Posts Tagged ‘IgE-mediated’

Allergens in Food
Anyone with true food allergy or coeliac disease needs to be very careful about avoiding certain foods. The information given here is aimed mainly at such people, rather than those with food intolerance (see p. 74), who can usually tolerate small amounts of their offending foods. However, some of the basic information given here is relevant to those with food intolerance as well.
There are different levels of sensitivity even among those with true food allergy. The ‘exquisitely sensitive’ can react to unbelievably minute traces of the food, and for them life is especially difficult. The same is true of some coelicacs, who can be affected by the tiniest quantity of gluten.
These people are a small minority. The level of vigilance required of such people will not be necessary for most people reading this book, so don’t get things out of proportion. While it is vital to be sensible about avoiding your problem food, it is also important not to become over-anxious.
Buying basic ingredients
Cooking for yourself is the safest way to eat for those with true food allergy and coeliac disease. There are relatively few hazards, but do beware of well-meaning assistants in health-food shops who try to sell you some exotic package of grain or flour – spelt or kamut or triticale, for example – reassuring
you that it is ‘definitely not wheat’. Be well informed about the different forms of your problem food and the names under which it is sold (see pp. 172-5).
Oils made from foods such as corn or peanut sometimes cause concern. Ordinary refined oils have been so thoroughly processed that they actually contain no allergenic proteins, so you can safely use these. Bottles of gourmet walnut oil and almond oil are a different story however, and should be avoided if you have nut allergies. Sesame oil is not purified either and can provoke serious reactions. With any oil, if you are unsure how safe it might be, go by the smell. Oils that smell or taste like the food from which they are made could well contain allergens.
Those with allergy to tuna can usually eat tinned tuna because the processing makes it safe. The allergens in fresh fruit and vegetables are generally inactivated by cooking too, so jams and tinned fruits tend to be safe – but test very cautiously. Cooking does not have much effect on other food allergens, apart from eggs. In rare cases, cooking can create allergens (see box on p. 186).
If you share your kitchen with others, and are highly sensitive, check that all cooking utensils are truly clean before use. Coeliac should watch out for breadcrumbs in the butter dish, jam or toaster. Where small children are allergic to a food, it may be best to keep the culprit out of the house entirely.
Genetic engineering and food allergy
Many people with food allergies are very concerned about the possibility that genetic engineering could introduce allergens from one plant species into another. This concern seems to be shared by government officials and those in the food industry, who are being extremely vigilant and cautious at present. As long as this attitude continues, there should be little danger to food allergy sufferers.
Finding food in funny places
If you are suffering some inexplicable reactions to non-food items, it might, just possibly, be a food reaction. Some latex gloves contain the milk protein casein, for example, added as a manufacturing aid.
Buying packaged foods
There are several different issues here:
• the need to read labels carefully for allergenic ingredients described by unfamiliar names (see p. 172)
• errors in the packaging used (see pp. 174-5)
• contamination by minute traces of a food substance due to processing machinery not being cleaned adequately. Cartons of fruit drink have occasionally been contaminated with traces of milk because the same production lines were used for packaging milk drinks. Tofu desserts made in ice-cream factories can also become contaminated with milk. These tiny traces of a food will only affect the most highly sensitive individuals, but contamination by nuts can involve large pieces and affect anyone with nut allergy (see p. 174).
• foodstuffs which are used as part of the production process
and leave a tiny residue in the finished item (see p. 174).
Be very cautious indeed about ready-made food that is unlabelled, such as that from bakeries and home-made stalls. Egg is frequently used as a glaze on baked products, nuts may lurk within, and milk or wheat can turn up in the most unlikely places.
Restaurants, cafes and takeaways
The majority of fatal and near-fatal incidents involving people with true food allergy are due to restaurants, cafeterias and canteens. Takeaways can also be a problem except in the case of the large chains such as McDonald’s, where ingredients are standardised. It is alarming that highly allergenic foods (e.g. peanut) are sometimes used – yet far from obvious – in recipes and sandwich fillings where they would simply not be expected. Anyone with peanut or shellfish allergy should be ultra-cautious about Chinese, Thai or Malaysian cooking – but those with milk allergy should find a haven here, because milk is not part of these culinary traditions.
The simplest solution is to eat very plainly when you go out –steak and salad, for example. Steer clear of casseroles and thick soups, where you can’t see what’s in it (the occasional chef throws in peanut butter to thicken the mix…). Food wrapped in pastry is best avoided for the same reason. Desserts and cakes are risky for anyone with nut, egg or milk allergy.
You must insist on accurate information about the food before you taste it. If the counter staff, the waiter or the waitress
is unsure of the ingredients, ask them to check with the chef, or with the label on pre-packaged food. Be persistent and never eat anything unless you are sure. Make eye contact with the person concerned, and learn to be a good judge of character. Your life could depend on telling the difference between the waiter who knows the facts about the food and the waiter who is being blandly reassuring for the sake of a quiet life.
It is a great mistake to pick out the pieces of offending food – kiwi fruit from a fruit salad for example – and eat the rest. There is often enough allergen left behind to cause anaphylaxis in the highly allergic individual.
Those who are extremely sensitive to the offending food must also consider the problem of contamination in the kitchen. Grills and fryers in restaurants and canteens can become contaminated with fish allergens or nut allergens (e.g. from nut cutlets) and these can be transferred to fried potatoes or other foods, provoking anaphylaxis in the highly allergic individual. One person with fish allergy died in this way. Sesame seeds can also contaminate equipment, work-surfaces or bakery counters.
Parties and buffets
Milk, egg, shellfish or nut allergies can make it especially hazardous to eat buffet or party food. Regard everything with suspicion. Cocktail snacks with nuts or peanut paste hidden inside are a particular problem.
When fish allergy isn’t fish allergy
Anisakis is a parasitic worm that infests fish and can sometimes survive the
cooking process to infect humans. The worms are easily thrown off by the human immune system, but the body is primed to make IgE antibodies should
it ever encounter Anisakis again. Another meal of parasitised fish – even if the Anisakis worms are all dead this time, and only the allergens remain
will provoke a massive IgE-mediated reaction, leading to anaphylactic shock. This problem is usually misdiagnosed as allergy to fish itself.
Other inconsistent reactions to food can be due to contaminants such as antibiotics, preservatives, other food additives or (especially in the case of shellfish) naturally occuring toxins.

