Posts Tagged ‘skin prick tests’

Allergens and irritants at work
Some workplaces have very high concentrations of allergens in the air, especially if proper safety procedures are not being followed. Occupational allergies can begin with symptoms in the nose, such as sneezing, blockage or constant streaming (allergic rhinitis). You may also suffer with itchy or watery eyes (conjunctivitis), a cough, sweating and a feverish feeling. Alternatively, direct contact with the allergen can produce a skin rash (dermatitis) or itchiness and swelling (contact urticaria/nettle rash and angioedema).
If you work somewhere with an allergy risk (see pp. 133-4), be vigilant for such symptoms and see your doctor immediately. These symptoms can be the forerunners of occupational asthma, which is a serious and potentially irreversible problem. Some allergens, such as latex, can even produce anaphylactic shock (a life-threatening allergic collapse).
Skin-prick tests (see p. 91) can show if you have an allergy to a substance encountered at work.
Acting promptly gives you the best possible chance of recovery and is vital if you have occupational asthma. Only if exposure to the allergen stops promptly do you have a good chance of shaking off the asthma. See your doctor as soon as possible and ask for a referral to a chest specialist, so that a definite diagnosis can be made. This is essential if you are going to make a claim for compensation.
Far too many people with occupational asthma are just sent off with an inhaler when they first see their doctor. By delaying the moment when work is identified as the source of the problem, and the exposure to the allergen is stopped, drug treatment can turn occupational asthma into a disabling lifelong problem. Although drugs can be helpful in speeding your recovery once exposure to the allergen
Latex allergy
Sensitisation to latex usually occurs at work (see pp. 133-4), or as a result of having many surgical operations. But latex allergy sometimes occurs in allergy-prone people even though they don’t work in a high-risk job and haven’t had many operations. Some doctors think that if a child with severe allergies needs surgery, this should be done in latex-free conditions, even though the child has no allergy to latex, because of the risk that the operation will sensitise.
Latex can cause either contact dermatitis (see p. 55) or a Type I allergy, whose symptoms can include urticaria, asthma and anaphylaxis. Latex allergy often goes undiagnosed. Once sensitised, you may react to balloons, elastic bands, condoms and household gloves. Latex in the air,
due to powdered latex gloves being used, can be a hazard for someone who is highly sensitive, as can latex traces in food (see box on p. 175). Medical treatment may be problematic (see p. 98 and box on p. 249). Cross-reactions to certain foods can occur (see p. 15 and p. 51).
For those avoiding latex, there are non-latex gloves (see p. 57), and non-latex condoms. Immunotherapy (see pp. 164-9) may be useful in severe cases: it can reduce sensitivity and eliminate cross-reactions to foods.
Other hazards
This article (pp. 132-5) deals mainly with allergens at work, that is, substances which provoke classical allergies (Type I reactions). In addition, there are skin irritants and antigens in workplaces which can provoke contact dermatitis (see p. 56) or contact urticaria (see p.50).
Some of the most dangerous workplace substances are those that bring on asthma but are not allergens. These are usually called low-molecular-weight asthmagens. The most notorious of these are platinum salts, isocyanates (used in cement, in the manufacture of foam, plastics and varnishes, and for spray-painting cars, aeroplanes and boats), colophony (used as a solder in electronics), glutaraldehyde (used in hospitals for sterilisation procedures), and persulphate (used in hairdressing). Powerful respiratory equipment, supplying air from outside the area (see p. 135) is needed if you work with some of these substances, e.g. isocyanates for spray-painting cars.
has ended, they should not be seen as a way of allowing you to go on working with the offending allergen or asthmagen.
If it seems plausible that your allergies or your asthma are related to your work, your doctor should be able to give you a sickness certificate, so that you can have some time away from the workplace, to see if you recover. The medical service at your workplace may be better at diagnosing occupational asthma than your own doctor, but be cautious. In some workplaces they do operate as they should and offer genuinely confidential treatment. But there have also been cases of information being passed to the management, and workers with the early signs of occupational allergies and/or asthma being dismissed on a pretext, or made redundant, to avoid a possible compensation claim. Most occupational health services claim to be independent, but they actually have to earn the trust of the workforce. Before you make any move, ask your colleagues for their views, especially those who have worked there for many years.
Choosing a job
If you have any tendency to allergies, or come from an allergy-prone family, you should be very choosy about where you work. Try to avoid workplaces where there is heavy exposure to allergens, especially airborne allergens which can provoke asthma:
• Bakeries and flour mills, where the allergens concerned may be wheat proteins in the flour, or enzymes added to the flour mix. These allergies can take years to begin.
• Other food-processing works, particularly those dealing with tea, soyabeans, other beans (e.g. gram flour), shellfish and fish (especially if automated gutting machines are used without adequate ventilation). Food preparation and sandwich-making can cause contact urticaria, if there is prolonged contact with a particular foodstuff (e.g. tomatoes).
• Farms, docks and cotton mills – or any other workplace generating dust from plant products. On farms, it is the dust from grain and hay that is often responsible, although mould spores (see p. 121) can also be the culprit. Allergies to mites (found in hay, grain and flour) sometimes occur and eczema is the most common symptom – often called simply ‘grain itch’.
• Saw mills and joineries, because of the wood dust, especially that from hardwoods and from red cedar (Thuja plicata).
• Paper recycling plants, if there is a lot of paper dust in the air.
• Detergent and pharmaceutical factories handling enzymes – these are added to ‘biological’ washing powders and are potential allergens. The risks are less these days, as the enzymes are in granule form rather than powder.
• Factories processing natural products such as psyllium or ispaghula, which are used as laxatives. Anyone who has been sensitised should avoid taking medicines containing the offending substance in the future, because these can sometimes provoke a dangerous anaphylactic reaction.
• Hospitals, clinics and dental surgeries, mainly due to latex rubber, used in gloves and equipment. Although nursing staff and surgeons are most susceptible, other staff including hospital administrative workers can occasionally be affected. Fears about the spread of the HIV virus has led to a huge increase in the use of latex gloves in medicine and dentistry, and a consequent epidemic of latex allergy. The main problem is with powdered latex gloves, which release 15,000 times as much allergen into the air as unpowdered gloves. Unpowdered, low-allergen gloves greatly reduce the risk of latex allergy developing, and non-latex gloves are even better. There are moves to ban the import of powdered latex gloves into Britain. They are already being phased out in hospitals and other medical facilities, but progress is slow in some areas.
• Other workplaces where powdered latex gloves are used, including
Making the workplace safe for everyone
Note that these choices about employment are for the individual employees to make for their own protection - an employer cannot refuse to take anyone on because they have allergies or come from an atopic (allergy-prone) family.
The reasoning behind this is that the workplace should be safe for everyone, as far as possible. As many as one in three of the population may be susceptible to allergies, and it is clearly wrong to bar all such people from major industries. Current thinking, in most countries, is that the focus should be on getting allergens and asthmagens out of the air, not keeping the more vulnerable workers out of the workplace.
hairdressers, dental surgeries, pathology laboratories and police stations. Construction workers wearing rubber gloves are also at risk. Someone who has been sensitised by powdered latex gloves may then react to other items (see box on p.132). Those severely affected can have great problems in daily life and with medical treatment, so anyone with a strong tendency to allergy should strenuously avoid becoming sensitised.
• Factories making or using rubber items may also expose workers to the risk of latex allergy. Anything made by the ‘dipping method’ (e.g. balloons, condoms, elastic bands and gloves) is highly allergenic. Moulded rubber items, such as tyres, are much less of a problem. Neoprene and other synthetic rubber items are not allergenic.
• Chiropody and podiatry clinics, where there is a risk of allergic reactions to the fungus that causes athlete’s foot. It is inhaled on skin flakes from the patients’ feet.
• Laboratories and other workplaces where animals are kept. In the case of mice, rats and other rodents, the allergen is found in the animals’ urine, and becomes airborne as the urine dries. Insects and spiders (e.g, those reared for biological pest control), are also allergenic due to small airborne particles from their bodies. Those working closely with bees (either honeybees or bumblebees, now reared for pollinating glasshouse crops) are liable to be stung frequently, and this can lead to sting allergy (see pp. 60-61).
• Hairdressing salons, where many different items are used that are potentially allergenic, including latex gloves (see above), permanent-wave solutions and henna. The risks of contact dermatitis are also high (see p. 55).
• Greenhouses, where the enclosed conditions can lead to high levels of allergens from plants, moulds and insect pests. There may also be exposure to pesticide sprays or their residues, which can greatly aggravate any underlying tendency to allergies.
If you have ever suffered from atopic eczema, work situations that can bring on contact dermatitis should also be avoided (see p. 55).
Taking a risky job
If circumstances force you to take a job with an allergy risk, observe all the safety procedures that are in place, and where you have the option of turning on extractor fans, wearing protective gear, or simply opening doors and windows, always do so. If the safety procedures seem inadequate, talk to your trade union Safety Representative, or the local Health and Safety Executive which can run a check on safety procedures in your workplace. This will be presented to the employer as a routine check, so they need never know that a member of the workforce has contacted the HSE.
Whatever you do, if you are in a risky job, don’t smoke. At a salmon processing plant in Scotland, 40% of the smokers developed allergies (resulting in asthma) to the fish allergens in the spray from the fish-gutting machine. Non-smokers - who formed the overwhelming majority of the workers - were not affected at all. In United States cotton mills, smokers are affected by levels of cotton dust in the air that are legally defined as ’safe’, while nonsmokers remain unaffected.
Passive smoking at work is also an important issue. A recent US study showed that non-smokers were more likely to develop asthma if they worked alongside a smoker. Your employer has a duty to provide you with clean air. This includes ensuring that other employees do not impose their cigarette smoke on you.
Respiratory equipment
Where respiratory equipment is needed, your employer must provide this, and it must be the right equipment for the job. It should be inspected, tested, cleaned and repaired after each use, and filters should be replaced regularly. All this is your employer’s responsibility, but check that it is being done, and always look the mask over before you put it on.
Two different types of respiratory equipment are currently in use:
• Those that give you a supply of air from outside the work area, either from a compressed-air cylinder, or via an air-hose (airline) supplied with fresh air. In Britain these are called breathing apparatus.
• Those that use the surrounding air but filter it to remove allergens and asthmagens. In Britain these are called respirators. (In some countries this term describes any kind of respiratory equipment.) Ordinary respirators may pose problems for some asthmatics because they cannot breathe in strongly enough to draw sufficient air through the filter. Powered respirators can be the answer: they have a battery-powered unit to help with pulling in the air.
There are government regulations concerning the type of equipment required for each type of allergen and asthmagen. Large companies generally follow these regulations, but small businesses, such as local sawmills, joineries and car-repainting workshops, may not even know about them.
Any respiratory equipment that has a face mask must form a tight seal with your face. Facial hair will prevent this, and so will stubble, so shave carefully. Faces vary enormously in shape, and if your face mask does not fit, ask for a different type of mask or a different type of respiratory equipment. Persist until you get one that’s right for you.
Carry out a ‘fit check’ each and every time you wear the mask. For example, with respirators, you can check the fit by covering the air intake completely with your hand and breathing in sharply: if the mask fits properly, it should collapse onto your face, and remain stuck to your face for several seconds. Look at the manufacturer’s instruction booklet as there may be a specific fit check recommended for the equipment you are using.
If there is any difficulty in breathing through the respiratory equipment, the replaceable filter cartridge or the equipment itself should be replaced. You should also take action immediately if you can smell the substance being handled – but never rely on this as a danger sign, because an extremely small amount, way beyond the detection capacity of the human nose, may be very damaging indeed to your health.
