Sophisticated –omics approaches will be reviewed in this manuscript, but currently they are not being used in clinical practice.
Sophisticated –omics approaches will be reviewed in this manuscript, but currently they are not being used in clinical practice.Tags: Aleister Critical Crowley Essay In Star Upon West WorksRunaway Jury Essay QuestionsHow To Make Yourself Do HomeworkCreative Writing TeachersBusiness Plan Competition ListCover Letter Athletic DirectorEssays On Relationships With ParentsHistory Dissertation Structure
• Does the child have the treatable trait of (usually short-acting, β-2 agonist sensitive) reversible airflow obstruction?
And conversely, does the child have the untreatable trait, meaning treatment should be discontinued, of fixed airflow obstruction?
The result has been the specific, molecular therapies (2–4), none of which would have come to the bedside if they had been tested on every child with a chronic wet cough.
It is also important, but largely outside the scope of this chapter, to set airway disease in the context of extra-pulmonary co-morbidities such as obesity, and environmental and lifestyle factors, such as adverse environmental exposures and adherence (5).
Additionally, the pathophysiology of risk domains must be considered: these are risk of an asthma attack, risk of poor airway growth, and in pre-school children, risk of progression to eosinophilic school age asthma.
Phenotyping the airway will allow more precise diagnosis and targeted treatment, but it is important to move to endotypes, especially in the era of increasing numbers of biologicals.There is only a weak correlation at baseline between eosinophilic inflammation and bronchial hyper-responsiveness (6, 7).The anti-Ig E monoclonal omalizumab reduces airway eosinophilia, but has no effect on bronchial hyper-responsiveness (8), whereas the anti-TNF monoclonal etanercept reduces hyper-responsiveness but has no effect on airway inflammation (9).The conventional view of at least school age and adult asthma is that the root cause is airway inflammation, which leads to airway hyper-responsiveness, and, secondary to repeated episodes of inflammation, airway remodeling.However, a critical review of the evidence shows that this view is untenable.Furthermore, there are domains of risk, which also need to be considered in any discussion of pathophysiology: • Risk of acute asthma attacks, which may be fatal • Risk of impaired trajectories of lung growth, which may sometimes but not inevitably be associated with asthma attacks • (in pre-school children) risk of progressing from episodic wheeze to eosinophilic atopic school age asthma • A fourth risk, about which little is known and will not be discussed here, is the risk of failing to remit Clearly not all are relevant to all pediatric airways diseases: the hallmark of CF is the effects of the airway being too dry [“low volume hypothesis” (11)] and infection and neutrophilic inflammation, whereas some at least of the asthmas are dominated by eosinophilic airway inflammation.What is also clear is that we need modern–omics or genetic tools to try to dissect out these components—and these are sadly lacking.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.