Posts Tagged ‘Skin-prick’

The simplest and most certain test for any sensitivity reaction is to expose the person concerned to the substance under suspicion and see what happens. This is known as a

challenge test. With true allergies, challenge tests are powerful tools, but they are also alarmingly close to reality. The risk of provoking a severe reaction requires a very

cautious approach.
By comparison, an indirect test – a roundabout way of seeing how the body responds, such as the skin-prick test (see p. 91) – has the advantage of rarely producing dangerous

reactions. The downside is that indirect tests can be misleading, precisely because they are not like the real-life situation. No indirect test is perfect – there are always

false positives and false negatives (see box on p. 91).
Challenge tests
If you undergo a challenge test with food or an airborne allergen, you will also be given dummy challenges with an innocuous substance which is indistinguishable from the item

being tested. Neither you, nor the tester who is scoring the reaction, should know which is which. This is called a double-blind trial because, to eliminate all possible bias,

both of you are in the dark. (The full name is a ‘double-blind placebo-controlled trial’ – the dummy challenge is also called a ‘placebo challenge’ or ‘control challenge’.)
The double-blind trial is a standard medical procedure and does not imply that the doctors think you are faking symptoms. Psychological forces are powerful things, and just

thinking that you might react to a test can be enough to produce a reaction – the process that generates the symptoms is largely unconscious.
Food challenge
A food challenge – eating the food that is under suspicion – is a key test for food intolerance (see p. 197). It is sometimes used for food allergy and other forms of food

sensitivity too, as a follow-up to skin tests. Some allergists use a food challenge only if the skin test is at odds with actual events reported by the patient. Other allergists

use food challenge more readily, to confirm skin-test results, and to assess the severity of the reaction.
Extreme caution must be exercised with immediate food allergy, because of the considerable risks involved. The test must be done under medical supervision with resuscitation

equipment to hand. A challenge test should never be done for true food allergy without some careful preliminary tests on the face and the lips (see box on p. 23). Even if these

tests produce no reaction, only tiny amounts of the food should be eaten to begin with.
Bronchial challenge
This type of test involves inhalation of an airborne allergen – such as pollen – suspected of causing asthma. Bronchial challenge carries the risk of provoking a severe asthma

attack, and few doctors use it unless there are compelling reasons to do so – such as demonstrating that someone’s asthma is due to an allergen encountered at work.
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.

No single factor lies behind the allergy epidemic — the causes are many and various (see p. 20). What this means for parents interested in allergy prevention is that there is no

single measure which will ensure that your children do not develop allergies. Instead there are a great many different things that can be done, each of which reduces the risk to

some extent. The more of these you do, the lower the risk becomes.
Avoiding allergens
Starting before the birth is best, if you want to reduce allergen exposure for your child (see p. 240). But if you have missed the boat with that one, don’t despair – there is

still a lot to be gained by reducing allergen exposure at a later stage.
If you are ridding your home of allergens after the child’s birth, bear in mind that things will get worse before they get better– there will be a temporary surge in airborne

allergen as a result of the clean-up operation, and you will need to protect the child from this. The best strategy is for the child to be away for a few days while the work is

done, especially if you are taking out carpets, furniture or mattresses. Remember to protect yourself as well, if you are allergy-prone (see p. 109).
One of the most important steps you can take to reduce allergen levels is improve the natural ventilation of your home. This lowers the humidity (assuming you don’t live in an

extremely humid climate), which helps combat both moulds and dust mites. Ventilation also flushes out allergens in the air, especially cat, dog and mould allergens. Half the

problem with modern houses is that the airtight seals around doors and windows, introduced to conserve heat and save energy, turn the indoor air into a rich stew of allergens

and irritants.
House-dust mite
Avoiding high levels of house-dust mite in the home is one of the most valuable things you can do to reduce the risk of allergies in your child. Not only is house-dust mite a

powerful allergen in its own right, it may also act as an agent provocateur as far as the immune system is concerned (see p. 12), and may help to initiate allergic reactions to

other potential allergens – such as those from pets or indoor moulds.
Even if you do nothing else to protect your new baby from mite allergen, at least buy a new mattress and pillow for the cot, with ready-fitted allergen-proof covers. Do the same

for the portable crib, if you have one. Choose anti-mite products that are designed for babies and are guaranteed safe – there is a risk of suffocation with some loose covers

sold for older children and adults (see p. 245).
You may want to eliminate house-dust mite from your own bed as well as the baby’s, because there will probably be times when you take the baby into bed with you for a feed or a

cuddle – and times when, as a toddler, he or she just barges in! It is good to know that your child is still breathing air free from dust-mite allergen in these circumstances.
Deal with your own bed as soon as you can. Some doctors believe that lowering your exposure to dust mite during pregnancy may reduce the risk of sensitising your baby before

birth (see p. 241).
When taking anti-mite measures with your own bed, make sure that there is no risk of suffocation to the baby from the allergen-proof materials used. Microporous membranes based

on plastic could, if sucked onto the baby’s face during sleep, cause suffocation. Loose covers on duvets are worrying in this respect. Buy a new duvet with a built-in

allergen-proof cover, for preference, or a duvet that can be laundered at 60°C or above.
All the other measures for combating dust mites, described on pp. 114-17, will help to protect your child. Buy a good anti-allergen vacuum cleaner if you possibly can, and keep

your baby out of the room while vacuuming if you can’t (open the windows too). Make sure the baby only has new soft toys, preferably washable ones (see p. 116).
It is also an excellent idea to reduce dust-mite levels in the carpets and soft furnishings (see p. 117), because children tend to have very close contact with these in their

early years. A crawling baby, motoring enthusiastically around the sitting room floor, is stirring up the stockpile of dust-mite allergen that is found in any carpet, and

