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Background/Introduction Obstructive sleep apnea (OSA) is one of the most common respiratory disease which is considered as a risk factor for cardiovascular disease and death. Although coexistence of OSA and arterial hypertension may be attributed to well-known common environmental risk factors for both diseases, a genetic background should be considered. LEPR rs1137101 polymorphism was reported to be associated with coronary artery disease and heart failure. Left ventricular hypertrophy is a part of hypertension-mediated organ damage assessment and an independent risk factor for adverse outcome in patients with hypertension. Purpose This study is aimed to establish the relationship between LEPR rs1137101 polymorphism and left ventricular hypertrophy in patients with OSA and arterial hypertension. Methods Consecutive patients with newly diagnosed OSA confirmed by polysomnography underwent genotyping for the single nucleotide polymorphisms of LEPR (rs1137101). LVH was diagnosed using standard 12-lead electrocardiogram according to the current European Society of Cardiology guidelines. Logistic regression was used to assess the relationship between LEPR rs1137101 polymorphisms and LVH. Results From 600 subjects diagnosed with OSA, 427 subjects with hypertension were included for further analysis (25.1% women, 74.9% men). In analyzed subpopulation mean age was 58.5±9.4 years, body mass index 33.7±6.6 kg/m2, apnea-hypopnea index 43.1±23.6/hour. In 34 (8.0%) subjects LVH was diagnosed. Genotyping revealed, that 123 (28.8%) subjects were LEPR rs1137101 AA homozygotes, 202 (47.3%) LEPR rs1137101 A/G heterozygotes and 102 (23.9) LEPR rs1137101 G/G homozygotes. Logistic regression showed, that LEPR rs1137101 A/A polymorphism vs A/G and G/G was associated with increased risk of LVH (odds ratio: 2.08, 95% confidence interval: 1.02–4.25, p=0.03). The relationship was significant also after adjustment for age, sex, apnea-hypopnea index and current smoking status (odds ratio: 2.28, 95% confidence interval: 1.08–4.83, p=0.03). Conclusions Our study shows a possible link between the polymorphism of the LEPR rs1137101 polymorphism and LVH in patients with OSA and arterial hypertension. Acknowledgement/Funding The study received financial support from the Polish National Science Centre (710/N-COST/2010/0)

INTRODUCTION Although the coexistence of type 2 diabetes mellitus (T2DM) and obstructive sleep apnea (OSA) may be attributed to environmental risk factors common for both diseases, a genetic background should also be considered. Data on the role of genetic factors in the development of T2DM in patients with OSA are lacking. OBJECTIVES The study was aimed to evaluate the prevalence of polymorphisms of selected genes that are known to be associated with diabetes or obesity in patients with OSA and concomitant T2DM and to assess these polymorphisms in the context of OSA severity. PATIENTS AND METHODS Consecutive patients with newly diagnosed OSA confirmed by polysomnography underwent genotyping for the following single nucleotide polymorphisms (SNPs): SREBF1 rs11868035, HIF1A rs11549465, APOA5 rs3135506, TCF7L2 rs7903146, and FTO rs16945088. The frequency of genotypes was compared between patients with and without concomitant T2DM and was analyzed with regard to OSA severity. RESULTS A total of 600 patients with newly diagnosed OSA were enrolled to the study. Of these, 121 patients (20.2%) were diagnosed with T2DM (97 men and 24 women; median age, 58 years; range, 52-64 years). The prevalence of T2DM was significantly lower in APOA5 rs3135506 GG homozygotes than in CG heterozygotes (18.8% vs 33.3%, P = 0.02). APOA5 rs3135506 CG heterozygotes were at higher risk for developing T2DM (adjusted odds ratio, 2.64; 95% confidence interval,1.38-5.04; P = 0.003). No significant differences were found for the genotype distribution of the other investigated SNPs. CONCLUSIONS Our study shows a possible link between the polymorphism of the gene encoding APOA5 and T2DM in patients with OSA.

