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Biomedical subjects

Raimundas Sakalauskas

Publications and source records attributed to Raimundas Sakalauskas.

At least 19 recordsLinked to original sources

Changes in cough reflex sensitivity after cessation and resumption of cigarette smoking.

Previous studies have shown that healthy cigarette smokers have diminished cough reflex sensitivity compared to healthy nonsmokers. We have recently demonstrated that cough reflex sensitivity is enhanced soon after smoking cessation, suggesting that diminished cough sensitivity in smokers results from chronic cigarette smoke-induced desensitization of airway cough receptors. In this study, we evaluated cough reflex sensitivity to capsaicin (C(5)) in 11 chronic smokers who had discontinued smoking for at least 2 weeks, and then resumed smoking. Two weeks after smoking cessation there was a significant enhancement of cough reflex sensitivity; mean (+/-SEM) log C(5) decreased from 1.77+/-0.18 to 1.47+/-0.14 (p=0.01). All subjects resumed smoking after 2-12 weeks of abstinence. Repeat capsaicin cough challenge was performed 14-23 days after resumption of smoking. Mean log C(5) increased compared to the last value obtained during the smoking cessation period: 1.42+/-0.15 vs. 1.77+/-0.16 (p=0.0004). Mean log C(5) after resumption of smoking returned to almost exactly the baseline value. Our findings suggest that the sensitivity of airway cough receptors is a dynamic phenomenon, promptly affected and modulated by changes in environmental conditions, such as the presence or absence of cigarette smoke.

Administration, Cutaneous↗

Dyspnea perception and reversibility of methacholine-induced unlimited airway narrowing in asthmatics.

The hypothesis was that asthmatics might experience impaired perception of dyspnea and salbutamol-induced reversibility during unlimited airway narrowing. A total of 38 asthmatics (18 to 59 years of age) were examined. All patients underwent the methacholine challenge test. According to the dose-response curve to methacholine, they were categorized as having either unlimited airway narrowing (UAN group) (n = 20) or response plateau (RP group) (n = 18). Reversibility of methacholine-induced bronchoconstriction was measured 20 minutes after the inhalation of 400 microg of salbutamol to compare postbronchodilator FEV1 with baseline FEV1. Dyspnea perception was evaluated using the Borg Scale to calculate a perception score at a 20% decrease in FEV1 (PS20) and the slope alpha of the regression line between the changes in Borg scores and the reduction in FEV1 as percentage of the baseline value. Subjects in the UAN group exhibited significantly lower PS20 compared with the RP group (1.45+/- 0.23 vs. 2.84 +/- 0.35, p = 0.002); the mean of the slope values was higher in the RP group than it was in the UAN group (0.150 +/- 0.015 vs. 0.095 +/- 0.006, p = 0.003). Salbutamol-induced reversibility was significantly lower in the UAN group (81 +/- 1.4 % of baseline FEV1) compared with patients from the RP group (91 +/- 1.1% of baseline FEV1; p < 0.001). In conclusion, asthmatics during methacholine-induced unlimited airway narrowing exhibit diminished perception of dyspnea and lower bronchial reversibility to the baseline 20 minutes after inhalation of salbutamol. This suggests that more careful monitoring of the lung function for timely recognition of asthma deteriorations and adequate bronchodilatory therapy during severe acute attacks should be recommended for such patients.

Adolescent↗

[The rate of isolation of Klebsiella pneumoniae producing extended-spectrum beta-lactamases and resistance to antibiotics].

