For anyone interested in either respiratory diseases or allergy this was a really fascinating meeting of the experts in the field.
The asthma-rhinitis connection
First to speak was Dr Glennis Scadding, from the Royal National Throat, Nose and Ear Hospital, who made the point, so often ignored by both asthma and rhinitis specialists, that the nose is part of the same respiratory system as the lungs, so the connection between rhinitis (a nasal condition) and asthma (a respiratory one) is very close.
For example, 80% of asthmatics also have rhinitis while those with allergic rhinitis are three times more likely to develop asthma. Moreover, 20-25% of asthmatics also have rhino-sinusitis, which involves the sinuses and causes facial pain as well as the blocked nose and mouth breathing of simple rhinitis. Both of the latter, which also increase the chances of contracting a virus, will have a deleterious effect on asthma.
Studies suggest that asthmatics who suffer from allergic rhinitis need fewer hospital visits if they are receiving treatment for the rhinitis.
The usual treatment is intra- nasal steroids although there is a concern about steroid load as these patients may also be on steroids for asthma and/or eczema - and 80% of what goes into the nose finds its way into the stomach and the liver.
Alternative treatments which show promise are allergen-
specific immunotherapy (see below) and anti-IgE drugs (see below).
Asked whether she had tried any nutritional interventions Dr Scadding said that she had not but that she was a great believer in warm salt water nasal douches.
Allergic sensitisation and asthma
Professor Adnan Custovic, professor of allergy at the University of Manchester, maintained that allergic sensitisation was crucial in asthma.
Although there are a huge number of people who are sensitised to allergens (house dust mite, pollen, cats, dogs etc) but who do not have asthma or any symptoms of asthma, there is a strong correlation between the level of allergic sensitisation and the presence of asthma.
The severity of the asthma may also depend on which allergen the patient is sensitised to. Sensitivity to moulds, for example, usually suggests more severe disease. And the severity of the disease will also be closely linked to the level of exposure to the allergen.
Viral infection will also be relevant so, while an asthmatic who is exposed to a high level of allergens will make an increased number of hospital visits, an asthmatic exposed to high levels of allergens and a virus will make even more.
Because lung function that is set very in early childhood persists into adult life it is very important to identify allergic sensitisation that could lead to asthma as young as possible. Three year olds who were atopic had poorer lung function than non-atopic children, even though they had no symptoms of asthma or wheeze.
Genetic predispositions are entirely dependent on environmental factors so, depending on the latter, genetics can either predispose or protect. Thus although allergy is really important for some patients, it is not for all. Treatments need to be individualised to patients - one size really does not fit all.
Proteins versus sugars
Dr Tom Platts-Mills is head of the Asthma and Allergic Disease Center at the University of Virginia.
He pointed out that asthmatic children taken to the Alps improve not only because of the reduction in their exposure to mites but because they take more exercise, eat different (better?) food etc. So although exposure to allergens is important it is not the only factor.
Other interesting points:
• Allergic asthma is becoming more common; intrinsic (non-
allergic) asthma is not.
• There are basically four cat allergens and over 20 dust mite allergens - yet it takes a far higher exposure to cat proteins to induce allergy than it does to mite allergens.
This could be explained by the fact that dog and cat proteins are, in evolutionary terms, far closer to human proteins than those of mites, cockroaches etc. So it may require a higher exposure to the relatively similar dog or cat proteins than to the less similar mite proteins to trigger a reaction.
• In New Zealand 50-55% of households have cats and asthma rates are three times higher than they are in Germany, for instance. Yet,
although New Zealanders have high levels of IgE antibodies to mites, they have none to cats. This suggests that high exposure may have induced tolerance to cat proteins.
• On the other hand, high exposure to a potential allergen (such as the Asian lady beetle which has recently invaded the US) can trigger an IgE mediated allergy at any point in life.
• IgE antibodies are not only created in response to a protein; they can also be created to a carbohydrate - specifically galactose, which is a non-human sugar. We all carry antibodies to it. Humans need an enzyme (galactose alpha 1-3 galactose transferase) to process this sugar, but it would appear that only certain blood groups carry it. Raised levels of IgE to galactose do not show up in skin or prick tests; they appear to be related to anaphylaxis, but not to allergy.
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