BACKGROUND: The impact of treating OSA on renal function decline is controversial. Previous studies usually included small samples and did not consider specific effects of different CPAP modalities. The aim of this study was to evaluate the respective influence of fixed and autoadjusting CPAP modes on estimated glomerular filtration rate (eGFR) in a large sample of patients derived from the prospective European Sleep Apnea Database cohort. METHODS: In patients of the European Sleep Apnea Database, eGFR prior to and after follow-up was calculated by using the Chronic Kidney Disease-Epidemiology Collaboration equation. Three study groups were investigated: untreated patients (n = 144), patients receiving fixed CPAP (fCPAP) (n = 1,178), and patients on autoadjusting CPAP (APAP) (n = 485). RESULTS: In the whole sample, eGFR decreased over time. The rate of eGFR decline was significantly higher in the subgroup with eGFR above median (91.42 mL/min/1.73 m(2)) at baseline (P < .0001 for effect of baseline eGFR). This decline was attenuated or absent (P < .0001 for effect of treatment) in the subgroup of patients with OSA treated by using fCPAP. A follow-up duration exceeding the median (541 days) was associated with eGFR decline in the untreated and APAP groups but not in the fCPAP group (P < .0001 by two-way ANOVA for interaction between treatment and follow-up length). In multiple regression analysis, eGFR decline was accentuated by advanced age, female sex, cardiac failure, higher baseline eGFR, and longer follow-up duration, whereas there was a protective effect of fCPAP. CONCLUSIONS: fCPAP but not APAP may prevent eGFR decline in OSA.

INTRODUCTION Melatonin secretion, one of the main factors controlling the sleep-wake rhythm, may be disrupted in patients with sleep disorders. OBJECTIVES The aim of the study was to evaluate the profile of circadian melatonin secretion in patients with obstructive sleep apnea (OSA) and to assess the impact of 2-day and 3-month treatment with continuous airway pressure (CPAP) on diurnal and nocturnal serum melatonin levels. PATIENTS AND METHODS Serum melatonin levels were evaluated in 71 untreated patients with OSA and 18 healthy controls at 6 time points: 10 AM, 2 PM, 6 PM, 10 PM, 2 AM, and 6 AM. The measurements were repeated after 2 days and 3 months of CPAP treatment. RESULTS Melatonin secretion rhythm was altered in 25.4% of the patients with OSA. In patients with preserved secretion rhythm, the serum melatonin level was significantly lower at 2 AM and 6 AM, compared with healthy controls: 68.2 pg/ml (interquartile range [IQR], 30.1-109.8 pg/ml) vs 109.1 pg/ml (IQR, 63-167.9 pg/ml), P = 0.02 and 40.8 pg/ml (IQR, 20.8-73.2 pg/ml) vs 67.7 pg/ml (IQR, 32.7-131.7 pg/ml), P = 0.04, respectively. Melatonin levels did not change significantly after the 2-day and 3-month CPAP treatment. However, at 3 months, a shift of the peak melatonin concentration to 2 AM was observed in patients with an altered secretion rhythm. CONCLUSIONS OSA has a significant effect on serum melatonin levels. Neither short-term nor long-term CPAP treatment significantly changes melatonin concentrations; however, our results seem to indicate that a 3-month CPAP treatment may be helpful in restoring the physiological rhythm of melatonin secretion in patients with OSA.

INTRODUCTION Melatonin secretion, one of the main factors controlling the sleep-wake rhythm, may be disrupted in patients with sleep disorders. OBJECTIVES The aim of the study was to evaluate the profile of circadian melatonin secretion in patients with obstructive sleep apnea (OSA) and to assess the impact of 2-day and 3-month treatment with continuous airway pressure (CPAP) on diurnal and nocturnal serum melatonin levels. PATIENTS AND METHODS Serum melatonin levels were evaluated in 71 untreated patients with OSA and 18 healthy controls at 6 time points: 10 AM, 2 PM, 6 PM, 10 PM, 2 AM, and 6 AM. The measurements were repeated after 2 days and 3 months of CPAP treatment. RESULTS Melatonin secretion rhythm was altered in 25.4% of the patients with OSA. In patients with preserved secretion rhythm, the serum melatonin level was significantly lower at 2 AM and 6 AM, compared with healthy controls: 68.2 pg/ml (interquartile range [IQR], 30.1-109.8 pg/ml) vs 109.1 pg/ml (IQR, 63-167.9 pg/ml), P = 0.02 and 40.8 pg/ml (IQR, 20.8-73.2 pg/ml) vs 67.7 pg/ml (IQR, 32.7-131.7 pg/ml), P = 0.04, respectively. Melatonin levels did not change significantly after the 2-day and 3-month CPAP treatment. However, at 3 months, a shift of the peak melatonin concentration to 2 AM was observed in patients with an altered secretion rhythm. CONCLUSIONS OSA has a significant effect on serum melatonin levels. Neither short-term nor long-term CPAP treatment significantly changes melatonin concentrations; however, our results seem to indicate that a 3-month CPAP treatment may be helpful in restoring the physiological rhythm of melatonin secretion in patients with OSA.