OBJECTIVE: To determine the relationship between the production of extended-spectrum beta-lactamases (ESBLs) in Klebsiella pneumoniae (K. pneumoniae) strains resistant to third-generation cephalosporins and resistance of these strains to antibiotics used. MATERIAL AND METHODS: A total of 157 cultures of K. pneumoniae resistant to third-generation cephalosporins were obtained from bronchial secretions of patients treated in intensive care units (ICUs) at Kaunas University of Medicine Hospital (KUMH). The secretions were cultured, and antibacterial susceptibility was tested in the Laboratory of Microbiology at KUMH according to the recommendations of the National Committee for Clinical Laboratory Standards (NCCLS). Using a method of double-disc synergy test, K. pneumoniae strains possibly producing ESBL were considered for further testing by means of E-tests. The resistance to carbapenems, piperacillin, gentamycin, amikacin, and ciprofloxacin was compared between ESBL-producing and non-ESBL-producing K. pneumoniae strains resistant to third-generation antibiotics. RESULTS: Almost one-third of K. pneumoniae strains (n=28, 32.8%) were resistant to third-generation cephalosporins in 2001 and 50.0% (n=36)--in 2004 (p<0.05). Half of the strains (n=7, 50%) were producing ESBLs in 2001 and 50% (n=12)--in 2004. All strains of K. pneumoniae were susceptible to carbapenems. Resistance rates to piperacillin and gentamicin were higher in ESBL-producing strains compared with non-ESBL-producing strains (94.7% (n=18) vs. 15.8% (n=3) (p<0.05) for gentamicin and 100% (n=19) vs. 36.8% (n=7) (p<0.001) for piperacillin, respectively). No significant differences were found in the resistance rates to amikacin and ciprofloxacin. CONCLUSIONS: The resistance of K. pneumoniae strains, isolated from bronchial secretions of patients treated in ICUs at KUMH, to third-generation cephalosporins increased significantly during the period of 2001-2004. However, the proportion of ESBL-producing strains remained unchanged. Resistance to certain antibacterials could be suspected if ESBL production is present - higher rates of resistance to piperacillin and gentamicin were found in the group of ESBL-producing K. pneumoniae strains.

Amikacin↗

[Genetic features during chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease is one of the leading causes of mortality, which is caused by the interaction of genetic susceptibility with environmental factors (especially smoking); however, genetic features of chronic obstructive pulmonary disease still remain unknown. The only proven genetic risk factor is severe deficiency of plasma protease inhibitor, alpha-1 antitrypsin. A large number of candidate genes for chronic obstructive pulmonary disease have already been identified in many experimental and clinical studies; however, polygenic etiology of chronic obstructive pulmonary disease is the main reason for conflicting molecular and genetic findings. This review describes the correlation between single nucleotide polymorphism of alpha-1 antitrypsin, alpha-1 antichymotrypsin, microsomal epoxide hydrolase-1, matrix metalloproteinases-1,-9,-12, glutathione S-transferases, heme oxygenase-1, tumor necrosis factor-alpha, transforming growth factor-beta, interleukins-1,-4,-13, beta2-adrenergic receptor, G-globulin genes and chronic obstructive pulmonary disease. Regions on chromosomes 1, 2, 12, and 17 are indicated as candidate chromosomal regions influencing the decrease in spirometric parameters. Genome-wide scan shows direct evidence for linkage of decreased FEV1/FVC ratio to one or more genes on chromosome 2q influencing the development of airflow obstruction. Genetic markers on chromosome 12p suggest evidence for linkage of FEV1 to this region, and observations on chromosome 1p show the relationship between FVC and genes of this region. All these findings also need to be proven, and linkage analysis among combinations of gene candidates for chronic obstructive pulmonary disease has to be done.

Genetic Linkage↗

Clinically equivalent bronchodilatation achieved with formoterol delivered via Easyhaler and Aerolizer.