Keep your mask on throughout the work period. If you find this impossible, talk to your employer or
line manager about getting a different kind of respiratory equipment – a powered device, for example, that assists the inflow of air.
No form of respiratory equipment provides complete protection against allergens and asthmagens: there is always the chance of some small amount getting through. This is why respiratory equipment should not be used by those who have already developed occupational asthma but want to stay in their job.
Those who really cannot change jobs (e.g, farmers) are sometimes able to use a powered respirator helmet, which allows them to go on working despite the allergen. But this is not an ideal solution from a purely health point of view. Farmers can also improve matters, where moulds are the source of allergens, by keeping all harvested crops dry and thoroughly ventilated.
A lasting problem
As long as you catch the problem early, and are no longer anywhere near the allergen, your symptoms should disappear completely, but remember that you may still be highly sensitive to the allergen, even years afterwards. For a year or two at least, avoid contact with it again, even in tiny amounts. If someone else in your family works at the same place, they may bring home traces of the allergen on their clothes and hair: ask them to leave their workclothes outside the house and shower on arriving home.
With occupational allergies to airborne food particles, it is possible that the affected individual will later react to the same food when eaten. Experiment very cautiously, especially if the allergen is fish or shellfish.
The allergy may persist long after the job has ended. In one case, doctors found that a woman who had developed ‘baker’s asthma’, while working briefly in a bakery when young, was still allergic to the enzyme additive in bread 20 years later. She suffered an asthma attack whenever she ate bread.

Many countries have special schools for children with severe asthma and other allergies. Italian children are sent to one in the Italian Alps, where there is no trace of pollen, house-dust mite, or animal allergens. After nine months these children are a great deal healthier and more active - all their lung function tests are vastly improved. Blood tests show that they are actually less allergic to common allergens than before.
You may not be able to do quite this well at home, but all allergens and irritants can be avoided to some extent. Even if you can’t eliminate them completely, you can certainly reduce your exposure.
Before you start, it is important to be clear about exactly what affects you, otherwise you will be wasting a lot of effort. For example, people who are allergic to dust mite often think that a dusty house will necessarily be worse for them than an apparently clean house, but this is not so (see p. 115). Or they may say ‘Oh, I got asthma on holiday, because the roads were so dusty and I’m allergic to dust,’ forgetting that only house dust contains dust mites. The road dust may have acted as an irritant, and helped to spark the asthma attacks, or it may have contained pollen or mould spores - but it does not contain dust mites or their allergens. Blaming the wrong thing for the asthma attack means that the real culprit is not identified.
If you are not absolutely sure what causes your allergies, skin-prick tests (see p. 91) can identify the allergen. These are especially recommended if your reactions to the presumed allergen are inconsistent, or you don’t respond to the anti-allergen programmes described here. For example, a few people who react to house dust are not allergic to dust mites, but to something else in the dust such as wool fibres or mould spores, or particles from cockroaches, house
flies, carpet beetles or a long-departed cat. Even pollen that has accumulated in house dust can provoke allergic reactions - if you are not an over-keen duster, it can still be there long after the pollen season.
If you have hayfever, knowing which pollens cause your symptoms (and learning to recognise the plants concerned) is useful. You will probably need skin-prick tests to be sure. ‘Hayfever’ can even be a seasonal mould allergy in some people (see p. 27).
Tackling allergens is now big business. There are a lot of people out there competing for your money and false claims are common, especially for anti-mite products. Only a few manufacturers are deliberately misleading, and most false claims probably stem from ignorance or wishful thinking, but be very sure you know the facts about your allergen before you buy.
Air cleaners are a good example. A really good quality air cleaner (which uses a HEPA filter - a High Efficiency Particulate Air filter) is an expensive purchase and, as the advertising tells you, it takes out very small particles with staggering efficiency. But this is entirely irrelevant if the source of those particles is no distance at all from your nose - your mite-infested pillow, for example, or the cat on your lap.
Something else that advertisements for air cleaners rarely mention is that unless you reduce allergen production - tackling mould growth in the house, for example, or keeping the dog outside - the filter can’t help much. In short, air cleaners do have their uses for some allergens, but they can’t work miracles.
The products mentioned here, if not available in your locality, can be bought mail-order from specialist suppliers of anti-allergy products (see p. 255). Note that some offer both very good products and distinctly doubtful products, so judge each item on its individual merits. Ask to see scientific evidence that it works.
Don’t be taken in by vague statements such as anti-allergenic’ - get the facts. This label is often used on pillows with synthetic filling, for example, and people assume that it refers to dust-mite allergy, whereas it simply means that the pillow does not contain feathers. But unless you are allergic to feathers, there is no reason to avoid feather pillows. (In fact, if not covered with mite-proof covers, synthetic pillows collect more dust-mites than feather pillows, because the fabric used for the cover is less tightly woven and the mites and skin particles get in more easily.)
Bad advice is also a hazard. Some of it just wastes your time and effort, but some could actually increase your exposure to the allergen. Advice to vacuum floors daily, or to vacuum beds, is commonplace but this achieves little and it means breathing much more allergen unless you have the right kind of vacuum cleaner. One health magazine even advised its readers with dust-mite allergy to ‘air mattresses by regularly turning them’. This will not affect mite numbers at all, but it will shoot massive amounts of mite allergen out of the mattress and into the nose and lungs.
Ridding your house of allergens and irritants is, in itself, a hazardous procedure because more of the offending substances will be released into the air during the work. If you take up carpets or remove mattresses, dust-mite allergens and mould spores will be churned up in their millions. Just bundling up a duvet will produce invisible clouds of dust mite allergen - and cat allergen, if your pet once slept on the bed.
Ideally, the allergic individual should not do the work, nor be in the house until it is 100% complete and the house has been very thoroughly aired. This is particularly important for those with chronic sinusitis and mould growth in the house, because of the risk of fungal infections in the sinuses (see p. 32).
If you are an allergy sufferer and have absolutely no choice but to do the work yourself, or to be present, then you should get a good quality dust mask and wear it throughout - only take it off when you go outdoors. Those with atopic eczema and sensitivity to airborne allergens should cover their skin carefully -with clothing, not barrier cream.
An ordinary hardware-shop dust mask is not adequate for most allergens - it only takes out really big particles and lets through all the common airborne allergens except pollen. You need a more serious sort of mask, designed for workplace use and conforming to official standards. Before buying one, ask what is the smallest size of particle that it filters out (at 90% efficiency, or better). Compare this with the particle size of your allergen (given in the articles that follow).
You must be able to breathe well through the mask when physically active, and it must fit tightly against your face, forming a seal at all edges. Beards and moustaches tend to prevent this - as does stubble.
Masks that combine an activated carbon filter with a dust filter will take out gases and chemical vapours as well as particles. Cycle shops now sell such masks -or try an industrial supplier. Such a mask can be useful if you are affected by traffic exhaust or industrial pollution as well as an allergen, for example, or if you are exposed temporarily to wet paint or other fumes at home. Activated carbon masks should also filter out the irritant substances from oil-seed rape plants.
Some people who try the anti-allergen programmes feel much better quite fast. But generally these are long-term strategies - you may not reap any benefits for a few weeks, and the improvement may be small at first. Sometimes it takes several months for the full effects to be felt, so be persistent.

Skin-prick tests
This is an indirect method of detecting true allergic reactions. It is one of a family of skin tests that use a similar approach. The three different tests in this family are known as: skin-prick tests or prick tests, puncture tests, and scratch tests.
For the skin-prick test - the technique used in Britain - a small drop of liquid containing an allergen, such as grass pollen, is placed on the arm. The doctor makes a small prick in the skin, under the drop of liquid, allowing a minuscule amount of the allergen to get into the skin. A positive reaction is recorded if a red bump develops soon afterwards. For accuracy, the bump must be compared to positive and negative controls (see below).
The puncture method is very similar to the skin-prick test but uses a slightly different technique for breaking the skin. The term prick-puncture test covers both techniques.
With the scratch method, the skin is scratched lightly, and the allergen solution is then applied over the scratch. This method gives less consistent results than prick-puncture testing.
It is important to include a negative control in the test - a skin-prick test with plain salt water (saline). This should not produce much of a bump - if it does, the skin is clearly over-reactive and the tests more difficult to assess. The doctor should also include a positive control - a skin-prick test with histamine, the substance that plays a central role in allergic reactions. This should always produce a bump. If it does not, the skin is decidedly under-reactive, and the tests are invalid.
Taking antihistamines will make the skin under-reactive, and you should stop taking them before the testing, for a period ranging from a day to several weeks - it varies depending on the particular antihistamine. Ask your doctor for specific instructions about stopping these and other drugs before testing.
Skin tends to be over-reactive to testing in people with dermatographism (see p. 52). Blood tests for specific IgE,
such as RASTs (see p. 92), are needed for anyone who has this condition. Eczema sufferers with a rash over large areas of the body may also require blood tests, if there is too little clear skin for testing.
Skin-prick tests can produce both false positives and false negatives (see box below). Some allergic diseases will give a lot of false negatives and relatively few false positives, while for others the reverse is true. The allergen itself influences the rates of misleading reactions: for example, tests for soya allergy are notoriously unreliable, whereas those for peanut are far more accurate. The age of the person being tested also makes a difference. With all these influences at work, interpreting the test responses is a real art, and the doctor’s experience counts for a lot.
All sorts of people offer skin-prick tests, including alternative practitioners. Get them done by a qualified doctor, preferably by an allergist, who will know how to make sense of the reactions.
Note that the purpose of these tests, and of blood tests for specific IgE, is to identify the allergens that are bringing on your symptoms, not to predict how strongly you will react to those allergens. The tests may give some indication of the intensity of your reaction, but they cannot be regarded as a good guide to how you will respond to the allergen in the future.
The safety record of skin-prick tests is very good. Occasionally a systemic reaction (anaphylaxis) occurs with these tests, but there are no records of any deaths. Nevertheless, if you suffer from severe asthma or have experienced anaphylactic shock in the past, it is advisable for the doctor to have adrenaline and resuscitation equipment available. Those with strong allergic reactions to latex may also react badly if they are tested with an allergen that cross-reacts with latex (e.g. cypress pollen), not just when tested with latex itself. Taking beta-Mockers (see box on p. 150) increases the risk of a life-threatening reaction for anyone in these higher-risk categories.
False positives and false negatives
Apart from challenge tests, none of the tests used for allergy works with 100% accuracy. Most give both false positives and false negatives.
A false positive means that there is a positive test but no actual reaction when the allergen is encountered (e.g. eaten or inhaled). A false negative means that there is a negative test result despite a genuine reaction (as shown by a challenge test, for example).
A test that gives relatively few false positives has good positive predictive value - in other words, if it suggests you are allergic to something, you probably are.
A test that gives relatively few false negatives has good negative predictive value. If it comes up negative, you are probably not allergic to that allergen.
Some tests for allergic reactions show good positive predictive value but poor negative predictive value, while for other tests the reverse is true.
Fresh is best
The fruit and vegetable allergens that provoke Oral Allergy Syndrome (see p. 63) are chemically unstable, so commercially produced extracts for skin-prick testing quickly lose their potency and give false-negative results. Most allergists now favour using a drop of fresh juice from the fruit or vegetable concerned.
Intradermal tests
These tests (also called ‘intracutaneous tests’) put allergen more deeply into the skin than prick-puncture tests. The skin tends to react more when penetrated to this depth, so there are more false positives. There is also a greater risk of a serious reaction which may require emergency resuscitation. Don’t undergo these tests if you are taking beta-Mockers (see box on p. 150).
