Background.Bronchiectasis is a progressive chronic disease associated with an increased risk of mortality.Objectives.To identify the prevalence of comorbidities in patients with bronchiectasis and the impact of these comorbidities on mortality. Materials and methods.A cohort of 93 patients with computed tomography (CT)-confirmed bronchiectasis admitted consecutively to a tertiary teaching hospital was observed over a period of 5 years.All patients were carefully observed for comorbidities and mortality.Results.A total of 43 men (46.2%) and 50 women (53.8%) with a median age of 66.0 years (interquartile range (IQR) 59.7-74.0years), and a median of 3 comorbidities at baseline (IQR 1-5) were observed.The mortality rate during the observation period was 16%.The median number of comorbidities was significantly higher in the group of non-survivors (5 (IQR 3-5.75)) compared with survivors (3 (IQR 1-4); p = 0.0100).The burden of comorbidities was associated with an increased hazard of death: having 4 or more comorbidities was associated with an increased risk of death compared to patients with 2 or 3 coexisting illnesses (hazard ratio (HR) = 1.35 (95% confidence interval (95% CI) [0.41, 4.41]); p = 0.0494).The Bronchiectasis Aetiology Comorbidity Index (BACI) was a significant predictor of death in patients with severe bronchiectasis.Conclusions.We found a significant number of comorbidities in patients with bronchiectasis.In these patients, the comorbidity burden has an impact on mortality.The BACI is a useful tool for the clinical assessment of patients with severe bronchiectasis.

Background Recent studies indicate that chronic kidney disease (CKD) is a comorbidity in patients with obstructive sleep apnea (OSA). We hypothesized that the use of the classical muscle-dependent, creatinine-based equation to estimate glomerular filtration rate (GFR) in patients with OSA may be inaccurate due to the extreme body mass index (BMI) of some patients. The aim of this study was to establish the role of cystatin-C-based estimation of GFR for the detection of CKD in patients with OSA and typical comorbidities. Methods Two hundred and forty consecutive patients with newly diagnosed OSA were enrolled into this cross-sectional study. In all patients estimated GFR (eGFR) was calculated with chronic kidney disease-epidemiology collaboration group (CKD-EPI) equations using creatinine and cystatin-C. All patients were examined for comorbidities. Results In obese patients with OSA significant differences between GFR estimations based on creatinine and cystatin were found: eGFR based on muscle-dependent creatinine measurement was significantly higher than the muscle-independent eGFR based on cystatin-C measurement. Conclusions GFR can be routinely screened for using creatinine-based estimations (eGFRcreat). In a selected group of patients with OSA with BMI over 30 kg/m2 the addition of cystatin-C for assessment of eGFR is suggested.

The findings of numerous studies and analyzes conducted in many countries have proven that obstructive sleep apnea (OSA) negatively affects the psychophysical abilities drivers. Therefore, in Commission Directive 2014/85/EU of July, 1 2014, OSA was recognized as one of the most important risk factors for car accidents. The implementation of said Directive by Member States is to contribute to reducing the risk of such accidents. The implementation of the Directive in Poland has resulted in enacting the Ordinance of the Minister of Health of December 23, 2015 amending the ordinance on medical examinations of applicants for a driving license and drivers. Although Annex 2 to that regulation sets out the detailed conditions for a medical examination for OSA, it does not regulate or clarify the issue of tools and methods for suspecting OSA in a moderate or hard form. Therefore, it was necessary to develop standards of management for doctors authorized to perform medical examinations of drivers and applicants for a driving license in the case of suspected OSA. The paper presents an algorithm of proceedings that streamlines the case-law process in the above-mentioned cases, which was developed by the Polish Society of Occupational Medicine in cooperation with the Polish Respiratory Society, the Nofer Institute of Occupational Medicine in Łódź and the Polish Sleep Research Society. Med Pr. 2020;71(2):233-43.

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.

