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The aim of the study was to compare REM-dependent and REM-independent, obstructive sleep apnea syndrome (OSA) patients in relation to their daily sleepiness assessed by Epworth sleepiness scale (ESS). The study included 1863 consecutive patients, who were referred to a sleep centre with a presumed diagnosis of OSA. Following polysomnography, 292 patients fulfilled criteria for either REM-dependent OSA (REM-OSA, n = 102) or REM-independent OSA (nREM-OSA, n = 190). Both study groups were matched regarding sex and age. REM-OSA group had two times lower median apnoea-hypopnea index (AHI) compared to nREM-OSA (p < 0.001), yet day-time sleepiness measured by ESS was similar: median score 9.0 (6.0–11.0) and 8.0 (4.8–11.0), p = 0.109, respectively. Subsequent post-hoc ANCOVA analysis, with covariates (BMI, percent of total sleep time spent in REM stage, percent of total sleep time spent in the supine position), has shown statistically significant difference between study groups regarding AHI (p < 0.001) and no difference regarding ESS score (p = 0.063). Despite two times lower AHI, patients with REM-OSA present with similar day-time sleepiness as those with REM independent OSA. Daily sleepiness may be stronger associated with apneas/hypopneas occurring in REM than nREM sleep.

Attention deficit hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder that not only affects attention and behavior but is also intricately linked with sleep disturbances and immune system dysregulation. Recent research highlights that individuals with ADHD frequently experience sleep problems, which in turn exacerbate ADHD symptoms and contribute to cognitive and emotional difficulties. Immunological alterations, including elevated proinflammatory cytokines and hypothalamic–pituitary–adrenal axis dysfunction, have been observed among ADHD patients, suggesting a biological interplay between inflammation, sleep, and neurodevelopment. Genetic and environmental factors further modulate these relationships, influencing the onset and progression of the disorder. Thus, there is a need to find a key connecting such topics and the most vulnerable subjects in order to contribute towards a more personalized approach. This review examines the complex relationships between sleep, immunology, and ADHD, and explores the underlying mechanisms that involve circadian rhythm genes, neuroinflammation, and neurotransmitter imbalances. Our review outlines therapeutic strategies, emphasizing the importance of integrated pharmacological, behavioral, and lifestyle interventions to improve sleep quality, regulate immune responses, and ultimately enhance the overall management of ADHD.

Obstructive sleep apnea (OSA) is a chronic respiratory disorder characterized by intermittent hypoxia and is strongly associated with the development of type 2 diabetes mellitus (T2DM). Despite this link, the molecular mechanisms underlying OSA-related metabolic dysregulation remain incompletely understood. The aim of the study was to investigate the role of hypoxia-sensitive microRNAs, sirtuin 1 (SIRT1), and adiponectin in the metabolic profile of OSA patients, with and without T2DM. A total of 87 participants were stratified into three groups: OSA, OSA + T2DM, and healthy controls. Blood samples were collected in the evening and morning, and after continuous positive airway pressure (CPAP) therapy. Expression levels of miRNAs and SIRT1 were measured via RT-qPCR; adiponectin was quantified by ELISA. Significantly reduced expression of miRNA-181a and miRNA-199a was observed in the OSA + T2DM group compared to OSA (p = 0.035 and p = 0.042, respectively). In contrast, SIRT1 expression was highest in the OSA + T2DM group (p < 0.01), while adiponectin concentrations was lowest in this group and the highest among healthy controls (p = 0.001). Despite increased SIRT1 in OSA + T2DM patients, the parallel increase in adiponectin was not observed. Additionally, expression of SIRT1 was significantly increased in OSA patients who were taking metformin (n = 23) vs. patients without metformin (n = 32) 77.315 vs. 437.08 (p = 0.037). CPAP therapy had significant influence only on miRNA-181a—expression was increased after long-term treatment (p = 0.047). Increased miRNA-181a expression in patients with OSA is related to decreased SIRT1 expression, which may lead to T2DM development. Surprisingly, the expression of SIRT1 is significantly higher and expression of hypoxia-sensitive miRNAs is significantly lower in patients with already developed T2DM, which might be explained by metformin intake.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in the regulation of synaptic plasticity and metabolic processes, including glucose metabolism and insulin sensitivity. In patients with obstructive sleep apnea (OSA), recurrent episodes of intermittent hypoxia may stimulate BDNF expression as a compensatory neuroprotective response. OSA is associated with metabolic disturbances, such as increased insulin resistance and a higher risk of type 2 diabetes. Continuous positive airway pressure (CPAP) therapy may influence both BDNF levels and metabolic outcomes. The aim of this study was to evaluate changes in BDNF concentration and glucose metabolism in patients with OSA, with particular emphasis on the effect of long-term CPAP therapy. Sixty-six adult patients with OSA confirmed by polysomnography were enrolled and divided into severe (s-OSA) and non-severe (ns-OSA) groups. Fasting blood samples were collected to measure glucose, insulin, and BDNF concentrations. Patients with s-OSA were re-evaluated after 12 months of CPAP therapy and further classified as compliant (sc-OSA) or non-compliant (snc-OSA) based on recorded device usage. The same biochemical parameters were assessed after the 12-month follow-up. Baseline BDNF levels were significantly higher in the s-OSA group compared to the ns-OSA group (20.1 ng/mL vs. 8.1 ng/mL, p = 0.02) and correlated with the apnea–hypopnea index (AHI, r = 0.38, p = 0.02). In the nsc-OSA group, BDNF concentrations increased significantly after 12 months (16.2 ng/mL vs. 35.5 ng/mL, p < 0.001), while no significant change was observed in the sc-OSA group (24.4 ng/mL vs. 27.4 ng/mL, p = 0.33). Among sc-OSA patients, a significant improvement in insulin resistance was noted, although no significant changes were observed in fasting glucose or insulin levels. Increased BDNF levels were observed in patients with s-OSA compared to ns-OSA. Compliant CPAP therapy was associated with reduced insulin resistance and no further BDNF increase, in contrast to non-compliance, suggesting a beneficial effect of CPAP on glucose metabolism and BDNF regulation. These findings support the hypothesis that both neurotrophic and metabolic responses in OSA may be modulated by disease severity and therapy adherence.