Blood tests for IgE
There are blood tests that look at the total amount of IgE (the allergy antibody), which is sometimes useful in diagnosis. But more important are blood tests for specific IgE – against egg or grass pollen or latex, for example. There are different ways of measuring the IgE in the blood, the most commonly used being a radio-allergosorbent test or RAST.
Research shows that RASTs are no more accurate than skin-prick tests in confirming real-life allergic reactions. However, they are useful for patients who can’t discontinue their antihistamines without developing severe symptoms, and for those with dermatographism or very severe eczema (see p. 91).
Patch tests
These tests, used primarily for contact dermatitis, are similar to straightforward challenge tests, because the suspect substances are applied directly to the skin.
The test substances are placed on the skin – usually on your back – in small chambers. They are held in place with sticky tape, and left there for several days. Ideally, the reaction of the skin should be checked three times: after two days, again the next day, and again the day after that. It really is worth going back for all these separate visits, because the accuracy of the test increases greatly with repeated checking.
The substances chosen for testing are a standard set of antigens that most commonly cause contact dermatitis. This standard set will pick up 60-80% of all sensitivity reactions in contact dermatitis. If you have substances that you suspect may be causing symptoms, such as cosmetics, the doctor can usually test for these too.
You should not be tested while you still have a rash, as the testing will probably make the existing rash flare up, even though the test patches are applied well away from the rash.
Use of steroid creams and any light treatments (including exposure of the test area to ordinary sunlight) must stop at least a week before testing starts, or the results will not be accurate.
Interpreting patch tests requires a huge amount of skill, plus extensive knowledge of the finicky details of the different test substances. You need a dermatologist with considerable experience in this area.
False positives (see box on p. 91) can occur, especially if you react very strongly to one of the substances tested – some people develop what dermatologists call an ‘angry back’, and this generates false positives to various other substances being tested at the same time. Should you be told that you are sensitive to a great many different things, you may want to query this reading of the test. Ernest N. Charlesworth, an allergist and dermatologist at the University of Texas, describes patients who ‘develop into environmental cripples’ after being told that they are definitely sensitive to multiple antigens, on the basis of misinterpreted false-positive patch tests.
False negatives (see box on p. 91) are also possible, even with very careful testing. Should this occur, a type of challenge test known as a ROAT (Repeat Open Application Test) is possible. The suspect substance is applied to the inner fold of the elbow twice a day for a week. Get your doctor’s agreement before trying this test.
Endoscopy and biopsy
Miniaturised cameras and sophisticated fibre-optics have allowed modern doctors to do something that their predecessors could never have imagined possible – look right inside the human body. This procedure is called endoscopy, and it has a useful role in a few sensitivity reactions.
Looking inside the sinus cavities can assist in understanding exactly what is going wrong in chronic sinusitis. Inspecting the digestive tract can be valuable in several of the non-IgE immune reactions to food, such as coeliac disease (see p. 70) and eosinophilic gastroenteritis (see p. 72).
A biopsy is often carried out at the same time as endoscopy.
s involves taking a small sample from the affected area, such as
I ning of the gut, and studying it in detail under a microscope.
One purpose of a gut biopsy is to look for characteristic :goes of damage to the lining of the gut – such as the distinctive charges produced by untreated coeliac disease. A biopsy can also reveal what kind of immune cells are present. Abnormal numbers of certain immune cells, for example, eosinophils (see p 19), may suggest a particular diagnosis.
Another way of looking at what kind of immune reactions are going on, used for lung diseases, is a bronchoalveolar lavage – iterally a ‘washing out’ of the airways and lungs, allowing immune cells to be collected and studied. This diagnostic technique is lased for Heiner’s Syndrome (see p. 72).
Tests for food intolerance
The only really effective way of testing for food intolerance is an el ruination diet (see pp. 194-7). This is the gold standard. However, it is neither easy nor quick – which has led to a constant search for alternative tests.
The proposed alternatives are all indirect tests, that is to say, non-dietary. The results of the tests are used as a basis for an avoidance diet. In other words, the foods that give a positive test result are avoided.
Some of these tests use samples of hair or blood, others use pulse testing, pendulums, or muscle strength tests (’applied kinesiology’). A few of these tests do show some promise. Pulse tests, and a blood test called the ‘lymphocyte transformation test’. for example, can give a general indication of sensitivity reactions – sometimes. However, even in the most expert hands, these do not give a result that is accurate enough to be useful.
Of the other tests that are available, most have not been evaluated at all objectively.
Many of them are advertised directly to the public, and one of the problems with this approach is that the testing company starts by assuming that food is the problem. The same is usually true of ‘dietary therapists’ and others in the alternative health field offering tests of this kind.
Almost everyone who undertakes such tests is given a fairly long list of foods which have come up positive in the tests. This does not fit with the evidence from medical trials in which a group of people with irritable bowel or migraine (typical food intolerance symptoms) undertake an elimination diet. A significant proportion of them always find that they do not have food intolerance. Of the rest. many find that they react to one or two foods only. The long lists of foods produced by the commercial tests are, to put it mildly, implausible.
With tests that require a sample of blood, sending off two blood samples from the same person, under different names, is a simple way of assessing the tests’ validity. This exercise has been tried several times with different testing companies, and every time two completely different lists of foods have been sent back.
Covert studies of this kind have also shown that the tests overlook genuine reactions. In one alarming case, a woman with a true allergy to peanuts was assured by a ‘dietary therapist’ that she really could eat peanuts safely.
Many people with food intolerance will tell you that they did well after following a diet based on such tests – and they may well have done. Given that common foods such as wheat and milk are regular offenders in food intolerance, and that these foods very frequently feature on the lists of positive test results generated by commercial testing companies, quite a few people should do well. The problem is that these people may also be avoiding many other foods quite unnecessarily.
Furthermore, if people have sensitivities to some other foods that are not on the list, they will be missing out. They could enjoy a far better level of health if all the foods causing symptoms were Identified and removed from their diet.
In the end, an elimination diet is both cheaper and far more likely to give the right answers.
Testing for IgG antibodies
In diagnosing food intolerance, a few doctors offer tests for a type of antibody called IgG. This antibody is formed to any food molecules that get Into the bloodstream after a meal – and some do, even in entirely healthy people. So finding IgG antibodies to food molecules is not indicative of any disease at all. It occurs in everyone and is perfectly normal.
Nevertheless, some doctors feel that by measuring the level of IgG antibodies to foods, they can get a general idea of the permeability of the gut wall (which might possibly be true) and of particular foods that could be causing intolerance reactions (very doubtful – the tests just tell you what you eat most, and you know that already).
This test does measure something real, unlike some of the alternative tests for food intolerance. But the relevance of what it measures to the health of the individual concerned is partial and indefinite. A recent study of IgG testing for irritable bowel syndrome has confirmed this view.
In short, blood tests for IgG antibodies to food molecules seem like very poor value for money, and potentially misleading, whereas an elimination diet is a far more precise way of pinpointing food intolerances.

Tony had suffered from hayfever since childhood but rarely took any medicines. Outside the grass-pollen season, he was fine, free of allergies and very fit. Then, when he was 35 he bought a run-down cottage in the country. The cottage was very damp and dirty.
The previous owner of the cottage, an elderly man, had died, and everything was much as he had left it. Tony moved in with his wife in late summer, and they began pulling out all the old carpets and furniture. Many of the windows would not open and there were dank musty cupboards and attics to be cleared. Dust filled the air – and Tony’s nose. He began to sneeze a little and within a few days he had a strange and unfamiliar feeling of tightness in his chest. During the following weeks, harvesting began in the surrounding fields, with several huge combine-harvesters working away all day and night. Tony noticed that, when out of doors, his eyes began to stream and the tightness in his chest became more noticeable. A few more days passed, and Tony found it harder to breathe, so he reluctantly went to see the doctor. The diagnosis was asthma. Skin-prick tests showed that Tony had allergic reactions to house-dust mite and moulds.
Tony’s case shows how someone who is already sensitised to an allergen – pollen in this case – may be vulnerable to developing new sensitivities, and new symptoms. It was almost certainly the dust mite and mould spores in the cottage that sparked off the trouble, followed by the mould spores from the cereal leaves, dispersed during harvesting.
For people with a tendency to allergies, the dangers of heavy exposure to potential allergens are something to bear in mind. It is surprising how many people with asthma had their first major attack while away from home, sleeping on an old sofa or in a friend’s dusty spare room. The dose of dust-mite allergen that you get from an ancient mattress or eiderdown can be massive.
Managing your allergy symptoms
As well as avoiding the development of new allergies, you need to manage your existing symptoms, and make sure that they interfere with your life as little as possible. For this you need good information and advice, support from your doctor, optimal drug treatment, and careful avoidance of your allergens.
Quite often people have all the information and drug treatment they need, but they still don’t stay on top of their health problems. There can be two distinct reasons for this: either they are not wholehearted about wanting to be well (ambivalence) – or they have never really accepted that they are ill (denial).
Ambivalence
Sometimes being ill has certain benefits – or being entirely well has certain disadvantages. Our state of health determines how people treat us, especially within the family, and the expectations people have of us. It may be comforting to be ill because others are more supportive then, or it may be less risky, because we are not forced to try things (such as sports or other physical activities) at which we might fail or look foolish. Being ill as a child often sets up a pattern for how we interact with the world, which revolves around caution, the comforts of familiarity, and holding back from new situations.
These habitual patterns can survive in the mind long after any real advantages have evaporated. Many people become stuck with a way of thinking and living where ill-health is a cornerstone of their existence. Doctors at the Chelsea and Westminster Hospital in London, who have developed a radical programme for treating atopic eczema (see pp. 46-8), have noticed this in their patients. ‘Old habits die hard and living with a little bit of eczema is a very tempting prospect for many patients, rather than clearing the skin completely…. As atopic skin disease begins for many in the first year of life, causing sometimes understandable alarm and despondency in the parents, the child learns how relevant their condition can be in their relationship with the external world, and with their parents in particular. Before they are able to speak, they have a powerful means of gaining parental attention which can have long-standing effects in the development of their personality. For some, to live without eczema is understandably a daunting prospect. This can be consciously appreciated and spontaneous-y referred to by some patients, while for others the issue will be buried from view, deep in their unconscious.’
If any of this rings bells with you, try to tackle the problem at source. Such mental blocks are not immovable. Indeed, simply recognising that the block is there can start to change things for some people.
Others may need professional help to overcome these longstanding habits of mind. Counselling or cognitive therapy can be very valuable, and your doctor may be able to help in locating a suitably qualified person for this.
Denial
At the opposite end of the spectrum are those who want to deny that they have any kind of health problem. Often these people cannot quite accept that they have a long-term disease, such as eczema or asthma, so they forget to take their drugs, apply creams to their skin, or carry their inhalers. Ironically, these people frequently wind up having far more trouble with their allergies than they need to, and a very poor quality of life, simply because they neglect preventive treatments.
To be really well, you first have to admit that you do have allergies, and then sort out your conflicting feelings about what this means. Again, counselling, cognitive therapy or some other kind of psychotherapy can be helpful.
Dealing with doctors
The decisions that your doctor makes about your treatment are ones in which you should be fully involved. Quite a few allergy patients don’t feel happy about their doctor’s treatment plan, but they never say so to the doctor’s face.
