Emphysema- and airway-dominant COPD phenotypes defined by standardised quantitative computed tomography.

EvA (Emphysema versus Airway disease) is a multicentre project to study mechanisms and identify biomarkers of emphysema and airway disease in chronic obstructive pulmonary disease (COPD). The objective of this study was to delineate objectively imaging-based emphysema-dominant and airway disease-dominant phenotypes using quantitative computed tomography (QCT) indices, standardised with a novel phantom-based approach.441 subjects with COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1-3) were assessed in terms of clinical and physiological measurements, laboratory testing and standardised QCT indices of emphysema and airway wall geometry.QCT indices were influenced by scanner non-conformity, but standardisation significantly reduced variability (p<0.001) and led to more robust phenotypes. Four imaging-derived phenotypes were identified, reflecting "emphysema-dominant", "airway disease-dominant", "mixed" disease and "mild" disease. The emphysema-dominant group had significantly higher lung volumes, lower gas transfer coefficient, lower oxygen (PO2 ) and carbon dioxide (PCO2 ) tensions, higher haemoglobin and higher blood leukocyte numbers than the airway disease-dominant group.The utility of QCT for phenotyping in the setting of an international multicentre study is improved by standardisation. QCT indices of emphysema and airway disease can delineate within a population of patients with COPD, phenotypic groups that have typical clinical features known to be associated with emphysema-dominant and airway-dominant disease.

Acceptance of home support and integrated care among advanced COPD patients who live outside large medical centers.

BACKGROUND: Poor self-management constitutes a risk factor for COPD deterioration. Patients from rural areas located at a considerable distance from large medical centers frequently need home-support in advanced stages of the disease. Integrated care has been proposed as a comprehensive model for appropriate treatment, coordination and holistic support. The aim of the study was to assess whether home visits provided by trained assistants are needed and accepted by advanced COPD patients living in rural areas a to evaluate whether an individual short educational program can actually improve such patients' knowledge of COPD and inhaler use. METHODS: Thirty patients with severe or very severe but stable COPD participated in one-month home-assistance interventions twice a week. RESULTS: The total value ≥70 of SGRQ (St George's Respiratory Questionnaire) was recorded in 18 (60%) patients. At the beginning of the study, the patients' knowledge of COPD and inhalation techniques was highly unsatisfactory. Significant improvement in all items (p=0.00) was obtained after the intervention. The risk for poor self-management was high. All patients had at least one 'factor' that indicated the need for home-support. A total of 240 visits (100%) were completed. Patients expressed high acceptance for home-based support delivered by medical assistants twice a week for one month. No patients opposed this kind of care and most of them expressed interest in receiving it in the future. CONCLUSIONS: The results suggest a compelling need for home care and demonstrate full acceptance of this kind of support on the part of advanced COPD patients.

Causes of deaths in COPD patients in primary care setting--a 6-year follow-up.

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.

Methotrexate as a single agent for treating pulmonary sarcoidosis: a single centre real-life prospective study.