inhaling it in full measure. An adult walking around the same room has a far lower exposure, because dust-mite allergen, being relatively heavy, stays near the ground.
The best option is to go for non-carpet flooring, which doesn’t encourage dust mites. Parents tend to worry about the hardness of this, for a baby or toddler. In fact babies are

far more robust than we generally believe, and a hard floor is no problem for a small child who has never known the luxury of carpeting.
If you really hate the idea of your baby having anything other than carpet to play on, the next best option is to get new carpet, so that you start with zero dust mites. You

must then prevent dust-mite numbers from building up too much, by means of good ventilation, or with the use of a powerful dehumidifier (see p. 117).
Although the first year is the most vulnerable time for your baby, you mustn’t let your guard drop too much as time passes. The moment when a toddler moves from a cot to a ‘big

bed’ is sometimes the beginning of allergy symptoms because, after carefully protecting their child from dust mites in infancy, parents then put him or her into a bed with a

used mattress. This sudden exposure to a high dose of
dust-mite allergen can be the start of asthma. Get a new mattress if you can, and put allergen-proof covers on it. Alternatively, put allergen-proof covers on the existing

mattress.
Moulds
Mould spores are another potent allergen, and you should avoid bringing up a vulnerable child in a damp house if you can, because moulds will be growing there in abundance. Some

new research suggests that heavy exposure to mould allergens in childhood makes allergies in general much more likely. Even in a house that is not obviously damp, it is a good

plan to reduce indoor humidity (see p. 119). Carpets and furnishings that are full of mould spores (see p. 122) should be replaced.
Pets
What about pet allergens – should you find another home for your cat or dog when you are expecting a baby? This is a difficult question because the latest research shows that

pets are a double-edged sword as far as allergies are concerned.
A baby with allergic tendencies who is born into a house with a resident cat or dog is more likely to show allergic reactions to cats or dogs some years later. On the other

hand, there is research showing that having a pet in the house reduces the risk of allergies overall, especially for a child with no brothers or sisters. This is probably

because the pet boosts household levels of endotoxin (see p. 21), and generally makes the environment less hygienic for the child, fulfilling the same anti-allergy role as

brothers and sisters would in the early life of a child (see p. 246).
If you are planning to give your child the kind of grubby childhood that seems to protect against allergy (see p. 246), the additional protection provided by a pet is probably

unnecessary. Or, you could view your pet as having both pros and cons, and decide to keep it, while implementing all the other anti-allergy measures described here. If you do

this, ensure that the house is well ventilated (so pet allergens don’t build up to very high levels) and keep the pet out of the child’s bedroom so that he or she is not

breathing huge amounts of pet allergen while asleep. You could also wash the pet regularly (see p. 125) to reduce allergen levels.
If your child begins to show any signs of allergy to the pet, you must then find it another home.
Avoiding irritants
As well as increasing ventilation and eliminating cigarette smoke from the home completely, it may be worth evicting certain specific items that produce irritant gases.
The main ones are:
•    gas cookers (if you can’t afford to switch to an electric cooker, at least improve the ventilation in your kitchen as much as possible)
•    easy-clean plastic wall coverings and flooring
•    materials such as chipboard and MDF, which give off formaldehyde.
The evidence regarding the possible role of these in increasing the risk of allergies and asthma is described on pp. 128-9. In addition, although there is no evidence on this

point, common sense would suggest getting rid of any plastic or lacquered items that have a powerful smell.
Generally speaking, although traffic pollution can act as an irritant, it seems to play a lesser role in causing allergies and asthma than most people imagine. However, it may

sometimes play a part, especially if there are high levels of diesel fumes in the air (see p. 131).
Infections - friend or foe?
A large group of Italian military cadets were recently studied by doctors interested in the causes of allergy. By taking blood samples and testing them for antibodies to common

infections, the doctors could see what diseases the men had been exposed to early in life. At the same time, the young conscripts were assessed for allergies.
Allergies were least frequent among the young men with antibodies against three common infections that are dispersed via food and faeces – Hepatitis A, Toxoplasma gondii and

Helicobacter pylori. Only one in twelve of the cadets in this group had allergies.
Among the men with no antibodies against any of these infections, the rate of allergy was nearly three times as high – one in five of these cadets had allergies.
The doctors who carried out this experiment believe that these three infections are not necessarily important in themselves, but that they identify individuals who were ‘reared

in an environment that provides a higher exposure to many other orofecal or foodborne microbes’. In other words, they grew up in the kind of household where washing your hands

before meals wasn’t considered too important.
This study adds to the growing body of evidence (see p. 21) which shows that an over-clean environment during childhood encourages the development of an allergic disposition.
Those with lower rates of allergy include:
•    children raised on farms with livestock. The more exposure the children have to farm animals, the less the likelihood of them developing allergies.
•    children from homes with high levels of bacterial endotoxin in the household dust (see p. 21)
•    children who have fewer baths, and wash their hands less often (see p. 21)
•    children with brothers and sisters, especially those with older siblings. Some of the protection here may be due to the impact of the mother’s hormones and immune system

on the foetus in the womb: these effects change with successive pregnancies. But close contact with older siblings, and thus exposure to more microbes, probably plays a part.
•    children who go into kindergarten, nursery school or day care with other children at an early age – this is only valuable for children without brothers and sisters
•    children with pets at home – the benefits are much more pronounced for children without brothers and sisters.
The Italian study is especially important because, for the first time, it gives detailed information about the kinds of infections that make a difference in allergy prevention.