BACKGROUND: User-friendly devices for the delivery of asthma drugs are needed to enhance treatment compliance. Formoterol inhalation powder has been developed to Easyhaler multidose powder inhaler to enable the treatment of all asthma severities with the same device. OBJECTIVES: This double-blind, double-dummy, single- dose, placebo-controlled, cross-over study aimed to demonstrate the non-inferiority of the bronchodilating effect of formoterol 12 microg delivered via Easyhaler versus via Aerolizer. In addition, dose responses following placebo, 12-microg and 48-microg doses of formoterol via Easyhaler were compared. Furthermore, onset and duration of action, and safety of formoterol inhaled using the two inhalers were compared. METHODS: Sixty-seven adult asthmatic subjects showing >or=15% increase in forced expiratory volume in 1 s (FEV(1)) after short-acting sympathomimetic inhalation were enrolled and completed the study. The study comprised screening and 4 treatment days, with each subject inhaling a single 12-mug dose of formoterol via Easyhaler, a 12-microg dose via Aerolizer, a 48-microg dose via Easyhaler or placebo. Repeat spirometry and vital sign measurements were performed for 12 h during treatment days. The primary efficacy variable was the area under the flow volume curve (AUC(0-12)) of FEV(1). Secondary efficacy variables comprised maximum FEV(1 )(FEV(1max)), forced vital capacity (FVC), and the need of rescue medication during the treatment days. Safety was evaluated by determining blood pressure, heart rate and the number of adverse events (AEs). RESULTS: Results showed the non-inferiority of the bronchodilating effect of 12 microg formoterol via Easyhaler compared to Aerolizer. The Easyhaler-Aerolizer ratio for AUC(0-12) of FEV(1 )was 0.991 (95% confidence interval from 0.969 to 1.013). No statistically significant differences emerged for secondary efficacy variables. A statistically significant dose response was seen following placebo, 12- and 48-microg doses in FEV(1). No safety differences emerged for the 12-microg dose inhaled via Easyhaler or Aerolizer, but the incidence of AEs was higher following formoterol 48 microg and placebo treatments. CONCLUSIONS: Formoterol delivered via Easyhaler was therapeutically equivalent to Aerolizerat the 12-microg dose. The 48-microg dose via Easyhaler demonstrated statistically significantly greater bronchodilation but showed an increased occurrence of AEs.

Adult↗

Airway allergen exposure stimulates bone marrow eosinophilia partly via IL-9.

BACKGROUND: Interleukin (IL)-9 is a Th2-derived cytokine with pleiotropic biological effects, which recently has been proposed as a candidate gene for asthma and allergy. We aimed to evaluate the therapeutic effect of a neutralizing anti-IL-9 antibody in a mouse model of airway eosinophilic inflammation and compared any such effect with anti-IL-5 treatment. METHODS: OVA-sensitized Balb/c mice were intraperitoneally pretreated with a single dose (100 microg) of an anti-mouse IL-9 monoclonal antibody (clone D9302C12) or its vehicle. A third group was given 50 microg of a monoclonal anti-mouse IL-5 antibody (TRFK-5) or its vehicle. Animals were subsequently exposed to OVA on five days via airways. Newly produced eosinophils were labelled using 5-bromo-2'-deoxyuridine (BrdU). BrdU+ eosinophils and CD34+ cell numbers were examined by immunocytochemistry. After culture and stimulation with OVA or PMA+IC, intracellular staining of IL-9 in bone marrow cells from OVA-exposed animals was measured by Flow Cytometry. The Mann-Whitney U-test was used to determine significant differences between groups. RESULTS: Anti-IL-9 significantly reduced bone marrow eosinophilia, primarily by decrease of newly produced (BrdU+) and mature eosinophils. Anti-IL-9 treatment also reduced blood neutrophil counts, but did not affect BAL neutrophils. Anti-IL-5 was able to reduce eosinophil numbers in all tissue compartments, as well as BrdU+ eosinophils and CD34+ progenitor cells, and in all instances to a greater extent than anti-IL-9. Also, FACS analysis showed that IL-9 is over-expressed in bone marrow CD4+ cells after allergen exposure. CONCLUSIONS: Our data shows that a single dose of a neutralizing IL-9 antibody is not sufficient to reduce allergen-induced influx of newly produced cells from bone marrow to airways. However, in response to allergen, bone marrow cells over-express IL-9. This data suggest that IL-9 may participate in the regulation of granulocytopoiesis in allergic inflammation.

Animals↗

The role of beta(2)-adrenergic receptors in inflammation and allergy.