Obturacyjny bezdech podczas snu (OBPS) jest stosunkowo młodą jednostką chorobową, której patomechanizm oraz wpływ na zaburzenia metaboliczne oraz endokrynologiczne ciągle pozostają tematem badań klinicznych [...]

OSA increases the risk of arterial hypertension (AH) and coronary heart disease (CHD). One of the directions for the research aimed at the identification of patients particularly susceptible to serious cardiovascular complications is the assessment gene polymorphism of the genes associated with an increased risk of cardiovascular diseases. Aim: Evaluation of some genetic polymorphisms that may affect the incidence of cardiovascular disease in patients with obstructive sleep apnea. Material and Methods: We enrolled 600 patients (449M, 151F) aged 54.4±10.3 yrs with OSA. The following gene polymorphisms were evaluated by real-time PCR in peripheral blood: ALOX5AP (arachidonate 5- lipoxygenase-activating protein), LPL (lipoprotein lipase), SREBF1 (sterol regulatory element binding transcription factor 1), SREBF2 (sterol regulatory element binding transcription factor 2), APOA5 (apolipoprotein A-V) and FTO (fat mass and obesity associated protein). Correlations between these polymorphisms and the diagnosis of CHD, myocardial infarction and AH were evaluated. Results: AH was diagnosed in 427 (71.2%), CHD in 127 (21.2%) and myocardial infarction in 26 (4.3%). We observed a statistically significant correlation only for SREBF1 homozygous GG gene and coronary heart disease (in 72 out of 127 patients were homozygous GG, p Conclusions: Determination of polymorphism of SREBF1 and FTO genes may be useful in assessing the risk of cardiovascular complications in patients with OSA.

Obstructive sleep apnea syndrome (OSAS) is characterized by complete cessation of inspiratory flow (apnea) or upper airway airflow limitation (hypopnea) with increased respiratory muscle activity, which is repeatedly observed during sleep. Hypothyroidism has been described as a rare cause of OSAS, but it is considered to be the main cause of breathing disorders during sleep in patients in whom an improvement of OSAS is observed after thyroid hormone replacement therapy. Nevertheless, euthyreosis due to thyroxine replacement in patients with OSAS often does not improve the breathing disorder and treatment with continuous positive airway pressure is usually applied. The aim of this study was to assess thyroid function in patients with OSAS. We studied 813 patients in whom severe OSAS was diagnosed; the mean apnea-hypopnea index was 44.0. Most of the patients were obese (mean BMI 33.1 ± 6.6 kg/m2) and had excessive daytime sleepiness (ESS 12.8 ± 6.6). With the thyroid stimulating hormone (TSH) concentration as the major criterion, hypothyroidism was diagnosed in 38 (4.7%) and hyperthyroidism was diagnosed in 31 (3.8%) patients. Analysis of basic anthropometric data, selected polysomnography results, and TSH, fT3, and fT4 values did not reveal any significant correlations. In conclusion, the incidence of thyroid function disorders seems to be no different in OSAS than that in the general population. We did not find correlations between TSH activity and the severity of breathing disorders during sleep.

Obstructive sleep apnea (OSA) is one of the most often sleep disturbance. Not treated patients have 2–3 times more risk for death because of the cardiovascular diseases. Leptin and homocysteine are the risk factors for cardiovascular diseases. Treatment by nCPAP has positive influence for health care and reduction of hyperten-sion in this group. The aim of this study was to evaluate an effect of 3 weeks nCPAP therapy on a serum leptin and homocysteine con-centrations in patients with OSA. Material and methods: The study group consisted of 48 male patients in the age x = 51.2 ± 7.5 years old, OSA was diagnosed by polisomnographic study The leptin concentration was evaluated by RIA methods (HUMAN LEPTIN RIA KIT), the homocysteine concentration was evaluated by Axis Homocysteine EIA test. Patients were treated by nCPAP during 3 weeks. Only 29 patients were effectively treated for this time. The compliance was: 5.07 ± 1.81 h. Results: In the group of 29 patients the serum leptin and homocysteine concentration before and after treatment were 11.05 ± 5.59 ng/mL vs. 11.07 ± 7.16 ng/mL i 10.98 ± 2.79 μmol/L vs. 10.34 ± 2.99 μmol/L. In the all study group the statistical important correlation between leptin and AHI, mean and minimal saturation overnight, fibrinogen econcentration, BMI, WHR, waist circumference, heart rate and between homocysteine and heart rate were observed. Conclusions: 3 weeks therapy does not have any effect on leptin and homocysteine concentrations in the studied group of patients with OSA. Serum leptin concentration correlates with AHI, TMB90, as well as with mean and minimal saturation during a sleep. This indicates a potentially higher risk of cardiovascular diseases in the studied group.

