Ograniczanie wyników

Czasopisma help
Autorzy help
Lata help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 44

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  chronic obstructive pulmonary disease
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Content available remote

Non-invasive ventilation in chronic obstructive pulmonary disease

100%
Non-invasive ventilation (NIV) via nasal or full face mask can be applied in respiratory failure due to chronic obstructive pulmonary disease (COPD) both in the acute and long-term settings. In acute exacerbation of COPD with respiratory failure it may be considered as a standard treatment. There is strong evidence that NIV might reduce intubation, complication, and mortality rate in patients with acute hypercapnia (PaCO2 >45 mmHg). The method is cost effective and reduces hospital stay. NIV might be also useful in the weaning of COPD patients from invasive ventilation. On the other hand, for severe stable disease the data concerning a positive effect of NIV are less convincing. Preliminary evidence suggests that NIV improves gas exchange, sleep quality and quality of life and might reduce the need for hospitalization. Especially, COPD patients with substantial chronic hypercapnia (PaCO2 >55 mmHg) and/or nocturnal hypoventilation, and those with repeated exacerbations may profit from NIV. In any case, NIV is a very valuable and effective tool in the non-pharmacological treatment of COPD. Every clinician who is involved in the management of COPD patients with respiratory insufficiency should be able to apply this technique.
4
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Experiences of a Slovak PhD pioneer

