ConclusionThe web‐based version of the C‐ACT and ACT is reproducible and comparable with the paper‐based version in assessing asthma control. Most children and their parents prefer the web‐based version. Pediatr. Pulmonol. © 2011 Wiley‐Liss, Inc.
Food allergy is an increasingly prevalent problem in westernized countries, and there is an unmet medical need for an effective form of therapy. A number of therapeutic strategies are under investigation targeting foods that most frequently provoke severe IgE-mediated anaphylactic reactions (peanut, tree nuts, and shellfish) or are most common in children, such as cow's milk and hen's egg.
Approaches being pursued are both food allergen specific and nonspecific. Allergen-specific approaches include oral, sublingual, and epicutaneous immunotherapy (desensitization) with native food allergens and mutated recombinant proteins, which have decreased IgE-binding activity, coadministered within heat-killed Escherichia coli to generate maximum immune response. Diets containing extensively heated (baked) milk and egg represent an alternative approach to food oral immunotherapy and are already changing the paradigm of strict dietary avoidance for patients with food allergy. Nonspecific approaches include monoclonal anti-IgE antibodies, which might increase the threshold dose for food allergen in patients with food allergy, and a Chinese herbal formulation, which prevented peanut-induced anaphylaxis in a murine model and is currently being investigated in clinical trials.
The variety of strategies for treating food allergy increases the likelihood of success and gives hope that accomplishing an effective therapy for food allergy is within reach.
Advancing our understanding of mechanisms of immune regulation in allergy, asthma, autoimmune diseases, tumor development, organ transplantation, and chronic infections could lead to effective and targeted therapies. Subsets of immune and inflammatory cells interact via ILs and IFNs; reciprocal regulation and counter balance among Th and regulatory T cells, as well as subsets of B cells, offer opportunities for immune interventions.
Here, we review current knowledge about ILs 1 to 37 and IFN-γ. Our understanding of the effects of ILs has greatly increased since the discoveries of monocyte IL (called IL-1) and lymphocyte IL (called IL-2); more than 40 cytokines are now designated as ILs. Studies of transgenic or knockout mice with altered expression of these cytokines or their receptors and analyses of mutations and polymorphisms in human genes that encode these products have provided important information about IL and IFN functions.
We discuss their signaling pathways, cellular sources, targets, roles in immune regulation and cellular networks, roles in allergy and asthma, and roles in defense against infections.
2010 was marked by rapid progress in our understanding of the cellular and molecular mechanisms involved in the pathogenesis of allergic inflammation and asthma. Studies published in the Journal of Allergy and Clinical Immunology described advances in our knowledge of cells associated with allergic inflammation (mast cells, eosinophils, dendritic cells, and T cells), as well as IgE, cytokines, receptors, signaling molecules, and pathways.
Studies used animal models, as well as human cells and tissues, to advance our understanding of mechanisms of asthma, eosinophilic esophagitis, food allergy, anaphylaxis and immediate hypersensitivity, mast cells and their disorders, atopic dermatitis, nasal polyposis, and hypereosinophilic syndromes. Additional studies provided novel information about the induction and regulation of allergic inflammation and the genetic contribution to allergic inflammation.
Critical features of these studies and their potential effects on human atopic disorders are summarized here.
Exacerbations are a frequent cause of morbidity and mortality in COPD. It is crucial to identify risk factors for failure after treatment of exacerbations of COPD. This study evaluates the COPD severity score (COPDSS) as a predictor of clinical failure, together with other severity, activity and quality of life measurements, in patients with exacerbated COPD.
Method : Multicenter, prospective, observational study in ambulatory patients with exacerbation of COPD. The patients completed the COPDSS, the London Chest Activities of Daily Living (LCADL) and the EuroQol 5D (EQ-5D). A follow-up visit was scheduled one month after presentation with the exacerbation to assess the clinical evolution.
Results : A total of 346 patients were included (mean age 68.5 years (SD = 9.5 years and 90.7% male) and mean FEV1(% predicted) 46.9% (SD = 17)). After one month, 28.2% of episodes were classified as failures, with half of them requiring hospital admission. Patients who failed were more frequently active smokers, with more severe dyspnoea at presentation and worse lung function. They had significantly worse scores of COPDSS, LCADL, EQ-5D index and EQ-5D visual analogue score (VAS) and shorter mean time walking per day. ROC analysis of relationship between COPDSS and failure gave AUC 0.72, which improved only to 0.77 when the other significant variables in univariate analysis were considered.
Conclusions : Clinical failure after ambulatory treatment of exacerbation of COPD is frequent. Usual markers of severity (impaired lung function, active smoking and severe dyspnoea) are associated with failure; however, a short severity questionnaire (COPDSS) provides better predictive value than the usual variables.