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SUMMARYObstructive sleep apnea syndrome (OSAS) is associated with cardiovascular morbidity and mortality. Inflammatory processes associated with OSAS may contribute to cardiovascular morbidity in these patients. C-reactive protein (CRP) is an important serum marker of inflammation. We tested the hypothesis that patients with OSAS have increased plasma CRP.After 173 male subjects underwent polysomnography, 94 were considered to have OSAS (apnea-hypopnea index (AHI) > 5), 38 cardiovascular disease (CVD), and 56 without CVD. Seventy-nine subjects were considered not to have OSAS (AHI < 5) and from among these 57 patients without CVD were enrolled as control subjects.Serum CRP levels were significantly elevated in the OSAS + CVD group compared to the two other groups (P < 0.05). When we evaluated the association between the serum CRP level and severity of OSAS, CRP levels were positively correlated with AHI in OSAS patients (r = 0.61, P < 0.001) OSAS, as a marker of inflammation and cardiovascular risk, is associated with elevated levels of CRP. According to these results, the link between cardiovascular morbidity and OSAS may be explained by the coexistence of other cardiovascular risk factors such as circulating CRP levels. (Int Heart J 2005; 46: 801-809) Key words: CRP, Sleep apnea, Inflammation OBSTRUCTIVE sleep apnea syndrome (OSAS) is a common disorder that affects both children and adults. It is characterized by periods of breathing cessation (apnea) and periods of reduced breathing (hypopnea). Both types of events have similar pathophysiology and are generally considered to be equal with respect to their impact on patients. There are several methods of quantifying the severity of the disorder such as measuring the number of apneas and hypopneas per hour of sleep (the apnea-hypopnea index: AHI), the severity of oxygen desatFrom the

The mechanisms of nocturnal asthma are intimately related to circadian rhythms, which influence inflammatory cells and mediators, hormone levels and cholinergic tone. Nocturnal airway narrowing in asthma is sometimes associated with sleep disorders, such as obstructive sleep apnea syndrome (OSAS). The aims of this study were to evaluate the association of nocturnal asthma and OSAS, and investigate the influence of continuous positive airway pressure (CPAP) therapy to improve nighttime symptoms in asthmatic patients with OSAS. Forty-three asthmatic patients who had nocturnal symptoms in spite of the optimal medical treatment according to the Global Initiative for Asthma guidelines and associated with snoring were studied. Pulmonary function tests (PFTs), asthma nighttime symptom scores, and polysomnography were performed on all patients. We treated the patients with an apnea-hypopnea index (AHI) 15 (moderate-severe OSAS) (n=16) with CPAP during 2 months. After 2 months, PFT, asthma nighttime symptom scores were reperformed. There was no significant difference in PFT values before and after CPAP treatment in OSAS patients. Asthma nighttime symptom scores were improved significantly (P<0.05) after CPAP treatment. In conclusion, in some patients with nocturnal asthma, OSAS may be responsible disease for nocturnal symptoms. In this condition, CPAP improves nocturnal symptoms without amelioration in PFT abnormalities.

Background: Leptin is a hormone with well-investigated functions concerning body composition, energy homeostasis and feeding behavior in humans. The obstructive sleep apnea syndrome (OSAS) is strongly associated with obesity, which is known to be closely associated with hyperleptinemia. More recently, ghrelin, a hormone that also influences appetite and energy homeostasis, has been discovered. Objectives: The aim of this study was to investigate serum leptin and ghrelin levels in obese patients with OSAS in comparison with equally obese controls without OSAS. Methods: Thirty untreated obese patients with moderate-severe OSAS (apnea-hypopnea index: AHI ≧15) and 22 obese controls (AHI <5) were studied. To confirm the diagnosis, all patients underwent standard polysomnography in our sleep disorders center. Serum samples were taken at 08:00 h in the morning after overnight fasting. Results: Significantly higher serum leptin levels were found in OSAS patients compared to controls (p = 0.012), but there was no significant difference in serum ghrelin levels between OSAS patients and controls. Serum leptin levels were significantly correlated with body mass index in both OSAS patients (r = 0.55, p = 0.002) and controls (r = 0.46, p = 0.028), but only in OSAS patients was the leptin level significantly correlated with AHI (r = 0.38, p = 0.036). Conclusion: These data support findings suggesting that leptin is a hormonal factor affected by OSAS and not determined by obesity alone. Further studies are needed to investigate the relationship between serum ghrelin and OSAS.