Aim: The aim of this study was to identify the patients with increased level of FCOHb in the group of LTOT patients declaring themselves as current non-smokers. Materials and methods: Retrospective analysis of arterialized capillary blood gases of 118 consecutive LTOT pts, assessed during a period of apparent clinical stability. The measurements were performed on Point-of-Care blood gases analyzer during one summer month when air pollution in the city of study was reported as low. Results: 62 males (52.5%) and 56 females (47.5%) with mean age 72.0±6.9 yrs were studied. In this group 26 (22%) patients presented with increased FCOHb, higher than 1,5% in arterialized capillary blood. Results are listed in Table 1. FCOHb significantly correlated; positively with: Hb, HCO3, pCO2; negatively with: FO2Hb, p50c. Conclusion: 22% LTOT patients declared themselves as a currently non-smokers have increased level of FCOHb what can suggest unreported active or passive smoking. Increased level of FCOHb corresponds with indices of diminished oxymetry results in this group. The measurement of FCOHb during routine visits patients in LTOT clinic may have clinical importance.

Introduction: Obstructive sleep apnoea (OSA) in an independent risk factor for arterial hypertension development. Both OSA and arterial hypertension frequently coexist, thus common genetic background can be suspected. Material and methods: We enrolled 600 participants with diagnosis of OSA in all stages of severity from 2 tertiary care outpatient clinics in Warsaw, Poland. All patients undergone polysomnography and were evaluated for the diagnosis of hypertension. Gene polymorphisms for genes encoding ALOX5AP, SREBF2, ADRA2A, APOA5 and TCF7L2 were analyzed in blood samples. Chisquare and Mann-Whitney tests were used for comparisons. Results: Data of 449 (74.8%) men and 151 (25.2%) women were analyzed. Arterial hypertension was diagnosed in 427 (71.2%) participants. In the hypertensive patients with OSA median age was 59 (53–64) years, BMI 32.8 (28.9– 37.3) kg/m2, AHI 39 (24–60)/hour. Among tested genes only TCF7L2 polymorphism ([C/T] rs7903146) was linked to increased incidence of arterial hypertension. Conclusions: Results of our analysis suggest potential relationship of TCF7L2 polymorphism ([C/T] rs7903146) and development of hypertension in patients with OSA, although further studies regarding impact of genetic in comparison with traditional risk factor for hypertension are needed.

Previous studies confirmed relationship between intermittent hypoxia in OSA subjects and metabolic syndrome. The aim of this study was to compare prevalence metabolic abnormalities in moderate (AHI=15-29.9), severe (AHI=30-49.9) and very severe OSA (AHI ≥50). We studied 1068 OSA pts (AHI – 42.1±21, BMI – 34.4±6.4 kg/m2, mean SaO2 – 90.6±5.8%, age – 56.1±10,4 years). Moderate OSA had 400 pts (37.5%), severe OSA - 306 pts (28.6%) and very severe – 362 pts (33.9%). Comparison of these groups is shown in table. Conclusions: Incidence of metabolic disturbances increased with OSA severity. Subjects with AHI ≥50 were younger, more obese and had higher frequency of diabetes, arterial hypertension and presented with more severe desaturation during night and lower PaO2 during daytime.

Rationale: Some studies have demonstrated an association between chronic kidney disease (CKD) and obstructive sleep apnea (OSA). It was suggested that glomerular filtration rate estimations (eGFR) based on serum creatinine may be influenced by muscle abnormalities observed in OSA patients. Aim: The aim of this study was to compare the prevalence of CKD in OSA pts using eGFR estimations based on both cystatin C and creatinine serum concentrations. Materials and methods: A cohort of 240 pts with newly diagnosed OSA was enrolled into the study. Results: 185 males (77%) and 55 females (23%) with mean age = 56.8 ±9.9 yrs, Apnea-Hypopnea Index (AHI) 38.7±21.7/hour, Epworth sleepiness scale (ESS) 11.2± 5.7 were examined for CKD. Results of eGFR in studied group are listed below. Weak correlations were observed between eGFR estimated using cystatin C and: proBNP (R -0.24, p=0.0061), total cholesterol (R =0.16, p=0.015) and ESS (R -0.16 p=0.015). Conclusion: We have found a signs of CKD in a significant number of studied OSA pts. eGFR based on cystatin C increased prevalence and severity of CKD in OSA pts. Additional eGFR masurements based on cystatin C should be considered in OSA pts.