The military cadets were also checked for antibodies to measles, mumps, rubella, chickenpox and herpes. None of these infections gives protection against allergies – only

infections carried in food and faeces do.
Exactly what practical use you make of these discoveries is up to you. For most of us, the importance of hygiene was so firmly instilled during our own childhood that it is

quite hard to suddenly become more relaxed about it. But do let your children play in the garden, if you have one, and don’t worry so much about how dirty they get. Encourage

them to do some gardening – medical researchers believe that harmless bacteria in the soil may be particularly important in educating the immune system away from allergies (see

p. 21). Let them play with pets, as long as the animals are not carrying harmful parasitic worms (talk to your vet about whether pets should be treated for parasites). Ease up

or, hand-washing and, if this is your first baby, make sure he or she plays with other children as early in life as possible.
A few chest infections do seem to increase the risk of asthma, notably Respiratory Syncytial Virus (RSV). If this Infects babies, it provokes an IgE-reaction (see box on p. 12)

which may encourage the development of allergies. Unfortunately, there is very little you can do to protect your child from this common virus, but it makes sense not to take the

baby to a hospital for unnecessary trips (visiting relatives, for example) because RSV infections are often picked up in hospital.
Taking care with antibiotics
The possible role of antibiotics in making allergies more likely to develop is an exceedingly controversial topic. Before making any practical decisions in this respect, you

must consult your doctor. Never go against your doctor’s advice, if he or she thinks that antibiotics are necessary.
Several different studies have now produced evidence of a link between antibiotic use before the age of one or two, and the later development of allergies, asthma or both. The

best of these studies was carried out by doctors in Oxford, who followed 1900 children up to the age of sixteen. Among children at risk of allergy (because their mothers had

allergies) taking antibiotics before the age of two was linked with an increase in the rate of allergy from 32% to 54%. The more courses of antibiotics a child received, the

greater the risk.
The type of infection for which the drugs were prescribed was not important, as far as the risk of allergy was concerned, but the type of antibiotic did make a difference.

Broad-spectrum antibiotics, which kill a wide range of bacteria, were more risky –suggesting that the depletion of friendly bacteria in the gut (see p. 204) could be responsible

for increasing the allergy risk. Penicillins seemed less likely to promote allergies than erythromycin or cephalosporins.
This research is not widely known, as yet. And because there is a widespread assumption that giving an antibiotic can do no harm, even if it is unnecessary, antibiotics are

sometimes prescribed when they serve no purpose. In particular, antibiotics are often given for virus infections, especially in childhood, despite the fact that antibiotics are

of no value whatever against viruses. Research shows that doctors are sometimes responding to pressure from anxious parents when they prescribe antibiotics – it is difficult for

some parents to accept that a virus infection cannot easily be treated and just has to ‘run its course’. (Although there are drugs that combat viruses, these are expensive and

produce unpleasant side effects – they are reserved for very serious virus infections such as hepatitis.)
Obviously. when a child needs antibiotics to deal with a serious infection there can be no question about giving them. This is why you should always follow your doctor’s advice.

But it is also worth asking the doctor the following questions before giving antibiotics to your child:
•    are you sure that this is a bacterial infection, and not a virus infection?
•    would it be possible to do tests and check that it is a bacterial infection, before prescribing antibiotics?
•    what is the chance of the child overcoming the infection without antibiotics?
•    would it be dangerous to wait and see if the infection clears up naturally?
Vaccination
The same Oxford research team that investigated antibiotics (see left) also looked at the question of vaccination and allergy. They found a link between vaccination for

pertussis (whooping cough) and increases in asthma, eczema and hayfever. However the increases were not large, and a study from Sweden found that whooping cough vaccination did

not have any effect on rates of allergy and asthma. And researchers in Ethiopia have found that whooping cough vaccination actually reduces the risk of allergy in their country.
This is clearly a complex issue. The contradictory results from different parts of the world suggest that the ‘big picture’ is what counts here – the overall combination of

childhood infections, antibiotic treatment and exposure to harmless bacteria such as those in the soil or from animals. Depending on this big picture, vaccination against

whooping cough may push the allergy risk one way or the other.
There are many other arguments both for and against vaccination and, given our current state of ignorance about the possible effect on allergy, these other considerations are

probably more relevant. Discuss the matter in detail with your doctor before making a decision.

Doctors in Japan recently tried a very simple experiment in allergy prevention. They chose babies suffering from atopic eczema who were allergic to foods, but not allergic to

house-dust mite. Dividing the babies into two groups, the doctors put special allergen-proof covers, designed to protect against house-dust mite (see p. 115), on the mattresses

of all the babies in the first group. Babies in the second group were given ordinary cotton covers.
When the babies were one year old, they were tested again for allergy to house-dust mite. Two out of three children in the second group now gave a positive skin test to

house-dust mite.
By comparison, only one in three of the children from the first group gave a positive skin test. In other words, using the anti-allergy covers for these high-risk children had

cut by half the number who developed an allergic reaction to dust mite.
As this experiment shows, even if a child has already developed allergies, it is not too late to bring protective measures into play. Indeed, an allergy problem in infancy, such

as atopic eczema, can be seen as a warning sign to parents, telling them that they should reduce the child’s exposure to allergens as much as possible.
As well as reducing dust-mite levels, you should minimise your child’s exposure to moulds at home by limiting indoor humidity (see p. 119) and cleaning up any existing mould

growth (see pp. 122-3). This will lessen the chance of mould allergy developing.
Try to avoid staying, even temporarily, in any house that is damp or has old carpets and mattresses. When you are moving house, or carrying out any kind of renovation work,

remember that this will stir up a lot of dust-mite and mould allergens. Protect your child by arranging for a stay away from home.
This pro-active approach should not just apply to airborne
allergens, but also to food, in the opinion of some experts. They
suggest that any child with a true allergy to cow’s milk or egg
should not be given peanuts, tree nuts, fish or shellfish until three
years of age, to avoid sensitisation to these potent food allergens.
Pets are a more difficult issue, with both pros and cons as
regards allergy-prone children (see p. 245). If you decide to keep
your cat or dog, always ventilate the house well, and wash the animal regularly if you can (see p. 125). Be alert for your child developing an allergic reaction to your pet –

