C-reactive protein and sleep disordered breathing. Sleep

Sleep Disorders Clinic, Stanford University, Stanford, CA 94305, USA.
Sleep (Impact Factor: 4.59). 01/2005; 27(8):1507-11.
Source: PubMed


Over a 2-month period, to evaluate serum levels of C-reactive protein (CRP) in new patients with obstructive sleep apnea syndrome (OSAS), upper airway resistance syndrome (UARS), and absence of important comorbidity, as well as in normal controls.
Cross-sectional analysis.
Sleep disorders clinic.
239 successively monitored subjects: 156 subjects were diagnosed with OSAS, 39 with UARS, and 54 controls.
Clinical information (neurologic, general medical, and otolaryngology examination), body mass index, neck circumference, hip-waist ratio, Epworth Sleepiness Scale, 3 fatigue scales, Sleep Disorders Questionnaire, serum CRP, and polysomnography were collected. Analysis of variance indicated a significant difference between the groups for diastolic blood pressure, respiratory disturbance index, lowest SaO2, and body mass index. The mean serum CRP level was normal in all 3 groups. Only 15 (14 OSAS and 1 UARS) out of 239 subjects had high serum CRP values. CRP levels were significantly correlated with body mass index, esophageal pressures, hip-waist ratio, neck circumference, and blood pressure. Only body mass index was significantly associated with high CRP values; multiple regression showed: adjusted R2 = 0.115, beta = 0.345, P <.001. When men and women were considered separately, body mass index was again significantly associated with high CRP levels.
Obesity is a risk factor for high serum CRP levels in patients with sleep-disordered breathing, as in the general population.

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    • "Subsequent studies have shown increased levels of CRP in patients with OSA that were independent of body mass index (BMI).45–47 Conversely, two studies found that obesity per se, rather than OSA, is a better predictor of CRP.48,49 Furthermore, a large community study failed to detect an independent association between CRP and OSA after adjustment for BMI,50 suggesting that the OSA-CRP relationship may be primarily driven by obesity. However, the Icelandic Sleep Apnea Cohort (n = 454)51 recently found that OSA severity is an independent predictor of IL 6 and CRP levels but interacts with obesity such that this association is found only in obese OSA patients. "
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    ABSTRACT: Obstructive sleep apnea (OSA) is increasingly being recognized as a major health burden with strong focus on the associated cardiovascular risk. Studies from the last two decades have provided strong evidence for a causal role of OSA in the development of systemic hypertension. The acute physiological changes that occur during apnea promote nocturnal hypertension and may lead to the development of sustained daytime hypertension via the pathways of sympathetic activation, inflammation, oxidative stress, and endothelial dysfunction. This review will focus on the acute hemodynamic disturbances and associated intermittent hypoxia that characterize OSA and the potential pathophysiological mechanisms responsible for the development of hypertension in OSA. In addition the epidemiology of OSA and hypertension, as well as the role of treatment of OSA, in improving blood pressure control will be examined.
    Nature and Science of Sleep 05/2013; 5:43-52. DOI:10.2147/NSS.S34841
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    • "Inflammation plays also a major role in the development and progression of atherosclerosis. It has been repeatedly reported that OSA patients have increased serum levels of inflammatory substances [27] [28] [29] [30] [31] [32] [33] and adhesion molecules [14] [34] [35] and that chronic hypoxemia in OSA patients can activate specific inflammatory pathways [36] [37] that could facilitate the atherosclerotic process [38] [39]. CPAP treatment may also influence reversibility of these findings [40]. "
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    ABSTRACT: Coronary artery disease (CAD) and obstructive sleep apnea (OSA) are both complex and significant clinical problems. The pathophysiological mechanisms that link OSA with CAD are complex and can influence the broad spectrum of conditions caused by CAD, from subclinical atherosclerosis to myocardial infarction. OSA remains a significant clinical problem among patients with CAD, and evidence suggesting its role as a risk factor for CAD is growing. Furthermore, increasing data support that CAD prognosis may be influenced by OSA and its treatment by continuous positive airway pressure (CPAP) therapy. However, stronger evidence is needed to definitely answer these questions. This paper focuses on the relationship between OSA and CAD from the pathophysiological effects of OSA in CAD, to the clinical implications of OSA and its treatment in CAD patients.
    Pulmonary Medicine 04/2013; 2013(20):768064. DOI:10.1155/2013/768064
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    • "In particular, significant elevations in serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) have been seen in patients with OSA [18,24-29]. However, some studies did not show elevation of CRP in patients with OSA [30,31]. "
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    ABSTRACT: BACKGROUND: Obstructive sleep apnea (OSA) is associated with coronary artery disease (CAD). Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to CAD in patients with OSA. Treatment with continuous positive airway pressure (CPAP) has been shown to change levels of inflammatory markers. We analyzed data from published studies by a systematic meta-analysis. OBJECTIVE: To asses if treatment for sleep apnea by CPAP will affect levels of inflammatory markers.Data resources: PubMed, Embase and Cochrane library. METHODS: Study eligibility criteria full text English studies of adult, human subjects, addressing values of at least one of the inflammatory markers before and after CPAP treatment. We used the definition of OSA as an apnea-hypopnea index (AHI) of >= 5/h, reported values in mean and standard deviation or median with range.Participants: Adult, humanInterventions: CPAP treatment for OSAStudy appraisal and synthesis method: A total of 3835 studies were reviewed for inclusion, while 23 studies pooled for analysis. A total of 14 studies with 771 patients were pooled for C-reactive protein (CRP); 9 studies with 209 patients were pooled for tumor necrosis factor-alpha (TNF-alpha); and 8 studies with 165 patients were pooled for interleukin-6 (IL-6).Endpoint definitions: The following inflammatory markers were chosen: CRP, TNF-alpha, and IL-6. RESULTS: C-reactive protein: Study level means ranged from 0.18 to 0.85 mg/dl before CPAP treatment and 0.10 to 0.72 mg/dl after CPAP treatment. Mean differences, at a study level, ranged from -0.05 to 0.50. The pooled mean difference was 0.14 [95% confidence interval 0.08 to 0.20, p < 0.00001]. There was heterogeneity in this endpoint (df = 13, p < 0.00001, I2 = 95%).Tumor necrosis factor-alpha: Study level means ranged from 1.40 to 50.24 pg/ml before CPAP treatment and 1.80 to 28.63 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -1.23 to 21.61. The pooled mean difference was 1.14 [95% confidence interval 0.12 to 2.15, p = 0.03]. There was heterogeneity in this endpoint (df = 8, p < 0.00001, I2 = 89%).Interleukin-6: Study level means ranged from 1.2 to 131.66 pg/ml before CPAP treatment and 0.45 to 66.04 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -0.40 to 65.62. The pooled mean difference was 1.01 [95% confidence interval -0.00 to 2.03, p = 0.05]. There was heterogeneity in this endpoint (df = 7, p < 0.00001, I2 = 95%)Limitations: Only published data. Studies pooled were mainly small, non-randomized trials. CONCLUSION: Sleep apnea treatment with CPAP improves levels of inflammatory markers.
    Journal of Inflammation 03/2013; 10(1):13. DOI:10.1186/1476-9255-10-13 · 2.02 Impact Factor
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