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Dr Candice Royal, paediatrician and allergist, presented first, on asthma.
Over 300 million people have asthma and it is the most common chronic disease of childhood.
It is a heterogenous group of conditions involving chronic airway inflammation and bronchial hyper-reactivity. Publications cite many different phenotypes with varying pathophysiological pathways.
Implications for management
- Corticosteroid responsiveness
- Control with other suppressors of airway type 2 (T2) inflammation - Leukotriene receptor antagonists (LTRA), long-acting beta2-agonist inhaled corticosteroid (LABA-ICS) combinations
- Expanding group of biological therapies that target specific pathways to T2 inflammation
Key features of T2 - low inflammation
- Sputum neutrophilia or paucigranulocytic type
- Activation of effector T-helper-cells (Th1 and/or Th17)
- Imbalance of Th17/ regulatory T-cells (Treg) may play a role in severe steroid unresponsive asthma
- Is the neutrophil merely an effect of high-dose corticosteroid use?
ICS - formoterol as reliever
Mild asthmatics are at risk of serious adverse effects:
- Acute asthma
- Near-fatal asthma
- Asthma mortality
- Adverse events in OCS.
Short-acting β-agonist (SABA) reliever therapy has adverse effects and reduced efficacy with overuse. There is often poor adherence to daily Inhaled corticosteroids (ICS) in mild asthmatics.
ICS-formoterol as reliever decreased exacerbations by 60-64% (O’Byrne et al NEJM 2018).
At each visit assess for control:
- Is the diagnosis correct?
- Is the treatment adequate?
- Is the patient adherent?
- Is the technique correct?
- Are there environmental factors that can be addressed- irritants/ allergens
- Are there co-morbidities that are impacting on control?
- No daytime symptoms
- No nocturnal symptoms
- Able to exercise
- No exacerbations
- Minimal SABA use
- No impact on ADLs.
Assess for type 2 inflammation:
- Eosinophilia >150U/L
- Positive immunocaps or skin prick tests
- Sputum >2% eosinophils
- Fractional exhaled nitric oxide (FeNO) >20ppb.
- Sop ineffective add-on therapies.
Severe asthma management
T2 high - consider LAMA, LTRA, low-dose OCS, address irritants/ allergens.
T2 high - Biologics available
T2 low - Review diagnosis.
Address irritant exposure, such as smoking, as well as obesity. Consider high-resolution computed tomography and bronchoscopy.
Add on: LAMA, azithromycin, low-dose OCS and bronchial thermoplasty.
Global health burden
We have a clear understanding of T2 high asthma with good clinical guidelines including a rapidly expanding group of biological therapies to provide tailored therapy.
Immunopathogenesis and phenotypes of T2 low asthma is less clear.
Where to from here?
We need consensus regarding the clinically meaningful asthma phenotypes based on immuno-pathogenesis and improvement in our understanding of T2- low asthma. This would translate into clinical guidelines to enhance asthma care.
We are ONE: Allergic rhinitis and the United Airway
Prof Claudia Gray, Associate Professor in paediatrics and paediatric allergologist in Cape Town presented next. Allergic rhinitis (AR) is a reaction involving immune system to things that should be harmless, mostly aeroallergens.
Cardinal symptoms of include itch, sneeze, rhinorrhoea and congestion. There is ocular involvement in a large percentage.
Allergic rhinitis is not to be sniffed at. There are debilitating physical symptoms and local complications such as otitis media and sinusitis. Atopic complications include asthma worsening, poor sleep quality and emotional and scholastic implications.
Allergic rhinitis classification is by aetiology: seasonal or perennial, and by duration of symptoms and severity of symptoms: ARIA (Allergic Rhinitis and its Impact on Asthma).
Treatment of AR: what makes a good treatment?
How do intranasal steroids work?
Glucocorticoids penetrate the plasma membrane and bind to cytosolic glucocorticoid receptor. The complex translocates into nucleus and binds to DNA in ‘steroid-responsive gene’ regions.
They activate anti-inflammatory genes and repress pro-inflammatory genes.
Intranasal steroid strengths: multiple sites of action. However, they take 3-6 hours to start working, with a maximal effect after 2-4 weeks.
Antihistamine strengths: multiple anti-histamine actions. However, they do not act on other cytokines and chemicals. They have a rapid onset of action - within 5-15 minutes.
Anti-leukotriene strengths - rapid onset of action, within 24 hours, reduces nasal blockage and they are useful if a patient has both asthma and AR.
However, they are not as good for itching/ sneezing and there are potential neuropsychiatric side effects (however these are rare).
Focus on AR treatment
Over 70% of patients with moderate to severe AR require multiple therapies to achieve effective symptom relief.
Myth: It is easy to tell allergies and infection apart.
Both viral colds and allergies can present with a runny nose, cough, sneezing and red eyes
Common colds can last up to three weeks, hence are easily confused with an ‘allergy’.
Some unique features of the common cold are that it is often with lethargy, low-grade fever, achiness, mucous often starts as clear, then opaque, then even yellow after a while. It often sweeps through families (‘goes viral’). The patient is usually completely better between colds.
The picture can be even more clouded in young children, who can catch 10-12 colds per year, so are seemingly ‘always sick’. Intercurrent infections are one of the most common causes of allergy/asthma flares.
Allergies and Covid-19
There was initial concern of asthma/AR increasing susceptibility to Covid-19 but this has not borne out in clinical practice. Could it be the opposite?
Could asthma/allergies reduce the risk of Covid-19? Biomarkers of Th2 inflammation inversely related to angiotensin-converting enzyme 2 (ACE-2) receptor expression.
Does the protective effect of IL-13 in eosinophils reduce ACE-2 receptors?
However, poorly controlled AR carries the risk of touching the nose a lot, rubbing, sneezing, fiddling with mask, and could increase the transmission of viruses to self and others.
Myth: Allergic inflammation can already be in the nose and airways before the patient has symptoms
Allergy medications work best if they are already in the system at the time of allergen exposure.
Myth: If you use only one brand of allergy medication, it will stop working after a while because you build up tolerance.
There is no evidence of building up a tolerance to a specific antihistamine/ nasal corticosteroid.
A variable response to treatment involves the waxing and waning nature of the disease, intercurrent infection and an increase in allergen exposure.
Myth: Inhaled corticosteroids are the safest and most effective means to treat allergic rhinitis and asthma. Absorption systemically is minimal if doses are used prudently.
The patient would have to be taking inhaled corticosteroids for several months to get the equivalent steroid exposure to a short course of oral steroids.
Myth: Young children cannot be tested for environmental allergies until they are two or three.
Young children can get environmental allergies, especially if atopic/ family history. Testing is accurate from 3-4 months age. Testing helps differentiate recurrent infections from allergies. The pattern of exposure determines reactivity.
The united airway
This is the concept that upper and lower airways, which are anatomically and immunologically related, form a single organ, and reflect a single underlying disease at different sites of the respiratory tract.
Other inflammatory conditions include eosinophilic conditions causing chronic rhinosinusitis with polyposis and eosinophilic asthma, and neutrophilic conditions: chronic rhinosinusitis and neutrophilic asthma/ chronic obstructive pulmonary disorder.