The incidence of ischemic heart disease (IHD) in patients with OSAS is estimated at around 20%. This greatly affect a common risk factors for both diseases: male gender, obesity, age and diabetes and hypertension. Attention is drawn to the possibility of genetic determinants of IHD. The aim of study was to answer the question whether the presence of polymorphisms of selected genes possibly related to IHD may be useful to isolate the group of patients with OSAS, especially vulnerable as a complication of IHD. Materials and methods. The study included 600 people with OSAS, which was isolated in patients with IHD (127 people). The remaining 473 individuals were observed as a control group. The polymorphism of three genes were evaluated to find possible influence on the occurrence of IHD or myocardial infarction as follows: SREBF1 (sterol regulatory element binding transcription factor 1), REBF2 (sterol regulatory element binding transcription factor 2) and HIF1 (hypoxia inducible factor 1, alpha subunit). Results. Analysis of relationship between polymorphisms of selected genes and the diagnosis of IHD in the whole group of patients with OSAS showed a relationship only for the gene SREBF1 finding the lowest frequency of its occurrence in AA homozygotes (at 13.6%) and twice with GG homozygotes (26.1%). Conclusions. Rating polymorphisms studied genes did not reveal their relationship to the occurrence of IHD in patients with OSAS, both in the whole group as well as separate subgroups.

Introduction: Metabolic syndrome (MS), which is connected with enlarged cardiovascular risk, is common in patients with OSAS. The aim of the study was to estimate the prevalence of MS in patients with OSAS according to two definitions of MS (criteria from NCEP-ATP III from 2001 versus criteria from IDF 2005). Material and methods: Materials consisted of 155 males and 18 females with OSAS (mean AHI 44 ± 22 h−1), obesity (BMI 31.8 ± 5.0 kg/m2), aged 53.9 ± 9.3 years (mean ± SD). Serum lipids, glucose, body mass index (BMI), waist circumference (WC) and waist-to-hip ratio (WHR) were measured in all patients. Results: According to first definition (NCEP—ATP III from 2001), MS was diagnosed in 98 patients (56% of the whole group—MS1 group) compared to 120 patients (69% of the whole group—MS2 group) diagnosed according to the second definition (IDF from 2005), p < 0.05. No differences in BMI and WC between the groups were found. Significant differences in WHR were noted (MS1 group: 1.005 ± 0.05 vs. MS2 group: 1.027 ± 0.06, p < 0.05). Patients from the MS2 group had higher cholesterol HDL compared to the MS1 group (52.3 ± 12.1 mg/dl vs. 42.3 ± 12.1 mg/dl, p < 0.05). Serum triglyceride concentrations were significantly higher in the MS1 group than in the MS2 group (228 ± 122 mg/dl vs. 122 ± 49 mg/dl, p < 0.05). There were no differences in OSAS severity between the MS1 and MS2 group. In both groups weak correlations between diagnosis of MS and AHI were f ound (r = 0.19 for MS1 and r = 0.21 for MS2, p < 0.05) They are, however, clinically insignificant. Conclusions: The IDF definition from 2005 of metabolic syndrome indeed increases the frequency of diagnosis of metabolic syndrome in patients with OSAS. We did not observe essential clinical correlation among the degree of OSAS severity and recognition of metabolic syndrome in the MS1 or in the MS2 group.

In OSAS patients CPAP therapy decreases cardiovascular morbidity and mortality. Homocysteine and leptin may play a role in development of ischaemic heart disease (IHD) in patients with OSAS. The aim of the study was to assess the influence of 3 month CPAP therapy on cardiovascular risk factors in patients with OSAS without IHD (pure OSAS) and with OSAS and IHD.Therapy with CPAP was started in 42 OSAS without IHD (pure OSAS) and 23 OSAS and IHD patients. Plasma concentration of homocysteine, serum concentration of leptin, C-reactive protein (CRP), fibrinogen, lipids, and markers of visceral adiposity (MVA) were measured before and after treatment.There were no significant changes in homocysteine, leptin, fibrinogen and CRP concentrations in neither group. In OSAS and IHD no change in serum lipids and MVA were found. In pure OSAS group total cholesterol and LDL cholesterol concentrations significantly decreased (202.5 ± 38.5 mg/dl v. 186.7 ± 33.5 mg/dl, p = 0.001 and 127.3 ± 32.9 mg/dl v. 116.4 ± 26.9 mg/dl, p = 0.02, respectively). Triglycerides did not significantly change (p = 0.09). There were no significant changes in BMI (30.4 ± 3.8 v. 30.6 ± 3.6, p = 0.5), waist circumference (108.5 ± 8.0 cm v. 107.0 ± 7.5 cm, p = 0.09) and waist to hip ratio (1.03 ± 0.04 v. 1.01 ± 0.03, p = 0.07).Three month CPAP therapy did not change homocysteine and leptin concentration in neither group. However, it significantly decreased serum lipids concentration in patients with pure OSAS, but not in patients with OSAS and IHD, suggesting beneficial effects of CPAP therapy on cardiovascular risk factors.

