Nonatopic Asthmatic Patients Research Articles

OX40 ligand: a potential costimulatory molecule in atopic asthma

Objective: We aimed to assess the percentage of peripheral blood B-lymphocytes expressing OX40 ligand (OX40L) in adult atopic and non-atopic asthmatic patients, and in healthy controls. Methods: This case–control study included 15 atopic asthmatic patients, 15 non-atopic asthmatic patients, and 15 healthy controls. Atopic status was determined by skin prick test reaction to the most common locally-encountered allergens. For all subjects, pulmonary function tests and measurement of total serum immunoglobulin E (IgE) levels by ELISA were performed. In addition, the percentage of B-lymphocytes expressing OX40L was assessed by flow cytometry in all three groups. Results: OX40L expression was significantly higher in atopic asthmatics than in non-atopic asthmatics and controls, but did not differ significantly between non-atopic asthmatics or controls. Among atopic asthmatics, OX40L expression correlated positively with total serum IgE levels, but not with age, disease duration, or values of forced expiratory volume in the first second. Conclusion: The over-expression of OX40L in atopic asthmatic patients appears to be linked to markers of the atopic status as total serum IgE, and signifies the vital role of OX40L in the atopic mechanism. Further large-scale studies are needed to investigate the role of OX40L in other atopic diseases and its relation to disease activity and severity.

Can anti IgE treatment be used in non-atopic asthma patients; thoughts of a case about the role of IgE in asthma

Can anti IgE treatment be used in non-atopic asthma patients; thoughts of a case about the role of IgE in asthma

The interleukin-4 − 589C/T polymorphism and the risk of asthma: A meta-analysis including 7345 cases and 7819 controls

BackgroundA number of studies assessed the association of −589C/T polymorphism in the promoter region of interleukin-4 (IL-4) with asthma in different populations. However, the results were contradictory. A meta-analysis was conducted to investigate the association between polymorphism in the IL-4 and asthma susceptibility. MethodsDatabases including Pubmed, EMBASE, Wanfang Database, China National Knowledge Infrastructure (CNKI) and Weipu Database were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. ResultsThirty-four studies involving 7345 cases and 7819 controls were included. Overall, significant association between −589C/T polymorphism and asthma was observed for TT+CT vs. CC (OR=1.26; 95% CI 1.12–1.42; P=0.0001; I2=26%). In the subgroup analysis by ethnicity, significant associations were found among Asians (OR=1.36; 95% CI 1.07–1.73; P=0.01; I2=0%) and Caucasians (OR=1.30; 95% CI 1.09–1.54; P=0.004; I2=53%) but not among African Americans (OR=1.20; 95% CI 0.72–2.00; P=0.48; I2=48%). In the subgroup analysis by atopic status, no significant association was found among atopic asthma patients (OR=1.20; 95% CI 0.92–1.34; P=0.27; I2=6%) and non-atopic asthma patients (OR=0.97; 95% CI 0.73–1.28; P=0.81; I2=0%). ConclusionsThis meta-analysis suggested that the IL-4 −589C/T polymorphism was a risk factor of asthma.

Leptin, Adiponectin, and Ghrelin Levels in Female Patients with Asthma during Stable and Exacerbation Periods

Objective. The mechanisms underlying the relationship between obesity and asthma have not been fully established. Data in the literature suggest that adipose tissue-derived hormones may be implicated. However, no definite conclusions regarding the role of leptin and adiponectin with asthma are available. No studies have examined the role of ghrelin in asthma. Methods. We assessed the circulating concentrations of leptin, adiponectin, and ghrelin in 32 postmenopausal stable asthma patients, 37 female asthmatics during exacerbations and 8 weeks later, and 22 controls. We examined the relationship between the three peptides and indexes of pulmonary function, airway inflammation, and atopy. Results. Stable asthma patients exhibited higher leptin and lower ghrelin concentrations compared with controls. Patients with severe asthma had higher leptin and lower adiponectin levels versus patients with mild to moderate asthma. Both leptin concentrations and leptin/adiponectin ratio served as markers for discriminating asthma patients from controls on the one hand, and severe from mild to moderate asthmatics on the other. Leptin levels were inversely correlated with both FEV1/FVC and FEF25–75 in patients with mild to moderate asthma. Atopic asthma patients had higher leptin concentrations than nonatopic asthma patients. There was a positive correlation between serum leptin and total IgE levels in atopic asthmatics. Finally, serum leptin levels and leptin/adiponectin ratio were significantly increased during asthma exacerbations, while adiponectin and ghrelin levels were significantly decreased. Conclusion. Our findings suggest that leptin, adiponectin, and ghrelin may play a significant role in the pathogenesis of asthma during both stable state and asthma exacerbation, independent of obesity.