don’t turn a blind eye to the symptoms, as parents sometimes do because they are reluctant to accept that the child has become allergic to the family’s much-loved pet. If your

child does develop an allergy to the pet, the best option is to find the animal another home as quickly as possible (see p. 124).
Breast-fed babies with atopic eczema
Although breast-feeding is a good way of protecting children against atopic eczema, it is no guarantee. Sometimes babies become sensitised to food, in spite of being breast-fed,

and then they may react to traces of that same food, eaten by the mother and coming through in her breast milk.
Skin-prick tests (see p. 91) may help to identify the foods responsible for the eczema. Otherwise, a simple elimination diet by the mother, as used for colic (see p. 203), may

pinpoint the offending food. Keeping that food out of the mother’s diet will often clear the baby’s eczema.
Sometimes a breast-fed child’s eczema remains severe, despite the elimination of suspect foods from the mother’s diet. In this case, what should be done? New research from Or

Erika Isolauri – a staunch advocate of breast-feeding – suggests that the best option at this point is to stop breast-feeding promptly. Her research team found that breast-fed

children with persistent eczema had a slower growth rate. If these babies are switched to hypoallergenic formula – either an extensively hydrolysed formula or an artificial

amino-acid formula (see box on p.66) – their eczema symptoms usually subside, and their growth picks up.
Is vaccination safe for those with allergies?
The influenza vaccine and a few others (e.g. yellow fever) are grown in eggs and are not usually given to people with egg allergy. Measles vaccine is grown in cells taken from

eggs and may contain a minute trace of egg allergen, but only those who are extremely sensitive will react: there should be resuscitation equipment available for children who

have had anaphylactic reactions to egg and for those with severe asthma as well as egg allergy. Some vaccines come in vials with latex seals that are designed to be pierced by

the needle of the syringe. A different method should be used for latex-allergic patients. Smallpox vaccine (for bio-terrorism threats) is dangerous for children with atopic

eczema.
Never too late?
The role of modern ultra-clean lifestyles in promoting allergies is now well established (see p. 21). If your child already has allergies, it may seem as if these discoveries

have come too late to help —but that is not the case. Some research suggests that the battle for supremacy between Th1 and Th2 cells (see p. 11) — the unseen power struggle

which decides whether a child will be allergy-prone — is not really settled until some time between the ages of five and seven years. So there is still some potential for

intervening right up to this age. Some studies have suggested that the immune system can be pushed away from an allergic disposition at an even later age, right into adulthood,

by exposure to endotoxin, a bacterial product found around livestock and in `lived-in’ homes.
Several research groups are working on vaccination strategies (for example, using extracts of soil bacteria) that might also be able to achieve this. The initial results are

promising and they suggest that these vaccines can even help adults with allergies. Unfortunately, such treatments will not be available for many years. In the meantime, you can

probably reduce your child’s chance of developing new allergies, and perhaps make the existing ones less severe, by easing up on hygiene (see p. 246).
Fresh air and exercise
With the boom in watching TV and videos, and playing on computer games, some modern children hardly go outdoors at all. As far as allergies and asthma are concerned, there are

two big disadvantages to being a juvenile couch potato. For a start, the couch is also home to dust mites in their millions, and secondly the child is not running about and

using his or her lungs to the full. Airways that are never stretched (because the child never gets out of breath) lose their youthful flexibility in time. Once this has

happened, the airways can never be stretched to their full capacity. Some doctors believe that this may make asthma more likely to develop, or help to make it more severe once

it has developed. Inactivity also encourages obesity, which increases the risk of asthma developing.
Getting outside and running around, or engaging in other vigorous exercise, should be encouraged for any child with allergies. Obviously, you should balance this against the

need to protect the child from pollution peaks and (if your child has hayfever) pollen peaks. Children with exercise-induced asthma should use their reliever inhalers to allow

them to take exercise (see p. 41).
Keep the air at home free from irritants such as nitrogen dioxide (see p. 128), formaldehyde, air fresheners, paint, polish and strong-smelling cleaning fluids. These may

encourage new allergies to develop, and can make existing asthma worse.
Medical treatments
Antihistamines may have a preventive role in very young children with allergies. A study of one- to two-year-olds with atopic eczema found that the antihistamine cetirizine,

taken daily for 18 months, halved the chances of the children developing asthma later.
The children who benefited in this study were those with several risk factors for becoming asthmatic. They had moderate to severe atopic eczema, at least one close relative with

allergies, and allergic sensitisation to pollen or house-dust mite, as shown by skin-prick tests (see p. 91).
The cetirizine was taken at fairly low doses and had no bad effects on the children in this study. What is more, it seemed to benefit their skin as well as reducing the risk of

asthma: those taking the drug had less need of high-strength steroid creams. There is some controversy about the validity of these results, so few children with atopic eczema

are receiving antihistamines at present.
No one yet knows if other antihistamines might have the same effect as claimed for cetirizine. Ketotifen, which is an atypical antihistamine (see p. 159), may do so.
Immunotherapy may also have a protective effect. One study, involving children suffering from nasal allergies, found that those given immunotherapy were less likely to develop

asthma (see p. 165). Another study shows that immunotherapy for children with mite allergy halves the risk of their developing new allergic reactions to other allergens.

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.

