The platelet-to-lymphocyte ratio reflects the severity of obstructive sleep apnea syndrome and concurrent hypertension.
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ABSTRACT:
SUBMITTER: Song YJ
PROVIDER: S-EPMC4750799 | biostudies-other | 2015
REPOSITORIES: biostudies-other
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Project description:Study objectivesThe association of mild obstructive sleep apnea (OSA) with important clinical outcomes remains unclear. We aimed to investigate the association between mild OSA and systemic arterial hypertension (SAH) in the European Sleep Apnea Database cohort.MethodsIn a multicenter sample of 4,732 participants, we analyzed the risk of mild OSA (subclassified into 2 groups: mildAHI 5-<11/h (apnea-hypopnea index [AHI], 5 to <11 events/h) and mildAHI 11-<15/h (AHI, ≥11 to <15 events/h) compared with nonapneic snorers for prevalent SAH after adjustment for relevant confounding factors including sex, age, smoking, obesity, daytime sleepiness, dyslipidemia, chronic obstructive pulmonary disease, type 2 diabetes, and sleep test methodology (polygraphy or polysomnography).ResultsSAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and nonapneic snorers (52% vs 45% vs 30%; P < .001). Corresponding adjusted odds ratios for SAH were 1.789 (mildAHI 11-<15/h; 95% confidence interval [CI], 1.49-2.15) and 1.558 (mildAHI 5-<11/h; 95%, CI, 1.34-1.82), respectively (P < .001). In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in the polygraphy (odds ratio, 1.779; 95% CI, 1.403-2.256; P < .001) and polysomnography groups (odds ratio, 1.424; 95% CI, 1.047-1.939; P = .025).ConclusionsOur data suggest a dose-response relationship between mild OSA and SAH risk, starting from 5 events/h in polygraphy recordings and continuing with a further risk increase in the 11- to <150-events/h range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify participants with OSA according to cardiovascular risk.
| S-EPMC7849667 | biostudies-literature
Project description:This meta-analysis is aimed to investigate the association between the neutrophil-to-lymphocyte ratio (NLR) and obstructive sleep apnea (OSA). The PubMed, Web of Science, Google Scholar, and Cochrane Library databases were searched to collect all relevant articles. The pooled standardized mean difference (SMD) with a 95% confidence interval (CI) was calculated using the random effects model. In addition, subgroup analysis and meta-regression analysis were performed. Eleven eligible articles containing 2,259 patients with OSA were included in this study. Pooled outcomes revealed that the NLR was significantly higher in patients with OSA than in controls (SMD 0.62, 95% CI 0.29-0.94, P?=?0.002). In subgroup analyses, differences in the NLR between patients and controls increased with worsening OSA grades. Furthermore, meta-regression analysis showed that differences in mean BMI exerted a significant effect on differences in the NLR (P?=?0.0003). In summary, our meta-analysis demonstrated that the NLR in OSA patients was significantly higher than that in controls, and the difference was larger in patients with severe OSA. These results indicate that the NLR may be a reliable marker for detecting systemic inflammation and predicting disease severity in patients with OSA.
| S-EPMC7331605 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO
Project description:BACKGROUND:Cardiac involvement is a rare and potentially fatal presentation of sarcoidosis. Obstructive sleep apnea may complicate sarcoidosis. CASE PRESENTATION:We report a case of a sarcoidosis patient with cardiac involvement presenting with ventricular arrhythmias. Besides medical and invasive measures of therapy, the patient failed to respond fully. The patient was subjected to overnight polysomnography and diagnosed with concurrent obstructive sleep apnea syndrome. Following continuous positive airway pressure therapy, we observed a significant improvement of ventricular arrhythmias while methylprednisolone was further tapered. CONCLUSIONS:To our knowledge, this is the first report of cardiac sarcoidosis further implicated by OSAHS and presenting as ventricular arrhythmias that underlies the need for extensive testing in cardiac sarcoidosis in patients not responding to immunosuppressive therapy.