Utility of fractional exhaled nitric oxide (FENO) measurements in diagnosing asthma

To facilitate the use of fractional exhaled nitric oxide (F(E)NO) as a clinical test, F(E)NO measurements need more clarification. We sought to evaluate the yield of F(E)NO measurement for the diagnosis of asthma and identify the determinants of F(E)NO in children. Two hundred forty five consecutive steroid-naïve patients aged 8-16 years with symptoms suggestive of asthma were included. Children were evaluated using F(E)NO measurements, questionnaires, skin prick tests, spirometries, and methacholine challenge tests. Asthma was diagnosed in 167 children. The sensitivity, specificity, and positive (PPV) and negative predictive values (NPV) of F(E)NO measurements for the diagnosis of asthma at the best cutoff value of 22 ppb were 56.9%, 87.2%, 90.5%, and 48.6%, respectively. At a cutoff value of 42 ppb, specificity and PPV were all 100% but at the cost of very low sensitivity (23.4%) and NPV (37.9%). Both atopy and asthma were identified as independent risk factors associated with high F(E)NO. The association of asthma with high F(E)NO was found only in atopic children because F(E)NO was low in non-atopic children regardless of asthma status. Although highest F(E)NO was observed in atopic asthmatic patients, 28% of these patients had F(E)NO values lower than 22 ppb. Atopic asthmatic patients with low F(E)NO values and non-atopic asthmatic patients were responsible for false-negative cases that might contribute to low sensitivity of F(E)NO measurements in diagnosing asthma. High specificity of F(E)NO measurements may help identify patients with atopic asthma among subjects with respiratory symptoms.

Methacholine challenge test: Diagnostic characteristics in asthmatic patients receiving controller medications

The methacholine challenge test (MCT) is commonly used to assess airway hyperresponsiveness, but the diagnostic characteristics have not been well studied in asthmatic patients receiving controller medications after the use of high-potency inhaled corticosteroids became common. We investigated the ability of the MCT to differentiate participants with a physician's diagnosis of asthma from nonasthmatic participants. We conducted a cohort-control study in asthmatic participants (n= 126) who were receiving regular controller medications and nonasthmatic control participants (n= 93) to evaluate the sensitivity and specificity of the MCT. The overall sensitivity was 77% and the specificity was 96% with a threshold PC(20) (the provocative concentration of methacholine that results in a 20% drop in FEV(1)) of 8 mg/mL. The sensitivity was significantly lower in white than in African American participants (69% vs 95%, P= .015) and higher in atopic compared with nonatopic (82% vs 52%, P= .005). Increasing the PC(20) threshold from 8 to 16 mg/mL did not noticeably improve the performance characteristics of the test. African American race, presence of atopy, and lower percent predicted FEV(1) were associated with a positive test result. The utility of the MCT to rule out a diagnosis of asthma depends on racial and atopic characteristics. Clinicians should take into account the reduced sensitivity of the MCT in white and nonatopic asthmatic patients when using this test for the diagnosis of asthma.

