mice cognitive dysfunction.

Relationship between obstructive sleep apnoea syndrome and gastrointestinal diseases: a systematic review and Meta-analysis.

Studies exploring the association between obstructive sleep apnoea syndrome (OSA) and gastrointestinal diseases (GID) are important for enhancing clinical outcomes. This study aimed to systematically assess the association between these two diseases. Adhering to PRISMA guidelines, a comprehensive literature search was conducted across databases including PubMed, Web of Science, Willey Library, Cochrane Library and Scopus. This search focused on English literature published up to January 2024. Literature screening, quality assessment (using the NOS scale) and data extraction were performed by two independent researchers. Statistical analyses were performed using the meta-package of the R.4.2.2 software. An initial screening of 2178 papers was conducted and 11 studies were included. Meta-analysis results showed a significant association between OSA and GID (p < 0.01). Subgroup analyses further indicated a stronger association between OSA and GID in Asian populations compared to Europe and the United States. In addition, both benign and malignant GID were significantly associated with OSA, with a pronounced association for malignant GID than for benign GID. The results of publication bias analysis revealed no significant bias (Begg's test p = 0.45, Egger's test p = 0.60). This study uncovers a notable association between OSA and GID, especially in Asian populations, suggesting that clinicians should consider the potential connection between these two diseases during diagnosis and treatment. However, due to the heterogeneity and limitations of the study, these conclusions need to be further validated through more comprehensive research.

[Cervicogenic dysphagia: a case report]. / Tservikogennaya disfagiya: sluchai iz praktiki.

The article presents a case of pharyngeal dysphagia and obstructive sleep apnea syndrome caused by degenerative-dystrophic changes in the cervical spine with the formation of large cervical osteophytes at the C3-C6 level. Osteophytes caused deformation of the posterior wall of the hypopharynx and narrowing of its lumen by 20-25% from the level of the arytenoid cartilages to the upper parts of the epiglottis. CT scan also showed the intervertebral disc heights lost, as well as osteophytes at the posterolateral margins of the vertebral bodies (disc osteophyte complex). Osteosclerosis in combination with facet arthrosis caused spinal and foraminal stenosis.

Mechanical Interactions Between the Upper Airway and the Lungs that Affect the Propensity to Obstructive Sleep Apnea in Health and Chronic Lung Disease.

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive narrowing and collapse of the upper airways during sleep. It is caused by multiple anatomic and nonanatomic factors but end-expiratory lung volume (EELV) is an important factor as increased EELV can stabilize the upper airway via caudal traction forces. EELV is impacted by changes in sleep stages, body position, weight, and chronic lung diseases, and this article reviews the mechanical interactions between the lungs and upper airway that affect the propensity to OSA. In doing so, it highlights the need for additional research in this area.

Does Obstructive Sleep Apnea Lead to Progression of Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) have important bidirectional relationships that influence the pathophysiology of each disorder. The slim hyperinflated "pink puffer" phenotype of COPD protects against OSA, whereas the heavier "blue bloater" phenotype predisposes to OSA by fluid retention. OSA may aggravate COPD by promoting airway inflammation. COPD-OSA overlap patients have lower quality of life and are at higher risk of cardiovascular comorbidity than either disorder alone due to greater nocturnal oxygen desaturation and sympathetic activation. Management of OSA with positive airway pressure improves COPD outcomes that include lower exacerbation rates compared to untreated patients.

Untreated Obstructive Sleep Apnea in Interstitial Lung Disease and Impact on Interstitial Lung Disease Outcomes.

Subjects with interstitial lung disease (ILD) often suffer from nocturnal cough, insomnia, and poor sleep quality. Subjects with ILD and obstructive sleep apnea (OSA) seem to have relatively mild symptoms from sleep fragmentation compared to subjects with only ILD. The overlap of ILD, OSA, and sleeping hypoxemia may be associated with poor outcome, even though there is no agreement on which sleep parameter is mostly associated with worsening ILD prognosis. Randomized controlled trials are needed to understand when positive airway pressure (PAP) treatment is required in subjects with ILD and OSA and the impact of PAP treatment on ILD progression.