75%
It has all started 10 years ago, at my first WON CA Europe conference in Istanbul in 2008, where I became amazed by so many general practitioners, who performed and presented their scientific work there. However it took me 7 years since the idea to start my PhD studies until it´s final completion in 2017. My PhD journey wasn´t straight, but rather twisty, with 2 interruptions. In 2011 I started to earn my basic research skills at 2 courses. The first one was the European General Practice Research Network (EGPRN) course in Nice and the second University of Crete´s research workshop in Slovakia lead by Professor Christos Lionis. The easiest part of my PhD studies was the clinical one – administering questionnaire and performing spirometry with my patients at my rural general practice. I also enjoyed teaching medical students at undergraduate as well as postgraduate level. I gave lectures at national conferences and published articles about general medicine in Slovak scientific journals, focusing on prevention, patient safety and respiratory diseases, especially COPD. I also contributed to two medical text books. My research was presented as posters or oral presentations at 3 WONCA Europe conferences, where I found a great space for sharing research ideas and results. Final results of my PhD thesis are going to be presented at Krakow conference. Even though I was a fruitful author of publications, reaching the goal of an international publication was the most difficult part for me, not achievable without a help of experienced colleague, Austrian general practitioner, Professor Gustav Kamenski.
Inhaled corticosteroids have a high level of topical anti-inflammatory activity. However, in patients with COPD these drugs have been reported to exert limited effects. A reduction in histone deacetylase (HDAC) activity is suggested to prevent the anti-inflammatory action of corticosteroids. Cigarette smoke is known to reduce HDAC expression. The aim of this study is to compare the outcome of corticosteroid therapy in both smoking and non-smoking COPD patients. Twenty-three smoking patients and 18 ex-smoking patients with COPD were treated with inhaled corticosteroids for a period of 2 months. Blood and induced sputum samples were collected before and after treatment. Values of FEV1 %-predicted did not change upon the therapy, but there was a trend to improve in the ex-smokers (63.1 64.8%-pred.), compared with a decrease in the smokers (63.3 61.6%-pred.). The levels of the pro-inflammatory cytokine IL-8 increased in the group of smokers from 379 ±78 to 526 ±118 ng/ml. Although not significant, a slight decrease from 382 ±70 to 342 ±62 ng/ml was observed in the group of ex-smokers. The neutrophil related elastase activity showed similar effects after steroid treatment, it went up from 36.4 ±12.0 to 113.5 ±9.7 nmol/l in smokers, and decreased from 346.2 ±72.1 to 131.1 ±6.5 nmol/l in ex-smokers with COPD. These results support the evidence that inhaled corticosteroids have no anti-inflammatory effects in COPD patients, but only when these patients are still smoking. Smoking cessation seems the best therapy for COPD patients.
Inhaled corticosteroids (ICS) are widely used for the treatment of COPD despite of controversial statements concerning their efficacy. The use of N-acetylcysteine (NAC), a mucolytic drug with antioxidant properties, is less clear, but it may counteract the oxidant-antioxidant imbalance in COPD. The aim of this study was to evaluate whether treatment of COPD patients with ICS or NAC is able to improve inflammatory indices and to enhance lung function. ICS treatment enhanced protective markers for oxidative stress such as glutathione peroxidase (GPx) (51.2 ±5.8 vs. 62.2 ±8.6 U/g Hb, P<0.02) and trolox-equivalent antioxidant capacity (TEAC) (1.44 ±0.05 vs. 1.52 ±0.06 mM, P<0.05). NAC decreased sputum eosinophil cationic protein (318 ±73 vs. 163 ±30 ng/ml, P<0.01) and sputum IL-8 (429 ±80 vs. 347 ±70 ng/ml, P<0.05). The increased antioxidant capacity prevented an up-regulation of adhesion molecules, since the levels of intracellular adhesion molecule 1 (ICAM-1) correlated negatively with GPx (P<0.0001) and TEAC (P<0.0001). On the other hand, expression of adhesion molecules was promoted by inflammation, reflected by a positive correlation between the levels of IL-8 and ICAM-1 (P<0.0001). The effects of treatment on lung function were only reflected in the FEV1 values. The absolute value of FEV1, both before and after salbutamol inhalation, increased from 1690 ±98 to 1764 ±110 ml, and 1818 ±106 to 1906 ±116 ml, respectively, after ICS (P<0.05) . Ten weeks after treatment, FEV1 values dropped to 1716 ±120 ml post-salbutamol (P<0.05). When followed by treatment with NAC, these values decreased even further to 1666 ±84 ml. These results suggest that ICS improved lung function in COPD patients with moderate airflow obstruction, beside a minor improvement in the oxidant-antioxidant imbalance leading to a lesser expression of ICAM-1. Treatment with NAC decreased some inflammatory parameters and had indirectly an inhibitory effect on the expression of adhesion molecules.
Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alphalpha/IL-1ß) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alphalpha/IL-1ß-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alphalpha/IL-1ß- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.