Essential role of beta(2)-adrenoreceptor (beta(2)AR) in airway relaxation is well established. Nevertheless, beta(2)AR seems playing an actual role in allergy and inflammation. Interaction between beta(2)AR and proinflamatory cytokines in airway smooth muscle has been revealed. Being located on proinflamatory cells, beta(2)ARs may influence function of these cells in vivo. It was clear established, that stimulation of beta(2)AR inhibits release of proinflamatory mediators from mast cells, influences T-cell growth and function, eosinophil survival and function, including GM-CSF- or PAF-induced degranulation. Stimulation of beta(2)ARs, located on alveolar macrophages and epithelial cells, has ambiguity influence on their regulation and function, including phagocytosis and mediator secretion, in vivo. Vascular responses, resulting in inhibition of plasma exudation were confirmed, but modulation of sensory nerves via beta(2)AR is not certain yet. beta(2)AR-agonists are effective in treatment of immediate allergic reactions, but desensitisation of beta(2)ARs on inflammatory cells may result in paradoxical effects, especially in asthma. In summary, it is clear that beta(2)ARs may play an anti-inflammatory role in vitro. Unfortunately, in vitro data have shown limited applicability in vivo; therefore further research in this field is required.

Adrenergic beta-2 Receptor Agonists↗

Genetic polymorphisms in chronic obstructive pulmonary disease.

Etiology of chronic obstructive pulmonary disease remains unknown but, despite some inconsistencies in reports on inflammatory cells, mediators and proteases involved in the pathogenesis of chronic obstructive pulmonary disease, genetic risk factors were proposed as a cause of susceptibility to the disease. Results of many studies suggested polygenic inheritance, with the genetic component consisting of several genes of a small effect each, rather than of single major gene. We are going to review the clinical importance of alpha-1 antitrypsin, glutathione S-transferase, microsomal epoxide hydrolase, matrix metalloproteinase, tumor necrosis factor-a, alpha-1 antichymotrypsin, alpha 2-macroglobulin, cytochrome P4501A1, heme oxygenase-1 genes polymorphisms associated with susceptibility and progression of the chronic obstructive pulmonary disease.

Alleles↗

[Aberrant promoter methylation of tumor suppressor genes in serum from lung cancer patients: frequency and correlation with clinicopathological characteristics].

OBJECTIVE: The aim of this study was to determine aberrant promoter methylation of tumor suppressor genes in genomic serum DNA from lung cancer patients and to evaluate the association between methylation of genes and clinicopathological characteristics. MATERIALS AND METHODS: Genomic serum DNA from 46 lung cancer patients and 14 healthy control persons was examined. Nested methylation-specific PCR approach was used for detection of methylated genes in serum. RESULTS: Aberrant promoter methylation in serum from lung cancer patients was detected in 2.3% (1/43) for O6-methylguanine-DNA-methyltransferase, in 11.1% (5/45) for p16INK4a, in 41.3% (19/46) for retinoic acid receptor beta, in 4.5% (2/44) for RAS association domain family 1A, in 40.9% (18/44) for fragile histidine triad, in 34.9% (15/45) for p14(ARF), in 6.5% (3/46) for adenomatous polyposis coli 1A, in 78.1% (25/32) for Ecad, in 5.7% (2/35) for adenomatous polyposis coli 1B, in 0% (0/36) for death associated protein kinase. None of the death associated protein kinase, O6-methylguanine-DNA-methyltransferase, p16INK4a, fragile histidine triad or adenomatous polyposis coli 1A promoter regions were positive for methylation in serum DNA from healthy persons. A total of 78.3% of the samples from lung cancer patients had methylation in at least one of the genes tested. The methylation status of fragile histidine triad was associated with that of p14ARF(p=0.021), as was retinoic acid receptor beta--with that of adenomatous polyposis coli 1A (p=0.04). Methylation of adenomatous polyposis coli 1A was detected more frequently in tumor with pleura involvement (p=0.079), retinoic acid receptor beta was observed more frequently in undifferentiated tumor than in better-differentiated tumor (p=0.029). The methylation status of RAS association domain family 1A and fragile histidine triad showed a tendency to be associated with an advanced tumor size. In addition, tumors with an advanced pathological stage showed epigenetic alteration of the RAS association domain family 1A promoter with a higher frequency. The methylation index was also associated with an advanced tumor size (p=0.033). CONCLUSION: Approximately 80% of the samples from lung cancer patients had methylation of the tumor suppressor gene and it might be associated with more aggressive tumor. Detection of epigenetic alterations in serum may provide basis for the early and noninvasive lung cancer diagnosis and customized therapy.