INTRODUCTION: The first-line therapy in chronic sarcoidosis, according to WASOG/ATS/ERS recommendations, is GCS. This therapy is associated with significant adverse effects and finally does not alter the natural history of the disease. The objective of our study was to evaluate the efficacy and safety of monotherapy with MTX, as an alternative to GCS, in progressive pulmonary sarcoidosis. MATERIAL AND METHODS: An open prospective real-life, single-centre trial was performed on 50 patients with biopsy proven sarcoidosis, 28M and 22F, mean age 45.55 ± 8.9 years. The average duration of disease before MTX therapy was 12.34 ± 20.49 years, GCS therapy in the past was applied in 41 patients. All patients received MTX (10 mg or 15 mg weekly) between 2004 and 2013 because of chronic progressive pulmonary sarcoidosis. Therapy was planned for 24 months. Patients underwent regular clinical evaluation, pulmonary function assessment, exercise ability testing (6MWT), and chest radiography for therapy effectiveness every six months and side effects monitoring every 4-6 weeks. Forty-nine patients were included for statistical analysis of treatment efficacy. They were retrospectively allocated to "MTX responder" group if an improvement of 10% of FEV1, FVC, TLC, or 15% of DLCO from the initial value was documented for at least one parameter or "non-responders" if the patient did not meet the above-mentioned criteria. RESULTS: Duration of treatment ranged from 6 to 24 months, mean time 60.75 ± 34.1 weeks. For the whole cohort significant improvement after MTX therapy was observed for minimal SaO2 (%) (p = 0.043) and for decrease of DSaO2 (%) (p = 0.048) in six-minute walk test. The results were significantly better for patients treated with 15 mg than for those treated with 10 mg weekly and for those who obtained a greater total amount of MTX during therapy. Significant difference of DLCO%pred was observed after six months of MTX therapy between groups treated 15 mg vs 10 mg weekly (73.27 ± 12.7% vs. 63.15 ± 16.4%, p = 0.03). Twenty-five patients (55%) met the criteria of "MTX responders" group. Patients who responded well to treatment had significantly lower TLC and FVC initial values comparing to "MTX non-responders". After treatment the only significant difference in PFT between groups was noted for DLCO%pred. Eleven patients (22%) stopped the treatment due to adverse events of MTX, mild hepatic abnormalities were observed in ten patients (20%), and concomitant infection was found in four patients. There were no patients with a fatal outcome. CONCLUSIONS: MTX as a single agent in the treatment of sarcoidosis has proved to be a safe and effective steroid alternative. Selected patients with chronic pulmonary sarcoidosis experience definite PFT improvements after MTX treatment. There is need to search for predictors of MTX treatment effectiveness.

Impact of mild anaemia on dyspnoea during exertion and exercise tolerance in patients with acute exacerbation of chronic obstructive pulmonary disease.

INTRODUCTION: Dyspnoea and decreased exercise tolerance are symptoms of acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Anaemia is a risk factor for reduced functional capacity and dyspnoea in stable COPD. There is limited information about the impact of anaemia on functional capacity and dyspnoea of patients during AECOPD. The aim of this study was to evaluate the impact of decreased blood haemoglobin concentration on the results of six-minute walking test (6MWT) in patients during AECOPD. MATERIAL AND METHODS: A post hoc analysis of data collected from prospective long-term studies on AECOPD. Haemoglobin concentration from the first obtainable hospital measurement were included in the assessment. 6MWT was performed after clinical improvement of the patient. Dyspnoea at baseline and after exercise and oxygen saturation (SpO(2)) during exercise was measured. RESULTS: (presented as means ± SD): 402 patients with exacerbation of COPD (COPD stage 3.5 ± 0.6) were examined. Patients with anaemia (26% of those studied, age 74.5 ± 8.2 years) achieved 258.1 ± 125.1 m during 6MWT, with exertional desaturation of 2.9 ± 2.6%. Patients without anaemia (74% of those studied, age 70.2 ± 8.7 years) achieved 271 ± 136.0 m during 6MWT with exertional desaturation of 3.8 ± 3.7%. The haemoglobin concentration did not correlate with 6MWT, dyspnoea during 6MWT, or exercise oxygenation and blood desaturation during exercise. CONCLUSION: Mildly decreased blood haemoglobin concentration did not influence the results of 6MWT in patients with AECOPD.

Fatal clinical outcome in a patient with sarcoidosis-lymphoma syndrome.