Coeliac Disease
During World War 11, there was no bread to be had in the Netherlands and people were forced to eat tulip bulbs. ‘My mother roasted them,’ one survivor recalls, ‘and they tasted delicious then, because we were so hungry I suppose. I cooked some years later, just to taste them again, and they were absolutely disgusting.’
While most of the population was thin and unwell on this starvation diet, a few children were actually healthier than before. An observant Dutch doctor noted that these were the children who, before the war, had suffered from constant diarrhoea, fatigue, poor growth and muscle wasting. They were suddenly stronger and, his enquiries revealed, their diarrhoea had vanished. But when the food situation improved at the end of the war, all their old problems returned. By carefully experimenting with the diet of these patients, the doctor discovered that eating wheat and rye caused the symptoms. Subsequent research has revealed that both contain a collection of proteins, referred to as gluten, which are the source of coeliac disease.
Belly disease
Coeliac disease (or celiac disease) is an old name which simply means ‘belly disease’. It is derived from the Greek word for’belly’ — koilia. Once the cause of the symptoms became understood, a new name was devised — gluten-sensitivity enteropathy — but it has not really caught on. Other terms that you may come across are non-tropical sprue and coeliac sprue, based on the close resemblance of the symptoms to those of tropical sprue. This disease, found in those who live or have lived in the tropics, is probably caused by bacterial infection. There is no causal link with coeliac disease.
Symptoms
The symptoms of coeliac disease are:
• diarrhoea, with pale, bad-smelling stools
• in a few patients, constipation rather than diarrhoea, but this is very rare
• bloating and wind
• damage to the lining of the intestine. This is of a characteristic type: the complex folded structures (the villi) of the intestinal lining are destroyed. Additionally, huge numbers of immune cells are present.
• the loss of the villi results in failure to absorb nutrients from food (malabsorption) causing poor growth in babies, and weakness and weight-loss in adults.
• poor appetite, especially in babies. This can greatly reduce the diarrhoea.
Coeliac disease usually appears in babies during weaning, a few weeks after cereals are introduced, but it can also begin for the first time in adults. The tendency to coeliac disease is genetically inherited, so it runs in families.
Where coeliac disease runs in the family, another disease, dermatitis herpetiformis, is also likely to occur. Dermatitis herpetiformis has the same basic mechanism as coeliac disease but very different symptoms:
• an intensely itchy rash, sometimes with tiny blisters; the rash is symmetrically distributed on the buttocks, shoulders, scalp, and the outer surfaces of the knees and elbows
• the same characteristic damage to the lining of the intestine as seen in tests for coeliac disease, though generally less severe
• diarrhoea, in some cases, but not all. About 5% of those with coeliac disease actually go on to develop dermatitis herpetiformis. Most people have either one or the other.
Both diseases are caused by the same gene, which results in sufferers developing antibodies against one of their own proteins, an enzyme called tissue-transglutaminase. The job of this enzyme, which is found in the intestines, is to assist with the breakdown of gluten.
If no gluten is present, the enzyme does not arouse the interest of the immune system. It is the process of gluten digestion, in which a particular peptide is produced from gluten, that provokes the autoimmune reaction. (A peptide is any short length of protein chain, obtained from the complete protein chain by digestion.)
