Search

Aim of the Study: The aim of this study was to evaluate granzyme B, perforin and FasL expression in peripheral blood mononuclear cells (PBMCs) in lung cancer patients and in paraneoplastic neurological syndromes (PNS)., Clinical Rationale for the Study: Cellular immune response is activated as part of anti-tumour reaction of the malignancy-bearing host. Paraneoplastic neurological syndromes (PNS) are defined as indirect effects of cancer on the nervous system and are considered immune-mediated. Such stimulation of the immune system may limit the aggressiveness of cancer and the development of metastasis, and thereby improve survival. Granzyme B and perforin pathway, and Fas ligand (FasL) - Fas receptor interaction play an important role in cytotoxic response., Materials and Methods: Fifty-two patients were included in the study: 28 subjects with PNS and 24 subjects with lung cancer. PNS cases were diagnosed according to the Graus criteria. The presence of onconeural antibodies (anti-Hu/anti-Ri/anti-Yo/anti-Ma/Ta/anti-CV2/anti-amphiphysin/anti-myelin/anti-neuroendothelium/anti-MAG/anti-GAD) was detected with indirect immunofluorescence and confirmed with Line Blotting. The expression of granzyme B, perforin and FasL was detected in PBMCs with ELISA., Results: PPBMC-FasL expression was increased in lung cancer compared to other patient groups. The granzyme to FasL ratio was significantly higher in lung cancer patients with peripheral than with central PNS involvement. In a multiple regression model, sex was an independent factor influencing PBMC expression of granzyme and perforin., Conclusions: FasL expression in PBMCs is up-regulated in lung cancer patients. The interplay between granzyme B and FasL may be involved in the development of PNS at the level of the peripheral and the central nervous systems in different manners. Gender is associated with PBMC expression of granzyme B and perforin in lung cancer patients., Clinical Implications: The novel findings that we report broaden the current knowledge on PNS pathomechanism, with aspects that have not been previously explored. Our findings provide a rationale for further exploration of the granzyme B/FasL pathway with regards to its potential diagnostic value. However, our study is preliminary and needs further research, especially in the context of the prognostic value of the proposed markers.

Introduction: Taking into account important role of apoptosis in COPD pathogenesis, we wanted to asses the serum levels of markers involved in apoptosis regulation, including apoptosis inducers such as TNF-a, sFasL or p53 protein and apoptosis inhibitor bcl-2 and, in addition, to compare these markers with selected COPD parameters., Material and Methods: In 181 patients (60 women) with COPD (age was 62.2+ 9.37 years; FEV1% 55.2 + 19.98 %) and in 29 controls (11 women), serum levels of TNF-a, sFasL, p53 and bcl-2 were evaluated by the enzyme-linked immunosorbent assay (ELISA) method., Results: In COPD patients the mean sFasL level was 0.092 ± 0.077 ng/ml and mean TNF-a level was 2.911 ± 3.239 pg/ml. There were no differences in serum sFasL and TNF-a in COPD patients and control group. TNF-a and sFasL did not correlate with COPD parameters such as FEV₁%, BMI, RV% (percentage of predicted value of residual volume) or BODE. Although we tried to evaluate bcl-2 and p53 protein serum levels with two different tests, measurable levels of bcl-2 were only detected in 15 patients and p53 in only 3 patients. Bcl-2 values were from 0.418 to 11.423 ng/ml and p53 from 90.772 to 994.749 pg/ml., Conclusions: We didn't observe any differences in serum levels of pro- and antiapoptotic markers in COPD patients and the control group or correlations between the markers studied and COPD parameters.

Chronic obstructive pulmonary disease (COPD) is characterised by persistent airflow limitation and extrapulmonary comorbidities, which contribute to the overall severity. Some risk factors, with tobacco smoking as the most serious one, lead to a chronic, systemic inflammation that plays the main role in the pathogenesis of COPD and comorbidities, including cardiovascular diseases (CVD). The course of COPD is diverse; it depends on pathologies in the respiratory system and on other organ dysfunctions. CVDs are the most commonly recognised comorbidities in COPD patients. The severity and natural course of COPD, as well as quality of the patient's life, are influenced by them. CVDs are frequently the reason for hospitalisation and may lead to death. They are also an important prognostic factor. Comorbidities may prolong exacerbation of COPD. On the other hand, COPD is an independent risk factor of CVD. The prevalence of COPD is high in patients suffering from coronary artery disease, and airflow limitation is a major risk factor for chronic heart failure. These complex interactions between heart and lung can be denoted as 'cardiopulmonary continuum'. These dependencies are not recognised in detail. Currently research is being done, which attempts to explain these complicated relations. For many years COPD and CVD were not connected. Today it is known that patients suffering from COPD must be provided comprehensive care. It is necessary to monitor the risk of CVD and their influence on the COPD course. Careful and proper treatment of all diseases is essential. An interdisciplinary team with good cooperation should prepare a plan of COPD treatment with simultaneous therapy of comorbidities.