Objective: Serotonergic neurons innervating motoneurons increase their firing rates in response to respiratory challenges, and long-term facilitation of respiratory activity in response to hypoxia is serotonin (5-HT) dependent. Polymorphism of the genes which code for 5-HT receptors may affect functions of the serotonergic system, and may be associated with obstructive sleep apnea syndrome (OSAS). The objective in this study was to assess the significance of T102C and –1438G/A polymorphisms of the 5-HT_2A receptor gene in OSAS. Methods: Fifty-five patients with OSAS and 102 healthy volun teers were included for genetic analyses of T102C and –1438G/A polymorphisms of the 5-HT_2A receptor gene. Results: For the T102C polymorphism, there was no significant difference between the patients and controls and both genders (p > 0.05). For the –1438G/A polymorphism, the A/A and G/A genotypes were overrepresented in the patients and controls, respectively (p = 0.045). In the control group, the genotypes of both genders were not significantly different (p > 0.05). In the patients, the A/A and G/A genotypes were overrepresented in males and females, respectively (p = 0.035). Concerning males, the A/A genotype was overrepresented in patients (p = 0.007). Conclusion: Serotonergic mechanisms appear to be related to OSAS. The T102C polymorphism of the 5-HT_2A receptor gene is not associated with OSAS. However, the –1438G/A polymorphism is associated with OSAS occurrence, especially in male patients. This polymorphism may also be associated with different OSAS incidences of both genders.

In the light of the present study, we speculate that OSAS is an independent risk factor for the progression of chronic kidney disease, which is a growing health problem. Further randomized-multicenter prospective studies are warranted to evaluate this relationship.

STG polymorphism appears to be associated with the occurrence of OSAS, especially in male patients. Absence of association of between genetic variants and polysomnography findings may suggest that some mechanisms other than STG polymorphism are involved in OSAS pathophysiology. Our results need confirmation in a larger group of patients with OSAS.

Background: The obstructive sleep apnea syndrome (OSAS) is closely associated with cardiovascular and metabolic disorders. Objectives: The aim of this study was to evaluate the influence of OSAS on plasma adiponectin levels independent of obesity in our study group. We also investigated the association between plasma adiponectin, plasma tumor necrosis factor-α (TNF-α), obesity, cardiovascular disease (CVD) and OSAS. Methods: The patients were classified into controls or OSAS patients according to the apnea-hypopnea index (AHI): patients with an AHI <5 constituted the control group (n = 32) and patients with an AHI ≧5 constituted the OSAS group (n = 106). Plasma TNF-α and adiponectin levels were measured in both groups. Results: Plasma adiponectin levels were negatively correlated with AHI, body mass index (BMI) and SpO₂ <90% and positively correlated with minimum oxygen saturation. The plasma levels of TNF-α were positively correlated with SpO₂ <90%, BMI and fasting plasma glucose levels. In addition, there was a significant negative correlation between plasma TNF-α and adiponectin levels in theOSAS group. Compared with thenon-obese OSAS group, subjects with obesity and OSAS had lower adiponectin levels and SpO₂ <90%, and higher TNF-α levels. Obese OSAS patients had higher rates of CVD with lower plasma adiponectin levels when compared with obese control subjects. Conclusion: Serum adiponectin is significantly lower in patients with OSAS and it is independent of obesity. This might explain the high incidence of CVD and metabolic syndrome in patients with OSAS.