Introduction: Continuous positive airway pressure (CPAP) treatment reduces cardiovascular morbidity and mortality in patients with obstructive sleep apnoea syndrome (OSAS). Homocysteine and leptin may play a role in the development of ischaemic heart disease (IHD) in these patients. The aim of the study was to assess the effects of 3-month CPAP treatment on the risk factors of IHD in patients with OSAS without co-existing IHD (OSAS without IHD) and on OSAS with co-existing IHD (OSAS with IHD). Material and methods: CPAP treatment was commenced in 42 patients with OSAS without IHD and in 23 patients with OSAS with IHD. Baseline and end-of-treatment levels of homocysteine, leptin, C-reactive protein (CRP), fibrinogen, lipids parameters and visceral obesity related parameters were determined. Results: No significant changes in the levels of homocysteine, leptin, fibrinogen or CRP in either of the study groups were observed at the end of the treatment. No changes in lipid parameters or the degree of obesity were observed in the OSAS with IHD group. A significant reduction in total and LDL-cholesterol levels were observed in the OSAS without IHD group (202.5 ± 38.5 mg/dl v. 186.7 ± 33.5 mg/dl, p = 0.001 and 127.3 ± 32.9 mg/dl v. 116.4 ± 26.9 mg/dl, p = 0.02, respectively). There were no significant changes in body mass index (30.4 ± 3.8 kg/m2 v. 30.6 ± 3.6 kg/m2, p = 0.5) or the amount of visceral fat, as measured by waist circumference (108.5 ± 8.0 cm v. 107.0 ± 7.5 cm, p = 0.09) and waist-to-hip ratio (1.03 ± 0.04 v. 1.01 ± 0.03, p = 0.07). Conclusions: Three-month CPAP treatment did not affect the levels of homocysteine or leptin in patients with OSAS, although there was a significant reduction in lipid parameters in patients with OSAS without co-existent IHD, which confirms the beneficial effect of this method of treatment on the risk factors of IHD.

Obstructive sleep apnea syndrome (OSAS) patients are at risk of cardiovascular complications. The aim of this study was to assess the effect of treatment with continuous positive airway pressure (CPAP) on the response to symptom limited exercise test. Methods: twenty nine OSAS patients (1 F, 28 M), mean age 50.7 ± 9.7 yrs with body mass index of 32.6 ± 4.5 kg/m2 participated in the study. OSAS was diagnosed by overnight polysomnography. Incremental cardiopulmonary exercise test (CPET) on a treadmill was performed twice: before and after 2–3 weeks of regular treatment with CPAP. Results: mean apnea + hypopnea index (AHI) before therapy was 57.6 ± 12 h−1. CPAP treatment did not change peak oxygen consumption (VO2max) (38.3 ± 9.0 vs. 38.9 ± 6.9 mlO2/kg/min, p = ns) or peak heart rate (153.4 ± 21 min−1 vs. 155.5 ± 22 min−1, p = ns). There were no significant changes in ventilation or gas exchange variables. However, a decrease in peak systolic blood pressure from 194.5 ± 24 mmHg to 186.7 ± 27.9 mmHg (p < 0.05) with CPAP treatment was found. During recovery a decrease in heart rate (at 1st minute and minutes 3–6) and mean arterial pressure (MAP) (minutes 4–7) with CPAP treatment was observed. Significant correlations between VO2max and AHI (r = −0.38, p < 0.05); MAP at peak exercise and: AHI, mean oxygen saturation (SaO2) during sleep, minutes of sleep with SaO2 < 90% (T90); MAP at recovery (minutes 3–8) and T90 before CPAP treatment were also noted. Conclusions: OSAS patients are not limited on exercise. Treatment with nasal CPAP attenuates circulatory response to incremental exercise on a treadmill.