Various anti-allergy drugs
An allergic reaction is a lengthy, complex process, and the various anti-allergy drugs all work on different stages of that process. That is why it often makes sense to use several different drugs for the same allergic condition: they each tackle the problem in their own way.
Steroids (see p. 140) intervene at a very late stage, quelling the inflammation that follows on from an allergic reaction. Using a steroid is rather like calling the fire brigade to put out a fire, whereas using an antihistamine (see p. 138) is like having fire-proof doors, to prevent the fire spreading at an early stage. Cromoglycate-type drugs (see below) intervene at an even earlier stage. They are like basic fire prevention - teaching children not to play with matches, or fitting smoke detectors.
Anti - leukotnene drugs (see p. 149) work at roughly the same stage of the process as anti-histamines but tackle an entirely different aspect of the allergic reaction.
Cromoglycate-type drugs
These drugs are also referred to as mast-cell stabilisers or mast-cell Mockers.
There are three drugs in this group, sodium cromoglycate (also spelled cromoglicate), nedocromil sodium, and lodoxamide. All operate at an early stage of the allergic reaction, stopping it before it actually starts. They stabilise the outer membrane of the mast cells (see box on p. 12), which prevents the allergic response from occurring.
Some common brand names
Common brand names of cromoglycate-type drugs include:
inhalers - Cromogen Easi-Breathe, Intal, Tilade
eye drops - Hay-Crom, Opticrom, Rapitil, Vividrin, Viz-on nose sprays - Rynacrom, Vividrin
capsules - Nalcrom
This is a far more satisfactory way of dealing with an allergic reaction than trying to tackle it after the reaction has occurred. But from a purely practical point of view, it has a drawback. I order to work at all, these drugs must reach the mast cells in advance of the allergen. They are of very little use if taken after the allergic reaction has begun.
For those who are taking cromoglycate-type drugs on a regular schedule, several times a day, it is very important to be conscientious about taking them on time. This maintains the protective effect of the drug, without any gaps.
If you are using these drugs on an ‘as-needed’ basis, you should take them 30 minutes before an allergen is encountered. or 30 minutes before a bout of exercise, if they are being prescribed for exercise-induced asthma. (Note that children sometimes respond differently, getting protection from these drugs immediately.)
The effect of these drugs takes time to build up. You should take them regularly for at least four weeks before deciding whether they are helping you or not.
One point in favour of cromoglycate-type drugs is that they are extremely safe, with few or no side effects in most people. Sadly, they do not work for everyone. A fairly high percentage of children respond well to them, but the response rate is much lower for adults. Nevertheless, adult allergy sufferers, especially those who need steroids to control their symptoms, should always be given the opportunity to try out these drugs. When cromoglycate-type drugs do work, they are very effective and almost always trouble-free, so they are a good alternative to steroids.
Both sodium cromoglycate and nedocromil sodium are available in inhaler form for asthma (see p. 157). Sodium cromoglycate is also available as nose drops for hayfever and other nasal allergies.
All three drugs are available as eye drops. Recent evidence suggests that sodium cromoglycate drops are less effective than the other two, particularly for the treatment of severe allergic conjunctivitis (inflammation of the eye).
Sodium cromoglycate is available in capsule form for food allergy. Note that these capsules are of very limited value in food allergy, and are certainly not a substitute for food avoidance. They do reduce sensitivity a little and can sometimes be helpful for those with multiple food allergies (see p. 67).
Side effects
There are no serious side effects at all for nedocromil sodium. cromoglycate can, very rarely, cause joint pain and swelling. An allergic reaction to the drug itself is even more uncommon. Stop taking the drug and see your doctor promptly if either of these occurs.
The only other side effects that have occasionally been reported are headache, nausea and vomiting. None of these indicates any damaging effect by the drugs – they are all minor side effects.
Eye drops containing these drugs may cause stinging and burning when inserted, but this is a minor side effect and usually wears off. Flushing and dizziness have sometimes been reported with lodoxamide eye drops.
Nose drops may also cause local irritation. This could be due to the drug itself, in which case it is a minor side effect. Alternatively, the irritation may be due to the preservative used or some other non-drug ingredient (see box on p. 33).
Occasionally cromoglycate nose drops cause bronchospasm – contraction of the airway muscles – but this tends to wear off quite quickly. Bronchospasm can also occur when cromoglycate-type drugs are inhaled (see p. 157).
Anti - leu kotriene drugs
These drugs, which have a set of very specific effects (see p. 159), were originally designed to treat asthma. Their potential for treating other allergic diseases is currently being explored:
•    Several studies show that they work well for perennial allergic rhinitis brought on by allergens such as house-dust mite. They also have some effect on hayfever, but standard treatment (such as antihistamines plus a steroid spray for the nose) is more effective.
•    They are especially useful for both rhinitis and asthma in patients suffering from triad (see box on p. 28). Research shows that they also reduce asthmatic reactions to very small test doses of aspirin, but they don’t give protection against anaphylaxis brought on by normal doses.
•    They have also been used successfully in cases of chronic urticaria and for some patients with delayed pressure urticaria. It seems plausible that they would also be helpful for chronic urticarla linked to aspirin sensitivity.
•    Preliminary trials suggest that these drugs might be useful in atopic eczema. Some studies show a very good response that allows a reduction in steroid creams.
•    Montelukast works very well for eosinophilic gastroenteritis and eosinophilic oesophagitis (see p. 72), according to some new studies.
For side effects of these drugs see pp. 159-60.