What seems to trigger the autoimmune reaction is this enzyme–peptide combination: the offending peptide, newly produced and still attached physically to the enzyme. There is something about the particular ‘chemical picture’ that this combination makes which outrages the immune system of individuals with a particular genetic make-up.
The impact of this autoimmune reaction on the intestinal lining is severe in coeliac disease, less so in dermatitis herpetiformis. What causes dermatitis herpetiformis is a particular type of antibody, called dimeric IgA, which is transported by the bloodstream from the gut to the skin. It is deposited in the skin all over the body, but for some reason only provokes inflammation in certain areas.
In rare cases, an IgE-mediated food allergy to wheat can co-exist with coeliac disease, making reactions more severe.
Secondary problems
Paradoxically, while the damaged gut lining of untreated coeliac disease makes a poor job of absorbing specific nutrients (e.g. iron and vitamins) in a form that the body can use, it also lets through far more intact, or partially digested, food molecules. These get into the bloodstream in such numbers that they can lead to idiopathic food intolerance (see p.74). Sensitivity to soya is a common problem, because it is so heavily used in gluten-free bread and other prepared food. Those with coeliac disease who have not improved fully, despite a strict gluten-free diet, often benefit from an elimination diet (see p. 194). This must be done under medical supervision.
Another possible effect of the intestinal damage is lactose intolerance (see p.79), producing a sensitivity to milk.
The frequency of schizophrenia is higher among those with coeliac disease than among the general population. Coeliacs not following a strict gluten-free diet are also vulnerable to other psychological problems. These might be linked to the effects of food-derived exorphins (see pp. 76-7) and other peptides on the brain. The increased permeability of the gut could play a part in this, allowing more exorphins to reach the bloodstream.
Diagnosis
A biopsy (see p. 92) is the only really reliable form of diagnosis. It is crucial that this is done before removing gluten from the diet, because the damage is repaired if gluten is avoided and the healing process is fairly rapid for some people (though in others it takes many months). If the intestinal lining reverts to a normal appearance quite quickly, an accurate diagnosis is never obtained, which can have serious consequences: if you or your child are coeliac, you need to know.
New blood tests can also be helpful in diagnosis, but they do not give the unequivocal result obtained with a biopsy.
Research from the United States suggests that coeliac disease is under-diagnosed in some countries compared to others – for example, Italy screens children routinely but the States does not. Some authorities suspect that there is a great deal of ‘hidden’ coeliac disease in the States, and this could be true in other countries as well. There is no routine screening of children in Britain.
The symptoms of coeliac disease are not always distinctive. Many cases are first detected when patients with rather non-specific symptoms are discovered, by a blood test, to be anaemic.
Treatment
There are no drug treatments for coeliac disease and avoiding gluten religiously is the only way to remain well. Those who are lax about their gluten-free diet may be more vulnerable to certain cancers of the digestive tract.
A strict gluten-free diet is not easy to follow (see p. 177). The most severely affected coeliacs are so sensitive to gluten that they react violently to even a tiny amount: this is known as coeliac shock and can be fatal.
A gluten-free diet is also the treatment for dermatitis herpetiformis, but at the outset the rash can be controlled with the highly effective drug dapsone.