The usual pattern is to accept what the doctor prescribes without any argument, but then halve the dose of tablets, or only put the cream on once a day instead of twice, or not use the Inhaler at all. Some people stop and start their drugs in a random way because they never quite make up their minds about whether drugs are a good thing or not.
This approach to allergies invariably leads to worsening symptoms. The risks are greatest with complex problems such as
atopic eczema or chronic sinusitis, where a vicious circle can easily be set up if the disease is not brought under control, and for those with a life-threatening condition such as asthma. In the case of asthma, neglecting preventative treatment can be fatal.
It is far better to say what you think in the surgery, and discuss any misgivings you may have about drugs with the doctor. That way you can agree on a treatment regime that you are prepared to stick to – which may or may not involve drugs. Most doctors would far prefer a little plain speaking at the outset to having a patient who is half-hearted about following the treatment plan and never really improves.
A more serious form of communication breakdown occurs when a doctor stops believing what a particular patient says. This usually occurs because the doctor has decided that some or all of a patient’s symptoms are due to psychological rather than physical causes. (This is far more likely to happen to those with intolerance or unusual forms of allergic reaction than to those with classical allergic diseases.) Sometimes doctors say what they think, but often they don’t – they just start treating the symptoms in a different way, or acting impatiently, or saying rather puzzling things that leave the patient trying to guess what is going on.
If you find yourself in such a situation, the main thing to do is stay very calm and be very rational. Getting upset, or challenging the doctor’s opinion in a manner that seems at all aggressive, instantly confirms the ‘psychological’ diagnosis. Unfortunately, insisting firmly that the symptoms are not psychological also confirms the diagnosis as far as many doctors are concerned (see p. 237) which can be extremely frustrating. To begin with, deal with the situation by informing yourself about your illness. Be tactful and patient but persistent with the doctor, trying all the time to keep the relationship pleasant and the channels of communication open. If, after giving it a fair try for some weeks or months, this approach isn’t working, you should look into the possibility of changing doctors (see p. 88).
Emergency alerts
An emergency alert bracelet or pendant should be worn by anyone who:
• is allergic to latex rubber, or to drugs such as penicillin
• has a severe allergy to insect stings
• suffers from exercise-induced anaphylaxis, or anaphylactic shock as a result of food allergy
• has very severe asthma attacks.
Key information is engraved on the bracelet, along with a telephone number which gives medical staff access to a computer database containing vital medical data about you. This valuable service is provided by a non-profit-making company called Medic Alert.
As everyone knows, a little knowledge is a dangerous thing. You can use the information in this book to help yourself, but it’s important to remember that there is no substitute for the comprehensive understanding of the human body that your doctor gained during many long years at medical school. Always check with your doctor before changing your diet, stopping your drugs, practising breathing exercises, taking a non-prescription medicine or trying any other experimental treatment.
The information about disease, diagnosis and treatment in this book falls into four categories:
• basic information about the disease that no doctor would disagree with
• the findings of new research, or research that has not become widely known, but which falls within the accepted medical model of the disease concerned. Your doctor may not know about some of this research (there is a terrifying amount of new information bombarding doctors every week, and no one can keep up with it all) but he or she won’t find it unbelievable.
• evidence from research that is entirely valid, but which is widely ignored or dismissed because it falls outside the accepted medical model of the disease concerned (see pp. 86-7)
• information based on the repeated observations of doctors, or of patients – this does not amount to scientifically valid evidence, but it’s included here if it seems plausible and if it could be useful to some readers.
You should be able to tell, from the context in which it is presented, which category any item of information falls into. When talking to your doctor about items that belong in the last two categories above, be prepared for a certain amount of scepticism or possibly outright dismissal.
The important thing to ask the doctor is if there is good reason why you should not try the suggested measures, in addition to your usual treatment – is there any risk involved, given your particular state of health? Make it clear that you want to try the additional treatment with an open mind and will drop it if it is not helping. Ask for the doctor’s help in assessing the effects of the treatment objectively.
Managing asthma
Of all the diseases described in this book, asthma is among the most difficult to live with, especially severe asthma. Learn to recognise asthma symptoms before they get out of hand, and take immediate action.
Studies of patients who die from asthma attacks find that the deaths could, in almost all cases, have been prevented. Factors contributing to fatal attacks include:
• heavy exposure to allergens just before the asthma attack
• cigarette smoking
• failure to use preventer drugs
• repeat prescriptions for inhalers being given without the patient seeing a doctor
• delays in seeing an asthma specialist
• depression in the asthmatic leading to neglect of treatment.
For the day-to-day management of asthma, you should have a written management plan prepared by your doctor or asthma nurse.
This should tell you how often to take your drugs under normal circumstances, and what to do if your symptoms change or you develop a cold or chest infection. The actual brand names of your drugs (or the colour of the inhaler) should be included on the management plan. Assuming you have a peak-flow meter – and you really should have one –specific peak-flow values should be included on your management plan, with instructions for how to respond if your peak flow falls to these levels.
Your plan should tell you how to recognise a severe attack coming on, and what to do at the various stages of the attack. (This personal management plan is specifically geared to you or your child. Although pp. 100-101 give generalised advice, your own plan is invaluable.)
Be sure that you know exactly how the advice in the plan relates to the sort of real-life situations you experience. No matter how good your plan, real life can sometimes be far more complex than anyone anticipates, so there may be times when it is difficult to know what to do. When this occurs, make a note of the situation, and the reasons why you are unsure how to implement the plan. Call your doctor immediately if your asthma is getting worse, and get the asthma attack under control. Save your notes and, at the next opportunity, check with the doctor what you should have done in those circumstances. This will help you to build up your detailed knowledge of how to manage your asthma, or that of your child.
Research shows that asthmatics can, with training, develop a greater awareness of how narrow their airways are – this helps you to detect worsening asthma before things get too serious. You can train yourself in this art by guessing what your peak flow will be and writing your guess down before you use your peak-flow meter (see right) each day. Over a period of weeks, you should find your guesses getting closer to the true value.
A key part of asthma control is having everything with you that you need in case of an attack. It’s tedious, but you have to do it. You should take your reliever inhaler with you wherever you go. Those with severe asthma can also benefit from carrying a collapsible spacer (ask your pharmacist or see p. 255 for contact details of suppliers).
For a long day out, or a stay away from home, check that you also have:
• your management plan
• your peak-flow meter
• your preventer inhaler
• steroid tablets, if you sometimes need these
• your doctor’s phone number.
A little lateral thinking may be needed regarding the problem of carrying all this kit around. One asthmatic friend of mine carries his inhalers in a trendy-looking camera bag that goes everywhere with him. Mothers of asthmatic children have solved the problem by making an ‘inhaler pouch’ from a sunglasses case and attaching it to a favourite belt or by enlarging the pocket in a teenager’s jacket to accommodate inhalers.
Anyone with severe allergies to food or insect stings should take similar steps, so that carrying their auto-injector everywhere is a simple matter.
Peak-flow meters
A peak-flow meter can detect narrowing of your airways – the beginnings of an asthma attack – before there are any obvious symptoms. It measures the maximum speed at which you can force air out of your lungs. The signs of worsening asthma include:
• a morning reading which is less than 75% of the evening reading
• average readings less than 75% of your best-ever reading. (If they get to less than 50% of your best reading, this is a severe and possibly life-threatening attack.)
To use a peak-flow meter:
• push the pointer to zero and hold the meter horizontally
• keep your fingers away from the scale and the pointer
• breathe normally before you start
• stand up and take a deep breath, but don’t puff your cheeks out and don’t hold your breath before you blow
• seal your lips tightly around the mouthpiece
• blow hard into the meter, as if blowing out candles on a birthday cake; don’t move your tongue while doing this
• repeat three times, and record the highest reading of the three.
You must learn how to use a peak-flow meter from your doctor or asthma nurse, who should also check your technique regularly – it is very easy to get into bad habits.

Immune reactions to food
`When I finally found someone who could say what was wrong with me, it was such a relief. I can’t tell you how much ill-health and pain and misery I’d had up to that point. I’m immensely grateful to the doctor who sorted the problem out for me. My life has been transformed.’
Richard has eosinophilic gastroenteritis, one of the rarer immune reactions to food. Like all rare diseases, it can escape diagnosis for a long time. IgE (the allergy antibody – see box on p. 12) is sometimes involved in eosinophilic gastroenteritis, but it is not an essential part of the reaction. Those who, like Richard, do not make IgE antibodies to the problem food will not give positive skin-prick tests. For them, the possibility of food being responsible for their symptoms may well be overlooked*.
Another difficulty for patients such as Richard is that most of the non-IgE immune reactions to food affect babies and children exclusively. A few of them can also occur in adults, but this is very rare, so it’s not something that automatically springs to mind when the doctor is searching for a diagnosis.
Eosinophilic diseases
The key event in these diseases is the arrival of large numbers of immune cells called eosinophils (see p. 19) in the walls of the digestive system. If the eosinophils converge on the tube leading down to the stomach (the oesophagus) the disease is called eosinophilic oesophagitis, and the symptoms include reflux (regurgitation) of food, occasional vomiting, refusing food (in babies), stomach pain and disturbed sleep.
If the stomach is the focus for the eosinophils, this is eosinophilic gastritis, and there is vomiting, pain, poor appetite and therefore poor growth. There can also be obstruction of the stomach outlet which may, in a few babies, produce pyloric stenosis (the main symptom is projectile vomiting).
When eosinophils flock to the intestines as well as to the stomach, the disease is called eosinophilic gastroenteritis. In
terms of symptoms, the picture is not much different from the previous condition, but there can be diarrhoea as an additional symptom, and babies may be irritable and puffy in appearance.
These conditions are most common in babies, but sometimes they continue through childhood. Very occasionally they occur in adults too.
Heiner’s Syndrome
This disease affects babies only, and is very rare. It is a severe form of cow’s milk sensitivity leading to wheezing and haemosiderosis (bleeding into the lungs). The child usually seems sickly, growth is slow, and there may be recurrent bouts of pneumonia. A full diagnosis requires blood tests to check for anaemia, examination of sputum under the microscope, and a biopsy or lavage (see p. 92) from the lung. The only effective treatment is to remove cow’s milk from the diet completely. Needless to say, this must be done under full medical supervision.
Other reactions to food
The cause of these diseases is not fully understood, but the immune system is clearly involved.
Dietary protein entero-colitis syndrome
In babies, the symptoms begin with general irritability and vomiting between one and three hours after a feed. Unless the offending food – usually cow’s milk – is withdrawn promptly, there will be bloating, diarrhoea (usually containing blood), anaemia, and poor growth. Older children have similar symptoms, while adults suffer terrible nausea, plus stomach pains and vomiting.
Nickel in food
Nickel and other metals in food may cause immune reactions for those with sensitivity to such metals (see pp. 55-6). The symptoms are usually in the skin, but there can be a few digestive symptoms too.
Dietary protein enteropathy
The main symptom here is diarrhoea, usually very severe. Often babies vomit their feed as well. Most have little appetite, and if the offending food is not withdrawn they suffer from poor growth, anaemia and other signs of malnutrition. This is because damage to the lining of the gut prevents nutrients from being absorbed properly. Older children show similar symptoms.
Dietary protein proctitis
This is a far less severe problem. The babies with this disorder look healthy, but there is inflammation in the bowel and small amounts of blood are passed with the faeces.
Diagnosis
There are two aspects to diagnosis:
• what kind of disease is it?
• what food or foods are causing the reaction?
Your doctor will probably try to answer the first question by looking inside the digestive tract with special equipment (endoscopy) and by taking a small sample – a biopsy (see p. 92).