INTRODUCTION:Office spirometry has been widely used in recent years by general practitioners in primary care setting, thus the need for stricter monitoring of the quality of spirometry has been recognized.MATERIAL AND METHODS:A spirometry counseling network of outpatients clinics was created in Poland using portable spirometer Spirotel. The spirometry data were transferred to counseling centre once a week. The tests sent to the counseling centre were analyzed by doctors experienced in the analysis of spirometric data. In justified cases they sent their remarks concerning performed tests to the centres via e-mail.RESULTS:We received 878 records of spirometry tests in total. Data transmission via the telephone was 100% effective. The quality of spirometry tests performed by outpatients clinics was variable.CONCLUSIONS:The use of spirometers with data transfer for training purposes seems to be advisable. There is a need to proper face-to-face training of spirometry operators before an implementation of any telemedicine technology.

Urinary albumin excretion is associated with endothelial dysfunction. Untreated OSA is risk factor for endothelial injury (oxidative stress, thrombosis, inflammation) and finally cardiovascular complications. The aim of this study was to estimate a frequency of albuminuria and association with concomitant diseases in OSA pts. We studied 159 subjects with moderate and severe OSA - AHI= 41.5±20.7, BMI=34.4±6.4 kg/m2, age - 57±10.6 years, mean SaO2=90.7±6.9% (114 males -71.7% and 45 females -28.3%). Albuminuria (> 20mg/L) was found in 33 subjects (20.8% - group 1). Comparison of groups with and without albuminuria (group 0) is shown in the table below. Logistic regression analysis revealed that only nephrolithiasis (OR- 0.1; 95%CI – 0.01-0.7; p=0.02) was independent predictor of albuminuria after adjusting for AH, CAD, HF, AF, Diabetes, AHI > 30 vs ≤30, T90 >30 vs ≤ 30. Conclusions: Albuminuria was found in 20% of OSA subjects. Main predictor of urinary albumin excretion was nephrolithiasis.

Some previous studies confirmed relationship between smoking and OSA pathophysiology (aggravation of snoring, upper airway inflammation, effects of nicotine on upper airway muscles). The aim of the study was to assess smoking habits in OSA subjects and relations between smoking and OSA severity, obesity and concomitant diseases. We studied 1163 OSA pts: AHI – 39.7±21.7, BMI – 34.2±6.4 kg/m2, mean SaO2 – 90.8±5.7%, age - 56.4±10.4 years. Majority of subjects were active or ex-smokers (781pts, 67.2%). We divide pts into three groups: nonsmokers (group 0- 382pts, 32.8%), smokers < 30 packyears (group 1-460pts, 39.6%) and smokers ≥30 packyears (group 2 - 321pts, 27.6%). Comparison between groups is shown in the table. Conclusions: Majority of OSA subjects were active or ex-smokers (67.2%). Subjects who smoked ≥ 30 packyears were more obese and had higher prevalence of not only COPD but diabetes, heart failure and coronary artery disease, too.

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 <0.05) in the whole group. We found a higher incidence heterozygous AG for FTO gene in women with CHD (16.7% vs 6.3%, p <0.05) and in women with myocardial infarction (60% vs. 6.1%, p <0.0001). Conclusions: Determination of polymorphism of SREBF1 and FTO genes may be useful in assessing the risk of cardiovascular complications in patients with OSA.