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

Sinus cavities are something that most people just don’t know they have. It’s only when they start to

hurt that you find out where they are. ‘There is this terrible throbbing pain above and around my eyes,

and in my cheeks. It’s the most unpleasant feeling, but it’s hard to describe to anyone who hasn’t felt

it,’ says Gina, who suffers from chronic sinusitis (long-term inflammation of the sinus cavities).

There are no figures, but chronic sinusitis seems to be increasingly common.
A sinus cavity has no function, it is just empty space without which our skulls would be much heavier.

In other words, these airy spaces seem to have evolved simply to help us feel more ‘light-headed’. If

you have sinusitis, unfortunately, you feel just the opposite. ‘I had sinusitis for years,’ says Dr

Wellington S. Tichenor, a New York allergist who now specialises in treating chronic sinusitis. ‘I kept

working but felt like I wanted to die.’
Sinus cavities are lined with a membrane which is essentially similar to that lining the nose. It

contains immune cells and can produce mucus when necessary. Most of the time it doesn’t need to produce

much, because relatively few microbes or foreign particles get into the sinus cavities.
Any mucus that is produced should escape from the sinus cavities through narrow drainage channels,

called Ostia, leading to the nose. Unfortunately, the Ostia are very narrow – the diameter of a

pin-head – and U-shaped, making them prone to blockage. And that is not the only problem. These

drainage channels are situated at the top rather than the bottom of the main sinus cavities – this

arrangement was fine for our ancestors who walked on all fours, and therefore did not have to fight

gravity when clearing their sinuses. Sadly for
us, natural selection has not got around to reorganising things yet. It would be a completely hopeless

arrangement if not for the tiny hairs known as cilia, which lie like a carpet across the membranes

lining the sinus cavities. The cilia beat rhythmically. 18 times a second, to waft the mucus upwards to

the top of the sinus cavity.
This is a far-from-perfect system, and it is hardly surprising that it sometimes goes wrong. Chronic

sinusitis can begin in at least three different ways:
• The sinus membranes become inflamed due to an allergic reaction – 28 for likely airborne

allergens.
• The drainage channels from the sinus cavities become blocked due to events in the nose

(infection or allergy) or due to the growth of polyps (non-cancerous jelly-like lumps that can block

the drainage channels). When mucus cannot drain away, it stagnates in the sinus cavities encouraging

infection by bacteria or fungi. These infections cause inflammation.
• A bout of acute sinusitis (see box on p. 31), due to bacterial infection, never really goes

away and the persistent infection causes longterm inflammation. Note that this is unlikely: it is rare

for acute sinusitis not to clear up.
Whether the problem begins through allergy or blockage or infection, once it has begun a vicious circle

can be set up all too easily. Mucus output increases when there is inflammation, blocking the drainage

channels even more, so the sinus cavities become clogged up and increasingly uncomfortable. More mucus

pooling in the sinus cavities perpetuates any existing infections and fosters new ones.
All this infection results in more severe inflammation, causing the membranes which line the sinus

cavities to swell up. Inflammation also makes polyp growth more likely. The cilia may be lost or

severely depleted, and the mucus gets thicker. All this means yet more blockage. To cap it all, there

can be allergic reactions to some of the microbes involved (see right), fuelling the inflammation

further.
The body’s own attempts to clear the sinuses are defeated, and the problem is also very resistant to

medical treatment. This may make depressing reading, if you have chronic sinusitis, but don’t despair.

Understanding the complexities of the problem is a large part of the battle. Chronic sinusitis is not

invincible, if you have a good doctor to help you - that means a doctor who also understands these

complexities.
The symptoms of sinusitis are:
• pain and a sense of swelling or unpleasant fullness around the cheeks, or over and between the

eyes
• earache or headache; pain around the teeth
• reduction in the senses of smell and taste
• sore throat
• coughing, particularly at night
• post-nasal drip (mucus from the back of the nose running into the throat and airways)
• bad-smelling breath
• feverishness
• for some people, severe fatigue, poor concentration and even (but very rarely) psychiatric

symptoms
• irritability, especially in children.
Note that any of these symptoms can be caused in other ways, and even if you have several of them, you

may not necessarily have sinusitis. On the other hand, sinusitis can go unrecognised - to some people

it may seem like nothing more than a lingering cold.
Acute or chronic?
In medical terms, ‘acute’ means short-lived, while ‘chronic’ means long-lasting.
Acute sinusitis — a short, sharp dose of it, lasting less than 3-4 weeks - usually follows on from a

cold. Colds are caused by viruses, but a bacterial infection can follow, and it is the bacteria that

move into the sinus cavities and cause trouble. Some people are far more susceptible than others and

have an attack of sinusitis after every cold.
Chronic sinusitis means symptoms lasting more than three months, according to some authorities, but the

time point is a little arbitrary. This article deals with chronic sinusitis.
If your sinusitis has been going on for between four weeks and three months you will obviously be

asking ‘Is this acute or chronic?’ At this point, no one can say, but you would certainly be wise to

seek some expert medical treatment now, on the basis that it could be the start of chronic sinusitis.

