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Objective. The aim of the study was to assess links between family relationships and severity of dyspnea identified in asthmatic adults. Materials. A total of 131 consecutive, non-selected patients with asthma participated in the study: 88 women (67.18%) and 43 men (32.82%). The mean age of the studied patients was 49.87 years, SD = 13.73. The majority of the study population consisted of patients with grade II (37.74%) and IV (34.91%) of the disease in terms of severity (according to the GINA classification, 2006). Study protocol. All patients underwent functional respiratory tests. The subjective severity of dyspnea was assessed according to the ten-tier Borg scale. To evaluate family functioning values, the Family Assessment Questionnaire (FAQ) was used. Spouses of the asthmatic patients also completed questionnaires. Results. A significant relationship was identified between the values of the dimension: affective expression (assessment of the family performed by the asthmatic patient) and the severity of dyspnea (p = 0.03, r = -0.24) as well as between values of the dimensions: affective expression and affective involvement (as assessed by the spouse of the patient) and severity of dyspnea (p = 0.01, r = 0.39; p = 0.02, r = 0.34, respectively). The relationship between the severity of dyspnea declared by the patient and the FAQ dimension: Task accomplishment (as assessed by the spouse of the patient) was borderline (statistical significance [p = 0.06]). Conclusions. (1) A relationship can be observed between the functioning of the asthmatic patient's family and the severity of the patient's declared dyspnea. Dyspnea constitutes a specific form of emotional communication in the inter-spouse relationships. (2) An analysis of the severity of dyspnea in asthmatic patients should take into account the context of the functioning of the patient's family. [ABSTRACT FROM AUTHOR]

Background Eosinophils are one of the major effector cells in bronchial asthma. Their infiltration of airways correlates with the asthma severity. Recruitment and activation of eosinophils are partially mediated by integrins α4β1 and α4β7. Collagens type I and IV constitute important components of extracellular matrix and vascular basement membrane, respectively. Therefore, collagen-binding integrins (α1β1 and α2β1) may also play a role in eosinophil lung infiltration. Objective To evaluate the possible presence of α1β1 and α2β1 integrins on peripheral blood eosinophils from asthmatic subjects. Methods Collagen receptors were studied on eosinophils separated by immunomagnetic CD16-negative method from healthy donors ( n=13) and patients with moderate persistent atopic bronchial asthma ( n=15). Surface receptor identification was performed by flow cytometry and cell adhesion assay. Results Eosinophils isolated from the patients showed increased expression of both α1β1 and α2β1 integrins as compared with healthy controls. Moreover, adhesive function of eosinophils to collagen type IV was inhibited by snake venom disintegrins: viperistatin and obtustatin. These disintegrins contain KTS active motif and are specific inhibitors of α1β1 integrin. Conclusion We demonstrated for the first time that collagen receptors: α1β1 and α2β1 integrins are overexpressed on the surface of peripheral blood eosinophils of asthmatic subjects. Further studies may reveal potential application of KTS-disintegrins or their structural analogs for therapy of bronchial asthma. [ABSTRACT FROM AUTHOR]

Background GP2015 is a proposed etanercept biosimilar. Objectives To demonstrate equivalent efficacy, and comparable safety and immunogenicity of GP2015 and the etanercept originator ( ETN, Enbrel®) in patients with moderate-to-severe chronic plaque-type psoriasis. Methods In total, 531 eligible patients were randomized 1 : 1 to self-administer GP2015 or ETN twice weekly subcutaneously. Patients with ≥ 50% improvement in Psoriasis Area and Severity Index ( PASI 50) at week 12 were rerandomized to continue the same treatment on a once-weekly dosing schedule or to undergo a sequence of three treatment switches between GP2015 and ETN until week 30. Thereafter, patients continued treatment with the product they had been assigned to last, up to week 52. Results The difference in PASI 75 (75% improvement from baseline PASI score) response rates at week 12 between GP2015 and ETN (primary end point) was −2·3%. The 95% confidence interval (−9·85 to 5·30) was well contained within the prespecified margin range of −18 to 18. The incidence of treatment-emergent adverse events up to week 52 was comparable between continued GP2015 (59·8%) and ETN (57·3%); switching treatments revealed comparable safety profiles. Antidrug antibodies, all non-neutralizing, were limited to five patients on ETN during treatment period 1, and one patient in the switched ETN group, who had been treated with GP2015 for 12 weeks at the time of the finding. Conclusions The EGALITY study demonstrated equivalent efficacy and comparable safety and immunogenicity of GP2015 and ETN. The study results provide the final clinical confirmation of biosimilarity and contribute to the totality of the evidence proposing that GP2015 is an etanercept biosimilar. [ABSTRACT FROM AUTHOR]

Background There is evidence that altered blood coagulation and fibrinolysis are involved in the pathogenesis of asthma. Increased thromboembolic risk has been reported in asthmatics. Objective To investigate whether enhanced thrombin generation and impaired fibrinolysis occur in asthmatics. Methods Plasma thrombin generation profile together with a computational assessment of thrombin dynamics and fibrinolytic capacity expressed as clot lysis time ( CLT) were determined in 164 consecutive patients with stable asthma and 72 controls matched for age, gender, weight and smoking. Results Asthma patients had 20.2% increased endogenous thrombin potential ( ETP), 41.4% higher peak thrombin concentration, 61% higher maximal prothrombin conversion rate, 15.5% faster rate of thrombin formation (all, P < 0.0001) and 10% lower thrombin decay capacity ( P = 0.0004) compared with controls. Asthmatics had also 14.4% longer CLT ( P = 0.001) associated with 21.3% higher plasminogen activator inhibitor-1 ( PAI-1) ( P < 0.0001), and 13% higher plasma α2-macroglobulin ( P = 0.0002). Using ETP and CLT above 75th percentile of the control values as the cut-off levels, we found increased risks of enhanced thrombin generation and hypofibrinolysis in asthmatics, also after correction for potential confounders. ETP and CLT were associated inversely with forced expiratory volume in 1 s/vital capacity ( FEV1/ VC) index, after adjustment for age and body mass index. Non-allergic asthma ( n = 70, 42.6%) was characterized by 17.5% longer CLT ( P = 0.02), which positively associated with PAI-1. Thrombin generation profile was not affected by allergy. Conclusion and Clinical Relevance Asthma is associated with enhanced thrombin generation and impaired fibrinolysis, which might contribute to thromboembolic events in this disease. [ABSTRACT FROM AUTHOR]