INTRODUCTION COPD is one of the most frequent respiratory diseases responsible for patients' disability and mortality. In 2005 a single primary care practice, COPD was diagnosed in 183 out of 1,960 eligible subjects ≥ 40 years (9.3%). The aim of this study was to assess mortality rate and causes of deaths in this group after 6 years. MATERIAL AND METHODS In 2011 we invited all 183 patients with COPD recognised in 2005. We performed spirometry, physical examination, questionnaire of respiratory symptoms, smoking habits, concomitant diseases and treatment. Information about deaths was taken from primary care register, furthermore, family members were asked to deliver medical documentation or death certificate. RESULTS In 2011 we studied only 74 subjects (40.4%), 43 subjects died (23.5%) and 66 subjects were lost from the follow-up (36.1%). Cardiovascular diseases were the most frequent causes of deaths - 21 subjects (48.8%) (heart attack - 8 patients and stroke - 8 patients). Respiratory failure in the course of COPD exacerbation was the cause of 10 deaths (23.3%). Neoplastic diseases lead to 9 deaths (20.9%) (lung cancer 7 patients). Renal insufficiency was responsible for one death (2.325%), and the causes of 2 deaths remained unknown (4.65%). Subjects who died (predominantly males) were older, had higher MRC score and lower FEV₁. CONCLUSIONS Study performed six years after COPD diagnosis revealed that 23.5% of subjects died. The main causes of deaths were the following: cardiovascular diseases (mainly heart attack and stroke), COPD exacerbations and lung cancer (more than 75%). Death risk in COPD patients was associated with age, male sex, dyspnoea and severity of the disease.

The prevalence of obstructive sleep apnoea (OSA) is estimated to be 3-7.5% in men and 2-3% in women. In mentally ill population it is even higher, as these patients are a high risk OSA group. The aim of the paper was a review of literature about the prevalence of sleep apnoea in patients with schizophrenia, bipolar disorder and recurrent depressive disorder.The available data show that OSA is present in 15-48% of patients with schizophrenia, 21-43% of patients with bipolar disorder and 11-18% of patients with recurrent depressive disorder. The lack of diagnosis of OSA in people with mental illnesses has multiple negative consequences. The symptoms of sleep apnoea might imitate the symptoms of mental illnesses such as negative symptoms of schizophrenia and symptoms of depression, they might as well aggravate the cognitive impairment. A number of the drugs used in mental disorders may aggravate the symptoms of OSA. OSA is as well the risk factor for cardiovascular and metabolic diseases which are a serious clinical problem in mentally ill people and contribute to shortening of their expected lifespan. From the point of view of the physicians treating OSA it is important to pay attention to the fact that co-existing depression is the most common reason for resistant daytime sleepiness in OSA patients treated effectively with Continuous Positive Airway Pressure (CPAP). CPAP therapy leads to significant improvement of mood. However, in schizophrenia and bipolar patients it may rarely lead to acute worsening of mental state, exacerbation of psychotic symptoms or phase shift from depression to mania.

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.

Cardiovascular diseases are most frequent complications of untreated OSA. The aim of this study was to compare OSA pts with CAD and without CAD. We studied 1048 OSA pts with moderate or severe disease (AHI - 42.1±21), mean age - 56.1±10.4 years, BMI - 34.4±6,4 kg/m 2, Epworth score - 11.3±5.8 points, mean SaO2 -90.6±5.8%. We found 812 pts without CAD (77.5%; group 1) and 236 pts with CAD (22.5%; group 2). Comparison of both groups is shown in table. View this table: Logistic regression analysis revealed that: heart failure (OR- 4.43; 95%CI – 2.74-7.15; p 60 vs ≤ 60 years (OR- 2.38; 95%CI – 1.82-3.12;p 125 vs ≤ 125 pg/ml (OR – 1.84; 95%CI – 1.27-2.67; p=0.001) and diabetes (OR-1.47; 95%CI – 1.007-2.14; p=0.045) were independent predictors of CAD after adjusting for AH, stroke, AF, COPD, BMI > 30 vs ≤30 and hyperuricaemia. Conclusions: Coronary artery disease was frequent in OSA pts (more than 20%). We found strongest association between heart failure and age and CAD in OSA patients.