Tackling chronic sinusitis before the problem becomes
entrenched and complex is a good plan.
Allergy and chronic sinusitis
Chronic sinusitis is not necessarily an allergic disease, but it can be connected with allergies (or

other forms of immune sensitivity) in various ways:
• Allergic reactions can occur in the sinuses, usually in conjunction with allergic reactions in

the nose.
• Even if the allergic reaction does not affect the sinuses directly, allergic reactions in the

nose can block the drainage channels from the sinuses, causing an accumulation of mucus there. This may

lead to sinus infections.
• Once sinusitis has begun, infectious fungi (moulds) in the sinuses may provoke allergic

reactions, or other forms of immune sensitivity. This allergy to ‘the enemy within’ fuels more

inflammation and more mucus production. Right now, allergic fungal sinusitis (as it is known) is a

source of heated debate - 32. Allergic reactions to some of the bacteria that are present may also

occur.
• Chronic sinusitis - however caused - can contribute to asthma. Research on children with both

sinusitis and asthma found that 80% no longer needed asthma drugs once their sinusitis had been

treated, and 85% no longer wheezed. The link may be due to post-nasal drip, increased mouth-breathing,

or to a nerve-connection between the sinuses and the airways (the sinobronchial reflex) which can

stimulate airway inflammation. Alternatively, the sinusitis may simply fire up the immune system with

messenger chemicals in the bloodstream, resulting in more powerful responses throughout the body.
• Chronic sinusitis can also be the root cause of long-standing nettle rash (chronic urticaria),

and treating the sinusitis can result in a prompt and remarkable clearance of the skin symptoms.
• Some people who have chronic sinusitis are sensitive to aspirin (see box on p. 28) - a

sensitivity which is also linked with asthma, nasal polyps, rhinitis and chronic urticaria. Avoiding

aspirin and all other aspirin-like drugs (151) may substantially improve the sinusitis.
Diagnosis
Because so many different factors can play a part in chronic sinusitis, diagnosis should, ideally,

consider the problem from several different angles:
• The sinuses are viewed using X-rays and CT scans (computed tomographic scans - they use X-rays

but give a much more precise picture). These reveal how badly swollen the sinus membranes are, which

sinus cavities are blocked, and how much mucus has collected in the sinuses.
• Endoscopy (92) may be used to look inside the sinus cavities. Polyps are best located by this

method.
• Where allergies seem to be part of the picture, the doctor may employ skin-prick tests (91) to

identify allergies to airborne allergens (from house-dust mites, moulds, pets, pollen, cockroaches,

etc.)
• Laboratory tests on samples taken from your sinus cavities will be used to show which bacteria

and/or fungi have set up home there. There may also be a hunt for the immune cells known as eosinophils

(19) or the typical debris which they generate. The presence of large numbers of eosinophils is one

indication of allergic fungal sinusitis (see below).
• Skin testing with fungi (moulds) found growing in the sinus cavities may also be tried if

allergic fungal sinusitis is suspected.
• In severe cases, there may be tests of immune function, to see whether this is depressed in any

way.
• Children may be tested for an inherited disorder affecting the cilia, or for cystic fibrosis -

mild forms may escape detection, and can produce both chronic sinusitis and wheezing.
The enemy within
The biggest controversy in sinusitis research at the moment concerns allergic fungal sinusitis. The

orthodox view of this condition is that:
• It affects a small minority of chronic sinusitis patients -fewer than 10%.
• There is a true IgE-mediated allergic reaction to the fungus (mould) growing in the sinus

cavities. This allergic reaction is detectable with a skin-prick test (91). Immune cells known as

eosinophils (19) are also key players in the inflammatory reaction to the fungus, but it is an

IgE-response to the fungus that draws the eosinophils into the sinuses.
• There is clear evidence of fungal infection in the mem- banes of the sinus cavities.
• There may also be ‘fungus balls’ - a solid mass of fungus inside the sinus cavity. Or there may

be ‘allergic mucin’, a dark sticky mucus containing fragments of the fungus.
A rare complication
In rare cases, the fungi involved in allergic fungal sinusitis can be invasive, spreading from the

sinuses to the surrounding bone. This problem needs prompt and thorough treatment with anti-fungal

drugs.
In 1996, researchers at the Mayo Clinic in Rochester, Minnesota, USA, caused a rumpus by claiming to

have identified a different form of allergic fungal sinusitis which is overlooked by standard

diagnostic techniques, and which affects 96% of patients with chronic sinusitis.
This is a staggering figure - 96% means, in effect, that they are claiming to have found the

fundamental cause of virtually all chronic sinusitis. ‘Up to now, the cause of chronic sinusitis has

not been known. Our studies indicate that, in fact, fungus is the likely cause of nearly all of these

