CPAP Does Not Reduce Inflammatory Biomarkers in Patients With Coronary Artery Disease and Nonsleepy Obstructive Sleep Apnea: A Randomized Controlled Trial

Hossain

Journal of Periodontology

et al. 2019

Background: Elevated levels of inflammatory biomarkers are consistently associated with chronic conditions, for which periodontitis and sleep are established risk factors. We examined the relationships between periodontitis, hours of sleep and white blood cell (WBC) markers among a nationally representative sample of US adults.Methods: Cross-sectional study using existing demographic, examination, laboratory and questionnaire data on 11,813 participants (5,814 men and 5,999 women, mean age ± SE; range: 52.74 ± 0.24; 30 to 80 years) from the 2009 to 2014 National Health and Nutrition Examination Surveys. Unadjusted, sex-and age-adjusted, as well as fully adjusted linear and logistic regression models were conducted in addition to generalized structural equations models, while considering sampling design complexity., odds ratios with their 95% confidence intervals, indirect effects and mediation proportions were estimated. Results:The weighted mean WBC count was 7,130 cells/µL, with the WBC 5-part differential estimated in terms of percentages of lymphocytes (29.50%), monocytes (7.99%), neutrophils (59.03%), eosinophils (2.84%), and basophils (71.88%). Furthermore, 36.2% of participants reported <7 hours of sleep and 49.8% had periodontitis. In fully adjusted models controlling for sociodemographic, lifestyle, and health characteristics, neither WBC markers nor periodontitis were related to hours of sleep.By contrast, periodontitis was directly related to WBC count and %neutrophils and inversely related to %lymphocytes, especially among men. However, the relationship of periodontitis with %neutrophils and %lymphocytes may be modified by hours of sleep, as it was specific to individuals reporting ≥7 hours of sleep. Conclusion:Periodontitis may be directly related to WBC count and %neutrophils and inversely related to %lymphocytes, especially among men and individuals reporting ≥7 hours of sleep, with implications for primary and secondary prevention. K E Y W O R D Sinflammation, leukocytes, periodontitis, sleep, surveys and questionnaires 582

Section: Discussionmentioning

confidence: 99%

Section: Covariatesmentioning

confidence: 99%

Periodontal disease, sleep duration, and white blood cell markers in the 2009 to 2014 National Health and Nutrition Examination Surveys

Hossain

Journal of Periodontology

et al. 2019

“…The pooling of eight published reports in adults with OSAS revealed that plasma IL-6 levels ranged from 1.2 to 131.7 pg/mL before CPAP treatment and signi cantly decreased to between 0.45 to 66.04 pg/mL after CPAP treatment [48]. However, among those studies, there was signi cant inter-individual heterogeneity [9] which may be related to the variance for IL-6 genes, environmental and/or lifestyle in uences [49,50]. Potential interactions between OSAS, obesity, and both genetic, environmental, and lifestyle factors, ultimately lead to a cascade of pathophysiological pathways, resulting in increased systemic in ammation, as illustrated by increased levels of IL-6 [9,50].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6 and vitamin D serum levels in patients with obstructive sleep apnea syndrome before and after long-term continuous positive airway pressure treatment

Kotsiou

Siachpazidou

Pastaka

et al. 2020

Preprint

Background: Hypoxia induces the production of adipocyte-derived mediators such as IL-6 in obstructive sleep apnea syndrome (OSAS). Low serum 25-hydroxyvitamin D (25(OH)D) levels have been linked to OSAS susceptibility. No data exist to assess whether there has been a correlation between vitamin D and IL-6 serum levels. The effect of CPAP therapy on IL-6 or 25(OH)D levels has yet to be investigated sufficiently in OSAS. We aimed at determining the serum levels of 25(OH)D and IL-6 in OSAS patients compared to non-apneic controls, investigating a possible correlation between 25(OH)D and IL-6 levels and evaluating the changes in IL-6 and 25(OH)D concentrations after twelve months of CPAP therapy in OSAS patients.Methods: 15 OSAS patients diagnosed by polysomnography and 15 non-apneic controls were included in the study. Serum IL-6 and 25(OH)D levels were measured before and after twelve-month CPAP therapy in the whole population and OSAS group, respectively.Results: IL-6 levels were significantly elevated in the OSAS group than the controls. IL-6 levels were positively correlated with OSAS severity, nocturnal hypoxemia, and body mass index (BMI). No difference was detected in 25(OH)D serum levels between groups. We found no correlation between IL-6 and 25(OH)D serum levels in two groups. No effect on IL-6 or 25(OH)D levels was detect after one year of effective CPAP therapy in OSAS patients.Conclusions: IL-6 levels were correlated with OSAS severity, hypoxemia, and BMI. No correlation between 25(OH)D and IL-6 levels and no effect of long-term CPAP on biomarkers were found in OSAS patients.

“…THUNSTRÖM et al [102] analysed the RICCADSA data regarding levels of high-sensitivity C-reactive protein, interleukin (IL)-6, IL-8 and tumour necrosis factor-α. The biomarkers were measured at baseline and after 1 year of follow-up in 220 patients randomised to CPAP or no CPAP.…”

Section: Treatment Effectmentioning

confidence: 99%

Obstructive sleep apnoea in acute coronary syndrome

2019

Obstructive sleep apnoea (OSA) syndrome affects about 13% of the male and 7–9% of the female population. Hypoxia, oxidative stress and systemic inflammation link OSA and cardiovascular and metabolic consequences, including coronary artery disease. Current research has identified several clinical phenotypes, and the combination of breathing disturbances during sleep, systemic effects and end-organ damage might help to develop personalised therapeutic approaches. It is unclear whether OSA is a risk factor for acute coronary syndrome (ACS) and might affect its outcome. On the one hand, OSA in patients with ACS may worsen prognosis; on the other hand, OSA-related hypoxaemia could favour the development of coronary collaterals, thereby exerting a protective effect. It is unknown whether positive airway pressure treatment may influence adverse events and consequences of ACS. In non-sleepy patients with OSA and stable coronary artery disease, randomised controlled trials failed to show that continuous positive airway pressure (CPAP) treatment protected against cardiovascular events. Conversely, uncontrolled studies suggested positive effects of CPAP treatment in such patients. Fewer data are available in subjects with ACS and OSA, and results of randomised controlled studies on the effects of CPAP are expected shortly. Meanwhile, the search for reliable markers of risk continues. Recent studies suggest that daytime sleepiness may indicate a more severe OSA phenotype with regard to cardiovascular risk. Finally, some studies suggest sex-related differences. The picture is still incomplete, and the potential role of OSA in patients with ACS awaits confirmation, as well as clear definition of subgroups with different degrees of risk.