A 62-year-old female suspected of malignant disease underwent a splenectomy that revealed noncaseating granulomas in the histological specimen. Chest X-ray (CXR) and lung CT scans suggested sarcoidosis stage II. TBLB showed noncaseating granulomas. A diagnosis of sarcoidosis was made. Initially no treatment was needed as partial remission on CXR and normal lung function were observed. During the follow up she underwent open lung biopsy and axillary lymph node biopsy because of radiological progression with presence of CXR opacities imitating metastases and recurrent lymphadenopathy. No malignant cells were found. Spontaneous partial resolution of disseminated changes on the CXR was observed. Because of progressive deterioration in lung function and the clinical course of the disease strongly suggesting the progression of systemic sarcoidosis, the patient was given steroid treatment, which initially resulted in partial remission of pulmonary disseminated changes, peripheral lymphadenopathy and improvement in lung function test. Eight months later severe deterioration in general condition, anaemia, leukocytosis, hypoxemia, massive hepatomegaly and recurrence of general lymphadenopathy along with progression of disseminated changes were found. She died before the final diagnosis was established. Post-mortem examination showed a nodal marginal zone B-cell lymphoma with monocytoid B-cells, according to WHO classification. The malignant cells were found in the jugular, mediastinal, paratracheal, paragastric, paraintestinal and retroperitoneal lymph nodes and they infiltrated the lungs, pleura, liver, thyroid gland and pancreas. No sarcoid granulomas were found in the autopsy.

The EvA study: aims and strategy.

The EvA study is a European Union-funded project under the Seventh Framework Programme (FP7), which aims at defining new markers for chronic obstructive pulmonary disease (COPD) and its subtypes. The acronym is derived from emphysema versus airway disease, indicating that the project targets these two main phenotypes of the disease. The EvA study is based on the concept that emphysema and airway disease are governed by different pathophysiological processes, are driven by different genes and have differential gene expression in the lung. To define these genes, patients and non-COPD controls are recruited for clinical examination, lung function analysis and computed tomography (CT) of the lung. CT scans are used to define the phenotypes based on lung density and airway wall thickness. This is followed by bronchoscopy in order to obtain samples from the airways and the alveoli. These tissue samples, along with blood samples, are then subjected to genome-wide expression and association analysis and markers linked to the phenotypes are identified. The population of the EvA study is different from other COPD study populations, since patients with current oral glucocorticoids, antibiotics and exacerbations or current smokers are excluded, such that the signals detected in the molecular analysis are due to the distinct inflammatory process of emphysema and airway disease in COPD.

[Autoimmunological pulmonary alveolar proteinosis--case report]. / Autoimmunologiczna proteinoza pecherzyków plucnych--opis przypadku.

Autoimmunological pulmonary alveolar proteinosis (APAP) is a rare interstitial lung disease with abnormal surfactant homeostasis. Autoimmunological pulmonary alveolar proteinosis is diagnosed most often in the third or fourth decade of life. Predominant symptoms are dyspnea and cough. In most cases, disease is mild but in more severe cases when dyspnea limits patient physical activity a treatment is required. The most common treatment procedure is a whole-lung lavage. We present a case study of 37 years old woman with the patchy consolidations in the chest radiograph. High resolution computed tomography (HRCT) image suggested hipersensivity pneumonitis. At the beginning due to limited disease symptoms no specific proceedings was implemented. After two year follow-up of non-resolving pulmonary changes the decision about open lung biopsy was made. On the basis of histological examination of samples and presence of anty GM-CSF antibodies the diagnosis of autoimmunological pulmonary alveolar proteinosis was established.

[Six-minute walk test in sarcoidosis patients with cardiac involvement]. / Test 6-minutowego chodu u chorych na sarkoidoze pluc z zajeciem serca.