problems,’ states Dr David Sherris, one of the researchers.
According to the Mayo Clinic team:
• The fungi (moulds) are growing in the mucus of the sinus cavities, not generally in the

membrane itself. They are not detected by normal diagnostic methods which tend to ignore the mucus. A

special method of collecting the mucus is required to detect the fungi.
• The immune reaction to the fungi is not usually an IgEmediated reaction, so skin-prick tests

are often negative.
• Finding evidence of unusual numbers of eosinophils is adequate for diagnosis of allergic fungal

sinusitis because the eosinophils are the prime movers in this sensitivity reaction to the fungi, as in

several other diseases (19).
‘We can now begin to treat the cause of the problem instead of the symptoms,’ says Dr Eugene Kern, head

of the research team. There is a lot of scepticism about these claims among other sinusitis

specialists, and so far no new treatment for chronic sinusitis has emerged.
The Mayo Clinic researchers say that they are in the process of developing a drug treatment, but that

it will take several more years before it is generally available. Existing anti-fungal drugs (taken in

capsule form) could not work on this particular form of allergic fungal sinusitis (if it exists)

because the drug does not get into the mucus. Any new treatment would probably involve inserting an

anti-fungal drug directly into the sinus cavities, which is far from easy.
All we can do for now is wait and see what emerges from the ongoing research. The current treatment for

allergic fungal sinusitis involves all the usual methods (see right) with special emphasis on steroids

to calm the inflammation, plus anti-fungal drugs where fungal infection is detectable in the membrane.

In some countries, immunotherapy is also used to reduce the immune reaction to the fungus, but this is

difficult to obtain in Britain (164).
Clearing moulds from your home may help (34). So may reducing the humidity in the house (119), as humid

conditions seem to be linked with allergic fungal sinusitis.
Treatment
Sinusitis can be very hard to treat, particularly if it has been going on for a long time. You need a

really committed attitude if treatment is to be successful.
All these treatments should be given at the same time:
1 Antibiotics for 2-3 weeks minimum (it takes this long because the antibiotic has such trouble getting

into the sinus cavities – if you are offered a shorter course, this suggests that the doctor does not

have enough expertise with chronic sinusitis, so you might be better off with someone else). It must be

the right antibiotic – commonly used ones such as penicillin, tetracycline and erythromycin are

unlikely to work because the bacteria are usually resistant to them.
2 Steroid drops in the nose to combat the inflammation. It is important to put these in correctly, so

that they have maximum effect (144) especially if you have polyps.
3 Irrigating the nose and sinus cavities daily with sterile salt water (saline). Your doctor will show

you how to do this.
4 Tablets that reduce the congestion in the nose.
5 Nose drops that reduce congestion, but for three days only (29).
6 Steam inhalations to loosen the mucus. There are special steam vaporisers on sale (ask at a

pharmacy), but you can just inhale steam from a bowl of boiling water, with a towel over your head to

keep the steam in. Adding eucalyptus oil to the water may help. For a quick-and-easy version, warm up a

damp flannel in the microwave and place it over your nose. Some doctors recommend having a steam

vaporiser beside the bed at night, when nasal blockage is most likely to occur, but if you have

allergies to house-dust mite or moulds this is not a good idea in the long term, as a damp bedroom will

favour both (and could encourage allergic fungal sinusitis).
7 A drug called guaifenesin which thins the mucus is used in some countries but rarely in Britain.

Alpha-methyl-cysteine is another drug that breaks up mucus. It is mainly used in chronic bronchitis but

some doctors also find it valuable in chronic sinusitis. If steam inhalations didn’t work – suggesting
that the mucus is too solid to be shifted – these drugs may be worth trying.
8 Anti-fungal drugs (taken by mouth) if allergic fungal sinusfis is suspected. Sometimes these have a

dramatic effect on chronic sinusitis that has previously resisted treatment.
You may also be given other drugs, such as steroid tablets. The new anti-leukotriene drugs (149) are

also being tried, with some success. As well as being taken by mouth, they can be applied directly to

the nose in an irrigation fluid, and may be helpful for those with nasal polyps.
Problems with nose drops
Nasal drops and washes contain preservatives and other non-drug ingredients. Some of these may act as

irritants – or the pH (acidity or alkalinity) of the preparation might cause problems. If you

experience burning or irritation after inserting drops or irrigating the sinuses, ask your doctor or

pharmacist about trying a different preparation.
Antibiotic resistance
Bacteria are becoming resistant to the effects of antibiotics: it is probably the biggest headache

facing modern medicine.
This is emerging as a particular problem in chronic sinusitis because many patients have been dosed

very regularly with antibiotics. Although most of the bacteria have been killed each time, the fact

that the sinus cavity is so clogged up with mucus, and so badly accessed by the bloodstream anyway,

means there is always some nook or cranny where a few bacteria survive because they have not been

exposed to the full lethal dose of the antibiotic. As you might expect, these survivors tend to be the