The Editors’ Choice

The Editors’ Choice

SICAM-1 and TNF-α in Asthma and Rhinitis: Relationship with the Presence of Atopy

Background. A genetically determined overproduction of specific immunoglobulin E (IgE) underlies many diseases like asthma or allergic rhinitis. IgE as well as tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule-1 (ICAM-1) play a critical role in the induction and maintenance of inflammation. While the correlation between IgE and atopy is inseparable, little is known about the correlation of atopy with markers of inflammation. Objective. We investigated the relationship between the serum concentrations of TNF-α, soluble ICAM-1 (sICAM-1), and the presence of atopy in patients with persistent rhinitis or asthma. Methods. Serum concentrations of sICAM-1, TNF-α, and total IgE were investigated in 64 adults with persistent allergic rhinitis, 17 subjects with nonatopic rhinitis, 90 patients with asthma, and 21 healthy individuals. Atopy was diagnosed on the basis of positive family history, skin prick tests, and serum IgE concentration. Results. Total IgE concentration was significantly higher in patients with atopic rhinitis or asthma when compared with nonatopic patients and healthy individuals and was the highest in patients suffering from severe atopic asthma who were not treated with systemic glucocorticosteroids. Although there were marked alterations in IgE in atopic and nonatopic patients, there were no significant differences between atopic and corresponding groups of nonatopic rhinitic and asthmatic patients in sICAM-1 and TNF-α concentrations. (sICAM-1 in rhinitis: atopic vs. nonatopic patients: 224.02 and 221.08 ng/ml, respectively, p > .05; in mild/moderate asthma: atopic vs. nonatopic: 306.22 and 326.39 ng/ml, respectively, p > .05; severe asthma without oral corticosteroids therapy: atopic vs. nonatopic: 418.03 and 468.09 ng/ml, respectively, p > .05; and severe asthma with oral corticosteroids therapy: atopic vs. nonatopic: 320.66 and 308.09 ng/ml, respectively, p > .05). Conclusions. Concentrations of sICAM-1 and TNF-α are significantly higher in patients with asthma compared with those observed in patients with rhinitis, but they are independent of the presence of atopy.

Chlamydophila pneumoniae, Mycoplasma pneumoniae infections, and asthma control

The influence of respiratory infections on asthma has not been fully understood. Acute viral and bacterial infections often lead to exacerbations. Less is known about the role of chronic infections, particularly with atypical pathogens. The aim of this study was to evaluate the impact of Chlamydophila pneumoniae and Mycoplasma pneumoniae infections on the control and severity of asthma. Spirometry, skin-prick tests as well as measurement of immunoglobulin G (IgG), IgM, and IgA against C. pneumoniae and M. pneumoniae (ELISA) were performed in 95 patients with persistent asthma and 58 healthy controls. Additionally, in the selected group of asthmatic patients, presence of C. pneumoniae and M. pneumoniae genetic material was tested in induced sputum (polymerase chain reaction [PCR]). IgA against C. pneumoniae was found in 42 (44.2%) asthmatic patients and 17 (29.3%) controls (p < 0.05). It was found more often in the group with uncontrolled asthma (p = 0.001) as well as in nonatopic asthmatic patients (p < 0.05). IgG was detected in 58 asthmatic patients (61%) and 21 (36.2%) controls, more often in cases of uncontrolled (p < 0.05) and nonatopic asthma patients (p < 0.05). Such correlations were not found in relation to M. pneumoniae infections. C. pneumoniae was detected by means of PCR in respiratory secretions of eight asthmatic patients (40%), and M. pneumoniae was detected in two asthmatic patients (10%). In conclusion, C. pneumoniae infections are more frequent in asthmatic patients compared with healthy individuals and in nonatopic asthmatic patients compared to atopic patients. Chronic infection is associated with poor control of asthma.