Effects of Obstructive Sleep Apnea on Airway Immunity and Susceptibility to Respiratory Infections.

Obstructive sleep apnea is a prevalent sleep disorder characterized by recurrent episodes of partial or complete upper airway collapse during sleep, leading to disrupted breathing patterns and intermittent hypoxia. OSA results in systemic inflammation but also directly affects the upper and lower airways leading to upregulation of inflammatory pathways and alterations of the local microbiome. These changes result in increased susceptibility to respiratory infections such as influenza, COVID-19, and bacterial pneumonia. This relationship is more complex and bidirectional in individuals with chronic lung disease such as chronic obstructive lung disease, interstitial lung disease and bronchiectasis.

Obstructive Sleep Apnea, Obesity Hypoventilation Syndrome, and Pulmonary Hypertension: A State-of-the-Art Review.

The pathophysiological interplay between sleep-disordered breathing (SDB) and pulmonary hypertension (PH) is complex and can involve a variety of mechanisms by which SDB can worsen PH. These mechanistic pathways include wide swings in intrathoracic pressure while breathing against an occluded upper airway, intermittent and/or sustained hypoxemia, acute and/or chronic hypercapnia, and obesity. In this review, we discuss how the downstream consequences of SDB can adversely impact PH, the challenges in accurately diagnosing and classifying PH in the severely obese, and review the limited literature assessing the effect of treating obesity, obstructive sleep apnea, and obesity hypoventilation syndrome on PH.

Obstructive Sleep Apnea and Sarcoidosis Interactions.

Obstructive sleep apnea (OSA) is very prevalent in sarcoidosis patients. Sarcoidosis of the upper respiratory tract may affect upper airway patency and increase the risk of OSA. Weight gain due to steroid use, upper airway myopathy due to steroids and sarcoidosis itself, and interstitial lung disease with decreased upper airway patency are other reasons for the higher OSA prevalence seen in sarcoidosis. Several clinical manifestations such as fatigue, hypersomnolence, cognitive deficits, and pulmonary hypertension are common to both OSA and sarcoidosis. Therefore, early screening and treatment for OSA can improve symptoms and overall patient quality of life.

Dyspnea and Quality of Life Improvements with Management of Comorbid Obstructive Sleep Apnea in Chronic Lung Disease.

Obstructive sleep apnea (OSA) has emerged as a significant and prevalent comorbidity associated with chronic lung diseases, including chronic obstructive pulmonary disease, asthma, and interstitial lung diseases. These overlap syndromes are associated with worse patient-reported outcomes (sleep quality, quality of life measures, mental health) than each condition independently. Observational studies suggest that patients with overlap syndrome who are adherent to positive airway pressure therapy report improved quality of life, sleep quality, depression, and daytime symptoms. Screening for and management of OSA in patients with overlap syndrome should emphasize the interconnected nature of these 2 conditions and the positive impact that OSA management can have on patients' well-being and overall health.

Hypoxic and Autonomic Mechanisms from Sleep-Disordered Breathing Leading to Cardiopulmonary Dysfunction.

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder. Its prevalence has increased due to increasing obesity and improved screening and diagnostic strategies. OSA overlaps with cardiopulmonary diseases to promote intermittent hypoxia and autonomic dysfunction. Intermittent hypoxia increases the risk for oxidative stress and inflammation, which promotes endothelial dysfunction and predisposes to atherosclerosis and other cardiovascular complications. OSA is associated with an increased sympathetic nervous system drive resulting in autonomic dysfunction leading to worsening of cardiopulmonary diseases. Cardiovascular diseases are observed in 40% to 80% of OSA patients. Therefore, it is essential to screen and treat cardiovascular diseases.

Is sleep bruxism in obstructive sleep apnea only an oral health related problem?

