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The study analysed post-acute COVID-19 symptoms and the pulmonary function test (PFT) results in patients surviving the native strain of the virus.The study was prospective; the inclusion criteria were positive PCR test for SARS-CoV-2 and age 18-100. Exclusion criteria were active respiratory infection, known or suspicious pre-existing pulmonary disease, cardiac failure, recent or acute pulmonary embolism, anaemia, and neuromuscular diseases. The recruitment period was 1The study involved 785 subjects (345 male) mean age 53.8 (SD 14.6). The disease severity groups were: mild (G1), moderate (G2) and severe/critical (G3). Anosmia was present in the acute disease phase in 45.2% of G1 patients, but only in 4.5% of G3 patients. Dyspnoea occurred frequently in more severe groups (40%, 51.8% and 63.7% for G1, G2 and G3 respectively), while cough and fatigue showed no relationship to disease severity. Females were more likely to experience persistent symptoms. PFT results were significantly decreased in more severe groups compared to the mild COVID-19 patients, diffusing capacity was 86.3%, 79% and 68% of predicted values in G1, G2 and G3 respectively.Anosmia during the acute phase was associated with mild disease, persisting dyspnoea was more frequent after more severe COVID-19. Females tended to have persisting symptoms in post-acute phase more frequently. PFT results showed decrease with disease severity.

A 33-year-old man with obesity, systemic arterial hypertension, and psoriasis who had been treated previously with little success by a pulmonologist for chronic unproductive irritant cough came to the outpatient pulmonary department because of profuse cough and short syncope (probably cough-induced). Chest radiography revealed widened mediastinum with lobular, polycyclic contours that was suspected to be a large mediastinal lymphadenopathy or mediastinal mass.

In Slovakia, NIPPV is a rapidly developing treatment method with increasing range of users. First guidelines - Slovak Guidelines for the Use of Non-Invasive Positive Pressure Ventilation came in practice in 2007 with partial revision in 2015. The amount of new knowledge and research results in this area justified the revision of the guidelines in 2019. Updated guidelines are based on widely accepted international guidelines with regard to local specifics. The document complies with the latest official ERS/ATS clinical practice guidelines for acute respiratory failure from 2017. A new important aspect in the document is the classification of acute indications into 3 categories: 1, Indications, which should be treated with NIPPV; 2, indications, where it is possible to consider NIPPV; and 3, those, where NIPPV is not recommended (regarding evidence based medicine). In addition, the guidelines extend the circle of specialists in the treatment of adult patients, but also the paediatric sector. We also highlighted the importance of comorbid sleep-related breathing disorders in other chronic respiratory conditions and the role of continuous positive airway pressure (CPAP) as their first line treatment, limitations of CPAP, and its failure justifying NIPPV use. Since NIPPV is often combined with oxygen therapy in chronic indications, guidance on safe use of oxygen therapy in NIPPV-treated patients has been also included. Support: VEGA 1/0220/17 , VEGA 1/0208/16; APVV-16-0158

Background: Systemic inflammation, endotoxaemia and oxidative stress may represent intermediate pathophysiological mechanisms involved in impaired sleep architecture. Aims: We investigated relationships between sleep architecture and serum endotoxaemia marker lipopolysaccharides-binding protein (LBP), oxidized low-density lipoprotein (oxLDL) and insulinaemia in patients with obstructive sleep apnoea (OSA). Methods: 66 women with OSA [age (mean±SD) 57.2±9.9 years, body mass index (BMI) 34.8±8.4 kg/m2, apnoea-hypoponea index (AHI) 37.4±37.5 events/hour] underwent overnight polysomnography. Serum biomarkers were analyzed using ELISA. Multivariate linear regressions assessed the independent correlates of slow-wave sleep (SWS) and rapid eye movement (REM) proportion of Total Sleep Time (TST). Results: Serum LBP levels were directly associated with TST duration, and inversely with the proportion of REM and SWS (Table). Moreover, OxLDL was inversely related to SWS, and serum insulin to REM sleep. LBP (P=0.047) and insulinaemia (P=0.013) were related to REM independently of age, AHI and BMI (R2=0.282, p Conclusions: Our results suggest that increases in circulating LBP and insulinaemia are related to reduced REM sleep in women with OSA. Further studies are needed to determine the role of various biomarkers in sleep architecture. Support: VEGA 1/0220/17, APPV-16-0158, VEGA 1/0208/16.

Backround: Obstructive sleep apnoea (OSA) is associated with increased arterial stiffness and endothelial dysfunction. OSA-related oxidative stress, systemic inflammation and endotoxemia may play a role in vascular derangements. Aims: We investigated effects of continuous positive airway pressure (CPAP) therapy on arterial stiffness, body composition, endotoxemia and oxidative stress. Methods: 40 subjects with OSA [age (mean±SD) 50±8 years, body mass index (BMI) 31.9±4.5 kg/m 2 ] free of cardiovascular diseases except for arterial hypertension were enrolled. Arterial stiffness was assessed by carotid-radial pulse wave velocity (PWV) (Complior®, France), body composition by measuring bioelectrical impedance (Bodystat 1500, UK). PWV, body composition, serum lipopolysaccharides-binding protein (LBP) and oxidized low-density lipoprotein (oxLDL), were measured at baseline and after 3 months of CPAP. Results: Compliance with CPAP was 4.1±1.8 hours/night. Reductions of PWV in association with reductions in oxLDL were observed after 3 months of CPAP (9.7±1.6 to 9.0±1.6 m/s, p=0.003; 501±186 to 381±174 ng/ml, p=0.002, respectively). Improvements in arterial stiffness were observed regardless body weight or body composition change. CPAP had no effect on an endotoxemia marker (serum LBP). Conclusions: Our results suggest that in patients with OSA without overt cardiovascular diseases, elimination of OSA by CPAP results in improvements in arterial stiffness in association with reductions in oxidative stress. Support: APVV-0134-11, VEGA 1/0863/15 and 1/0208/16, Ministry of Education, Slovakia.