High Serum Arginase I Levels in Asthma: its Correlation with High-Sensitivity C-Reactive Protein

Background. Much attention has been directed to the induction of arginase I in the lung of asthmatic mice. However, there is no agreement on the changes of serum arginase activity in asthmatic patients among previous studies. Objectives. The aim of this study was to evaluate the clinical relevance of serum arginase I in asthmatic patients. Methods. Serum arginase I was examined cross-sectionally in non-smoking asthmatic patients (n = 23) and healthy individuals (n = 30) using enzyme-linked immunosorbent assay (ELISA) and its correlations with several clinical parameters were investigated. Results. Serum levels of arginase I were significantly increased in asthmatic patients (mean ± SD 67.4 ± 41.0 ng/mL) compared with healthy controls (27.2 ± 12.9 ng/mL). In healthy controls, a difference in arginase I levels was not observed between sex groups but was observed between age groups. In asthmatic patients, serum arginase I levels were not different between groups of age, sex, and inhalation steroid therapy but were different between groups of atopic status. Non-atopic asthmatic patients revealed significantly high serum arginase I levels compared with atopic asthmatic patients and healthy controls although no difference was observed between atopic asthmatic patients and healthy controls. Spearman's correlation analysis showed that serum arginase I level had a significant negative correlation with age and a positive correlation with red blood cell numbers in healthy controls, whereas in asthmatic patients, it had significant positive correlations with alanine aminotransferase (ALT), high-sensitivity C-reactive protein (hs-CRP) and a negative correlation with immunoglobulin-E (IgE). Conclusions. High serum arginase I levels in asthmatic patients may be associated with airway inflammation in non-atopic asthma.

CD27 expression on lymphocyte and sCD27 levels in children with asthma

Background CD27, a lymphocyte specific member of the Tumour Necrosis Factor- Receptor (TNF-R) family is expressed on the majority of peripheral blood T cells. Activation of T cells via TCR/CD3 induces high CD27 surface expression and release of a soluble form (sCD27) of the molecule. sCD27 level increases in patients suffering from a variety of chronic inflammatory diseases. In the present study we aimed to measure both the serum sCD27 levels and CD27 expression on T cells in asthmatic patients, to evaluate the state of this molecule in allergic inflammation. Methods Forty-three patients with asthma were included in to the study. CD27 molecule expression and soluble form of this molecule were analysed in atopic asthmatic ( n:17) and non-atopic asthmatic ( n:13) patients receiving inhaled corticosteroid treatment, in asthmatic patients whose treatment ceased at least for 6 months ( n:13) and healthy control subjects ( n:14). Results There were no differences in the expression of CD27 molecule on peripheral blood lymphocyte nor in its soluble form sCD27 levels in sera between the atopic asthmatic and non-atopic asthmatic patients receiving ICS treatment, treatment free asthmatic patients and healthy control subjects. Conclusions Neither the soluble form of CD27 nor its expression on T cells seem to be a reliable marker of atopic or non-atopic asthmatic inflammation.

Increases in airway eosinophilia and a th1 cytokine during the chronic asymptomatic phase of asthma

Studies using allergen challenge models have suggested Th2 cytokines promote airway inflammation in asthma. We assessed mediators of airway inflammation during the chronic asymptomatic phase of asthma. Nine non-atopic asthma (NAA) patients, 19 atopic asthma (AA) patients, 20 atopic controls (AC), and 38 normal controls (NC) underwent sputum induction while asymptomatic. Sputum total cell counts and differentials were determined; levels of cytokines IL-4, IL-5, IL-13, GM-CSF, and IFN-gamma, and chemokines eotaxin (CCL11) and RANTES (CCL5) were measured by ELISA; and levels of eosinophil-derived neurotoxin (EDN) were measured by radioimmunoassay. NAA patients showed higher % eosinophils and total eosinophils compared to AA. NAA and AA patients showed higher IFN-gamma and EDN levels compared to AC and NC, with no differences in IL-4, IL-5, or IL-13 levels among the four groups. GM-CSF levels were higher in AA patients compared to AC or NC. In NAA, AA, and AC patients, % eosinophils and EDN levels correlated positively with IFN-gamma, GM-CSF, eotaxin, and RANTES, but not with IL-5 levels. Baseline airway inflammation of intrinsic and extrinsic asthma is characterized by eosinophilic inflammation and the Th1 cytokine, IFN-gamma. GM-CSF, instead of IL-5, and chemokines may coordinate airway eosinophilia during the chronic asymptomatic phase of asthma.

