Serum levels and gene expression of pentraxin 3 are elevated in COPD.

PURPOSE: Pentraxin 3 (PTX-3) is an acute phase protein that belongs to the pentraxin superfamily. It is synthesized locally at the site of inflammation and its levels are related to the damage of blood vessels. There are only a few studies examining the relationship between PTX-3 and chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the serum levels of PTX-3 and relative PTX-3 gene expression in COPD patients and their correlations with cigarette smoking history and lung function. MATERIALS/METHODS: A total number of 34 participants were enrolled into this study. Only stable patients without comorbidities were recruited. After obtaining written informed consent all planned procedures were performed (pre- and post-bronchodilator spirometry, blood samples for PTX-3 serum levels and PTX-3 gene expression measurements, demographical data, medical history, COPD patients were also asked for CAT and MMRC questionnaires). RESULTS: PTX-3 serum levels were significantly higher in the COPD group (29.22 (5.47) ng/ml vs. 14.64 (3.64) ng/ml). PTX-3 gene relative quantification (RQ) values were also significantly higher in the COPD group (0.15 (1.33) vs. -2.80 (1.99)). No differences in CRP serum levels were found between the control group and the COPD group. CONCLUSIONS: Our study demonstrates that serum levels of PTX-3 and the relative expression values of its gene are elevated in COPD, and can be related to cigarette smoking history.

Acute laryngeal dyspnea as first presentation of granulomatosis with polyangiitis.

Granulomatosis with polyangiitis (GPA) is a multi-organ disease which mostly affects lungs, kidney, and head and neck region. We report a rare case of acute laryngeal dyspnea and rapidly progressive pulmonary changes as first manifestations of disease. A 53 year-old woman presented with symptoms of two-week dyspnea, which aggravated rapidly in the preceding hours. Laryngological examination revealed subglottic infiltrations and vocal fold oedema which required urgent tracheotomy. During few days she developed gingival ulcerations and pulmonary infiltration with negative serum c-ANCA titers. The histopathological examination of subglottic and gingival biopsies and the clinical picture established the diagnosis of GPA. She was treated with prednisone and cyclophosphamide with recovery; however, during over 3 years of follow-up, pulmonary symptoms relapsed and subglottic stenosis persisted. The difficulties in diagnosis and treatment in this unusual presentation of GPA are outlined with conclusion that in patients with subglottic infiltration, which develops rapidly, even when this is a sole presentation of the disease, and when c-ANCA are negative, GPA should always be considered.

Association between asthma control test, pulmonary function tests and non-specific bronchial hyperresponsiveness in assessing the level of asthma control.

INTRODUCTION: Global Initiative for Asthma (GINA) reports emphasize the use of validated and simple tools in order to assess the level of asthma control, as the Asthma Control Test (ACT). However, an ACT does not include assessment of airway inflammation, which is better reflected when measuring nonspecific bronchial hyperresponsiveness (BHR). The authors aimed to find out if the level of asthma control quantified by an ACT correlates with BHR and pulmonary function tests. MATERIAL AND METHODS: 118 asthmatics participated in the study. All patients completed an ACT. The scores of the ACTs were compared with pulmonary function tests and BHR assessed with the methacholine challenge test and expressed as a provocative concentration of methacholine, inducing a 20% decline in the FEV1 (PC20 M in mg/ml). RESULTS: Patients with controlled asthma amounted to 52 (44%) while those with uncontrolled asthma amounted to 66 (56%). In patients with controlled asthma (ACT score ≥ 20) the mean geometric value of PC20M was 2.72 mg/ml (range from 0.25 to > 8.0), whereas 0.94 mg/ml (range from 0.28 to 8.0) (p = 0.02) was observed in patients with uncontrolled asthma (ACT score < 20). Almost 64% (21/33) of uncontrolled asthmatics achieved normal lung function (FEV1 > 80% pred. value) while 19% (5/26) patients with controlled asthma presented an FEV1 < 80% predicted value. Asthma duration in years in controlled asthmatics was significantly shorter than in uncontrolled patients (6.2 ± 8.9 vs. 12.0 ± 11.4, p = 0.005) CONCLUSION: In determining the most accurate level of asthma control it is reasonable to use an ACT in conjunction with BHR, which provides more accurate assessment of bronchial inflammation than ventilatory parameters alone.