Adolescent↗

[Diagnosis and management of chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease (COPD) is an increasing health problem and one of the leading causes of morbidity and mortality worldwide. Cigarette smoking remains the main risk factor. COPD is preventable, readily diagnosable and treatable disease. The appropriate and early use of spirometry for diagnosis is of importance. A comprehensive treatment plan for managing patients with COPD involves the use of pharmacological as well as nonpharmacologic interventions. Smoking cessation can substantially reduce the risk for the development or rate of progression of COPD. Bronchodilator therapy is a basis in symptomatic treatment. Inhaled steroids might reduce frequency and severity of exacerbation and can be effectively combined with long acting beta2 agonists. Pulmonary rehabilitation benefits most patients. Patients with hypoxemia suffering from more severe disease may require a long-term oxygen therapy. Surgical intervention may help a limited number of patients.

Adrenergic beta-Agonists↗

[Autoimmunity in pathogenesis of chronic obstructive pulmonary disease].

For years, smoking induced inflammatory reaction, comprised mainly of neutrophils and macrophages, has been accepted to be the major component in pathogenesis of chronic obstructive pulmonary disease. New developments in molecular and cell biology have provided scientists with new knowledge and understanding of inflammatory processes in lung. Recent reports have underlined the role of autoimmunity and T lymphocytes as a potential important factor, which takes place in the pathogenesis of chronic obstructive pulmonary disease. This article reviews potential mechanism of T cell mediated immune response in chronic obstructive pulmonary disease.

Antibody Formation↗

[Peculiarities of induced sputum inflammatory cell counts in allergic versus non-allergic asthma].

OBJECTIVE: According to the Global Initiative for Asthma (GINA, updated 2004), although non-allergic asthma has a different clinical profile than allergic asthma, it is not a distinct immunopathological entity. We aimed to investigate the peculiarities of inflammatory cell counts in induced sputum from patients with allergic and non-allergic asthma. METHODS: We investigated 41 steroid naive patients (mean age 51.8+/-1.5 years) with mild persistent asthma. Depending on the results of allergic anamnesis and skin prick test, patients were divided into the two groups: 21-with allergic asthma, 20-with non-allergic asthma. Spirometry, bronchial provocation test with methacholine (PD20) and sputum induction with hypertonic saline were performed. Cytospins of induced sputum were stained with May-Grunwald-Giemsa for differential cell counts. RESULTS. In samples from non-allergic asthmatics we detected a significantly higher number of total cells (1.97+/-0.33 vs 1.23+/-0.11x10(6)/ml, p<0.01), neutrophils (1.34+/-0.18 vs 0.41+/-0.06x10(6)/ml, p<0.01) and lymphocytes (0.36+/-0.04 vs 0.15+/-0.03x10(6)/ml, p<0.01), than in samples from allergic asthmatics. Number of eosinophils and macrophages did not significantly differ between two groups. In non-allergic asthmatics, number of lymphocytes correlated with PD20 (Rs=0.41, p<0.05); in allergic asthmatics, number of eosinophils in induced sputum correlated with PD20 (Rs=0.71, p<0.05). CONCLUSIONS: Our data suggest that lymphocytes might play a more important role in pathogenesis of non-allergic asthma, while eosinophils -- in allergic asthma.

Adult↗

[Lymphocyte subsets in patients with recurrent upper airway infections].

UNLABELLED: The aim of our study was to evaluate the digressions of lymphocyte subsets in patients with recurrent upper airway infectious diseases. METHODS: We studied 35 patients (mean of age 11.1+/-2.1 years) with recurrent upper airway infections. The first group consisted of patients, who had acute upper airway infections: rhinitis, pharyngitis, laryngitis and tracheitis more than 6 times per last year, sinusitis or otitis more than 4 times per last year. The control group comprised of 9 healthy subjects. Subsets of lymphocytes (CD3+, CD4+, CD8+, CD4+/CD8+, CD16+/56+ and CD19+) were detected by FACS Calibur cytometer. RESULTS: We found a significantly lower count of CD4+ lymphocytes in the patients' group compared to the control group (37.5+/-1.2 vs 45.7+/-3.1% of total lymphocytes, p<0.01). We did not find any significant differences of other lymphocyte subsets between patients and control groups. CONCLUSION: We propose that patients with recurrent upper airway infections have alterations of the cellular immunity -- decreased amount of CD4+ lymphocytes.