OSA is recognized as an risk factor for insulin resistance and diabetes. Plasma HbA1c concentration is an indicator of mean glycaemia over 2-3 month period (increased HbA1c may precede diabetes). We aimed to assess relationships between plasma HbA1c and OSA severity and complications in subjects without diabetes. We studied 455 OSA pts, mean age=56.3±11 years with moderate to severe OSA (AHI=40.5±21.4) and obesity (BMI=33.2±5.9 kg/m2). Normal HbA1c was found in 240 pts (52.75%), increased HbA1c (≥ 6%) was found in 215 pts (47.25%). Comparison of these groups is shown in the table. View this table: Multiple linear regression analysis confirmed significant correlation between plasma HbA1c and T90 (β=0.25; p=0.03) and Epworth score (β=0.12; p=0.01). Elevated plasma concentration of HbA1c in OSA pts without diabetes was related to some markers of body oxygenation: significantly lower mean overnight saturation, higher T90 and lower daytime PaO2. Conclusions: Increased plasma HbA1c concentration was very frequent (in about 50%) in a group of moderate to severe OSA pts without diabetes. Overnight desaturation time (T90) was mainly responsible for HbA1c elevation in this group.

Untreated OSA is a risk factor for cardiovascular morbidity. Arterial hypertension is one of the most frequent OSA complications. The aim of study was to compare hypertensive OSA pts and subjects without arterial hypertension. We studied 1164 OSA pts, mean age = 56.4±10.4 years, with obesity (BMI = 34.2±6.4 kg/m2) and moderate to severe disease (AHI = 39.6±21.7). We found 307 normotensive OSA pts (26.4%) and 857 OSA pts with arterial hypertension (73.6%). Comparison of both groups is shown in the table. View this table: Logistic regression revealed that: diabetes (OR- 3.05; 95%CI – 1.88-4.95; p 30 vs ≤ 30 (OR- 2.34; 95%CI – 1.67-3.28;p 125 vs ≤ 125 pg/ml (OR – 1.85; 95%CI – 1.23-2.79; p=0.003), hyperuricaemia (OR-1.83; 95%CI – 1.28-2.63; p=0.0009) and nocturia ≥ 2 vs 30 vs ≤30, T90 >30 vs ≤ 30. Conclusions: Arterial hypertension was very common in our group of OSA pts. The highest risk of arterial hypertension was related to diabetes and obesity.

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Arterial hypertension (AH) may affect up to 60% of patients with OSA. Therefore the identification of factors predisposing to AH in these patients seems to be of great importance. Aim: to assess genetic polymorphisms known to be associated with a greater risk of AH in patients with OSA. We enrolled 600 patients aged 54.4±10.3 yrs with OSA confirmed by polysomnography. The following gene polymorphisms reported to have a correlation with cardiovascular diseases and metabolic syndrome were evaluated by real-time PCR in peripheral blood: ALOX5AP (arachidonate 5-lipoxygenase-activating protein), LPL (lipoprotein lipase), SREBF2 (sterol regulatory element binding transcription factor 2), ADRA2A (adrenergic alpha-2A-receptor), APOA5 (apolipoprotein A-V), TCF7L2 (transcription factor 7-like 2) and LEPR (leptin receptor). We then searched for correlation between these polymorphisms and the diagnosis of AH in our patients. AH was diagnosed in 427 patients (71.2%). Only a significant correlation between AH and TCF7L2 polymorphism in the group as whole was found: the lowest AH incidence was found for TT homozygotes; particularly in patients with AHI > 30 (74% CC vs. 48% TT). Male AA homozygotes for ALOX5AP also had a higher risk for AH. Increased AH incidence was also noted in: GG SREBF homozygotes with BMI 30-35 kg/m2 and CG ADRA2A heterozygotes in patients with AHI 15-30. Conclusion: Only one gene polymorphism related with an increased incidence of AH in patients with OSA was found and it concerned the TCF7L2 gene (associated with diabetes mellitus). This correlation was specifically expressed in patients severe OSA.