Obstructive sleep apnea (OSA) is associated with dyslipidemia and increased cardiovascular risk. We assessed the effects of apolipoprotein E ( APOE) genotype on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particle size and lipid subclasses (separated by gradient gel electrophoresis) in patients with OSA. Stable patients (n = 181) prospectively recruited underwent full polysomnography. Both LDL particle size and LDL I proportion were reduced from ∊3∊3 homozygotes to ∊2 carriers and to ∊4 carriers (analysis of variance: P = .024; P = .040, respectively); carriers of the ∊4 allele of the APOE genotype had significantly lower LDL particle size and LDL I proportion compared to ∊3∊3 homozygotes ( P < .05 for both comparisons). Insulin resistance increased from patients with no OSA to those with mild–moderate and to those with severe OSA ( P < .001). In multivariate analysis, LDL size was independently predicted by APOE genotype, male gender, and the presence of metabolic syndrome (MetS; P = .001, P = .020, P = .027, respectively). The HDL particle size was not affected by APOE genotype. Our data demonstrate that both the ∊4 APOE genotype and MetS are independently related to smaller LDL size in patients with OSA.

Background: CD40, a transmembrane receptor of the tumor necrosis factor gene superfamily, is activated in response to cellular stress, including hypoxia, and orchestrates the process of inflammation via secondary messengers such as mitogen-activated protein kinase kinase 4 (MKK4) and c-Jun NH2-terminal kinases (JNK). Objectives: We hypothesized that CD40, MKK4 and JNK expression is increased in the adipose tissue of patients with very severe chronic obstructive pulmonary disease (COPD). Methods: In 20 patients with stable COPD, lung function was assessed using body plethysmography, and samples of subcutaneous adipose tissue were analyzed using real-time PCR. Body composition, including fat mass index (FMI), was assessed by bioelectrical impedance. Results: 12 patients in GOLD stage I–III (age 61.6 ± 8.6 years, 4 females, mean partial pressure of oxygen in arterial blood, PaO2, 9.38 ± 0.21 kPa) were compared to 8 patients in GOLD stage IV (age 62.6 ± 6.3 years, all male, mean PaO2 7.70 ± 0.37 kPa). Compared to patients in GOLD stage I–III, patients in GOLD stage IV had lower FMI (p = 0.004), being associated with significantly higher adipose tissue expression of CD40, MKK4 and JNK [ΔΔCt: 2.55 (1.99, 4.40) vs. 1.87 (1.63, 2.23), p = 0.013; 5.19 (3.13, 5.96) vs. 2.98 (2.82, 3.86), p = 0.002; 9.01 (5.12, 11.41) vs. 4.65 (4.42, 6.26), p = 0.001, respectively]. Log-transformed CD40, MKK4 and JNK expression was significantly inversely related to PaO2, respectively. Conclusions: Upregulation of proinflammatory CD40, MKK4 and JNK gene expression in adipose tissue in very severe COPD raises the possibility of a role of chronic systemic hypoxia in the pathogenesis of adipose tissue inflammation in COPD.

Summary Background Osteoprotegerin (OPG), a potent inhibitor of osteoclastogenesis, decreases bone resorption and has protective effects on bone mineral density (BMD). Recently we have shown that the adipose-tissue derived OPG relates to BMD in patients with chronic obstructive pulmonary disease (COPD), a condition associated with increased risk of osteoporosis. Objective Here we aimed to investigate the potential of circulatory OPG to reflect hip BMD in patients with COPD. Patients and methods In 56 subjects with COPD [age, 61.7 ± 6.7 years; forced expiratory volume in 1 s (FEV 1 ), 53.6 ± 19.2% predicted], total femur BMD was assessed by dual energy X-ray absorptiometry, serum OPG and β-crosslaps, a marker of increased bone resorption, by commercially available assays. Results From patients with normal hip BMD ( n = 32, T-score 0.1 ± 0.8) to those with osteopenia ( n = 14, T-score −1.6 ± 0.4) and osteoporosis ( n = 10, T-score −3.4 ± 0.7) serum OPG levels significantly increased (6.6 ± 1.8 versus 7.2 ± 2.9 and versus 8.6 ± 1.5 pmol/l, p = 0.036). In addition, hip T-scores were directly related to FEV 1 , and inversely to β-crosslaps ( R = 0.40, p = 0.002; R = 0.38, p = 0.01, respectively). In multivariate analysis, OPG independently predicted hip T-scores after adjustments for age, gender, FEV 1 , and β-crosslaps ( p = 0.011, adjusted R 2 = 0.354). Area under receiver operator curve for OPG as a discriminator of osteoporosis was 0.787 (95% CI, 0.653–0.921) ( p = 0.005). Conclusions Present results suggest that osteoporosis of the hip is associated with increased circulatory levels of OPG in patients with COPD. OPG might serve as a biomarker of this COPD-related comorbidity.

Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3±7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using real-time PCR. From underweight [n=9; body mass index (BMI)