 The bronchial epithelium is a very important factor during the inflammatory response, it produces many key regulators involved in the pathophysiology of asthma and COPD. Local influx of eosinophils, basophils, Th2 lymphocytes and macrophages is the source of many cytotoxic proteins, cytokines and other mediators of inflammation. These cells are attracted by eotaxins (eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26). Inhibitors of phosphodiesterase 4 (PDE4) are new anti-inflammatory drugs which cause cAMP accumulation in the cell and inhibit numerous stages of allergic inflammation. The aim of our study was to evaluate the influence of PDE4 inhibitors: rolipram and RO-20-1724 on the expression of eotaxins in human primary bronchial epithelial cells. Cells were preincubated with PDE4 inhibitors for 1 hour and then stimulated with IL-4 or IL-13 alone or in combination with TNF-α. After 48 hours, eotaxin protein level was measured by ELISA and mRNA level by real time PCR. These cells produce CCL24 and CCL26. PDE4 inhibitors increased CCL24 and CCL26 mRNA level irrespectively of the used stimulators. Rolipram and RO-20-1724 had no effect on eotaxin protein production in our experimental conditions. Thus PDE4 inhibitors have no effect on eotaxin protein expression in human primary bronchial epithelial cells. In vitro experiments should be performed using a primary cell model rather than immortalized lines.
Background. Cigarette smoking is a major public health problem, which leads to the formation of chronic obstructive pulmonary disease (COPD) and is one of the main causes of avoidable death and disability worldwide. Objective. The aim of study was analysis and comparison of the visceral fat in the body of the three groups of subjects (non-smokers, smokers and COPD patients) by Tanita Viscan 140. Material and Methods. The control group was composed of: (1) non-smokers (n=30), consisted of 13 males (43.4%) and 17 women (56.6%) - the average age was 52 ± 6.51 years and (2) smokers (n=30), consisted of 12 men (40%) and 18 women (60%) – the average age 46.53 ± 9.22 years. Study group consisted of patients with COPD (n=60), which consisted of 48 men (80%) and 12 women (20%). Mean age was 69.25 ± 9.90 years. The measurement of visceral fat by Tanita Viscan device 140, which uses bioelectrical impedance analysis to measure fat in the abdomen of the patient in the supine position. Results. High levels of visceral fat (women from 36.9% to 52.3% and more, men from 27.1% to 40.3% or more) were observed in 19 patients (3 women and 16 men), with 19 smokers (10 women and 9 men) and non-smokers in 22 subjects (10 women and 12 men). The average value of waist circumference measured with a Tanita Viscan 140 was in the group of patients 96.38 ± 12.27 cm, in the group of smokers 95.23 ± 10.12 cm and in group of non-smokers 96.86 ± 10.88 cm. Conclusions. The results of our work are of great importance for the health assessment not only among patients with COPD but also in the group of smokers. Therefore it would be appropriate to remind the general public, eg. by campaign for chronic obstructive pulmonary disease and its serious complications and reduce the life quality of these patients and thus help protect human health and in particular young people from the harmful effects of tobacco products.
The aim of the study was to evaluate the quality of life and its changes in patients with idiopathic pulmonary fibrosis (IPF), waiting for lung transplantation. Sixteen IPF patients, who qualified for lung transplantation, and 14 chronic obstructive pulmonary disease (COPD) patients on long term oxygen therapy, taken as a reference group, were assessed. The quality of life was estimated twice, using an SF-36-questionnaire, at the time of qualification for lung transplantation and 12 months later. The IPF and reference patients had similarly profound disturbances in lung function and arterial blood gas content. The IPF patients had a statistically greater score in their physical functioning (PF; 45 vs. 18), the role of limitations due to physical problems (RP; 43 vs. 11), social functioning (SF; 58 vs. 30), and the role of emotional limitations in everyday life (RE; 65 vs. 12) than the reference ones. After a year's observation, there were no differences in SF-36 questionnaire results, except for the role of limitations due to physical problems (RP). A correlation was noted between spirometry and blood gas results and SF-36 questionnaire results in IPF patients qualified for lung transplantation. There was a positive correlation between the partial pressure of oxygen (PaO2), on one side, and mental and general health, on the other. There also were positive correlations between FEV1 and SF and FEV1 and the level of bodily pain (BP). We conclude that the SF-36 questionnaire is a sensitive tool to assess the quality of life in IPF patients qualified for lung transplantation. The information gained can help assess the severity of the disease, clinical symptoms, and functional impairment in these patients.
The aim of our study was to evaluate cellular content in induced sputum in chronic obstructive pulmonary disease (COPD) in relation to the degree of airway obstruction, macrophage count, and phenotype. We compared the proportion of macrophages and cells expressing the following markers: CD11b, CD14, CD54, and CD71 in induced sputum obtained from patients with mild-to-moderate and severe COPD (n=29)], asymptomatic smokers (n=18), and nonsmokers (n=18). The differential cell count and macrophage phenotypes were examined in induced sputum by immunocytochemistry. We observed a greater proportion of neutrophils and eosinophils and an elevated macrophage count in patients with COPD and in smokers in comparison with nonsmokers. Macrophages in patients with severe airway obstruction were characterized by a significantly elevated expression of CD11b and CD14 markers. There were higher proportions of macrophages with expression of CD11b, CD14, CD54, and CD71 in induced sputum of smokers in comparison with nonsmokers. We concluded that macrophages are the cells involved in the inflammatory process caused by smoking in COPD. The macrophage phenotype with elevated CD11b and CD14 expressions was associated with severe airflow limitation.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.