Anti-IgE drugs
Since the antibody IgE (see box on p. 12) is such a crucial player in allergic reactions, developing drugs that disable this antibody should help allergy sufferers. The first such drug is omalizumab (brand name Xolair) which was licensed for use in the United States in 2003. It is expected to become available in Britain some time in the next few years.
Omalizumab binds to IgE antibodies and stops them from interacting with mast cells, so blocking any allergic reaction. The drug is given as a ‘depot injection’, just under the skin, every 2-4 weeks. It is gradually released from the injection site and moves around the body in the blood, mopping up IgE molecules.
At present, omalizumab is used for severe hayfever and for people with asthma who are not responding well to the usual treatments. It is only worth using if there is clear evidence that allergies play a part in the asthma. Patients who use omalizumab are often able to reduce their dose of inhaled steroids – and they suffer fewer serious asthma attacks and have better lung function. Some patients can even stop using steroids completely.
Other anti-IgE drugs are in the pipeline. Pilot studies show that one works very well for peanut allergy: after just four injections, sensitivity to the allergen falls sharply, reducing the risk of anaphylaxis from traces of peanut eaten accidentally.
More powerful anti-allergy drugs
Occasionally people with severe allergies, who are on constant high doses of steroid tablets, or who fail to respond to steroids, need treatment with powerful anti-inflammatory drugs, such as methotrexate or cyclosporin. These suppress the immune system, and extremely careful monitoring for side effects is needed.
Adrenaline (epinephrine)
Anyone who has suffered anaphylactic shock (see p. 58) should be carrying a special syringe, called an auto-injector, loaded with adrenaline. The injector is very simple to operate and is designed for emergencies. Most allergy sufferers, even children, can give themselves the injection – or a parent or other adult can give it.
Some asthmatics, and those with food allergy who suffer swelling of the throat, may be given adrenaline in inhaler form as well (see pp. 155-6). This can be useful as an additional treatment but it’s definitely not a substitute for an injector.
See pp. 98-9 for instructions on using adrenaline in a crisis.
Wherever you go, take your injector with you. Always keep it close at hand: you need to be able to use it within minutes of the allergic reaction starting. You may be unable to speak (and therefore unable to ask someone else to fetch it) quite soon after the attack begins. The injector must never be refrigerated. It can also be damaged by sunlight and excess heat.
If you live in the countryside or in an area with a poor ambulance sevice, or if you are going camping or hiking somewhere remote, ask your doctor for a second injector, or one that can deliver multiple injections. Also ask about the maximum number of injections that can be given, and never exceed this total. Some doctors believe everyone should have two injectors, just in case the first dose doesn’t do the trick and help is slow in coming.
It is vital that you are shown exactly how to use the auto-injector. Canadian researchers discovered that only one in four
Some common brand names
Common brand names of adrenaline preparations include: auto-injectors – Anapen, EpiPen
inhalers – AsthmaHaler Mist, Bronkaid, Epiphrine
health professionals got the technique correct when demonstrating how to use an auto-injector In this study, pharmacists were much the best as regards accurate instructions. Dummy injectors are useful for training purposes and most pharmacies have them.
When the adrenaline auto-injectors expire, they can be very useful for practising with, or for showing a new baby-sitter or teacher – practise on an orange or grapefruit.
If you are taking beta-blockers (e.g. for a heart condition or anxiety), adrenaline may not have much effect.
Heavy daily use of beta-2 relievers for asthma (see p. 152) will also make adrenaline less effective when you need it.
Side effects
The important side effects of adrenaline involve the heart. Anyone with a heart condition should be given special advice in advance by their doctor about using adrenaline. The same goes for people with diabetes, hyperthyroidism or high blood pressure, and anyone taking tricyclic anti-depressants. There are quite a few minor side effects from adrenaline, such as anxiety, trembling, nausea. sweating, dizziness and cold extremities. These soon wear off.
Drugs that can make you worse
Aspirin and its relatives have a very bad effect on some people with rhinitis and/or asthma (see box on p. 151). Unfortunately, recent research shows that paracetamol is not safe either. It makes asthma more likely to develop in those who do not yet have the disease, and increases the severity of asthma symptoms for those who do. Unlike aspirin, paracetamol affects everyone, because it lowers the levels of a natural antioxidant, called glutathione, which the body makes to protect the lungs from oxidants. The greatest effects are seen in people who take paracetamol regularly (once a week or more), but even an occasional dose makes some difference.
All the other drugs that can make you worse are prescription drugs, and your doctor should be alert to the dangers. But doctors are overworked and sometimes forget, so it is sensible to know about the risks for yourself. If you have any doubt about the drugs you are taking, ask a pharmacist.
Beta-blockers are a major hazard for people with allergies. They can make the airways contract, and can bring on a serious asthma attack. They also make anaphylaxis more likely in someone who already has allergic reactions (see p. 59) and they increase the risk of a severe reaction to
immunotherapy (see p. 166) or skin-prick tests (see p. 91). Beta-blockers are prescribed for high blood pressure, angina and other heart problems, migraine and thyroid disease. There are alternative drugs in all cases. Sometimes asthma develops in people who have been taking beta-blockers for years. The beta-blockers are not responsible for this, but once asthma has begun, they will make symptoms worse. Eye drops for the treatment of glaucoma may also contain beta-blockers and can have a bad effect on asthmatics.
ACE inhibitors, used for heart conditions, may cause a cough and airway narrowing. They may also increase the risk of a severe reaction to immunotherapy.