| S-EPMC7210663 | biostudies-literature
Project description:There is uncertainty over which characteristics increase obstructive sleep apnea syndrome (OSAS) severity in children. In candidates for adenotonsillectomy (AT), we evaluated the relationship of OSAS severity and age, sex, race, body mass index (BMI), environmental tobacco smoke (ETS), prematurity, socioeconomic variables, and comorbidities.Cross-sectional screening and baseline data were analyzed from the Childhood Adenotonsillectomy Trial, a randomized, controlled, multicenter study evaluating AT versus medical management. Regression analysis assessed the relationship between the apnea hypopnea index (AHI) and risk factors obtained by direct measurement or questionnaire.Clinical referral setting.Children, ages 5 to 9.9 y with OSAS.Of the 1,244 children undergoing screening polysomnography, 464 (37%) were eligible (2 ? AHI < 30 or 1 ? obstructive apnea index [OAI] < 20 and without severe oxygen desaturation) and randomized; 129 (10%) were eligible but were not randomized; 608 (49%) had AHI/OAI levels below entry criteria; and 43 (3%) had levels of OSAS that exceeded entry criteria. Among the randomized children, univariate analyses showed significant associations of AHI with race, BMI z score, environmental tobacco smoke (ETS), family income, and referral source, but not with other variables. After adjusting for potential confounders, African American race (P = 0.003) and ETS (P = 0.026) were each associated with an approximately 20% increase in AHI. After adjusting for these factors, obesity and other factors were not significant.Apnea hypopnea index level was significantly associated with race and environmental tobacco smoke, highlighting the potential effect of environmental factors, and possibly genetic factors, on pediatric obstructive sleep apnea syndrome severity. Efforts to reduce environmental tobacco smoke exposure may help reduce obstructive sleep apnea syndrome severity.Clinicaltrials.gov (#NCT00560859).
| S-EPMC3900616 | biostudies-literature
Project description:Hypertension and dementia are highly prevalent in the general population. Hypertension has been shown to be a risk factor for Alzheimer's dementia and vascular dementia. Sleep apnea, another common disorder, is strongly associated with hypertension and recent evidence suggests that it may also be linked with cognitive decline and dementia. It is possible that sleep apnea is the final common pathway linking hypertension to the development of dementia. This hypothesis merits further exploration as sleep apnea is readily treatable and such therapy could foreseeably delay or prevent the onset of dementia. At present, there is a paucity of therapeutic modalities that can prevent or arrest cognitive decline. In this review, we describe the associations between hypertension, dementia and sleep apnea, the pathophysiologic mechanisms underlying these associations, and the literature examining the impact of treatment of hypertension and sleep apnea on cognition. Potential areas of future investigation that may help advance our understanding of the magnitude and direction of the interaction between these conditions and the effects of treatment of high blood pressure and sleep apnea on cognition are highlighted.
| S-EPMC6636426 | biostudies-literature
Project description:Due to its effects, like an exaggerated negative intrathoracic pressure, sympathetic activation, systemic inflammation, oxidative stress, and endothelial dysfunction, obstructive sleep apnea (OSA) has been involved as a cause in multiple cardiovascular diseases. These diseases include coronary artery disease, hypertension, heart failure, and pulmonary hypertension (PH). Furthermore, OSA often coexists with chronic thromboembolic pulmonary hypertension (CTEPH) in clinical practice. However, few studies focus on OSA and its relationship with CTEPH. This study aims to determine whether OSA has an influence on the clinic status of patients with CTEPH, and to identify what possible factors are associated with OSA in CTEPH. Patients who were newly diagnosed with CTEPH and received overnight polysomnography (PSG) monitoring from September 2015 to December 2017 were enrolled. OSA was defined as apnea-hypopnea index (AHI) of ?5/h and the obstructive events at ?50%. Baseline clinical characteristics and parameters were collected and compared between CTEPH patients with and without OSA. In addition, logistic regression analysis was performed to identify possible factors associated with OSA in CTEPH. Fifty-seven patients with CTEPH were eventually enrolled. Among them, 32 patients were diagnosed