Acute Disease↗

[Influence of sensitization to pollen and food allergens on pollinosis clinical symptoms].

UNLABELLED: Geographic position and local plants of the country influence the profile of sensitization of the population to airborne allergens. The aim of this study was to evaluate the sensitization pattern to pollen and food allergens in adult patients with pollinosis in Lithuania. 101 patients (age 16-63 years) suffering from seasonal allergic rhinitis and 23.8% of them also diagnosed with concomitant seasonal asthma were investigated. Oral allergy syndrome (OAS) was diagnosed in 29.7% of cases. The sensitization to 21 species of tree-, grass- and weed-pollen and plant food allergens was determined by positive skin prick and prick-prick test. In serum levels of total IgE and timothy and orchard grass specific IgE were determined by immunoenzyme assay. 52.5% of patients suffered from spring-summer pollinosis. 91.2% of patients were sensitized to grass-pollen allergens, 79.3% -to tree pollen-allergens. 74.7% of patients were allergic to weeds. Pollinosis starting in the spring and lasting more than sixteen weeks was associated with increased probability of OAS (OR=7.1, p<0.001 and OR=3.1, p=0.01). Sensitization to hazelnut (OR=8.6, p=0.009), birch (OR=9.6, p=0.07), lamb's quarters (OR=5.2, p=0.04) allergens and twofold and more increase in serum IgE (OR=4.8, p=0.03) were considered the significant risk factors for pollinosis with OAS. More than two times elevated serum IgE increased the probability of seasonal asthma (OR=3.4, p=0.03). Sensitization to ragweed was associated with decreased risk for asthma (OR=0.26, p=0.03). CONCLUSIONS: Our data indicate that more than a half of patients (52.5%) had pollinosis symptoms during spring and summer seasons because of multiple sensitivity to pollen allergens. Sensitization to hazelnut, birch, lamb's quarters allergens, more than two times elevated serum IgE are significant risk factors for pollinosis with OAS. More than two times elevated serum IgE increased the probability of seasonal asthma, but sensitization to ragweed was associated with decreased risk for pollinosis with asthma.

Adolescent↗

[Peculiarities of nocturnal oxygen saturation in obstructive sleep apnea].

UNLABELLED: The aim of the study was to determine which factors are important for desaturation depth during sleep in obstructive sleep apnea (OSA) and to establish impact of nocturnal oxygen desaturation on the daytime sleepiness. 190 consecutive patients were included in the study (135 men and 55 women, mean age 52.59+/-11.31 and 58.93+/-8.85 years, respectively). Desaturation level depended on body-mass index and correlation with Epworth sleepiness scale (ESS) was statistically significant but not high (p<0.5). In the univariate analysis assessing factors important for severe daytime sleepiness (ESS more than 10), age and obesity were not statistically significant. A probability of severe sleepiness increased in male patients (odds ratio 3.52), and when microarousal index was more than 30 (odds ratio 6.12), apnea-hypopnea index more than 35 (odds ratio 4.25), mean desaturation less than 90% (odds ratio 4.09), maximum desaturation less 80% (odds ratio 3.06), general desaturation index more than 36 per hour (odds ratio 2.86), desaturation index during non-REM sleep more than 38 per hour (odds ratio 3.2). In the multivariate analysis only arousal index more than 30 per hour increased a probability of severe sleepiness in patients with OSA (odds ratio 4.97). CONCLUSIONS: Hypoxemia depth at night is an important factor for daytime sleepiness having obstructive sleep apnea, but the most important is microarousal index. Hypoxemia depth depends on initial saturation and patients' body-mass index.

Adult↗

[Consensus on asthma diagnosis and treatment in children and adults].

Asthma is a chronic airway disease that is a growing problem of public health. The current consensus is based on the Global Initiative for Asthma (GINA) and other guidelines for asthma, and adapted for Lithuania. This Consensus provides physicians with recommendations for asthma management in children and adults.

Adolescent↗

[Clinical and prognostic significance of tumor markers cytokeratin 19 fragment, carcinoembryonic antigen, and neuron-specific enolase in lung cancer].