Identifying the polymorphisms in the thymic stromal lymphopoietin receptor (TSLPR) and their association with asthma

The present study aimed to investigate whether the polymorphisms in the TSLPR gene are associated with atopic and asthmatic disease in the Korean population. We identified eleven single nucleotide polymorphisms (SNPs) and two variation sites in the TSLPR gene, including the promoter region. The genotype and allele frequencies of g.33G>C of the TSLPR gene in asthma patients were significantly different from the respective frequencies of the control group (P =0.006 and 0.003, respectively). Our additional analysis showed that the genotype and allele frequencies of the g.33G>C and g.19646A>G of the TSLPR gene were significantly associated in the atopic asthma patients rather than in the non-atopic asthma patients (genotype frequencies; P =0.0001 and 0.0003 respectively, allele frequencies; P =0.0005 and 0.0001 in that order). Our results suggest that the SNPs of the TSLPR gene could be associated with the susceptibility to atopic asthma in the Korean population.

Relationships between Severity of Chronic Rhinosinusitis and Nasal Polyposis, Asthma, and Atopy

The effect of comorbid conditions such as asthma and atopy on the severity of chronic rhinosinusitis (CRS) and the presence of nasal polyps (NPs) remains an area of investigation. We sought to elucidate the relationship among these entities. The study population included 106 consecutive patients who were referred to a multidisciplinary, university-based allergy and sinus clinic that underwent computed tomography (CT) scan, skin-prick testing, and had CRS. Data were analyzed to determine Lund-MacKay score (LMS), presence of NPs, asthma status, and sensitivity to seven classes of aeroallergens. Skin tests were positive in 52 cases and negative in 54 cases. Although, there was no statistical relationship between LMS and atopic status in the entire group, among the asthmatic subgroup, mean LMS was greater in nonatopic asthmatic patients than in atopic asthmatic patients. Asthmatic patients had a higher LMS than nonasthmatic patients (p < 0.0001). Asthmatic patients were more likely than nonasthmatic patients to have NPs (57.6% versus 25%; p = 0.0015), regardless of atopic status. Mean LMS was higher in NP patients compared with nonpolyp patients (p < 0.0001), independent of atopic status. Mean LMS was not affected by sensitivity to any particular allergen, with the exception of cockroach-allergic patients who were more likely to have an LMS of >10 (p = 0.0236) and had more severe maxillary sinus involvement (p = 0.0391). These data indicate a strong relationship between CRS severity, as measured by LMS, and chronic airway inflammatory diseases, asthma, and NPs. The association between LMS and atopic status appears weak. The present study suggests that CRS is an inflammatory disease that occurs independently of systemic IgE-mediated pathways.

Assessment of Spleen Tyrosine Kinase Expression in Basophils using Flow Cytometry