with OSA by PSG. CTEPH patients with OSA showed an older age, a higher body mass index (BMI), a higher hemoglobin level, a lower oxygen saturation and a worse World Health Organization functional class (WHO FC) (all P<0.05) when compared to CTEPH patients without OSA. In addition, sleep data including AHI, oxygen desaturation index and minimum oxygen saturation were also statistically different between two groups (all P<0.05). Adjusted for age, sex and BMI, hemoglobin [odd ratio (OR) =1.057, 95% confidence interval (CI): 1.001-1.117, P=0.046], oxygen saturation (OR =0.718, 95% CI: 0.554-0.929, P=0.012), N-terminal pro-brain natriuretic peptide (OR =1.001, 95% CI: 1.000-1.002, P=0.016), mean right atrium pressure (OR =1.284, 95% CI: 1.030-1.600, P=0.026), mean pulmonary arterial pressure (mPAP) (OR =1.087, 95% CI: 1.001-1.180, P=0.048), cardiac index (CI) (OR =0.058, 95% CI: 0.008-0.433, P=0.037), pulmonary vascular resistance (OR =1.004, 95% CI: 1.001-1.007, P=0.014) and WHO FC III-IV (OR =18.550, 95% CI: 2.363-144.128, P=0.005) were associated with OSA in CTEPH. Multivariate logistic regression analysis demonstrated CI (OR =0.051, 95% CI: 0.003-0.868, P=0.040) was independently associated with OSA in CTEPH in addition to age, sex and BMI. OSA may aggravate the clinical status of CTEPH patients to some degree. In turn, a worse hemodynamics, oxygenation state and cardiac function are associated with OSA in CTEPH after being adjusted for age, sex and BMI. Among them, CI is the most important parameter in indicating the coexistence of OSA and CTEPH.
| S-EPMC6236151 | biostudies-other
Project description:In vitro and animal models suggest that obstructive sleep apnea (OSA) increases cancer risk. However, the impact of OSA severity on cancer risk is poorly understood. We conducted a case-cohort study (a variant of the case-control study design), nested in a cohort of patients with a clinical diagnosis of OSA. OSA patients diagnosed between 2005 and 2013 were linked to a population-based cancer registry to identify cancers diagnosed subsequent to OSA between 2005 and 2015. Medical records were reviewed for a representative sample of 1162 OSA patients from this cohort (including 24 with subsequent cancer), and for an additional 304 OSA patients diagnosed with cancer; information regarding OSA severity indicators, including apnea-hypopnea index (AHI) was abstracted from these records. Adjusted Cox proportional hazards regression were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for associations of OSA severity indicators on cancer incidence. Compared with individuals in the lowest AHI category (5-14.9), indicating mild OSA, the adjusted HR (95% CI) for cancer incidence associated with having moderate (15-29.9) or severe (30+) OSA were 0.72 (0.40-1.29) and 0.87 (0.52-1.45) respectively. Associations with other severity indicators were not significantly associated with cancer. However, the proportion of patients with severe OSA (AHI ≥30) was consistently higher across numerous cancer sites relative to the subcohort, suggesting increased cancer risk relative to patients with less severe OSA. The absence of significant associations with OSA severity measures suggest that the underlying mechanisms deserve further investigation.
| S-EPMC6525275 | biostudies-literature
Project description:Tonsil hyperplasia is the most common cause of pediatric obstructive sleep apnea (OSA). Despite the growing knowledge in tissue immunology of tonsils, the immunopathology driving tonsil hyperplasia and OSA remains unknown. Here we used multi-parametric flow cytometry to analyze the composition and phenotype of tonsillar innate lymphoid cells (ILCs), T cells, and B cells from pediatric patients with OSA, who had previous polysomnography. Unbiased clustering analysis was used to delineate and compare lymphocyte heterogeneity between two patient groups: children with small tonsils and moderate OSA (n = 6) or large tonsils and very severe OSA (n = 13). We detected disturbed ILC and B cell proportions in patients with large tonsils, characterized by an increase in the frequency of naïve CD27-CD21hi B cells and a relative reduction of ILCs. The enrichment of naïve B cells was not commensurate with elevated Ki67 expression, suggesting defective differentiation and/or migration rather than cellular proliferation to be the causative mechanism. Finally, yet importantly, we provide the flow cytometry data to be used as a resource for additional translational studies aimed at investigating the immunological mechanisms of pediatric tonsil hyperplasia and OSA.
| S-EPMC8570126 | biostudies-literature