The prevalence of OSA rises with age, however it is also diagnosed in patients below the age of 35 years. Aim of the paper was the camparison of the severity and clinical features of OSA in young and elderly subjects. The study was a retrospective analysis of 561 subjects aged65 yrs and 319 subjects aged35 yrs who were investigated in our Sleep Laboratory between 1992-2005 due to snoring or daytime sleepiness. They all underwent full polisomnography or a limited recording. In patients with diagnosed OSA (AHI10) we initiated CPAP therapy.OSA was diagnosed in 383 (63,3%) older patients and in 144 (45,1%) younger patients. BMI was significantly higher in younger subjects than in older (32,2+/-6,9 vs 28,9+/-5,1 kg/m2). The prevalence of OSA among women was significantly higher in older patients than in younger (26,4 vs 5,8%). Younger patients with OSA had a significantly higher AHI (42,7+/-32,1 vs 32,2+/-18,4) and a longer duration of apneas expressed as percentage of total sleep time spent in apnea (31,6+/-23,2 vs 26,5+/-17,7%). CPAP therapy was initiated in 185 older patients and 41% of them continue therapy. In younger group patients CPAP therapy was started in 51 patients and 47% of them continue therapy. The mean therapeutic pressure was significantly higher in younger patients with OSA (9,2+/-2,2 vs 8,2+/-2,2 cmH2O).1/ OSA is more frequent in elderly patients ; 2/ in young patients OSA is more severe and requires higher pressures in CPAP therapy; 3/ OSA among women is four time more frequent in older patients than in younger.

Exhaled nitric oxide has been extensively investigated as a non-invasive marker of airway inflammation. Some authors have suggested that morning FENO in obstructive sleep apnea syndrome (OSAS) patients is elevated due to inflammation of upper airways, while others have not found any differences between patients and healthy subjects. The purpose of this study was to analyze concentration of exhaled nitric oxide (FENO) in OSAS patients. Methods: 119 (99 M, 20 F) consecutive patients of sleep laboratory participated in this study. Standard overnight sleep studies with polysomnography or portable screening device were carried out in the whole group: OSAS was diagnosed in 66 patients and 53 no-OSAS served as controls. FENO was measured on-line with a flow rate kept at 0.045–0.055 l/s, according to the recommendations of ATS using a chemiluminescence analyzer twice: before the sleep study (8–10 p.m.) and after termination of data collection (6–8 a.m.). There were no differences in age between patients and controls. Respiratory disturbance index (RDI) was 40.3 ± 24.9 in patients and 3.7 ± 2.8 in con-trols (p < 0.001). In OSAS patients both evening and morning FENO was significantly higher compared to controls(23.1 ± 14.8 ppb vs. 16.8 ± 9.8 ppb and 22.4 ± 13.2 ppb vs. 15.3 ± 8.1 ppb respectively, p < 0.05). Weak but statistically significant correlations for the whole group between morning FENO and mean and minimum arterial oxygen saturation (SaO2) during sleep and number of study minutes with SaO2 < 90% were observed. Lower evening FENO in OSAS patients with coexisting arterial hypertension when compared to normotensive OSAS patients was also noticed (19.1 ± 10.8 ppb vs. 27.1 ± 19.1 ppb; p < 0.05). Conclusions: The increase in FENO in OSAS patents may be caused by repetitive apneas and hypoxemia during sleep.

Aim: to evaluate usefulness of serum homocysteine concentration in assessing the risk of atherosclerosis in patients with OSAS. Materials and methods: 47 patients (mean age 50.6 ± 10.3 years, mean BMI 31.52 ± 6.04 kg/m2), with OSAS confirmed by polisomnography and 12 healthy snoring subjects (mean age 42.8 ± 16.8 years, mean BMI 26.9 ± 2.95 kg/m2) were enrolled to the study. OSAS patients were divided into two groups–subjects with normal blood pressure (group A, n = 32, mean age 51.3 ± 10.3 years, mean BMI 30.6 ± 4.4 kg/m2) and subjects with arterial hypertension (group B, n = 15, mean age 52.7 ± 9.8 years, mean BMI 31.4 ± 5.0 kg/m2). None of the study subjects was treated with statins or fibrates. Serum concentration of homocysteine, uric acid, glucose level and lipid profile was evaluated inall subjects. Results: We found significant abnormalities in the lipid profile in all the study groups. The mean concentrations ofcholesterol (mg/dL), triglycerides (mg/dL) and homocysteine (μmol/L) were as follows: 215.0 ± 34.2, 200.0 ± 173.0, 8.2 ± 2.9 in group A, 216.5 ± 43.1, 189.3 ± 138.8, 8.40 ± 1.67 in group B. 195.0 ± 32.9, 154.3 ± 133.0, 9.3 ± 2.1 in the control group. No significant correlation between the homocysteine concentration and level of cholesterol or triglycerides was found. Conclusions: the serum concentration of homocysteine seems not to be a good marker in the evaluation of the risk of atherosclerosis in patients with OSAS.