Polysomnography (PSG) is considered the gold standard in obstructive sleep apnea-hypopnea syndrome (OSAS) diagnostics, but its availability is still limited. Thus, it seems useful to assess patients pre-diagnostic risk for OSAS to prioritize the use of this examination. The purpose of this study was to assess positive (PPV) and negative (NPV) predictive values of the STOP BANG questionnaire (SBQ) in patients with presumptive diagnosis of OSAS. From a database of 1,171 (880 men) patients of a university based sleep center, 1,123 (847 men) met eligibility criteria and their SBQ scores were subject to the Bayesian analysis. The analysis of PPV and NPV was conducted at all values of SBQ for all subjects, but also separately for males and females, and for total sleep time (TS) and for sleep in the lateral position (LP). The probability of OSAS (AHI ≥ 5) and at least moderate OSAS (AHI ≥ 15) for TS was 0.766 and 0.516, while for LP the values were 0.432 and 0.289, respectively. Overall, due to low specificity, SBQ had low PPV for TS and LP. Negative test result (SBQ < 3) revealed NPV of 0.620 at AHI < 5 and 0.859 at AHI < 15 for TS, while in LP NPV values were 0.935 at AHI < 5 and 1.0 at AHI < 15, (n = 31), while SBQ < 4 generated NPV of 0.943 in LP (n = 105). SBQ did not change probabilities of OSAS to confirm or rebut diagnosis for TS. However, it is highly probable that SQB can rule out OSAS diagnosis at AHI ≥ 15 for LP.

ObjectivesThe study aimed to evaluate the diagnostic value of an original questionnaire for obstructive sleep apnea (OSA), the BOAH scale, and its ability to prioritize patients at high risk for OSA for polysomnography (PSG) examination.MethodsThe analysis included 273 patients referred to the Department of Sleep Medicine of the Royal Infirmary, Edinburgh, Scotland. The BOAH scale is comprised of 5 parameters: BMI (≥ 30 kg/m2 gives 1 point, ≥ 35 kg/m2 2 points), presence of witnessed apneas during sleep (1 point), patient age ≥ 50 years (1 point), and history of hypertension (1 point). Patients were divided into three study groups depending on OSA severity defined by the apnea-hypopnea index (AHI): at least mild (AHI ≥ 5), at least moderate (AHI ≥ 15), and severe (AHI ≥ 30) OSA based on polysomnography examination.ResultsIn the group of patients with severe OSA, the best BOAH cutoff point was 4 points based upon the Youden index. With 4 points, the area under the receiver operating characteristic (ROC) curve was 0.778 (95% CI 0.721–0.834). Sensitivity and specificity were 57% and 89%, respectively, yielding a positive and negative predictive value of 75% and 78%, respectively, for diagnosis of severe OSAS in a patient sample with a pre-test probability for severe OSA at 37%.ConclusionsThe BOAH scale in this group of Scottish patients performed comparably to other available questionnaires and scales while being shorter and simpler. The findings suggest that the BOAH scale should be considered as a useful instrument in OSA diagnosis and prioritization of high-risk patients for PSG examination.