A blood sample may also be taken to look for raised levels of immune cells and antibodies. Skin-prick tests or RAST tests (see pp. 91-2) will be tried to rule out the possibility of true food allergy – and because IgE may play a small part in these other forms of food sensitivity (in the eosinophilic diseases, for example).
Often the tests yield no very clear answers, especially in babies, and an exact diagnosis is not possible. But failure to answer the first question does not mean that the second question should be ignored. Pinpointing the culprit food or foods is vital.
Identifying the food is easier the younger the child, simply because the range of foods eaten is so much smaller. Cow’s milk is the most common offender when the disease affects young children – particularly bottle-fed babies, since standard infant formula is made with cow’s milk. Your doctor will prescribe an alternative formula (see box on p. 66) for you to try. For older children and adults, an elimination diet will probably be required to identify the food concerned. Among young children, likely offenders include soya, egg, wheat, rice, chicken or fish. A simple elimination diet, similar to that used for atopic eczema (see p. 198) may be adequate. You must have full medical supervision for this.
In the case of eosinophilic reactions, skin-prick tests may help identify the foods concerned, but are usually of limited value, so an elimination diet is again necessary. Where adults are affected by eosinophilic diseases, sensitivity to several different foods is likely, so identifying the offending foods usually requires the most exacting form of elimination diet, using an elemental diet for the exclusion phase (see box on p. 196). The symptoms are very slow to disappear: it can take up to eight weeks of avoiding the foods before your ailing digestive tract recovers. Don’t give up too soon.
Treatment
Avoidance is the only way here. Special infant formula (see box on p. 66) is required for cow’s milk sensitivity in babies.
In the case of eosinophilic reactions, some doctors may use steroid tablets as an additional treatment, just for a few weeks, to get the inflammation under control. Some new studies show that the anti-leukotriene drugs (see p. 149) are very effective for eosinophilic gastroenteritis.
Controversial topics
According to some doctors, a reaction to food may, on rare occasions, produce vasculitis (inflammation of the blood vessels).
Vasculitis itself is a well-recognised condition. The blood vessels are damaged by inflammation, and become more leaky. Symptoms often begin with a general swelling (angioedema), and an outbreak of small red blotches deep in the skin — especially on the legs — where small amounts of blood have escaped. These blotches later turn purplish, then yellow, before fading. This type of rash is known as purpura. Sometimes there are larger emissions of blood, resulting in spontaneous bruising.
Many different conditions can cause vasculitis, but only a few doctors would agree that food sensitivity is one of them. The inflammation could be caused by circulating immune complexes containing food antigens bound to antibodies (see p. 13). There is evidence, in some patients, of a direct effect on the cells called platelets that cause blood to clot.
Equally controversial is the suggestion that food sensitivity can be the cause of trouble for some children with kidney disorders. Some research groups have found that a few children with certain kinds of kidney disease recover on an elemental diet (see box on p. 196). All those affected have a classical allergic disease such as asthma or atopic eczema as well, and they tend to be sensitive to several different foods, plus pollen or other airborne allergens. Circulating immune complexes might be involved here, but no one is sure.
Some cases of food-related rheumatoid arthritis and palindromic rheumatism (see p. 76) could be due to immune complexes involving food molecules becoming deposited in the joints, but it is not the mechanism in all, or even most, of those affected.

FOOD SENSITIVITY IN ASTHMA, ECZEMA AND OTHER ALLERGIC DISEASES
In 1995, medical researchers in North Carolina, USA, asked over a hundred dermatologists how they treated atopic eczema. All used standard treatments such as moisturisers and steroid creams, but only 14% mentioned the possible role of food to the parents of children with eczema.
Between them, the dermatologists in this study treated about 17,000 children with atopic eczema per year. Using the most widely accepted estimates for food sensitivity in atopic eczema –38% of eczematous children are sensitive to food – one can calculate that there were over 5000 children in this study area who might perhaps have benefited from avoiding a problem food, but whose parents were never told about this treatment option.
North Carolina is by no means unique. The situation is much the same in other parts of the world, which adds up to millions of children and parents not even being told about a treatment that is frequently effective.
Other allergic diseases (see right) can also be triggered by food, although the percentage of patients affected is much lower than for atopic eczema. Here too, many doctors are unaware of (or sceptical about) the possible role of food.
These reactions are best described as ‘food sensitivity’. They cannot be called food allergy (see p. 62) if there are no symptoms in the mouth or gut and if skin-prick tests are negative – as is often the case. Negative skin tests suggest that the reaction is not IgEmediated (see box on p. 12).
However, in some children with atopic eczema. the skin-prick tests to culprit foods are positive. When these foods are eaten after a period of avoidance, such children sometimes suffer an
immediate reaction, with symptoms typical of true food allergy. For these individuals, their atopic eczema seems to be a symptom of IgE-mediated food allergy.
How can an atopic eczema reaction in response to food be IgE-mediated in one individual and not in another? Research is finally beginning to answer this question (see pp. 18-19).
The allergic conditions that may sometimes be induced, or simply aggravated, by a non-immediate reaction to food are:
• atopic eczema (atopic dermatitis)
• asthma
• perennial allergic rhinitis (constantly blocked or runny nose)
• chronic sinusitis
• secretory otitis media (’glue ear’).
In all of these conditions, many other causes exist. Except in the case of eczema, the other causes are far more likely than sensitivity to food. This fact will weigh heavily with your doctor, whose instinct, quite sensibly, is to look for likely causes first.
Taking asthma as an example, food sensitivity is relatively unusual as a primary cause, whereas allergy to airborne items. such as pollen or house-dust mite, is very common. Food probably affects only 8-10% of asthmatics overall, but is much more important for those with brittle asthma (the most severe and unstable form), affecting as many as 60% in a recent study.
The pollen connection
People who suffer from both birch-pollen allergy and atopic eczema may have worsening eczema when they eat certain fruits and vegetables, e.g. apples and carrots. These same foods cause Oral Allergy Syndrome (see box on p. 63) in some with birch-pollen hayfever, but they can aggravate eczema without causing Oral Allergy Syndrome.
Diagnosis
Consider other likely allergens first. Look at p. 28 for the airborne allergens that could play a part in perennial allergic rhinitis, chronic sinusitis, secretory otitis media (’glue ear’), and asthma. Only in the case of children with atopic eczema is food a prime suspect (between 38% and 69% of children with atopic eczema are affected by food), but even here there are a lot of other factors to consider (see pp. 43-4).
If you do decide to investigate the role of food, don’t abandon basic treatments in the meantime. By neglecting these. you could make the whole problem a great deal worse.
There are various clues that food is at fault:
• If you have other symptoms that suggest food intolerance (see p. 76). These problems often seem to go together with food-induced asthma or rhinitis.
• If you have noticed that a particular food makes your symptoms worse. Where there is intolerance to one food, there could well be intolerance to another, which you have not noticed.
• If you have exercise-induced asthma (see p. 41) and sometimes respond severely to exercise but sometimes have little or no reaction. Sensitivity to a food or foods may be instrumental in changing the response to exercise.
• If you have brittle asthma – but you must get your doctor’s consent for an elimination diet. Foods must be tested under medical supervision as severe life- threatening asthmatic reactions can occur on testing.
• If there are also digestive problems such as diarrhoea, vomiting or belching. This is a strong clue in the case of children with atopic eczema. Symptoms such as diarrhoea frequently precede atopic eczema, and it seems likely that a reaction to food in the gut increases the leakiness of the gut wall, allowing more food molecules through to the blood.
• If there is pronounced eczema around the mouth in children (but this can also be due to constant licking),
• For adults with atopic eczema, if there is a persistent rash on the hands, or the lips. Where there is a blistering rash on the hands that erupts at regular intervals, food is often the problem – or it may be metal contaminants of food such as nickel (see pp. 55-6). In general, food sensitivity is rarer among adults with atopic eczema than it is among children.
Skin-prick tests (see p. 91) for commonly eaten foods are worth
trying in all the diseases – if they give a positive result, they should
be noted, but if they give a negative one, they should be disre-
garded. The many alternative tests being marketed (see p. 93) are
highly inaccurate and unlikely to help.
Research from Tampere University Hospital in Finland suggests that babies are much more likely to give false-negative skin-prick tests for food than older children and adults with atopic eczema. The Finnish researchers found that 52% of babies with atopic eczema give a negative skin-prick test despite having a genuine reaction when tested by food challenge. In an attempt to tackle this problem, they have devised a patch test, similar to those used for contact dermatitis. The patch test, in which food is applied to intact skin and left there for two days, gives false negatives in only 39% of babies.
The best way to detect food-sensitive eczema, according to Dr Erika Isolauri. who heads the Finnish research team, is to use both tests, and take note of a positive reaction to either. This detects 80-90% of eczema-causing food reactions in infants.
Few other doctors are currently using patch tests for atopic eczema; because so much controversy surrounds this topic, and no standardised method has yet been devised. You may be lucky and find a specialist who does these tests.
To confirm the role of particular foods in atopic eczema, a food challenge test is essential, having first avoided the food carefully for two weeks. Great care is needed in testing (see p. 198).
If you cannot get suitable tests done. a simple elimination diet will be needed (see p. 198).
Treatment
There is a choice here, between avoiding the offending food, or eating normally and controlling the symptoms with drugs.
The difficulty comes when parents have to make this decision on behalf of their children. Unfortunately, there is insufficient evidence as regards the consequences of this decision. Treating food sensitivity can reduce the eczema symptoms substantially in the short term, but it does not necessarily improve the long-term prospects for the child. Orthodox doctors tend to think that eating a normal diet is much better for a child nutritionally and socially, and they have a point.
Doctors with a special interest in food sensitivity generally believe that treating the problem at source, rather than just suppressing the symptoms with drugs, must take the pressure off the child’s immune system, and give the child a better chance of growing out of sensitivity reactions in the long run.
The decision is yours – but it is vital that the diet is not more of an encumbrance than the disease itself, and that the child’s interests come first (see pp. 170-71). Whatever you do, don’t allow a child to become malnourished (see p. 198).

Atopic eczema
A Greek word meaning ‘to boil over’ or ‘to erupt’ is the source of the medical term ‘eczema’. It refers, of course, to the way in which the skin erupts into a rash, but it could equally well describe the eruption of controversy around this disease. No other allergic disease is quite such a cauldron of dissent - indeed, even the question of whether it is an allergic disease remains unresolved. These controversies directly affect the treatment of atopic eczema, so it is useful to understand them if you or your child have eczema.
The disagreement begins with the question of what causes atopic eczema.
Let’s start with the one point that everyone agrees on: dry skin plays a fundamental role. Those with atopic eczema have dry skin, not just in the eczematous areas, but in other parts as well, sometimes all over the body. The skin cells are less efficient than normal skin cells at retaining water.
Everyone would also agree that there is inflammation of the skin – a reaction that is produced by the immune system. But when it comes to the question of what starts off the inflammation there are huge differences of opinion among specialists treating atopic eczema – these specialists include dermatologists, allergists and paediatricians.
Since people with atopic eczema are atopic (allergy-prone), and most have
huge amounts of the allergy antibody, IgE, going round in their blood, it might
seem plausible that an allergic reaction to some external item kicks off the
inflammation. And when skin-prick tests (see p. 91) to common allergens such
as house-dust mite are tried, there are usually a large number of positive results.
But many of these turn out to be false positives – when tested more directly,
the allergen concerned does not actually play a part in causing the skin symptoms.