Assessment of leptin and resistin levels in patients with chronic obstructive pulmonary disease.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is the most common chronic lung disease in the world. The increasing severity of inflammatory processes in the respiratory tract leads to exacerbation of COPD. This process may be associated with changes in the synthesis of adipokines, the peptides that participate in immune processes. OBJECTIVES: The aim of this study was to identify more sensitive and specific laboratory markers useful in diagnosing inflammatory processes in patients with COPD. PATIENTS AND METHODS: The study involved 33 patients with COPD without exacerbation. During the previous year, 1 episode of exacerbation was reported in 15 patients and no exacerbations were reported in the remaining 18 patients. Serum concentrations of adipokines were measured using an enzyme-linked immunosorbent assay (ELISA). RESULTS: In patients with COPD, we observed a 2-fold increase in leptin levels compared with healthy controls (18.8 ±10.2 ng/ml vs. 9.06 ±4.33 ng/ml; P = 0.042). Mean resistin levels in these patients were also 2-fold higher than those in controls (8.24 ±4.18 ng/ml vs. 3.58 ±1.51 ng/ml, respectively; P = 0.027). Significant positive correlations between C-reactive protein (CRP) and leptin as well as CRP and resistin levels were observed in patients with COPD (r = 0.75 and r = 0.83, respectively; P <0.05). Moreover, a statistically significant negative correlation between the forced expiratory volume in 1 second (FEV1) and resistin was noted in this group (r = 0.62; P <0.05). There was no correlation between FEV1 and leptin levels either in patients with COPD or in healthy controls. CONCLUSIONS: A significant increase in leptin and resistin levels in patients with COPD may suggest that these adipokines are involved in the inflammatory process underlying the disease.

[Effect of natural allergens exposure on serum concentration of soluble form of intercellular adhesion molecule 1 in patients with seasonal airway allergy]. / Wplyw naturalnej ekspozycji na alergeny na stezenie rozpuszczalnej formy czasteczki adhezji miedzykomórkowej 1 w surowicy chorych z sezonowa alergia dróg oddechowych.

UNLABELLED: Chronic inflammation is a feature of bronchial asthma and allergic rhinitis. Intercellular adhesion molecules, especially ICAM-1 and its soluble form sICAM-1 present in systemic liquids play an important role in allergic inflammation. The aim of this study was to assess the effect of natural pollen exposure to plants on serum sICAM-1 concentration in patients with different clinical expression of seasonal allergy and to determine the relation between concentrations of these molecules to clinical symptom score and nonspecific bronchial hyperresponsiveness (BHR). MATERIAL AND METHODS: The study comprised 48 patients with isolated seasonal allergic rhinitis (SAR), 26 patients with seasonal asthma (SA) and 16 healthy volunteers. Serum s/CAM-1 concentration using an immunoenzymatic ELISA method and BHR to methacholine were measured twice, before grass season and during symptomatic period of SAR and SA. Clinical symptoms severity were evaluated by pointing method from patients diary cards. RESULTS: The study revealed no differences in mean concentration of serum sLCAM-1 between patients with SAR and SA but significant increase of serum sICAM-1 level during natural allergen exposure in all patients was observed. CONCLUSION: Serum concentration of sICAM-1 was not correlated to symptom score and BHR in both SAR and SA patients in and out of season.

[Correlation of serum concentration of tumor necrosis factor alpha, clinical course, ventilation and nonspecific bronchial hyperresponsiveness in patients with isolated seasonal rhinitis and seasonal asthma]. / Zaleznosci miedzy stezeniem czynnika martwicy nowotworu alpha w surowicy a przebiegiem klinicznym, wentylacja i nieswoista nadreaktywnoscia oskrzeli u chorych na izolowany sezonowy niezyt nosa i sezonowa astme.