INTRODUCTION: Cardiac involvement in sarcoidosis is of critical importance, due to the poor prognosis if this organ manifestation is left undiagnosed and untreated. The six-minute walk test (6 MWT) is a useful test to evaluate exercise tolerance of sarcoid patients. We aimed to assess the 6 MWT value in diagnosis, course and treatment monitoring of patients with cardiac sarcoidosis. MATERIAL AND METHODS: 47 patients were included: 22 with pulmonary sarcoidosis and cardiac involvement (13 women, 9 men), 25 with pulmonary sarcoidosis, with no changes in the heart (15 women, 10 men), and 18 healthy volunteers as controls (12 women, 6 men). Out of 22 patients with cardiac involvement 11 were treated for heart sarcoidosis with prednisone (9 pts - initial dose 60 mg daily and 2 pts - 40 mg daily). 11 pts in this group were not treated. In all patients sarcoidosis was confirmed histopatologically. Magnetic resonance imaging was used to diagnose involvement of the heart. In the studied groups we assessed: heart rate (HR), oxygen saturation, and distance in 6 MWT and Borg dyspnea score. RESULTS: Patients with cardiac sarcoidosis desaturated more during exercise (DSaO2max = 3.5 ± 3.2 vs. 0.38 ± 0.69; p = 0.004) and had a lower increase of HR in first minute during the 6 MWT (DHR1 = 21.81 ± 11.72 vs. 50.61 ± 12.35; p = 0.0001) when compared to healthy subjects. Significantly lower increase of HR in first minute of 6 MWT was observed in patients with cardiac sarcoidosis when compared to patients with pulmonary sarcoidosis with no cardiac involvement (DHR1 = 21.81 ± 11.72 vs. 38.8 ± 18.17, p = 0.01). After introduction of treatment in sarcoidosis group, significantly higher (p = 0.02) increase of HR in first minute of 6 MWT as compared to baseline test was observed. CONCLUSIONS: The six-minute walk test is useful in diagnosing cardiac involvement in sarcoidosis. The increase in HR during exercise and decrease degree of desaturation were a good predictors of the response to therapy.

[Prophylaxis in chronic obstructive pulmonary disease]. / Profilaktyka przewleklej obturacyjnej choroby pluc.

Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the world, is responsible for considerable morbidity and deterioration of quality of life of patients and their families. Prevention of COPD aims at reducing the burden of the disease. Prevention of COPD includes measures of tobacco control, reduction of the impact of harmful environment and the use of vaccination. However, despite proven efficacy of these methods, they are often inadequately applied.

[The impact of comorbidities on the length of hospital treatment in patients with chronic obstructive pulmonary disease]. / Wplyw chorób wspólistniejacych na dlugosc leczenia szpitalnegou chorych z zaostrzeniem przewleklej obturacyjnej choroby pluc.

INTRODUCTION: The aim of this study was to assess relationships of chronic obstructive pulmonary disease (COPD) comorbidities number, with the duration of hospital stay due to acute AE COPD in longitudinal prospective study. MATERIAL AND METHODS: We evaluated the number of re-hospitalizations, length of stay and number of comorbidities in 464 consecutive COPD patients admitted to the tertiary respiratory hospital due to AE COPD enrolled in longitudinal prospective study from 2005 to 2009 year. RESULTS: GOLD II stage COPD patients had 4.1 ± 1.2 comorbidities (p = 0.002), stage III 3.4 ± 1.3 and stage IV had 3.6 ± 1.2 comorbidities. Duration of hospital stay (medians) was longer in more severe patients. Duration of hospitalization correlated with urea level (r = 0.19 p 〈 0.001), pCO(2) (r = 0.193, p = 0.0003), HCO(3) (r = 0.25, p 〈 0.0001), haemoglobin (r = -0.18, p 〈 0.001), and hematocrit (r = -0.13, p = 0.008). The patients with the risk of readmission had more severe GOLD stage and were hypercapnic (pCO(2) = 47.6 mmHg v. 43.9 mmHg in those without hospitalization). CONCLUSIONS: The haemoglobin level, hypercapnia and renal function are predictors of prolonged hospitalization. Patients with more severe airflow limitation and higher pCO(2) have increased risk for readmission to the hospital. More severe disease stage, clinical diagnosis of cor pulmonale or bronchiectasis was related to longer hospital stay.

Gender specific airway gene expression in COPD sub-phenotypes supports a role of mitochondria and of different types of leukocytes.