This has led some specialists working with eczema, mainly dermatologists, to
What the words mean
Eczema is not a disease in itself. The word refers to a certain type of reddish rash — a rash which can be caused in a variety of ways. The type of eczema that affects people of an allergic disposition (atopics), is called either atopic eczema or atopic dermatitis.
The word dermatitis just means inflammation of the skin. Most doctors consider it to be synonymous with eczema, but some give it a slightly broader meaning.
believe that allergic reactions play little part in either initiating or perpetuating atopic eczema. In their view, the basic cause of atopic eczema is dry skin and a generally overwrought immune system, not specific allergic reactions.
To some of these doctors, positive skin-prick tests are all false positives in atopic eczema – that is, irrelevant to the disease process. A positive skin-test result, in their opinion, simply indicates that the skin of atopic eczema sufferers is in a highly sensitive state, not that the allergen concerned plays any causative role.
Allergists tend to take a different view of this, as you might expect. And recent research shows that they are correct – allergens often do play a significant part in provoking atopic eczema.
Research using direct challenge tests (see p. 90) has identified some of the things that could provoke such sensitivity reactions:
• house-dust mites, pollen or moulds
• cats, dogs, rabbits and other furry pets
• cow’s milk or other food – a prime suspect in babies and young children (see p. 68). The response to food is usually delayed, occurring some hours after the item is consumed.
With mite, pollen and pet allergens, the eczema symptoms can be provoked either by allergens falling on the skin, or by direct contact (e.g. mite allergens in the bed, skin contact with pets, or lying on grass for those with grass-pollen allergy).
The rash tends to occur on skin not covered by clothes, as you would expect. But it can sometimes occur only on particular exposed areas – usually the most sensitive areas of skin. For example, there are people who react to house-dust mite but have eczema on the eyelids only.
Additionally, experiments show that even when an airborne allergen is only inhaled it can sometimes provoke eczema symptoms. The allergen probably reaches the skin in the bloodstream. (Alternatively, it might provoke an immune reaction in the airways which generates chemical messages of the kind that promote inflammation – these then reach the skin in the blood.) This means that the skin reaction could occur anywhere on the body, not just on exposed skin.
In the case of food, the molecules of food that cause the trouble are probably being absorbed from the stomach without being completely broken down. They then reach the skin via the blood to provoke a reaction there. (Or, again, it could be an inflammatory messenger chemical travelling from the gut to the skin in the blood.)
When food gets directly onto the skin – which it frequently does with small children, of course – it can provoke a reaction that way too. This may be a slow eczema-causing reaction, or a much faster reaction known as contact urticaria (see pp. 50-51). Reacting to food with contact urticaria is quite common in children with atopic eczema – but the same food doesn’t necessarily provoke atopic eczema when it is eaten. (However, eating these foods can sometimes trigger anaphylaxis – see pp. 58-9. They should therefore be treated with great caution.)
At the same time as all this research – which shows for sure that allergens play a part in atopic eczema – others have been asking what actually happens when skin reacts to an allergen. Their studies have turned the accepted understanding of allergies upside-down. They show that when something like egg or pollen provokes atopic eczema, what is occurring isn’t necessarily an allergic reaction of the usual sort, with IgE and mast cells (see
box on p.12). Instead, other immune cells are causing the trouble. Sometimes IgE is involved, but without mast cells. Sometimes neither is involved. These revolutionary discoveries are described in more detail on pp. 18-19. One interesting realisation from this research is that in different eczema sufferers, different immune reactions may be producing the rash – even if they are reacting to the same allergen! This helps to explain why the results of skin tests are so inconsistent and puzzling.
The wandering rash
For a baby with atopic eczema, the face, and especially the cheeks, are commonly affected, but there may be a rash all over the legs, the backs of the arms, and the back. As the months go by, the rash settles on the lower legs, and spreads to the fold of the elbow, and then the fold at the back of the knees — by about three years of age, this flexure eczema is the main problem for most children.
In adults, eczema is often found in quite restricted areas, such as the hands, scalp, lips, eyelids or chest. It may be located around the nipples — a sensitive spot where rubbing by clothing is enough to initiate a rash.
Atopic eczema is always in a process of change, and different parts of the body may display different stages of the rash:
• The rash is red and usually dry at first, and there may be not a great deal to see. In this early stage the visible signs may be minimal, while the itchiness can be colossal. Sometimes there is oozing of clear fluid.
• Occasionally the first phase is more marked, with dense patches of small red bumps or tiny blisters. On the hands, these may merge to form larger blisters.
• Infections tend to change the appearance of the rash (see p. 44).
• With time the skin becomes thicker, paler and scaly. It may form leathery patches (called lichenification), especially if there is habitual scratching or rubbing. This is chronic eczema.
• When the eczema clears, there may be an area of skin that is lighter in colour, or darker, than the surrounding skin.
The next step
Whatever causes atopic eczema, it provokes the most horrendous itching, as every eczema sufferer knows. The itch cries out to be scratched, and scratching is the major cause of the visible rash. If left untouched, the skin does not erupt into eczema, although it may well turn red, and there are still distinct changes in the skin that can be seen with a microscope.
Once eczema has erupted, the skin is no longer an intact protective layer that neatly separates ‘in-here’ from ‘out-there’. The skin becomes more permeable and loses its own natural moisture far more readily, so the dryness gets worse. At the same time allergens and irritants penetrate far more easily, causing yet more inflammation.
Something else compounds the damage: once atopic eczema is established, the immune system starts making IgE antibodies to the body’s own proteins, especially those found in skin cells. This helps explain why atopic eczema can become so severe and so entrenched.
Infections — another vicious circle
When eczema erupts and the skin barrier is breached, infections often become a problem. A regular source of trouble is the bacterium Staphylococcus aureus, a cause of the infection impetigo. This microbe invades eczematous skin far more readily than healthy skin, causing a prolific ooze with golden-yellow crusting.
Staphylococcus aureus produces a toxin known as a ’super-antigen’ which revs up the immune system to even more furious effort. This effort does not, unfortunately, oust the bacteria, but it does make the skin inflammation even worse. To add to their woes, many who are afflicted with atopic eczema start making IgE antibodies against Staphylococcus aureus toxins.
Infection with fungi (yeasts and moulds) is also a problem in atopic eczema (see p. 49), and there may be sensitivity reactions to these fungi.
The herpes virus, responsible for causing cold sores, can also invade eczematous skin, though this is much rarer. It worsens the eczema and produces fever and general weakness. There may also be flocks of small red bumps, each with a tiny dimple or blister at the centre. Any symptoms of this kind indicate that the patient needs urgent treatment.
Irritants and stress
People with atopic eczema are far more susceptible to everyday irritants such as wool and rough synthetic fabrics, soap, and traces of detergent left behind in clothes. Chlorinated water, either in swimming pools or from the tap, can also aggravate the skin, and even ‘hard’ water (found in areas with chalk or limestone bedrock) may be a factor.
Some air pollutants may play a part in atopic eczema. Researchers in Germany have found that children living close to busy trunk roads, or in homes with a gas cooker and no extraction hood (see pp. 128-9), were more likely to develop eczema. Formaldehyde fumes, often found in modern houses (see p. 129), are sometimes a factor when eczema affects the face and hands.

A blocked or runny nose in Allergy
THAT LASTS ALL YEAR
`Everyone has heard of hayfever, but it’s news to most people that you can have this sort of problem all year round,’ complains Elizabeth. ‘Before we got the treatment sorted out, Benny was “the kid with the constant cold”, and I did notice other mothers looking less than enchanted at the prospect of his coming over to play.’
Benny suffers from allergic reactions to house-dust mites and cats which cause hayfever-style symptoms (26) all year round. This condition doesn’t even have a common name – the medical one is perennial allergic rhinitis – yet it is one of the most common allergic diseases.
Any airborne allergen that is found in the air all year round can cause perennial allergic rhinitis:
• House-dust mite is the number one suspect in most parts of the world. Particles from other insects, such as midges and mosquitoes outdoors, and cockroaches, house flies, bloodworms (used for fish food) or carpet beetles indoors, can also cause nasal allergies.
• Mould spores can be the problem: they are found both indoors and out.
• In some regions, certain types of pollen are airborne all year round (27).
• All pets other than fish produce allergenic particles (even snakes).
• Allergens encountered at work (133) can also produce symptoms in the nose. This is a warning sign gn you should not ignore – it often means that occupational asthma is on its way (132).
Occasionally, the offending substance is being eaten not inhaled. This is less common, so you should investigate inhaled allergens first, before trying an elimination diet (29).
Skin-prick tests (91) will help to identify any airborne allergens that are responsible, but where food is the culprit, skin-prick tests are often negative (69)
Triad and NARES
Diagnosis of perennial allergic rhinitis is complicated by the fact that there are two other conditions – called triad and NARES – which produce similar symptoms and involve the immune system but are not, strictly speaking, allergies.
Triad is so called because it involves three distinct symptoms:
• perennial rhinitis
• polyps in the nose – little fleshy growths that can kill your sense of smell
• asthma.
People with triad tend to collect all three symptoms gradually, in no fixed order, over a period of years or even decades. Many are sensitive to aspirin and related drugs, and almost everyone with triad develops this sensitivity eventually.
Aspirin sensitivity can come on very suddenly and produces a reaction akin to anaphylaxis (101). This can be fatal, so it is probably best to avoid all aspirin-like drugs if you have triad, even though you have not reacted to aspirin in the past Aspirin-like drugs are found in painkillers, arthritis drugs and cold remedies – check with a pharmacist before you buy (151).
If you have asthma, think twice about operations on the nose to remove polyps – they can make the asthma much worse.
The initial letters of Non-Allergic Rhinitis with Eosinophilia have been stretched a bit to get NARES. (This is a medical joke –the Latin word Hares means nostrils.) The problem is caused by eosinophils (19), which flock into the nose and cause severe inflammation. Some people with NARES go on to develop triad.
Collateral damage
Having the nose swamped with mucus can lead to knock-on problems in the ears, sinuses and airways.
If the tube that leads from the ear to the nose (the Eustachian tube) becomes blocked, then fluid cannot drain away from the middle ear. This is called secretory otitis media, or glue ear - it dulls the hearing and causes an unpleasant ‘popping’ sensation. The ears may also feel blocked and itchy, but if children have had this problem since they were tiny they may not complain because they assume that’s just the way ears are supposed to feel. Deafness is often the first sign anyone notices.
Sinusitis is another possible complication, because fluid from the sinuses should also drain into the nasal cavity. With the ouflow blocked, mucus builds up in the sinuses and can become infected by bacteria (30).
Post-nasal drip can also occur with perennial allergic rhinitis. The over-abundant mucus runs down the back of the nose, into the throat and then the airways. This produces a persistent phlegmy cough, which may occasionally be mistaken for asthma.
When the rhinitis is treated effectively, all these problems should sort themselves out, although additional treatment is usually necessary in the case of persistent sinusitis (33).
Treatment
Where an allergen such as house-dust mite or mould spores has been identified as the source of the problem, eradicating it from your house (see Chapter 4) will make a huge difference, and may avoid the need for drugs. If the allergen is unavoidable, immunotherapy (see pp. 164-8) or some alternative form of desensitisation (see pp. 210-13) could be very helpful.
Where drugs are needed, nose drops are best. They get the drugs right to the target so doses are minimal, which means very few side effects. The drugs used are:
• cromoglycate to prevent the allergic reaction before it starts (148)
• antihistamines to block the allergic reaction before it produces inflammation (138)
• steroids to calm down inflammation (144). Steroid nose drops are also useful for NARES and triad. If you are taking steroid drops continuously, your doctor should check the membranes inside your nose every six months. Make sure you put the drops in correctly, especially if you have polyps (144).