The prevalence of OSA rises with age, however it is also diagnosed in patients below the age of 35 years. Aim of the paper was the camparison of the severity and clinical features of OSA in young and elderly subjects. The study was a retrospective analysis of 561 subjects aged > 65 yrs and 319 subjects aged < 35 yrs who were investigated in our Sleep Laboratory between 1992–2005 due to snoring or daytime sleepiness. They all underwent full polisomnography or a limited recording. In patients with diagnosed OSA (AHI > 10) we initiated CPAP therapy. Results: OSA was diagnosed in 383 (63.3%) older patients and in 144 (45.1%) younger patients. BMI was significantly higher in younger subjects than in older (32.2 ± 6.9 vs. 28.9 ± 5.1 kg/m2). The prevalence of OSA amongwomen was significantly higher in older patients than in younger (26.4 vs. 5.8%). Younger patients with OSA had a significantly higher AHI (42.7 ± 32.1 vs. 32.2 ± 18.4) and a longer duration ofapneas expressed as percentage of total sleep time spent in apnea (31.6 ± 23.2 vs. 26.5 ± 17.7%). CPAP therapy was initiated in 185 older patients and 41% of them continue therapy. In younger group patients CPAP therapy was started in 51 patients and 47% of them continue therapy. The mean therapeutic pressure was significantly higher inyounger patients with OSA (9.2 ± 2.2 vs. 8.2 ± 2.2 cmH2O). Conclusions: 1/ OSA is more frequent in elderly patients ; 2/ in young patients OSA is more severe and requires higher pressures in CPAP therapy; 3/ OSA among women is four time more frequent in older patients than in younger.

Hypertension, coronary heart diseases, obesity, diabetes mellitus are often present in patients with obstructive sleep apnea (OSA). The aim of the study was to estimate the serum leptin concentration and sympathetic activity in patients with obstructive sleep apnea and in control group.51 persons (F6, M45) were included into the study. The control group (GK) consisted of 15 snoring person (15 M) in the age x = 44.19 +/- 14.60, study group (GB) consisted of 36 patients with OSA (6F, 30M) in the age 5 1.47 +/- 8.95 years.Leptin was measured by RIA methods using the HUMAN LEPTIN RIA KIT (LINCO Research, Inc).: adrenaline and noradrenaline were measured in the serum by HPLC methods (BIO-RAD).The serum concentrations of leptin (ng/mL), adrenaline and noradrenaline (pg/mL) in patients with OSA compared with control group were respectively 15.55 +/- 11.26 : 61.2 +/- 27.4: 523.2 +/- 165.1 vs 10.34+/- 6.86 : 47.7 +/- 27.3: 447.9 +/- 102.6. There was positive significant correlation between leptin concentration and BMI (r = 0,34) and serum leptin and adrenalin concentration (r = 0,34). The serum leptin concentration was significantly higher in the female group. In the male group there was tendency to increase leptin concentration together with degree of OSA grade estimated by AHI and AHI50 leptin concentration 12.23+/- 6.96 ng/mL vs AHI50 and leptin concentration 13.35 +/- 3.54ng/ml.1. In the group of patients with OSA the serum concentrations of leptin, adrenaline and noradrenaline were higher then in control group. 2. There are positive statistical significant correlation between serum leptin levels and BMI and serum adrenaline concentration in the study group. 3. The serum leptin concentration was higher in the female group. 4. There was tendency to increased leptin concentration in the study group together with degree of OSA grade estimated by AHI. 5. Our results confirm correlation between leptin and sympathetic activity and their influences on obesity and degree of OSA grade in studied group.