Chronic obstructive pulmonary disease (COPD) is a destructive inflammatory disease and the genes expressed within the lung are crucial to its pathophysiology. We have determined the RNAseq transcriptome of bronchial brush cells from 312 stringently defined ex-smoker patients. Compared to healthy controls there were for males 40 differentially expressed genes (DEGs) and 73 DEGs for females with only 26 genes shared. The gene ontology (GO) term "response to bacterium" was shared, with several different DEGs contributing in males and females. Strongly upregulated genes TCN1 and CYP1B1 were unique to males and females, respectively. For male emphysema (E)-dominant and airway disease (A)-dominant COPD (defined by computed tomography) the term "response to stress" was found for both sub-phenotypes, but this included distinct up-regulated genes for the E-sub-phenotype (neutrophil-related CSF3R, CXCL1, MNDA) and for the A-sub-phenotype (macrophage-related KLF4, F3, CD36). In E-dominant disease, a cluster of mitochondria-encoded (MT) genes forms a signature, able to identify patients with emphysema features in a confirmation cohort. The MT-CO2 gene is upregulated transcriptionally in bronchial epithelial cells with the copy number essentially unchanged. Both MT-CO2 and the neutrophil chemoattractant CXCL1 are induced by reactive oxygen in bronchial epithelial cells. Of the female DEGs unique for E- and A-dominant COPD, 88% were detected in females only. In E-dominant disease we found a pronounced expression of mast cell-associated DEGs TPSB2, TPSAB1 and CPA3. The differential genes discovered in this study point towards involvement of different types of leukocytes in the E- and A-dominant COPD sub-phenotypes in males and females.

[Prevalence of stroke in patients with obstructive sleep apnoea]. / Rozpowszechnienie udaru mózgu u pacjentów z obturacyjnym bezdechem sennym.

INTRODUCTION: Results of earlier population and clinical studies confirmed relationship between stroke and obstructive sleep apnea. Our previous study on epidemiology of sleep-disordered breathing in Warsaw based on 676 subjects, mean age 56.6 +/- 8.2 years, confirmed OSA in 76 subjects (11.3%) mean apnea hypopnea index (AHI) - 25.3 +/- 16.1 revealed low incidence of stroke in OSA group (2 pts; 2.6%) and in subjects without OSA (20 pts; 3.4%). The aim of this study was to assess prevalence of stroke in newly diagnosed OSA subjects qualified to CPAP therapy. MATERIAL AND METHODS: We studied 342 consecutive pts (263 males and 79 females)--mean age--55.4 +/- 10.1 years with severe disease--AHI 39.7 +/- 22.5 and obesity--body mass index 35 +/- 6.6. History of stroke was confirmed in 16 pts before continuous positive airway pressure (CPAP) introduction (4.7%) - group 1. Group 2 (without history of stroke) comprised of 326 pts (95.3%). RESULTS: Multiple linear regression analysis revealed significant correlation between stroke and time spent in desaturation below 90% during polysomnography-- T90 (beta = -0.22, p = 0.009), diabetes (b = 0.16, p = 0.006), Epworth sleepiness score (beta = 0.14, p = 0.02) and coronary artery disease (b = 0.14, p = 0.03). CONCLUSIONS: Stroke in OSA pts before CPAP treatment was related to overnight and daytime oxygenation, diabetes, daytime sleepiness and coronary artery disease. Incidence of stroke in our group was low (4.7%) and similar to previous data from population study.

[Obstructive sleep apnea in patient with Prader-Willi syndrome]. / Obturacyjny bezdech senny u pacjenta z zespolem Pradera-Williego.

Prader-Willi syndrome (PWS) is a genetic disorder caused by loss of function of genes situated within the 15q11-q13 region of chromosome 15. The disorder is characterized by central obesity, short stature, dysfunction of several hypothalamic centers. These symptoms lead to progressive metabolic, respiratory, circulatory and orthopedic complications. Because of the etiology of the disorder there is no known causal treatment. Patients should comply with dietary restrictions and behavioral modifications as it may reduce the risk of obesity related diseases. In this paper we present case of a 34-years old obese patient with PWS who was diagnosed with obstructive sleep apnea, and whom CPAP treatment was offered.