If you suffer stinging, burning or dryness, it might be due to preservatives in the drops, not the drug itself (see box on p. 33), so talk to your doctor about a different formulation.
Don’t use over-the-counter decongestant drops: they do nothing to treat the allergy or inflammation, and are little more than a ‘chemical crowbar’ to open up the nose. Your nose gets addicted to them in a few days, and when you stop using them you get ‘rebound congestion’ - absolute and total blockage. It does wear off eventually, but is unpleasant meanwhile. If you are suffering this problem at this very moment, don’t put more decongestant drops in - your nose needs to go ‘cold turkey’ to recover, not have its addiction fed!
If none of the anti-allergy drugs work, but decongestant drops do, then you probably have a non-allergic disease called vasomotor rhinitis. The symptoms are very similar to allergic rhinitis, but without the sneezing and itching. See your doctor again, because there is an effective treatment that uses anticholinergic drugs (see box on p. 156). Acupuncture (see below) can also be helpful.
An elimination diet (194) will diagnose any food reactions. It works wonders for some people with severe and unexplained perennial rhinitis, Including people with such a flood of mucus that they can scarcely work or live normally. You should certainly give this diagnostic diet a try if there are clues that suggest food is the culprit (69) or if no airborne allergen can be identified. Yeast - found in bread, beer and B-vitamin tablets -is quite often the culprit in rhinitis, but it could be any food.
Acupuncture is worth trying, to reduce the blockage in the nose and stem the flow of mucus, because the autonomic nervous system (see box on p. 235) plays some part in the symptoms of allergic rhinitis (and is the sole cause of the symptoms for those with vasomotor rhinitis). For those with severe sinusitis, osteopathy can be good for draining mucus from the sinuses.
Very occasionally, psychological or emotional reactions play a part in perennial allergic rhinitis, with symptoms getting significantly worse during stressful events. One possible manifestation of this is post-coital rhinitis, where sex brings on rhinitis (and sometimes asthma as well). In such cases, psychotherapy should be considered. (But check you are not just allergic to the dust mites in your bed first…)
A nose by any other name…
Rhinitis means inflammation (-itis) of the nose (rhin-). The same Greek word gives us rhinoceros - ‘nose-horn’.

`When I first arrived in Charlottesville in 1982, the senior allergist said “I’ve got to warn you that here in Virginia we have patients who have very severe fungal infection of their feet, and they also have urticaria. If you treat their feet, their urticaria gets better.”‘ Professor Tom Platts-Mills of the University of Virginia in Charlottesville is recalling how his innovative studies of fungal infections and allergy began. That surprising observation about athlete’s foot (a fungal infection) and urticaria (nettle rash) was made by his predecessor, Professor John Guerrant,
‘I followed his advice,’ Platts-Mills continues, ‘and found he was right. Then I started noticing asthmatics in our allergy clinic who also had fungal infections of their feet. They were mostly men with severe adult-onset asthma. We gave them skin-prick tests with the fungus Trichophyton and these were positive – showing they had an allergic reaction to it. So we tried treating them with anti-fungal drugs and the asthma got much better.’
This discovery is not an isolated instance. Research over the last decade or so has revealed that allergic reactions to long-standing infections (chronic infection is the medical term) are far more common than anyone expected. Infections by fungi are frequent offenders.
An infection becomes chronic because, although the immune system tries to rout the infectious agent, it never succeeds. Making IgE may be part of that futile defensive effort. Once the immune system starts making IgE against the allergens produced by the infectious microbe, new symptoms may begin, or existing allergic symptoms may get much worse. The link between the infection and the allergy is far from obvious, however. Both the allergens and the IgE can be carried in the
Fungal infections
‘Fungus’ means everything from an edible mushroom or a huge bracket fungus to the specks of mould on stale bread or a shower curtain. Fungal infections are caused, not by mushroom-like fungi, but by inconspicuous mould-like forms, or by yeasts (which are single-celled fungi).
Once they are flourishing, some fungal infections may be seen as whitish or creamy-coloured patches. But at an earlier stage, the fungi are so small that they cannot be seen without a microscope. They spread as invisibly as bacteria or viruses.
Some infectious fungi can exist in two different forms – a mycelial form (long thin strands, as in a mould) or a yeast form (single cells).
bloodstream, so the symptoms may be somewhere else in the body, far away from the site of infection.
If the symptoms of the infection itself are relatively mild, they may not receive medical attention. Infection-plus-allergy often explains severe long-term allergic problems for which no cause could previously be found. This is the kind of case that gets labelled as ‘intrinsic’ or ‘endogenous’, because all the allergy tests have proved negative. Most patients in this category have had years of simply being treated with steroids (often at high doses) to suppress the symptoms.
Sometimes the infection-plus-allergy is part of a larger picture, with other allergens or irritants also contributing to the symptoms, but with no stunning improvements when they are avoided because the allergic stimulus from the infection remains.
The links between allergy and fungal infections – all those that have been discovered so far – are described below. In such cases, anti-fungal drugs, taken by mouth, usually in capsule form, could be of value. However, they must be taken for an adequate length of time, normally several months.
Bear in mind that, with the possible exception of chronic sinusitis, an allergic reaction to fungal infection is a relatively uncommon cause of symptoms. It is important that, with the help of your doctor, you start with the more likely suspects such as airborne or contact allergens. These are described in detail, for each allergic disease, in the relevant sections of Chapter 2.
Asthma
the common causes and usual treatment of asthma.
Trichophyton – the fungus that causes athlete’s foot – can provoke allergic reactions that contribute to asthma, as already described. This fungus may also infect other parts of the body. Trichophyton diseases have names that begin with tinea (athlete’s foot, for example, is tinea pedis). Other terms you may come across are intertrigo (an itchy rash which develops in skin folds) and onychomycosis (also called `ringworm of the nails’ or tinea unguinum). The research on the link with asthma was published in a respected medical journal, The Lancet, but has been widely ignored, so if you think you have this problem, you may have to be quite persistent with your doctor. Very thorough treatment with anti-fungal drugs (swallowed in capsule form) is required.
Chronic urticaria
many possible causes of chronic urticaria.
Trichophyton infections in any part of the body (see above) can provoke allergies, producing chronic urticarla. A great variety of other infections, including fungal, viral and chronic bacterial
infections, can be the root of the problem in chronic urticaria . However, this may not be an allergic reaction. It could be a direct effect of the infection, provoking the immune system in such a way that it triggers mast cells by itself, without IgE.
Chronic sinusitis
 the causes and treatment of chronic sinusitis.
Long-standing (chronic) sinusitis may be due to a fungal infection with a subsequent allergy. This is now called allergic fungal sinusitis. Some doctors believe that a sensitivity reaction to fungal infection (not necessarily an allergic reaction) could account for 96% of chronic sinusitis. However this is widely disputed .
Atopic eczema (atopic dermatitis)
the causes and treatment of atopic eczema.
The Trichophyton fungus can infect eczematous skin, though this is far less common than infection by Staphylococcus aureus (see below). Among patients infected by it, there can be an allergic reaction to Trichophyton which then makes the eczema worse.
There can also be an IgE reaction to a yeast, Pityrosporum ovale (also called Malassezia ovalis), in atopic eczema. This yeast is a commensal – i.e. a natural, and normally harmless, inhabitant of healthy skin. The inflammation of eczema makes the immune system far more tetchy so that it reacts allergically to this yeast, an innocent bystander which it normally disregards.
Candida  can also provoke an allergic reaction in eczematous skin. This is a more complex story, because while Candida is a commensal in the gut, it does not normally live on the skin. However, it may flourish in the disturbed skin of eczema patients.
Those with atopic eczema may also develop an allergic reaction to toxins from Staphylococcus aureus, a bacterium that often infects skin which is inflamed by eczema and damaged by scratching. Antibiotics are needed to treat the infection .
Seborrheic dermatitis
Not so long ago, this disease – which causes a red, scaly rash on the forehead, nose and cheeks, and sometimes on the chest –was labelled ’cause unknown’. Now most doctors believe that the yeast Pityrosporum ovale could well have a role in causing it. This yeast is part of the normal skin flora (see above), but it is found in greater numbers on the skin of seborrheic dermatitis patients. As well as overgrowth of the yeast, there is an immune reaction against it, usually involving the antibody known as IgG, rather than Fungi in the lungs
One form of infection-plus-allergy has been well recognised for many years - allergic bronchopulmonary aspergillosis, often shortened to aspergillosis.
The problem starts with the fungus Aspergillus fumigates, a ubiquitous mould that is found in special abundance in damp straw, compost heaps, bird cages and any decomposing material. Its spores are everywhere, and most immune systems quickly defeat them, but in some people, especially those with asthma, the spores begin to grow in the lungs. The fungus is found in the lung mucus, but does not actually invade the lungs. However, an allergic reation then occurs to the fungus.
This disease often goes together with asthma, or can be mistaken for asthma. There are three clues that point to aspergillosis:
• rubbery plugs of phlegm, either golden-
brown or green in colour
• fever whenever the asthma is severe
• worsening symptoms despite treatment.
Allergic bronchopulmonary aspergillosis is treated with steroids to control the allergic reaction, and physiotherapy to clear the mucus from the lungs.
Anti-fungal drugs have not proved very effective in the past. There are some newer anti-fungal drugs that may well be more useful, such as itraconazole and terbinafine. These are not widely used for aspergillosis at present, except in patients who also have cystic fibrosis or an immune deficiency. Because there has been no large-scale trial of these drugs, they are not usually given to people who simply have aspergillosis. However, they are sometimes prescribed for people who are unable to take steroids, or are not responding to steroid treatment. Anti-fungal drugs may become more widely used in the next few years, so it is worth discussing the possibility of this treatment with your doctor.
the allergy antibody IgE. Only about 12% of people who suffer from seborrheic dermatitis make IgE against the yeast.
One problem with seborrheic dermatitis is that, while it may improve with anti-fungal treatment, it usually comes back when the treatment stops. Doctors have therefore been looking for ways of keeping seborrheic dermatitis at bay after a successful course of anti-fungal treatment. One method that seems to work is to use a good anti-dandruff shampoo, in place of soap, to wash your skin once a week.
A medical earthquake
The recent discoveries about infection-plus-allergy have not posed any serious challenge to conventional thinking about allergy, because a disease of just this kind - aspergillosis (see box at left) - was already well known. A far more fundamental shake-up of traditional ideas about allergy and sensitivity has been necessitated by new research into atopic eczema. It is little short of an earthquake in the basic concepts of allergy and sensitivity.
To understand the extent of this earthquake, you need to know about the time-honoured system for classifying hypersensitivity reactions, which recognises four distinct types:
• Type I hypersensitivity — the IgE-mediated allergies  such as hayfever.
• Type II hypersensitivity - irrelevant to allergy, these antibody reactions mainly occur after transplant surgery, if the transplanted organ is rejected.
• Type III hypersensitivity - caused by a massive overload of antibodies and antigen in the blood. It is a feature of certain infections and autoimmune diseases, and can also occur in allergic reactions, though this is rare (13).
• Type IV hypersensitivity - the odd man out, because antibodies are not involved, or are not of central importance. Immune cells that can launch a direct attack are the movers and shakers here. These attacking-cells are sensitised for a particular antigen, such as dust mite or lanolin. Type IV hypersensitivity is a very slow reaction. Generally speaking, 48 hours pass, after an encounter with the offending substance, before the symptoms appear. The most common form of Type IV hypersensitivity is contact dermatitis (54).