The aim of this study was to determine if there are changes in laboratory investigations which allow to recognize coagulation disturbances associated with inhaled glucocorticoid therapy.The study group consist of 26 patients with stable asthma (5 male, 21 female) without risk factors of venous thrombosis, mean age 45 +/- 14 years. 15 patients were treated with 500-1000 mg beclomethasone daily, 11 patients received a daily dose of 1000-2000 microg of beclomethasone. The laboratory investigations included: hemoglobin concentration (Hb), hematocrit (Ht), platelet count (PLT), red blood cell count (E), white blood cell count (L), percentage of eosinophils (Eos%), fibrinogen (Fib), D-dimer concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), prothrombin index (Quick), INR and von Willebrand factor (vWF).An elevated concentration of D-dimers was detected in 4 patients (15%) the others investigated coagulation parameters were within normal range. We found a significant correlation between the dose of inhaled glucocorticosteroid and the PT, prothrombin index and INR.The results revealed no evidence of increased fibrinolytic activity in subjects with stable bronchial asthma treated with inhaled glucocorticosteroids.

The aim of the study was to evaluate the short-term variability of FENO in healthy subjects.33 healthy volunteers (26 F, 7 M) aged 32.6 +/- 9.5 yrs with body mass index (BMI) of 23.3 +/- 3 kg/m2 participated in the study. Exhaled nitric oxide was analyzed on 5 consecutive days with a chemiluminescence analyzer (NIOX, Aerocrine, Sweden) according to the ATS recommendations. The exhalation flow was between 0.045 and 0.055 l/s. The measurements were performed at the same time of the day and the subjects were asked to refrain from eating and drinking for at least one hour before the analysis.The mean value of FENO for the whole group was 13.9 +/- 5.4 ppb, there were no correlations between FENO and age, BMI, sex or the concentration of ambient nitric oxide. Day-to-day coefficient of variation was 13.3 +/- 5.3% (range 4.6 - 23.9%), the value of pooled SD - 2.1 ppb and ICC (intraclass correlation coefficient) was 0.84. No relationship was observed between variability of FENO and intervals between measurement of exhaled nitric oxide and intake of food or beverages.Chemiluminescence analysis of FENO with NIOX is a highly reproducible method, however one has to take into account the possibility of about 13% variability of FENO within 5 days.

Exhaled nitric oxide is a marker of airway inflammation and it is significantly decreased by glucocorticosteroid therapy, especially in patients with asthma.Evaluation of changes in FE(NO) in asthma and COPD exacerbation.17 patients with acute asthma and 19 patients with an exacerbation of COPD were enrolled to the study. FE(NO) (chemiluminescence, on-line, restricted breath technique measurement in accordance with the ATS recommendations) was performed for five consecutive days following admission to hospital. Results of the following additional blood investigations: peripheral white blood cell count, ESR, C-reactive protein level, arterial blood gases, spirometry or peak expiratory flow were also analyzed.The average value of FE(NO) on admission was 41.5+/-10.7 ppb (95% CI: 18.8-64.2 ppb) asthma patients and 28.6+/-5.4 ppb (95% CI: 17.4-40.0 ppb) in COPD patients. In asthma patients a significant decrease of FE(NO) on the third day of therapy was observed (41.5 vs 26.1 ppb, p0.05). We found a positive correlation between FE(NO) on admission and the peripheral blood eosinophil count. In COPD patients a significant decrease of FE(NO) on the 4th day was noted (28.6 vs 17.5 ppb, p0.05). FE(NO) in both groups was higher than that of 19 healthy volunteers previously studied in our laboratory (14.1+/-4.7 ppb; 95% CI: 11.8+/-16.4 ppb).Exacerbations of asthma and COPD are associated with an increased FE(NO). FE(NO) measurement is a useful tool in the assessment of treatment efficacy. Exhaled nitric oxide may indicate the intensity of allergic inflammation in patients with asthma.

Obstructive sleep apnea (OSA) is often accompanied by cardiovascular and metabolic disorders. The renin-angiotensin system plays an important role of the cardiovascular regulation. The activity of the angiotensin converting enzyme is genetically determined. The aim of the study was to estimate the relation between angiotensin converting gene polymorphism and cardiovascular diseases or familial history in patients with obstructive sleep apnea. 63 patients with OSA were enrolled to the study. Arterial hypertension was diagnosed in 30 cases, ischaemic heart disease in 5 cases and 10 patients suffered from both mentioned diseases.The observed ACE genotype frequencies in the study group were II: ID: DD: 23.81: 47.62: 28.57%, in the hypertension subgroup II: ID: DD--30.0: 46.6: 23.3%. No differences in the study group were observed in relation to familial history :DI:II--30.43: 43.48: 26.09% vs 25.64: 48.72: 25.4%.1. In the study group there was no association between ACE polymorphism and OSA. 2. There were also no association between the polymorphism of ACE and cardiac diseases or familial history of cardiac diseases in OSA group. 3. The polymorphism of ACE is not a risk factor for OSA.