Female hormones affect asthmatics, so taking the contraceptive pill or hormone replacement therapy (HRT) may make asthma worse. Progesterone-only contraceptive pills tend to cause fewer problems.
The drug isoniazid (INH), prescribed for tuberculosis, makes the body far more susceptible to histamine in foods (see p. 200).
An allergic reaction to a specific drug (e.g. penicillin) can also occur in some people, resulting in urticaria, or even anaphylactic shock.
Aspirin sensitivity
Aspirin sensitivity is not an allergic reaction, because neither IgE nor mast cells are involved. What causes this problem is a metabolic abnormality — a malfunction in one aspect of the body’s chemistry. The details of this are very complicated: you may want to skip the next three paragraphs and
simply read about how to cope with the problem.
The exact nature of aspirin sensitivity is still far from clear, but it seems to involve a relatively poor production of prostaglandins, combined with a plentiful production of leukotrienes. Both these substances are messenger chemicals which, broadly speaking, promote inflammation. But the details of their pro-inflammatory activities differ. It seems that, ideally, the body should have a harmonious balance between the two, and an imbalance produces problems.
Both prostaglandins and leukotrienes are manufactured from certain fats that are found in the diet. These fats, the raw materials, are worked on initially by two different enzymes — one that leads to the production of prostaglandins and another that leads to the production of leukotrienes.
If one of these enzymes is defective, it may mean that the other is oversupplied with raw materials, resulting in a serious imbalance between prostaglandins and leukotrienes. In those with aspirin sensitivity, or at risk of developing aspirin sensitivity, the enzyme that produces prostaglandins seems to be defective.
Even in the absence of aspirin, this imbalance in the production of prostaglandins and leukotrienes causes problems. It leads to symptoms such as chronic urticaria (see p. 51) or rhinitis, nasal polyps and asthma (a cluster of symptoms that is commonly called triad — see box on p. 28).
Taking aspirin can make the imbalance between prostaglandins and leukotrienes even worse in a person with this underlying abnormality. Aspirin exerts its painkilling effects by disabling the main prostaglandin-making enzyme — the enzyme that is already defective.
When someone with aspirin sensitivity takes aspirin, they may suffer worsening asthma, a severe asthma attack or — the worst-case scenario —collapse. This is a potentially fatal reaction, similar to anaphylaxis, requiring emergency medical treatment (see p. 101).
The greatest puzzle about aspirin sensitivity is why it often takes so long to develop in someone who already has the symptoms of triad —indicating the basic metabolic abnormality. It may be as much as 20 years from when someone has their first triad symptoms to when they begin reacting badly to aspirin.
If you have triad symptoms already, but no aspirin sensitivity yet, what should you do? Unfortunately, there are no safe tests for aspirin sensitivity at present — taking a small dose of aspirin and seeing what happens is very hazardous. It is probably best to assume that you are going to become sensitive to aspirin at some stage, and avoid all aspirin and aspirin-like drugs. Caution is the best plan here because aspirin sensitivity can come on very suddenly, and be life-threatening the very first time it occurs. Note
that some triad sufferers have polyps and rhinitis but no asthma until they actually develop aspirin sensitivity — a dose of aspirin suddenly brings on their first asthma attack plus other symptoms of aspirin sensitivity.
Avoiding aspirin itself is not difficult, but aspirin-like drugs pose more of a problem. Every year there are a number of deaths from these drugs. Some cases occur because a busy doctor momentarily forgets that a patient should not take these drugs. The drugs that need to be avoided are all known as non-steroidal anti-inflammatory drugs (NSAIDs), COX-1 inhibitors or COX-2 inhibitors. However you will not see any of these names on the packet. These drugs are very widely used for pain relief (e.g. in headache and backache remedies such as Nurofen), for the treatment of arthritis, and for several other inflammatory diseases.
There are dozens of non-steroidal anti-inflammatory drugs available, and many are sold under several different brand names. The list grows every year, as new drugs or new brands are launched. The only way to avoid these drugs is to be very cautious:
•    When buying any cold- or flu-remedies, painkillers, medicines for sprains or sports injuries (including those you apply directly to the skin), headache tablets or migraine tablets, always buy them at a chemist’s shop rather than a supermarket, and check with the pharmacist that they do not contain aspirin or aspirin-like drugs.
•    Be cautious also about remedies for an upset stomach. A few (e.g. Alka-Seltzer) contain aspirin.
•    Don’t take any drugs unless you are 100% sure of what they contain. Remember that the ingredients of a familiar brand name can sometimes change — read the label every time.
•    When a doctor prescribes any new drug, always mention that you are sensitive to aspirin, or that you have triad symptoms. Alternatively, check with the pharmacist when the prescription is filled.
•    Aspirin-free painkillers almost always contain paracetamol, a drug which can cause a severe reaction (similar to the collapse induced by aspirin itself) in about 5% of those with aspirin sensitivity. If you are taking paracetamol for the first time, start with half a tablet. Be sure that, for the next 2-3 hours, you have a way of getting to hospital quickly should you start to feel ill. (Note that paracetamol has another entirely separate effect, increasing the severity of asthma, and it is best not to take it too often — see box on p. 150.)
Avoiding all aspirin-like drugs will prevent you having anaphylaxis or severe attacks of asthma. Unfortunately, triad symptoms will not go away however careful you are about avoiding aspirin.
It is well worth trying the new anti-leukotriene drugs (see p. 149), especially if you have aspirin-induced asthma. They seem to help with triad symptoms by curtailing the activities of leukotrienes and so redressing the balance between leukotrienes and prostaglandins.