Mystery has always surrounded atopic eczema. Although it crops up in the same atopic families that suffer from hayfever and asthma, and high levels of IgE in the bloodstream are typical of the disease, the actual role played by allergies in causing the symptoms is far from obvious.
The results of skin-prick tests - the standard test for an IgEmediated reaction - are puzzling. Patients tend to give a lot of positive results, many of which don’t mean much - the substances concerned do not provoke actual symptoms. On the other hand, skin-prick tests are often negative for substances that clearly do cause symptoms in challenge tests. Many children who regularly get eczema when they drink cow’s milk, for example, give a negative skin-prick test to milk. This conundrum has puzzled allergists for decades.
New discoveries about eczema do not entirely solve the puzzle, but they do go some way towards an answer, by revealing an immune response that cuts across the traditional categories. The most surprising fact is that even where skin-prick tests are positive and milk-specific IgE is involved in milk-induced eczema, this is not necessarily a standard IgE-mediated allergy.
While IgE antibodies may be involved, they are not necessarily teamed up with mast cells, their usual partners in crime (see box on p. 12). Instead, the IgE molecules are attached to special skin cells called Langerhans cells and dendritic cells. These have the role of picking up the antigen and showing or ‘presenting’ it to attacking-cells in the skin (a task called antigen presentation which is the ‘go’ signal that starts off all immune reactions).
The involvement of these attacking-cells, which are sensitised for a particular antigen, was a big surprise when first discovered. It makes this resemble a Type IV hypersensitivity reaction rather than a Type I.
IgE is not essential here, it seems — some patients do not have IgE for the substance that triggers their atopic eczema — but when Langerhans cells and dendritic cells are associated with IgE they do become far more zealous. This excitement is communicated to the attacking-cells, which mount a more powerful attack.
It looks as if what really matters in atopic eczema is the presence of antigen-specific attacking-cells in the skin, plus the heightened activity of the Langerhans cells and dendritic cells. If the individual has IgE for the antigen, it can play a part, but it is not essential.
In other words, this reaction cuts across two different categories of immune response — Type I and Type IV. (However, the kind of antigens that provoke the reaction are typical of IgEmediated allergy, rather than the kind of antigens that provoke contact dermatitis.) This has been exploited in a new and more sensitive set of diagnostic tests for food-induced atopic eczema (69).
Why atopic eczema is a feature of atopic families is the crucial question that remains unanswered. One factor may be that high levels of IgE in the bloodstream (not IgE for a particular allergen, but total IgE) make the whole immune system more excitable and prone to over-react. The next few years will no doubt solve this part of the puzzle too.
Peace-keepers or aggressors?
`It is bad enough having a child on an ultra-strict diet — Tim can’t have even a trace of cow’s milk or else he becomes violently ill. What makes it worse is when people — teachers, for example —ask what’s wrong. I take a deep breath and say “eosinophilic oesophagitis” then watch their eyes roll in disbelief.’
Tim’s disease is caused by a particular type of immune cell called an eosinophil. In the right circumstances, eosinophils can be valuable — like IgE and mast cells, they are geared to destroying parasitic worms . They produce some very toxic substances to kill these invaders, and it is the toxins that cause serious symptoms for Tim and others like him.
Any disease with ‘eosinophilic’ in the name involves vast numbers of eosinophils converging on some unfortunate part of the body. The stimulus that attracts them often remains unknown but once there, the toxins they generate cause inflammation (140) of a particularly violent kind.
It is only in recent years that doctors have begun to distinguish between patients such as Tim and children with classical food allergy, and to understand the cause of Tim’s symptoms. Several different forms of eosinophilic food sensitivity are now recognised (72). The exact relationship with IgE-mediated allergy remains a puzzle, because some sufferers make IgE to the culprit food but others do not.
That is not all — the eosinophil is finally coming out of the shadows and being recognised as an important agent in classical allergic diseases as well.
The fact that eosinophils appeared during the aftermath of an allergic reaction had long been known, but their role was misunderstood. What confused researchers was that eosinophils can break down histamine, the substance that kick-starts allergic symptoms. This ability gave eosinophils the appearance of peacekeeping troops, coming in at the close of battle to restore order. In fact, eosinophils are major aggressors — they do a whole lot of other things besides breaking down histamine, most of them pro-inflammatory. They can release toxins, just as they do in eosinophilic diseases, and they attract other inflammatory cells into the area. In short, eosinophils play a big part in keeping allergic reactions going once the initial burst of activity is over. This `Late Phase Reaction’ is enormously important .

Cross Reactions in Allergy

For the rabbi’s doctor, discussing the results of the allergy tests with his patient, it was an embarrassing moment. An allergy is not inborn, it is an acquired reaction — a response by the immune system to a substance it has already encountered at least once. So, in theory, nobody can be allergic to a food they have never eaten.
Naturally enough, the rabbi had never eaten shellfish - like pork, it is a forbidden food in Judaism. But the nurse carrying out the skin-prick tests was unaware of this, and she had been told to test for all the common food allergens, so shrimp allergen was included. The test came up positive.
Fortunately, the rabbi had also been tested for inhaled allergens and had given a very strong positive reaction to house-dust mite. The likely explanation was clear: the rabbi had formed antibodies to a muscle protein of house-dust mite called tropomyosin, which is also found in shrimps and prawns. His antibodies against house-dust mite had cross-reacted with shrimp tropomyosin.
This does not mean that everyone who is allergic to house-dust mite will also react to shrimp. Firstly, they must have made antibodies to tropomyosin, rather than some other dust-mite antigen. Secondly, the antibodies must be recognising a particular feature of dust-mite tropomyosin that closely resembles (chemically speaking) a particular feature of shrimp tropomyosin.
The important point about antibodies is that, on the one hand, they achieve results by being specific for their antigen , but on the other, they do make mistakes. In the case of allergies, this is sometimes an added problem for patients but is rarely life threatening. More seriously, there are other conditions, like coeliac disease, where cross-reactions initiate attacks on the body’s own components, causing severe symptoms.
Antibodies make mistakes because they recognise antigens by homing in on tiny chemical markers, not by looking at the antigen as a whole (see box on p. 15). Although this is a nuisance for allergy sufferers, it can be a bonus in fighting diseases. For example,
Antigens and allergens
An antigen is anything which elicits an antibody reaction. Each antibody is specific for a particular antigen.
When they tend to cause allergies (by provoking IgE antibodies rather than other kinds of antibody -  these antigens are called allergens. Something such as grass pollen is both an antigen (because it elicits an antibody reaction) and an allergen (because it often elicits IgE antibodies in those who are allergy-prone).
when viruses (such as those that cause influenza) revamp their outer coat proteins to evade the immune system, the chances are that some antibodies will still recognise them because a few of the original chemical markers persist.
Understanding cross-reactions
Many cross-reactions are between related species, and this makes sense in biological terms. The tropomyosin story is a good example - not only is tropomyosin found in dust mite and shrimps, but it also occurs in other crustacean shellfish, such as crabs and lobsters, in molluscan shellfish such as clams and oysters, and in insects. If one goes back over 300 million years, all these animals were just a twinkle in the eye of some primeval invertebrate, the common ancestor of them all.
Tropomyosin is one of those triumphs of the evolutionary process - a protein that reached near-perfection hundreds of millions of years ago, in the long-vanished ancestral species, and remains so good at its job that it has only been tinkered with by natural selection since then, never radically altered. In other words, because it works so well, it has been ‘conserved’ by the various animal groups descended from the shared ancestor. Although there are some differences between the tropomyosins from different descendants, the similarities are considerable.
Relatedness counts here. Shrimps and prawns are pretty closely related, as anyone can see by looking at them. Their tropomyosins are extremely similar, as are many other allergens. You’re unlikely to be allergic to prawn but not shrimp. The more distant the relationship, the more differences accumulate in the antigens, so a cross-reaction between dust mite and shrimp is far less likely (the rabbi was unlucky).
Another conserved protein, parvalbumin, explains why people who are allergic to one type of fish are usually allergic to all kinds of fish (in spite of the fact that fish belong to several different families which are only distantly related). Those allergic to hen’s eggs will probably be allergic to the eggs of all birds, because the primary allergens (e.g, ovalbumin) are so similar.
These conserved proteins produce cross-reactions across huge gulfs, in terms of zoological and botanical relationships. Far more easily understood are the cross-reactions between close cousins, such as dust mite and storage mites, wheat and rye, pine pollen and pine nuts, or ragweed and sunflower (both members of the daisy family).
Relatedness can be useful in explaining cross-reactions, but often fails when it comes to predicting them. Some related species do not show as many cross-reactions as one might expect. Peanuts are legumes, and highly allergenic. One would expect some peanut-allergic individuals to be allergic to other members of the legume family, such as peas, beans, carob and soya. In fact, although some patients give positive skin-prick tests, very few show actual symptoms when they eat these foods. Where symptoms do occur, they tend to be mild.
Paradoxically, those who are allergic to peanuts very often develop an allergy to tree nuts, and this usually spans several different kinds of tree nuts – yet botanically all these are very distant relatives. No tree nut is a legume and while walnuts and pecans belong to one plant family, almonds belong to another, hazelnuts to another, cashews to a fourth, and Brazils to a fifth different plant family. Here relatedness seems irrelevant, and it is shared lifestyle (surviving as a nut-producing plant) that is crucial.
A nut is just an over-sized seed that has to survive being buried in the soil – either by the plant itself (in the case of peanuts) or by a nut-eating animal such as a squirrel. All nuts must resist rotting in the soil until the following spring, and therefore contain powerful bactericidal and fungicidal compounds. Some of these may have chemical similarities that cause cross-reactions.
These functional ‘lifestyle’ allergens of nuts may be even more widely shared, with many seeds having something similar: recent research shows potentially cross-reacting allergens in wheat, rye, hazelnuts, sesame and poppy. It is interesting that many of those developing new allergies to sesame or poppy are already allergic to wheat and nuts.
A few cross-reactions seem to defy any explanation, such as that between house-dust mite and kiwi fruit – this appears to be just a case of chemical coincidence. Other cross-reactions can appear equally bizarre but actually have a biological basis, notably that between latex (as used in medical gloves) and various fruits and vegetables, principally chestnut, banana, avocado and kiwi fruit. This cross-reaction is due to a shared enzyme called a chitinase that protects plants against insect pests. Latex, of course, comes from the sap of the rubber tree: the tree needs such insect-protection and its sap is richly laced with chitinase.
How antibodies work - and why they make errors
Antibodies are catapult-shaped, with two antigen binding sites at the ends of the two arms. The other end of the antibody molecule – the handle of the catapult – is free to bind to cell receptors.
When an antibody binds to its antigen there is a ‘chemical handshake’: a very specific recognition event involving one of the antigen binding sites and a particular small site on the antigen molecule called the epitope. The two lock together. Different antibodies may recognise different epitopes.
The antibody is recognising its antigen, but it is as if we recognised other people by homing in on one small part of them, choosing a different feature for each person, whatever is most distinctive about them – the quirky right eyebrow, the hook in the nose, or the mole on the cheek. The antibody does not ‘look at’ the whole antigen molecule, but simply recognises a characteristic cluster of chemical features at the epitope.
Cross-reactions can occur so readily because an antigen molecule only has to resemble another molecule in one or two small areas (the epitopes) for a mistake to occur.
antigen antibody molecule binding sites
cell receptor antigen molecule
epitope
surface of immune cell
(e.g. a mast cell)