This is the same research to one of the audio presentations I'll post later. The congress was mainly about higher up mechanisms of disease rather than about lower level presentation of symptoms. Focus remained on the interaction of environment, asthma, atopic dermatitis in relation to the allergic march, and how a worldwide approach will never yield a result because patients are a mix of endotypes, environment and individual reactions. Much emphasis was placed on component testing, I believe even the ACAAI sponsored speakers joined the broad opinion of moving forward on a more contextual, granular approach in treating allergic patients.
The author that will be heard later presenting in audio is Cezmi Akdis of Swiss Institute of Allergy and Asthma Research. I'll link to the audio once it's up. For now an open access paper. I think in the audio he may be the one at the conference who challenged the convention of clinical significance of SPT at 3mm.
http://www.jacionline.org/article/S0091-6749(13)00367-9/fulltext#sec6Endotypes and phenotypes of chronic rhinosinusitis: A PRACTALL document of the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma & Immunology
Chronic rhinosinusitis (CRS) is a complex disease consisting of several disease variants with different underlying pathophysiologies. Limited knowledge of the mechanisms of these disease subgroups is possibly the greatest obstacle in understanding the causes of CRS and improving treatment. It is generally agreed that there are clinically relevant CRS phenotypes defined by an observable characteristic or trait, such as the presence or absence of nasal polyps. Defining the phenotype of the patient is useful in making therapeutic decisions. However, clinical phenotypes do not provide full insight into all underlying cellular and molecular pathophysiologic mechanisms of CRS. Recognition of the heterogeneity of CRS has promoted the concept that CRS consists of multiple groups of biological subtypes, or “endotypes,” which are defined by distinct pathophysiologic mechanisms that might be identified by corresponding biomarkers. Different CRS endotypes can be characterized by differences in responsiveness to different treatments, including topical intranasal corticosteroids and biological agents, such as anti–IL-5 and anti-IgE mAb, and can be based on different biomarkers that are linked to underlying mechanisms. CRS has been regarded as a single disease entity in clinical and genetic studies in the past, which can explain the failure to identify consistent genetic and environmental correlations. In addition, better identification of endotypes might permit individualization of therapy that can be targeted against the pathophysiologic processes of a patient's endotype, with potential for more effective treatment and better patient outcomes.
Topic: Innate Immunity and Endotypes (Read 1925 times)