Interleukin 33 (IL-33) is an alarmin cytokine from the IL-1 family. IL-33 is localized in the nucleus and acts there as a gene regulator. Following injury, stress or cell death, it is released from the nucleus, and exerts its pro-inflammatory biological functions via the transmembrane form of the ST2 receptor, which is present mainly as attached to immune cells. In recent years, IL-33 became a focus of many studies due to its possible role in inflammatory disorders. Among respiratory disorders, the contribution of IL-33 to the development of asthma, in particular, has been most identified. Increased level of IL-33 in lung epithelial cells and blood serum has been observed in asthma patients. The IL-33/ST2 interaction activated the Th2 mediated immune response and further production of many pro-inflammatory cytokines. Single nucleotide polymorphisms in the IL-33 gene cause a predisposition to the development of asthma. Similarly, in chronic pulmonary obstructive disease (COPD), both increased expression of IL-33 and the ST2 receptor has been observed. Interestingly, cigarette smoke, a key inducer of COPD, not only activates IL-33 production by epithelial and endothelial cells, but also induces the expression of IL-33 in peripheral blood mononuclear cells. Knowledge regarding its contribution in other respiratory disorders, such as obstructive sleep apnea, remains greatly limited. Recently it was shown that IL-33 is one of the inflammatory mediators by which levels in blood serum are increased in OSA patients, compared to healthy control patients. This mini review summarizes current knowledge on IL-33 involvement in chosen chronic respiratory disorders and proposes this interleukin as a possible link in the pathogenesis of these diseases.

Glutamate and γ-aminobutyric acid (GABA) are the two main neurotransmitters in the human brain. The balance between their excitatory and inhibitory functions is crucial for maintaining the brain’s physiological functions. Disturbance of glutamatergic or GABAergic neurotransmission leads to serious health problems including neurodegeneration, affective and sleep disorders. Both GABA and glutamate are involved in the control of the sleep–wake cycle. The disturbances in their function may cause sleep and sleep-related disorders. Obstructive sleep apnea (OSA) is the most common sleep respiratory disorder and is characterized by repetitive collapse of the upper airway resulting in intermittent hypoxia and sleep fragmentation. The complex pathophysiology of OSA is the basis of the development of numerous comorbid diseases. There is emerging evidence that GABA and glutamate disturbances may be involved in the pathogenesis of OSA, as well as its comorbidities. Additionally, the GABA/glutamate targeted pharmacotherapy may also influence the course of OSA, which is important in the implementation of wildly used drugs including benzodiazepines, anesthetics, and gabapentinoids. In this review, we summarize current knowledge on the influence of disturbances in glutamatergic and GABAergic neurotransmission on obstructive sleep apnea.

Insufficient sleep duration may lead to a series of immune dysfunctions. One of the factors influencing this effect could be physical activity (PA). The study aimed to assess the impact of deprivation of sleep (DS) on selected inflammatory parameters. Seventy-seven participants completed the protocol consisting of polysomnography (PSG) conducted in a sleep laboratory and DS, monitored with an actigraph. PA was assessed with actigraphy, which categorized participants as active or inactive. White blood cells (WBC) values negatively correlated with sleep efficiency based on sleep diaries and PSG parameters (total sleep time, sleep efficiency, and REM duration), but regression analysis showed that WBC depends only on the sleep diary parameter. Granulocytes (GRA) positively correlated with REM latency, and negatively with sleep efficiency. After DS, all participants exhibited an elevated GRA count. The number of WBC and GRA increased also in the active group; inactive participants showed no changes in inflammatory parameters. The overall number of WBC depends primarily on the quality of sleep over a period of several days. Under the influence of sleep deprivation, the number of GRA increases, but the number of leukocytes depends on the level of physical activity during DS.