Early diagnosis of chronic obstructive pulmonary disease (COPD) allows increased opportunity for smoking cessation advice and treatment, which potentially improves prognosis. This single-centre, prospective cross-sectional study investigated whether screening CT scans could diagnose COPD without the need for pulmonary function testing (PFT).

One thousand one hundred and forty men, ex or current smokers (>16.5 pack year history), aged 50–75 years, already enrolled in a lung cancer screening trial, had low dose screening inspiratory CT scans, PFT and an additional expiratory scan. Pre-bronchodilatory forced expiratory volume in one second/forced vital capacity ratio <70% was used to diagnose COPD. Those with advanced disease, self-reported as unable to climb two flights stairs were excluded. CT emphysema, CT air trapping, body mass index, pack years and smoking status formed a diagnostic model to identify those with COPD.

Four hundred and thirty-seven (38%) subjects had COPD on PFT. The diagnostic model correctly diagnosed 274 patients...

This randomised, multicentre, double-blind, placebo-controlled trial evaluated the efficacy and safety of four different doses of BIBF 1120, a tyrosine kinase inhibitor, in order to investigate its effect on progression of idiopathic pulmonary fibrosis (IPF).

The annual rate of decline in forced vital capacity (FVC), the primary end-point of this study, in the highest dose subgroup compared with the placebo subgroup failed to show statistical significance. However, the authors were able to demonstrate that the changes in FVC from baseline, total lung capacity, oxygen saturations, acute exacerbations and quality of life were statistically significantly better in the group receiving the highest dose of BIBF 1120. Serious adverse events were similar between groups, but lower in the highest dosing regimen compared with placebo. The most common reason for discontinuation of the medication was gastrointestinal upset.

Of note, only 33% of the patients recruited fulfilled the criteria for definite IPF with...

This article reviews the international literature on the cost-effectiveness of immunotherapy for respiratory allergy. Included studies conducted an economic evaluation of immunotherapy for allergic rhinoconjunctivitis, allergic conjunctivitis, allergic rhinitis, asthma or allergic rhinitis in combination with asthma. Although there were few economic evaluations and these suffered from methodological shortcomings, the evidence appears to support the cost-effectiveness of immunotherapy as compared with pharmacotherapy for allergic rhinoconjunctivitis, subcutaneous immunotherapy as compared with pharmacotherapy for allergic rhinitis and immunotherapy as compared with pharmacotherapy for allergic rhinitis and asthma. One economic evaluation suggested that immunotherapy as compared with pharmacotherapy is unlikely to be cost-effective for asthma. The questions of the cost-effectiveness of sublingual vs subcutaneous immunotherapy and of the cost-effectiveness of immunotherapy for allergic conjunctivitis have not been resolved to date. The cost-effectiveness of immunotherapy depends on the duration of the clinical benefit of immunotherapy following treatment cessation, and on the break-even point of cumulative costs between immunotherapy and pharmacotherapy. There is a need for economic evaluations based on high-quality prospective and long-term clinical studies comparing immunotherapy with pharmacotherapy in real-life practice and comparing sublingual with subcutaneous immunotherapy.

BackgroundViral pathogen–associated molecular patterns, such as dsRNA, disrupt airway tolerance to inhaled allergens. Specifically, the Th2 and Th17 cell responses are induced by low-dose dsRNA and the Th1-dominant response by high-dose dsRNA.ObjectiveIn this model, we evaluate the role of TNF-α in the development of adaptive immune dysfunction to inhaled allergens induced by airway sensitization with dsRNA-containing allergens.MethodsA virus-associated asthma mouse model was generated via simultaneous airway administration of ovalbumin (OVA) and low (0.1 μg) or high (10 μg) doses of polyinosine–polycytidylic acid (poly[I:C]). The effect of TNF-α on Th2 airway inflammation was evaluated using TNF-α-deficient mice and recombinant TNF-α.ResultsTNF-α production was enhanced by airway exposure to low and high doses of poly[I:C]. After airway sensitization with OVA plus low-dose poly[I:C], TNF-α-deficient mice exhibited less OVA-induced airway inflammation than did wild-type (WT) mice. However, this did not occur upon sensitization with high-dose poly[I:C]. In terms of T-cell response, the production of IL-4 from lung T cells after OVA challenge was enhanced by airway sensitization with OVA plus low-dose poly[I:C] in WT mice, and this phenotype was inhibited by the absence of TNF-α. Moreover, the Th2 cell response induced by sensitization with OVA plus low-dose poly[I:C], which was abolished in TNF-α-deficient mice, was restored in these mice upon addition of recombinant TNF-α.ConclusionThe results of this study suggest that TNF-α produced by airway exposure to low-dose dsRNA is a key mediator in the development of Th2 cell response to inhaled allergens.