OBJECTIVE: To evaluate the clinical and prognostic significance of the tumor markers cytokeratin 19 fragment, carcinoembryonic antigen and neuron-specific enolase in lung cancer patients. MATERIALS AND METHODS: Serum levels of cytokeratin 19 fragment, carcinoembryonic antigen and neuron-specific enolase were measured using electrochemical luminescence immunoassay in 46 lung cancer patients. Serum levels of cytokeratin 19 fragment, carcinoembryonic antigen, and neuron-specific enolase higher than 3.6 ng/ml, 5.0 ng/ml and 13.0 ng/ml, respectively, were considered as elevated. RESULTS: Cytokeratin 19 fragment, carcinoembryonic antigen, and neuron-specific enolase were elevated in 19.6%, 43.5%, and 63% of patients, respectively. Elevated levels of neuron-specific enolase were detected more frequently in smokers than in ex-smokers (p=0.003). Likewise preoperative levels of carcinoembryonic antigen (p=0.023) and neuron-specific enolase (p=0.007) were statistically higher in smokers than in ex-smokers. A significant correlation was detected between the level of cytokeratin 19 fragments and smoking cumulative exposure (r=0.542, p=0.037). The number of patients with elevated levels of cytokeratin 19 fragment and neuron-specific enolase was higher in more advanced disease than in early lung cancer (p=0.036 and p=0.036, respectively). Preoperative levels of cytokeratin 19 fragment (p=0.017 and p=0.016, respectively) and neuron-specific enolase (p=0.03 and p=0.006, respectively) were significantly associated with more advanced disease and tumor size, as well as tumor histology in non-small cell lung cancer (p=0.03 and p=0.016, respectively). Preoperative levels of cytokeratin 19 fragments were higher in squamous cell carcinoma than in adenocarcinoma (p=0.026). Elevated preoperative serum levels of cytokeratin 19 fragment predict a poor prognosis for lung cancer patients (p=0.007). CONCLUSION: Alteration of serum tumor markers cytokeratin 19 fragment, carcinoembryonic antigen and neuron-specific enolase is associated with particular tumor histology, smoking habit, more advanced disease and poor prognosis.

Adenocarcinoma↗

Perception of dyspnea in asthmatics with normal lung function.

UNLABELLED: The perception of dyspnea varies widely among asthmatics and it is influenced by many factors. The aims of our study were to investigate the perception of dyspnea during methacholine-induced bronchoconstriction in asthmatics with normal lung function and to evaluate the influence of bronchial responsiveness, age and gender to dyspnea perception in these patients. A total of 192 outpatients (aged 16-77 years) with stable asthma and normal lung function were examined. Methacholine challenge test was performed to each patient. The provocative dose of methacholine that reduces forced expiratory volume in 1 sec. (FEV1) by 20% (PD20) was estimated. Dyspnea perception of bronchoconstriction was evaluated using a Borg Scale and calculating the perception score corresponding to a fall in FEV1 of 20% (PS20). According to PS20+/-1 standard deviation subjects were divided into three groups: hypoperceivers, normoperceivers and hyperperceivers. From the hypoperceivers group we set up asthmatics with PS20=0 and defined them as nonperceivers. We found out that 43 (22.4%) patients were hypoperceivers, 116 (60.4%)--normoperceivers and 33 (17.2%)--hyperperceivers. The nonperceivers presented 6.3% (n=12) of all subjects. PD20 positively correlated with PS20 (r=0.252, p<0.001). Hypoperceivers showed significantly higher bronchial hyperesponsiveness (PD20=174+/-28 microg) comparing with hyperperceivers (PD20=323+/-50 microg, p=0.013). Bronchial responsiveness to methacholine of nonperceivers (PD20= 106+/-31 microg, range 15-253 microg) was the highest and PD20 was significantly lower comparing with normoperceivers (p=0.005) and hyperperceivers (p=0.001). Age and gender had no significant effect on the perception of bronchoconstriction. CONCLUSION: The part of asthmatics with normal lung function has impaired perception of dyspnea. Dyspnea perception depends on bronchial responsiveness, but not on age and gender of these patients.

Adolescent↗