UNLABELLED: Tumor necrosis factor alpha (TNF-alpha) plays a central role in pathogenesis of many inflammatory diseases including asthma and allergic rhinitis. Its capability for cell activation, chemotaxis and upregulation of adhesion molecule expression on surface of inflammatory cells suggests that TNF-alpha may be responsible for bronchial hyperresponsiveness (BHR) and clinical symptoms of atopic diseases. THE AIM: Relationships between serum concentration of TNF-alpha and clinical course as well as nonspecific BHR in patients with isolated seasonal rhinitis (SR) and seasonal bronchial asthma (SA) were assessed. MATERIAL AND METHODS: The study was performed in 19 subjects with SR and 26 subjects with asthma sensitized to pollens, with measurable BHR during symptomatic phase of disease. Control group consists of 16 healthy volunteers. Serum concentration of TNF-alpha, ventilatory parameters, BHR to methacholine, asthma and seasonal rhinitis score were assessed two times--during and outside pollen season. RESULTS: Nonspecific BHR was find in 10 (21%) patients with SR and 18 (69%) patients with asthma symptoms out of season. In both groups postseasonal mean geometric values of PC20M were significant higher than during season. There were no marked changes in ventilatory parameters accompanied the increase in BHR. TNF-alpha concentration in serum in both groups of patients was significant higher than in healthy subjects. Further increase of its activity about 50-70% compared to baseline values was observed during pollen season. There was no correlation between serum concentration of TNF-alpha, BHR and symptom score. There is increased serum concentration of TNF-alpha in patients with seasonal airway allergy even in asymptomatic period of disease. CONCLUSIONS: Natural exposure to allergens causes significant increase of TNF-alpha concentration in patients with rhinitis and asthma. Although level of BHR and intensification of clinical symptoms coexist with changes in TNF-alpha concentration there is no correlation between them.

[Effect of fexofenadine--selective antagonist of histamine receptor (H1) on histamine-induced bronchoconstriction]. / Wplyw feksofenadyny--wybiórczego antagonisty receptorów H1--na skurcz oskrzeli wywolany wziewaniem histaminy.

The aim of the study was to evaluate the effect of single and repeated fexofenadine (120 mg/day) doses on histamine-induced bronchoconstriction. Sixteen patients with mild, stabile asthma were examined. Bronchial reactivity was estimated as histamine dose (in mg/ml) causing a 20% FEV1 fall. A significant blockade of histamine H1 receptors in the airways was observed from the 1st to the 3rd day of the study. In all patients treated with fexofenadine, histamine in 16 mg/ml dose failed to induce bronchoconstriction. After another three days without fexofenadine, bronchial responsiveness returned to the initial value. The study points out that fexofenadine blocks H1 receptors in the bronchial tree.

[Allergic inflammation in the development of nonspecific bronchial hyperresponsiveness in asthma]. / Zapalenie alergiczne w rozwoju nieswoistej nadreaktywnosci oskrzeli w astmie.

Bronchial hyperresponsiveness, an exaggerated bronchoconstrictor response to a variety of nonspecific stimuli, is regarded as one of the most important feature in bronchial asthma. It can be demonstrated by bronchial provocation tests with pharmacological or physical stimuli. The measured level of responsiveness to these agents is considered to reflect the lability of the airways and the severity of the disease. Acute exposure to allergen causes an increase of airway responsiveness. The significant correlation between the allergen-induced increase in hyperresponsiveness and the severity of the late asthmatic reaction suggests the same underlying mechanisms that include an influx of inflammatory cells in the airways occurring during late phase of response to allergens. Marked inflammation with infiltration of eosinophils and disruption of airway epithelium has been also described on autopsies of patients who died of acute asthma but also on bronchial biopsies of subjects with mild asthma. Development and persistence of increased nonspecific bronchial responsiveness are possibly associated with these inflammatory changes.