RATIONALE: In basophils, spleen tyrosine kinase (syk) expression correlates with maximal histamine release. This suggests that syk may play a role in determining the severity of atopic disease. Our goal was to develop a high throughput method of assessing basophil syk expression, sensitive enough to differentiate between syk levels in basophils from healthy and asthmatic donors.METHODS: Basophils from peripheral blood mononuclear cell (PBMC) samples were stained for intracellular syk using flourescein isothiocyanate (FITC) conjugated syk antibodies. The stained cells were then analyzed using flow cytometry. Basophils were identified as a lineage negative, CD123 positive staining population. PBMC were obtained from healthy non-atopic volunteers, asthmatic patients, and patients with Eosinophilic Gastroenteritis (EG).RESULTS: Basophils stained for syk had between 1.7 and 2.1 times greater fluorescence than isotype control samples. Staining of basophils from healthy controls, asthmatics, and EG patients did not reveal significant variations in syk expression between these groups. Syk staining of dendritic cells and B-cells was brighter than that of basophils.CONCLUSIONS: Using flow cytometry, we found no significant difference in basophil syk expression between healthy controls, asthmatics, and EG patients. However, Basophil syk fluorescence was only marginally above the noise level established by the isotype control. This suggests that flow cytometry may not be a sensitive enough method to accurately determine syk expression in basophils. RATIONALE: In basophils, spleen tyrosine kinase (syk) expression correlates with maximal histamine release. This suggests that syk may play a role in determining the severity of atopic disease. Our goal was to develop a high throughput method of assessing basophil syk expression, sensitive enough to differentiate between syk levels in basophils from healthy and asthmatic donors. METHODS: Basophils from peripheral blood mononuclear cell (PBMC) samples were stained for intracellular syk using flourescein isothiocyanate (FITC) conjugated syk antibodies. The stained cells were then analyzed using flow cytometry. Basophils were identified as a lineage negative, CD123 positive staining population. PBMC were obtained from healthy non-atopic volunteers, asthmatic patients, and patients with Eosinophilic Gastroenteritis (EG). RESULTS: Basophils stained for syk had between 1.7 and 2.1 times greater fluorescence than isotype control samples. Staining of basophils from healthy controls, asthmatics, and EG patients did not reveal significant variations in syk expression between these groups. Syk staining of dendritic cells and B-cells was brighter than that of basophils. CONCLUSIONS: Using flow cytometry, we found no significant difference in basophil syk expression between healthy controls, asthmatics, and EG patients. However, Basophil syk fluorescence was only marginally above the noise level established by the isotype control. This suggests that flow cytometry may not be a sensitive enough method to accurately determine syk expression in basophils.

CCL5/RANTES chemokine gene promoter polymorphisms are not associated with atopic and nonatopic asthma in a Spanish population

CCL5/RANTES, a member of the C-C chemokine family, is a potent eosinophil, monocyte, basophile and lymphocyte chemo-attractant at the site of inflammation. Recent studies revealed that a functional mutation at the -403 position in the promoter may have significance for atopic dermatitis, bronchial asthma, sarcoidosis, rheumatoid arthritis and HIV infection, and others. Another polymorphism in the -28 position has been reported. Our objective was to investigate the possible influence of the CCL5/RANTES promoter polymorphisms in the different types of bronchial asthma. CCL5/RANTES genotyping was performed by polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) in 306 asthmatic patients with non-atopic (n = 145) and atopic (n = 161) asthma and 242 controls. The 81.9% of the atopic asthma patients for -403G/A had the G allele and the A allele frequency was 18%. Of the non-atopic asthma patients, the G allele frequency was 79.7% and the A allele was 20.3%. Concerning the -28C/G polymorphism, the frequency of the CCL5/RANTES -28G allele in our patients is 2.8%, which is similar to Spanish adult population. After comparing patients with asthma, atopic patients, non-atopic patients and control population, we found no significant deviation in the distribution of the alleles or genotypes of CCL5/RANTES promoter polymorphisms in any tested comparison. Therefore, human CCL5/RANTES gene promoter polymorphisms are not associated with the different types of bronchial asthma in Spanish population.

Clinical aspects of the link between chronic sinonasal diseases and asthma

Chronic sinonasal diseases (CSDs) are common comorbidity of asthma. The aim of this study was to assess comprehensively CSD in a population of asthma patients and determine whether the clinical factors in both diseases were related to each other. Eighty adult stable asthmatic patients with sinonasal symptoms (SNSs) of 3 months and who were nonresponsive to aggressive medical treatment were prospectively investigated. All patients underwent a detailed ear, nose, and throat examination and were evaluated by paranasal sinus computed tomography (PNS-CT). The severity of asthma was compared with SNS scores (SNSSs) and sinonasal involvement on PNS-CT. Asthma was severe in 12.5%, moderate in 55%, and mild in 32.5% of cases. There were 15 (18.7%) patients in stage 0, 16 (20%) patients in stage 1, 21 (26.2%) patients in stage 2, and 28 (35%) patients in stage 3 according to PNS-CT scoring. There was no correlation between asthma severity and CT stages, total opacification scores (TOSs), anatomic variations, and SNSSs. Although SNSSs were similar in patients with nasal polyps (NPs) and without NPs, patients with NPs showed significantly higher TOSs and CT stages (p < 0.05). The presence of NPs and age and duration of disease were related to severity of asthma (p < 0.05). Nonatopic asthmatic patients had both more severe asthma (p = 0.05) and more extensive CT findings (p = 0.01). The use of clinical symptoms alone is not very reliable in predicting the presence or severity of CSD. Therefore, SNSs should be supported with objective criteria such as nasal endoscopy and PNS-CT scan. Furthermore, sinonasal involvement may exist independently from severity of asthma.