‘tough ones’ – those bacteria that are not just well hidden but also the least sensitive to the

antibiotic.
Repeat this process many times, with frequent courses of antibiotics (separated by intervals during

which the hard-to-kill bacteria multiply in numbers) and what happens? Eventually you breed a race of

bacteria that are completely resistant to one or more of the antibiotics taken.
If you ever get to this point with your sinusitis, treatment is going to be extremely difficult. That’s

why it is so important to treat infections really thoroughly, and get rid of them completely. Expert

medical help is essential for this treatment campaign.
Too many people with chronic sinusitis are careless about taking their antibiotics regularly, or feel

ambivalent about them and stop the course before it’s complete, or don’t see the doctor again when the

tablets are used up. This is courting disaster.
Don’t start antibiotic treatment for chronic sinusitis until you are sure you can see it through. If

you have doubts about taking antibiotics, try all the other treatments and self-help measures first.

They may be sufficient, especially if you find you have an allergy underlying the chronic sinusitis and

can tackle this successfully.
Should there be no improvement, you could then go on to the antibiotic programme: delaying this

treatment for a few months will do no harm. What is hazardous is starting the antibiotic programme and

then stopping, or not taking the drugs consistently.
Antihistamines may be prescribed to treat any allergic reactions, but some specialists feel that they

can also aggravate the problems. In their experience, antihistamines dry out the mucus so that it

sticks to the walls of the sinus cavities, rather than being ushered out by the cilia. Drying out the

mucus may make you feel better initially, by reducing the pressure inside the sinus cavities, but it

makes matters worse in the long run.
Anti-chollnergic drugs (156) are sometimes prescribed for chronic sinusitis, but they too can dry up

the mucus and should be used cautiously.
After three weeks, if the sinusitis has not improved substantially, a different antibiotic is given. If

there are any bacteria resistant to the first antibiotic infesting your sinus cavities, the new

antibiotic is intended to kill them off.
Should you still have sinusitis after another three weeks, you will be given yet another antibiotic.

Changing the antibiotic, and taking prolonged courses, is the best way of exterminating the bacteria

completely, which prevents the development of antibiotic-resistant bacteria (see box at left).
It is crucial that you always see the doctor promptly at the end of each course, so that there is no

gap between the courses – do not give the bacteria any opportunity to build up their numbers again. The

last antibiotic treatment should continue for at least a week after symptoms clear up.
Dealing with allergic reactions is also important:
• If you cannot get allergy tests, try to work out for yourself if an allergen is playing a part.

Ask yourself if there were any changes in your life before the sinusitis began, such as getting a new

pet, moving house, increased exposure to moulds or house-dust mite, or starting a new job with exposure

to allergens. When thinking about this, remember that allergies to newly encountered allergens do not

develop immediately – it may take up to two years. Try avoiding the allergen concerned and seeing if

you improve.
• Should you discover that an allergen is at the root of the problem, but have difficulty

reducing your exposure to the offending item, try to obtain immunotherapy (164) or another form of

desensitisation treatment (210).
• If you suspect allergic fungal sinusitis (32), it is well worth eliminating any mould growth in

your home (120). One research study showed that the moulds growing in a patient’s sinus cavities were

often the same as those growing in the patient’s house. It is possible that, by inhaling the mould

spores from moulds in their houses, sinusitis sufferers are continually reinfecting their sinuses.
Various other self-help measures can be valuable during this medical treatment:
• Reduce your exposure to cigarette smoke (including other people’s) to an absolute minimum.

Cigarette smoke acts as an irritant to the nose and sinuses, but, more importantly, it paralyses the

cilia, preventing them from shifting mucus out of the sinus cavities.
• Avoid breathing other irritants, especially ozone (130). Think about the chemicals you use both

at work and at home – could any of these be irritants that are aggravating your sinusitis?
• Don’t drink too much alcohol – it dries out the sinus membranes and makes matters worse.
• Drink plenty of water, to keep your mucus from becoming too dry and therefore hard to shift.
• Try to breathe through your nose as much as possible. The amount of oxygen in your sinus

cavities drops drastically if you breathe through your mouth, and the low oxygen level probably fosters

the growth of certain bacteria. Devices, such as nose clips, that help keep the nose open at night may

be worth trying.
• Spicy food can help to clear nasal and sinus congestion, so try eating chilli or hot curry

regularly.
• Some people find that garlic helps – either eaten or sniffed.
• If you suspect that your sinusitis might be related to food sensitivity (68) consider trying an

elimination diet to identify the culprit food.
• Observe your reactions immediately after eating – some foods, such as yeast and red wine, can

cause an immediate swelling of the nasal membranes in certain people. So can sulphite food additives.