BACKGROUND: The etiology of sleep bruxism in obstructive sleep apnea (OSA) patients is not yet fully clarified. This prospective clinical study aimed to investigate the connection between probable sleep bruxism, electromyographic muscle tone, and respiratory sleep patterns recorded during polysomnography. METHODS: 106 patients with OSA (74 males, 31 females, mean age: 56.1 ± 11.4 years) were divided into two groups (sleep bruxism: SB; no sleep bruxism: NSB). Probable SB were based on the AASM criteria: self-report of clenching/grinding, orofacial symptoms upon awakening, abnormal tooth wear and hypertrophy of the masseter muscle. Both groups underwent clinical examination for painful muscle symptoms aligned with Temporomandibular Disorders Diagnostic Criteria (DC/TMD), such as myalgia, myofascial pain, and headache attributed to temporomandibular disorder. Additionally, non-complaint positive muscle palpation and orofacial-related limitations (Jaw Functional Limited Scale-20: JFLS-20) were assessed. A one-night polysomnography with electromyographic masseter muscle tone (EMG) measurement was performed. Descriptive data, inter-group comparisons and multivariate logistic regression were calculated. RESULTS: OSA patients had a 37.1% prevalence of SB. EMG muscle tone (N1-N3, REM; P = 0.001) and the number of hypopneas (P = 0.042) were significantly higher in the sleep bruxism group. While measures like apnea-hypopnea-index (AHI), respiratory-disturbance-index (RDI), apnea index (AI), hypopnea-index (HI), number of arousals, and heart rate (1/min) were elevated in sleep bruxers, the differences were not statistically significant. There was no difference in sleep efficiency (SE; P = 0.403). Non-complaint masseter muscle palpation (61.5%; P = 0.015) and myalgia (41%; P = 0.010) were significant higher in SB patients. Multivariate logistic regression showed a significant contribution of EMG muscle tone and JFLS-20 to bruxism risk. CONCLUSION: Increased EMG muscle tone and orofacial limitations can predict sleep bruxism in OSA patients. Besides, SB patients suffer more from sleep disorder breathing. Thus, sleep bruxism seems to be not only an oral health related problem in obstructive apnea. Consequently, interdisciplinary interventions are crucial for effectively treating these patients. TRIAL REGISTRATION: The study was approved by the Ethics Committee of Philipps-University Marburg (reg. no. 13/22-2022) and registered at the "German Clinical Trial Register, DRKS" (DRKS0002959).

Elucidating the association of obstructive sleep apnea with brain structure and cognitive performance.

BACKGROUND: Obstructive sleep apnea (OSA) is a pervasive, chronic sleep-related respiratory condition that causes brain structural alterations and cognitive impairments. However, the causal association of OSA with brain morphology and cognitive performance has not been determined. METHODS: We conducted a two-sample bidirectional Mendelian randomization (MR) analysis to investigate the causal relationship between OSA and a range of neurocognitive characteristics, including brain cortical structure, brain subcortical structure, brain structural change across the lifespan, and cognitive performance. Summary-level GWAS data for OSA from the FinnGen consortium was used to identify genetically predicted OSA. Data regarding neurocognitive characteristics were obtained from published meta-analysis studies. Linkage disequilibrium score regression analysis was employed to reveal genetic correlations between OSA and related traits. RESULTS: Our MR study provided evidence that OSA was found to significantly increase the volume of the hippocampus (IVW ß (95% CI) = 158.997 (76.768 to 241.227), P = 1.51e-04), with no heterogeneity and pleiotropy detected. Nominally causal effects of OSA on brain structures, such as the thickness of the temporal pole with or without global weighted, amygdala structure change, and cerebellum white matter change covering lifespan, were observed. Bidirectional causal links were also detected between brain cortical structure, brain subcortical, cognitive performance, and OSA risk. LDSC regression analysis showed no significant correlation between OSA and hippocampus volume. CONCLUSIONS: Overall, we observed a positive association between genetically predicted OSA and hippocampus volume. These findings may provide new insights into the bidirectional links between OSA and neurocognitive features, including brain morphology and cognitive performance.