Asthma Research Paper

Asthma Research Paper-87
The recent Lancet Asthma Commission (1) was predicated on the assumption that the term “asthma” was no more a diagnosis than is “arthritis” or “anemia.” It is an umbrella term that should be used to describe a constellation of clinical symptoms, namely wheeze, breathlessness, chest tightness and cough, and should be followed by the question “what sort of asthma is this?

The recent Lancet Asthma Commission (1) was predicated on the assumption that the term “asthma” was no more a diagnosis than is “arthritis” or “anemia.” It is an umbrella term that should be used to describe a constellation of clinical symptoms, namely wheeze, breathlessness, chest tightness and cough, and should be followed by the question “what sort of asthma is this?

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Indeed, currently we are not even trying routinely to identify treatable traits in airway disease, instead haphazardly making diagnoses and embarking on therapeutic trials without making simple measurements in order objectively to phenotype the airway disease.

The three important treatable traits, which will be considered in turn, are: • Does the child have the treatable trait of eosinophilic airway inflammation which is likely to respond to inhaled corticosteroids (ICS)?

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Advances in -omics technology allow delineation of pathways, which will be particularly important in TH2 low eosinophilic asthma, and also pauci-inflammatory disease.

It is very important to appreciate the difficulties of cluster analysis; a patient may have eosinophilic airway disease because of a steroid resistant endotype, because of non-adherence to basic treatment, and a surge in environmental allergen burden.These are: • Narrowing to cause fixed obstruction • Narrowing to cause variable obstruction which changes spontaneously over time, and with treatment • Inflammation with various cell types predominant; inflammation may be harmful or beneficial • The tube may become infected with combinations of bacterial, viral and fungal pathogens • There may be increased “twitchiness” of the tube—this is different from variable obstruction.An increased reflex expulsive effort (cough) may not be accompanied by transient airflow obstruction • The tube contents may be abnormal: including being too wet, too many solids, or too dry.The National Asthma Council Australia expressly disclaims all responsibility (including for negligence) for any loss, damage or personal injury resulting from reliance on the information contained herein.The recent Lancet commission has highlighted that “asthma” should be used to describe a clinical syndrome of wheeze, breathlessness, chest tightness, and sometimes cough.Furthermore, there is no relationship between the extent of airway remodeling, specifically reticular basement membrane thickness, and the degree or duration of any inflammatory parameter (10).Indeed, there is evidence that remodeling may be protective under some circumstances, discussed in more detail below.The ultimate aim is to discover endotypes of asthma, but currently we have not yet got to this point.The importance of endotyping is illustrated by the extraordinary achievements when the endotypes and the gene-class specific sub-endotypes of cystic fibrosis (CF) were first separated from the generality of conditions with chronic airflow infection and inflammation.The next step is to deconstruct the airway into components of fixed and variable airflow obstruction, inflammation, infection and altered cough reflex, setting the airway disease in the context of extra-pulmonary co-morbidities and social and environmental factors.The emphasis is always on delineating treatable traits, including variable airflow obstruction caused by airway smooth muscle constriction (treated with short- and long-acting β-2 agonists), eosinophilic airway inflammation (treated with inhaled corticosteroids) and chronic bacterial infection (treated with antibiotics with benefit if it is driving the disease).

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