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.

Candidal Spores of the Fungus, Candida Albicans.
`As a small child Jason was plagued with ear infections which led to many courses of antibiotics,’ Hannah Mitchell recalls. ‘Eventually he started to get symptoms such as an upset stomach, itchy bottom, flu-like symptoms and extremely itchy eyes. The GP prescribed eye drops and when I put them in Jason screamed his head off. In the morning every single eyelash had fallen out. Jason’s health deteriorated and a few months later his eyebrows started to itch. Within two days every single eyebrow hair had fallen out. His eyes were worse and I was offered steroid eye drops again. Reluctantly I accepted.’
‘Putting the drops in caused Jason extreme pain. The red patches of skin around his eyes spread and the itching increased. I was at the end of my tether when I came across a book in the library about food-related illness…
What Hannah discovered from her reading was that, for many with diarrhoea, bloating, wind and an itchy bottom, the cause can be an overgrowth of yeasts in the gut, caused in part by repeated courses of antibiotics which kill off friendly gut bacteria in the gut flora (see p. 204) and allow yeasts to flourish. This is not mainstream medicine, which is why none of the doctors who had seen Jason mentioned the possibility of yeast overgrowth.
Yeasts are microscopic fungi, so anti-fungal drugs are needed to kill them. However, reducing the intake of sugar in the diet is also very effective because yeasts living in the gut thrive on sugar. Hannah took matters into her own hands, and tried out a diet containing no sugar and no yeast. (The reason for avoiding yeast in food is discussed below.) There was some improvement and, encouraged, she went back to the doctor and asked for anti-fungal drugs.
The doctor agreed, and to Hannah’s immense relief, the combination of diet and drug treatment worked for Jason – it cleared the diarrhoea, wind and itching, and eventually allowed his eyelashes and eyebrows to grow back. (Note that few other patients with yeast problems suffer hair-loss – this is a very exotic symptom – but yeast overgrowth can produce some other quite unusual reactions.)
The elusive culprit
So far, you will notice, I have not mentioned Candida. Among those doctors who study and treat this condition, this particular yeast was once considered the prime suspect. Indeed, the disease itself was called ‘candidiasis’. But the role of Candida is now considered doubtful by many.
Researchers such as Dr John Hunter, of Addenbrooke’s Hospital in Cambridge, have tried to find Candida in their patients without success. ‘I think now we have to reject the idea of Candida causing the symptoms,’ says Dr Hunter. ‘But I do believe that there is an imbalance in the gut flora – the micro-organisms that live in the gut. I believe that’s at the root of so-called “candidiasis”.’ This new evidence has not yet affected beliefs about candidiasis’ and ‘Candida’ in the complementary health field.
The fact remains that anti-fungal drugs have proved very helpful to many patients with the typical cluster of symptoms –diarrhoea, wind, bloating and an itchy anus – that were previously attributed to Candida. Given the effectiveness of these drugs, it seems probable that yeasts of some kind are playing a large part in this condition. So the term ‘yeast overgrowth’ is being used, rather tentatively at the moment, as a label for this condition. The yeasts concerned have not, as yet, been identified.
The facts about Candida
This box is about Candida as understood by conventional medicine, rather than ‘Candida’ and ‘candidiasis’ as understood by alternative medicine.
The yeast known as Candida lives naturally in the gut, usually causing no trouble. Problems are usually caused by Candida only when it sets up home in the throat, vagina or penis (’thrush’ infections). Such localised infections have well-defined symptoms and, in most cases, are easily treated with anti-fungal drugs. Patients with damaged immune systems, caused by anti-cancer drugs or AIDS, often develop more widespread Candida infections, but this never happens to people with a normal immune system.
Inhaling steroids and not rinsing out the mouth afterwards can make asthma sufferers more susceptible to Candida infections in the throat (see p. 145).
Other symptoms that have been linked to yeast overgrowth are:
• fatigue
• poor concentration
• irritability, depression and confusion
• headache or migraine
• severe premenstrual problems
• recurrent cystitis
• skin rashes
• aching muscles
• chronic urticaria.
Sometimes there is constipation rather than diarrhoea. Recurrent thrush – a genuine Candida infection in the vagina – can also be a feature of this problem. Occasionally allergic symptoms such as asthma seem to get worse with yeast overgrowth.
Is there an allergic reaction to the yeast?
Those with symptoms typical of yeast overgrowth may give a positive skin-prick test to Candida, but what this means is debatable. For one thing, not everyone with this condition gives a positive test. For another, some entirely healthy people give a positive skin-prick test to Candida. To complicate matters, there are a lot of cross-reactions (see p. 14) between different kinds of yeasts and moulds, due to similarities in their chemical constituents. So the positive skin-prick test does not mean that Candida itself triggered the original IgE-response.
The question of whether some kind of sensitivity reaction to yeasts is occurring in those with yeast overgrowth, and contributing to their symptoms, is an interesting one. The benefits from avoiding yeast in food (see Diagnosis and treatment) suggest that it may be – but this is a question that cannot be answered at present.
Diagnosis and treatment
Unfortunately, this is one of those ’suck-it-and-see’ conditions, where diagnosis and treatment are the same – you try the treatment for yeast overgrowth, and if it works you assume that the disease is, or was, yeast overgrowth. This is far from satisfactory, but is the best that can be done at present.
It is only worth trying this treatment if you have quite a number of the symptoms listed. Bowel problems and an itchy anus are characteristic, and if you have neither of these it is unlikely the treatment will help you.
A key part of the treatment is a no-yeast-no-sugar diet (see p. 205). This diet has been developed on a largely pragmatic basis, and seems to work – but why? The rationale for cutting out sugar is clear – it feeds yeasts in the gut. But why avoiding foods containing yeast should help is uncertain. Possibly the yeasty food supplies some special nutrient that benefits the yeasts living in the gut. Alternatively, there might, for some people, be a sensitivity reaction to the yeast in food (see left).
If it seems that you are on the right track, because there is some improvement with this diet, ask your doctor for anti-fungal drugs. You should take these in addition to the diet. Nystatin (see box below) is very safe for most people, since it is not absorbed from the gut. Bacterial replacers (see p. 205) may also be useful.
You may need a referral to a doctor who is knowledgeable about yeast overgrowth but try to avoid those doctors and alternative therapists who are part of the ‘Candida’ craze, and think that ‘candidiasis’ explains a huge variety of illnesses. You may not have yeast overgrowth at all, so you need someone with an open mind.
Eczema and yeasts?
Doctors have found that some children whose eczema looks very red, and is not responding to treatment, have IgE in the blood against a range of yeasts and other fungi (Candida, Trichophyton, Saccharomyces and Pityrosporum). Given the tendency to cross-reactions among fungi (see main text) it is not clear exactly what these reactions indicate. A proportion of these children get much better on anti-fungal drugs, including a drug called nystatin, which is not absorbed through the gut wall – so cannot reach the skin. The eczema improves, and at the same time there is a fall in levels of anti-fungal IgE in the blood. In other words, a treatment that can only affect fungi living in the gut benefits the skin. Exactly what is going on here is unknown, but the important point is that the treatment seems to work. This is a controversial topic, but since nystatin is an extremely safe drug, your doctor may be prepared to try it out. A course of 3-4 weeks is the minimum needed.

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’.