Nitric oxide in children with persistent asthma

To assess the difference in exhaled nitric oxide levels in atopic and nonatopic asthmatic patients treated with anti-inflammatory drugs, and to compare exhaled nitric oxide measurement with lung function tests. Cross-sectional study with 45 consecutively selected patients with moderate and severe persistent asthma, aged between 6 and 17 years, and treated with anti-inflammatory drugs for at least 1 year. The patients were split into two groups: atopic ones (with positive skin tests) and nonatopic ones. The clinical and functional assessments and the measurement of exhaled nitric oxide were carried out concomitantly. There was a male predominance (62.5%), with an age range between 6 and 13 years (mean of 10.4 years) in 85% of the patients. Neither the symptoms associated with asthma (p = 0.07), allergic rhinitis (p = 0.17), food allergy (p = 0.09), necessity of systemic corticosteroids (p = 0.10), antileukotrienes (p = 0.20) and antihistamines (p = 0.70), nor the three parameters used to assess lung function (FEV(1), FEV(1)/FVC and FEF(25-75%), p > or = 0.14) were statistically significant. The frequency of eczema (p < 0.005) and exhaled nitric oxide levels (p < 0.001) were higher among atopic patients. Results suggest that clinical and functional stability of asthma among atopic patients does not necessarily reflect an efficient control over the inflammatory process and a higher probability for recurrence after discontinuation of anti-inflammatory therapy.

Aberrant Expression of CC and CXC Chemokines and Their Receptors in Patients with Asthma

This study further elucidates the roles of selected chemokines (IP-10, MIG, and RANTES) and their receptors (CCR3, CCR5, and CXCR3) in asthma. We compared their profiles in six groups of participants-atopic cohort and nonatopic cohort (each including controls and asthmatic patients with or without steroid therapy). Plasma concentration of IP-10 was significantly lower while that of RANTES and the expression of CCR3 were higher in asthmatic patients (all p < 0.05). Plasma RANTES correlated positively with the GINA severity score in all asthmatic patients (r=0.27, p < 0.05), and with IL-13 in nonatopic asthmatic patients (r=0.46, p < 0.05). In asthmatic patients, the ex vivo release of IP-10 and MIG was attenuated in PBMC activated with allergen, mitogens and IL-18 (p < 0.05). In conclusion, plasma RANTES may be a surrogate marker for asthma and the diminished Th1 related CXC chemokine production may contribute to Th2 predominance in asthma.

Correction of metabolic disorders in patients with chronic obstructive pulmonary disease treated with Troventol

The study was aimed to investigate efficacy, safety, and ability of correction some metabolic disturbances in patients with chronic obstructive pulmonary diseases (COPD) at the North during therapy with Russian anticholinergic drug Troventol. Thirty-nine moderate COPD patients and 11 mild non-atopic asthma patients were observed. Good clinical efficiency was noted in 72.3 % and satisfactory effect was in 20.8 % of the patients after the Troventol alone therapy. The treatment resulted in normalization of reduced blood antioxidant potential due to increase in intercellular superoxiddysmutase erythrocyte level, ceruloplasmin and transferrin plasma levels. Troventol provided normalization of increased fluidity of the erythrocyte membrane lipid bilayer. Therapeutic doses of Troventol were well-tolerated and did not cause severe adverse effects.