Asthma must be treated early

Clinical Update: Asthma - Asthmatics are chronically undertreated and the longer the condition remains untreated, the more treatment resistant it subsequently becomes. Children who do not have their asthma treated are more likely to have persistent asthma into adulthood.

Occupational asthma studies show that people who are not removed within two years from occupations that are associated with the development or exacerbation of asthma are much more likely to be left with the condition permanently.
“The important thing is to treat early and aggressively, for a reasonably prolonged period of time,” said Prof Stephen Lane, Consultant Respiratory Physician at AMNCH, Tallaght.
Making sure that patients are started on preventive medications much earlier in their condition is a key element in asthma therapy. GPs may often prescribe inhaled steroids or anti-leukotrienes, but when the asthmatic symptoms are gone, patients tend to stop taking them. If medications are given very early on in the condition, there are great gains to be had in terms of avoiding permanent reductions in lung function, said Prof Lane.
If a patient lurches from one asthma exacerbation to the next, these episodes become more frequent. Patients begin to develop symptoms between exacerbations. They progress from intermittent symptoms to more persistent asthma and then there are permanent reductions in lung function. Problems arise: these patients need higher doses of inhaled steroids and they are much more medication-dependent.
Clinically, asthma is diagnosed by first taking a history. There may be a wheeze on examination. There may then be abnormal lung function studies that reverse after bronchodilator use. If the lung function is normal, a challenge test is done, to try to drop the lung function by a certain amount.
Prof Lane uses a pyramid schematic: at the base are the majority of Ireland’s 400,000 asthmatics. Most are diagnosed and treated on the basis of symptoms. It is only toward the peak of the pyramid that lung function studies become abnormal.
The healthcare system in Ireland has ready access to sophisticated inhaled steroids, long-acting bronchodilators and leukotriene modifiers – including montelukast and combination products such as budesonide/formoterol and salmeterol/fluticasone.
About 60 per cent of asthmatics have demonstrable allergies. Rather than it being something that can be controlled, the presence or absence of an allergy says more about the asthma’s mechanism. If the underlying mechanism can be targeted, the asthma in that patient can be modified. When there is asthma associated with somebody who is also allergic (has positive blood or skin allergy tests), that means that asthma has an allergic mechanism underpinning it.
There are different treatment approaches for allergic asthma. Omalizumab, for instance, is a monoclonal antibody that blocks the Immunoglobulin E (IgE) molecule (an antibody which is central to the genesis of allergic asthma). The allergy is mediated by IgE.
One area where Ireland could do better, in Prof Lane’s view, is funding the use of omalizumab in patients for whom it is indicated (such as very bad allergic asthmatics). Omalizumab works very well in two thirds of carefully triaged severe allergic asthmatics (mainly hospital based), Prof Lane said. Omalizumab would not be used on a patient who did not have positive allergy tests.
Asthma is a heterogenous condition: there are many different conditions feeding into a final common pathway of an airflow obstruction – a 12 per cent reversal in either peak flow or forced expiratory volume in one second (FEV1) rate, after a bronchial challenge (the definition of asthma).
The condition can be divided in terms of what brings on the asthma attack or treatment responsiveness. There are pharmacogenomic subtypes of asthma that are relevant too. With steroids, there are mutations in the promotor regions of the β2 agonist gene, which determine responsiveness to β2 agonists.
Of 1,000 people taking 5mg of Ventolin, all will respond in different fashions. The ones who are less responsive have mutations or polymorphisms in the promotor regions of the β2 receptor gene, which determine treatment responsiveness.