Granulomatosis with polyangiitis (GPA) is a rare disease of unknown aetiology, characterized by necrotizing inflammation of small and medium-sized vessels and formation of granulomas. The disease typically involves the upper and lower respiratory tracts and the kidneys, but it can occur in many other locations, often giving a surprising clinical picture. The majority of patients have autoantibodies against cytoplasm of neutrophils (ANCA), of which a pathogenetic role is postulated. The disease affects mostly middle-aged and elderly people, with a predominance of Caucasians. Before the era of immunosuppressive therapy GPA was associated with high early mortality. Nowadays, we have a treatment that gives remission in the majority of patients. The decision about the method of treatment should be made depending on the clinical form of the disease (local or generalized, refractory). Standard remission induction therapy in the generalized disease is cyclophosphamide in combination with steroids. This therapy, however effective, is associated with a number of side effects. In addition, some patients are resistant to standard therapy, and half of them experience relapses. Therefore, there is need for further research for alternative treatment and maintenance therapy. Currently, hopes are raised by biological agents. Among them, the best studied so far is rituximab, which found a place in the current recommendations of EULAR as an alternative drug for patients with refractory disease. The article discusses the clinical picture of GPA, diagnosis and currently recommended treatment.

Chronic obstructive pulmonary disease (COPD) is still a leading cause of death, with a huge socioeconomic impact. Disease is mostly caused by cigarette smoking, characterized by persistent and progressive airway inflammation with pathological changes in the lungs and extrapulmonary and systemic consequences. The standard methods for classifying disease (i.e. forced expiratory volume in 1 second measurement) do not reflect individual characteristics and clinical status of COPD patients, and do not provide information regarding disease activity or the underlying pathologic process. Regarding the clinical evolution and prognosis, several clinical characteristics have been correlated to biomarkers. New strategies for the management of COPD are required, not only for identifying the origin of the exacerbation episodes, but also for phenotyping, assessing prognosis and tailoring treatment for each patient. We have made major gains in biomarker knowledge over the past decade. There are large-scale studies presently underway to identify novel biomarkers in COPD. Results of these investigations may lead to the development of new drugs and other interventions to improve the health outcomes of COPD patients.

Introduction: Among the most common extrapulmonary manifestations of COPD are nutritional status disorders. The specific loss of weight, called cachexia, characterized by loss of lean body mass in some COPD patients is observed. The aim of the study was the quantitative and qualitative analysis of COPD patients' nutritional status disturbances., Material and Methods: Fifty-five patients in different stages of COPD--43 males and 12 females (mean age 62.31 +/- 11.08) and 32 subjects from a control group (mean age 57.43 +/- 8.79) participated in the study. In both groups nutritional status was assessed using different indicators such as PIBW--percentage of ideal body weight, BMI--body mass index, FFMI--fat-free mass index and FMI--fat mass index., Results: Malnutrition measured by PIBW, BMI, BMI percentiles, and FFMI was observed in 5.45%, 3.64%, 3.64% and 18.18% of COPD patients, respectively, and in the control group 3.12%, 0%, 3.12% and 3.12%, respectively. The BMI mean value did not differ significantly between groups. It was confirmed that cachexia assessed by FFMI occured more frequently in COPD patients than in the control group--19.05 kg/m2 vs. 20,55 kg/m2 (p = 0.04)., Conclusions: 1. Nutritional status disorders pose a serious problem, which concerns about 1/5 of the COPD population. 2. It is necessary to perform quantitative analysis of nutritional status (assessment of lean and fat mass) because indicators of body mass (PIBW, BMI) are not sufficient for cachexia detection. 3. Having normal body mass does not exclude the possibility of nutritional status disorders in COPD patients.

Unlabelled: The aim of the paper was evaluation of social aspects of tobacco smoking among Polish students., Material and Methods: The data from 671 students of Medical University and University in the age between 19 and 25 were collected using a specially prepared questionnaire. The following factors were analyzed: age and causes of first attempt of smoking, frequency of tobacco smoking in relation to the kind of high school and sex; students' behaviors connected with tobacco smoking and the knowledge of the consequences., Results: 53.8% tried to smoke at least once. 23.09% of the students smoked regularly (10.73%) or occasionally (12.36%). University students smoked significantly more often than medical students--32.79% and 18.64% (p < 0.05), respectively. Males smoked more frequently than females (insignificant difference). The first smoking experience usually occurred at the age of 18, but males started to smoke earlier (between 10 and 14) than females (between 18 and 21)--significant differences. The age of 18 was the most common time when smoking became regular. Most smokers (80%) were aware of tobacco-dependent health disturbances., Conclusion: 1. Every fifth student of medicine and every third University student smoke cigarettes. 2. Anti-tobacco prevention should be started very early--before the age of 10 and continued up to the age of 21. Special attention should be taken at the age of 18 years as this time was found to be especially dangerous for development of addiction.

The aim of the study was the estimation of in vitro susceptibility to antifungal agents of yeast isolated from sputum of 70 respiratory diseases patients using the disc-diffusion method-antimycogram. The following agents were tested: amphotericin B, 5-fluorocytosine, nystatin, ketoconazole, fluconazole. Only Candida strains were isolated from sputum, 82% of them were Candida albicans. We noted differences in susceptibility to antimycotics of Candida strains. The best antimycotic in vitro was 5-fluorocytosine. 54% of isolated Candida strains were resistant to 1 or more antimycotics.