[Evaluation of motivation to quit smoking in outpatients attending smoking cessation clinic]. / Ocena motywacji do rzucenia palenia u pacjentów poradni antynikotynowej.

INTRODUCTION: The success in smoking cessation depends not only on a method of treatment but also on patient motivation. The aim of this study was to estimate the motivation and the main reason to quit smoking among outpatients attending smoking cessation clinic. MATERIAL AND METHODS: One hundred and eleven patients (50 men and 61 women), mean age 58, filled in a motivation test, nicotine dependence test and a questionnaire of the clinic. RESULTS: The main motivation to quit was for the health reasons (83%). Mean motivation test result was 6.93; mean nicotine addiction evaluated in dependence test was 5.49. Eighty seven percent of patients were ready to quit smoking during one month (36% in 24 hours; 23% in one week; 28% in four weeks). There was no significant difference between men and women. CONCLUSIONS: The main motivation to quit smoking were the health reasons as well among men as women. There was no correlation between the readiness to quit smoking determined as time to quit attempt and the motivation test.

[Integrated care for patients with advanced chronic obstructive pulmonary disease]. / Zintegrowana opieka medyczna u chorych na zaawansowana przewlekla obturacyjna chorobe pluc.

Chronic obstructive pulmonary disease (COPD) is the third cause of mortality and disability (assessed by DALY) among patients above 60 year old. Severe and very severe COPD (FEV(1) = equal or less than 50% and 30% of expected value, respectively) is estimated at 20% of all COPD patients. Advanced COPD usually leads to physical and mental deterioration, the patients often manage with the problems caused by the disease and other comorbidities poorly. This leads to increased risk of COPD exacerbations and further deterioration of the patient's status, increased costs of medical care and eventually increased risk of death. Current organization of medical care for those patients does not provide adequate health and social support for them. However, it seems that introducing an integrated approach proposed by World Health Organization, could improve the situation of advanced COPD patients. In Poland, this kind of care has been provided in advanced cancer patients throughout stationary palliative care units and hospices during the last several years. This experience should be helpful in integrating actions of general practitioners and specialized nurses, as well as providing access for the specialists' consultations according to the individual needs of the patients. It should also allow for broad cooperation with auxiliary staff, such as social workers, medical assistants and volunteers, as well as psychologists and clergymen (especially in the terminal phase of the disease).

[Markers of fibrosis and inflammation in exhaled breath condensate (EBC) and bronchoalveolar lavage fluid (BALF) of patients with pulmonary sarcoidosis -- a pilot study]. / Markery wlóknienia i zapalenia w kondensacie powietrza wydychanego (EBC) oraz w plynie z plukania oskrzelowo-pecherzykowego (BALF) u chorych na sarkoidoze pluc - badanie pilotazowe.

INTRODUCTION: Sarcoidosis is a disease of unknown etiology. Little is known of predictive factors of fibrosis. It was suggested that PAI-1, uPA, TGF-beta1, VEGF, IL-8, TNF-alpha influence this process. AIMS: To assess airway inflammatory and fibrosis markers in EBC in sarcoidosis and the effect of fiberoptic bronchoscopy (FOB), bronchoalveolar lavage fluid (BALF), transbronchial lung biopsy (TBLB) and bronchial mucosa membrane biopsy on their production in the airways. MATERIAL AND METHODS: The study group consisted of 11 patients (5 women, 6 men; mean age 40 +/- 9 yrs, mean +/- SD) with sarcoidosis stage I-III. PAI-1 (ng/ml), uPA (ng/ml), TGF-beta1 (pg/ml), VEGF (pg/ml), IL-8 (pg/ml), TNF-alpha (pg/ml) levels were measured in BALF and EBC collected before and 48 hours after FOB. RESULTS: No significant changes in EBC levels of VEGF, PAI-1, TGF-beta1, TNF-alpha (respectively: 8.02 +/- 4.97 pg/ml; 1.1 +/- 1.2 ng/ml; 2909.7 +/- 206.6 pg/ml; 10.7 +/- 19.9 pg/ml) after FOB were observed when compared to baseline. In contrast, IL-8 concentration in EBC (pg/ml) decreased after FOB (0.073 +/- 0.13 v. 0.061 +/- 0.1, p = 0.006) and was significantly lower than in BALF (BALF 0.95 +/- 0.62, p < 0.05). Also, mean level of VEGF was higher in BALF than in EBC both pre- and post- FOB (BALF 66.38 +/- 36.95, EBC pre-FOB 6.75 +/- 3.67 and EBC post-FOB 8.02 +/- 4.97). Significant relationship between TNF-alpha in post-FOB EBC and BALF was also shown (b = 0.63, p = 0.04). CONCLUSIONS: FOB does not significantly affect levels of airway inflammation and fibrosis markers present in EBC before and after FOB; they were also comparable to the concentrations marked by BALF. The lack of correlation between markers levels in EBC and BALF indicates that these methods are not equivalent. Due to repeatibility, and less invasive, simple method of EBC test it seems reasonable to continue the research on the larger number of patients.

[Simultaneous detection of tumor cells and the positive result of genetic test for Mycobacterium tuberculosis in pleural effusion]. / Jednoczesne wykrycie komórek nowotworowych i materialu genetycznego pratków gruzlicy w plynie oplucnowym.

Pleural effusion is a frequently observed lesion in the course of respiratory diseases such as inflammatory process and cancer metastasis. Its cause may be either tuberculosis (the most common extrapulmonary location is the pleura) and malignant disease of the pleura. Confirmation of tuberculosis is often troublesome. The primary site of cancer may be also difficult to find despite the application of difficult diagnostic methods. Below we present history of 79-year-old female in whom carcinomatous cells and positive result of PCR for Mycobacterium tuberculosis in pleural fluid were discovered simultaneously suggesting the tuberculosis and cancer of unknown primary origin.

Evolution of upper airway resistance syndrome.

The question of whether upper airway resistance syndrome (UARS) is a distinct disease or an initial feature of obstructive sleep apnoea syndrome is still a matter of debate. We evaluated a retrospective group of UARS patients to determine the evolution of UARS over time and the relationship between clinical evolution and subjects' phenotype. Investigations were performed in 30 patients, in whom UARS was diagnosed between 1995 and 2000 by the use of full polysomnography (PSG) without oesophageal pressure (Pes) measurement. The time between initial and follow-up investigations was 6.6 +/- 2.6 years. All subjects had full PSG with Pes measurement and completed a sleep questionnaire, including the Epworth Sleepiness Scale. In 19 subjects, PSG results were compatible with UARS. In nine subjects, obstructive sleep apnoea-hypopnoea syndrome (OSAHS) was diagnosed. In two subjects, PSG did not demonstrate breathing abnormalities. The mean +/- SD apnoea-hypopnoea index in the UARS group was 1.5 +/- 1.7 h(-1) and 25.2 +/- 19 h(-1) in the OSAHS group (P < 0.01). The increase in body mass index (BMI) between initial and follow-up investigations in the UARS group was from 29.4 +/- 4 to 31 +/- 5.7 kg m(-2) (P = 0.014) and in the OSAHS group from 30 +/- 4.1 to 32.4 +/- 4.7 kg m(-2)(P = 0.004). Amplitude of Pes swings during respiratory events was significantly higher in OSAHS than that in UARS (P = 0.014). Our results suggest that UARS is part of a clinical continuum from habitual snoring to OSAHS. Progression from UARS to OSAHS seems to be related to an increase in the BMI.