Avoid such items if you are affected.
• Treating gastro-oesophageal reflux (acid regurgitation from the stomach after meals) can

improve sinusitis.
• See an osteopath. By gently manipulating parts of your face, a good osteopath may be able to

improve the drainage from the sinus cavities.
• Some patients experience good effects from acupuncture although there are no observable changes

on CT scans. Other alternative therapies, such as homeopathy or Chinese herbal medicines, have not been

investigated scientifically, but some patients report good results.
Prolonged courses of antibiotics destroy many of the beneficial bacteria in the intestine, and may

cause long-term bowel problems. It makes sense to take a bacterial replacer (205).
Surgery for sinusitis
Chronic sinusitis sufferers may be offered surgery to remove polyps, or to correct anatomical problems

such as a deviated septum (the central division of the nose).
These operations can be very useful, but if you have asthma try all other options first, because

surgery to the nose can sometimes make asthma much worse.
Surgery on the sinus cavities themselves is also a possibility, when sinusitis does not respond to

medical treatment. The operation enlarges the natural drainage channels, so that mucus drains away more

easily. This rarely cures chronic sinusitis completely, but it usually makes it much easier to manage.

Once the drainage channels are larger, antibiotics can be put directly into the sinus cavities, for

example, avoiding the need for antibiotic tablets.
Don’t agree to surgery unless other forms of treatment, such as allergen avoidance or immunotherapy,

have been tried to the full. Patients for whom surgery seemed to be the only answer have sometimes

found they did not need an operation once their allergies were treated.
If you decide on having an operation, make sure your surgeon has a proven track-record with this type

of surgery. Don’t be afraid to ask searching questions about how many operations of this kind the

surgeon has done, how many he or she carries out per year, and the complication rates (how often things

go wrong). It’s a delicate job, and you want a real expert.

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

 

What is Allergy?
Words matter, particularly in medicine. Using the same words to mean different things is a major difficulty for patients when discussing allergies with a doctor. Unfortunately, few patients realise this, and doctors are frequently too busy to explain what they themselves mean. The result can be a great deal of misunderstanding, confusion and mutual irritation.
Unclear meanings can also create problems if you start exploring other treatment options. The word `allergy’ is like one of those cats that eat at six different houses in the neighbourhood: everyone feels as if they own it exclusively. A conventional allergist will understand one thing by ‘allergy’, while a more unorthodox doctor may have a broader definition, and a herbalist or naturopath may be using the word in a completely different way again.
This is an absolute jungle for the medically unqualified, and it can be an expensive jungle if you are looking around for an answer to your health problems. With the help of this book, you should be able to make sense of all this, and understand the seemingly contradictory advice on offer.
The word allergy was coined in 1906 when it was used to mean altered reactivity - any change in the way the body responds to the environment, whether immunity to a disease already encountered, or a sudden fit of sneezing from pollen. Immunity to disease was soon shunted off into a separate category
altogether, leaving allergy with a narrower meaning:
any adverse reaction to substances that are normally harmless - definition 1. In this book, that meaning is covered by the word sensitivity.
One group of American doctors, who later became known as clinical ecologists, stuck with this definition. Their broad view of allergy is still found among some other doctors today, generally those whose approach to medicine is fairly unorthodox. It is a concept of allergy that is also shared by most practitioners of alternative medicine or complementary therapists.
The rift between the clinical ecologists and mainstream medicine came in the 1920s when the definition of allergy used by conventional doctors was narrowed further to mean reactions to harmless items where the immune system is definitely involved -definition 2. The term immune sensitivity is used in this book to convey that meaning.
In the 1960s, conventional allergists narrowed the definition of allergy again. It was an exciting time because the antibody known as IgE (sometimes called the allergy antibody - see box on p. 12) had just been discovered. The new, tighter meaning of allergy was
reactions to harmless items where IgE is involved -definition 3.
If asked to define allergy, most doctors would give the second of these definitions.
However, when they talk of ‘a tendency to allergy’, ‘allergy treatment’ or `the allergy epidemic’, doctors are generally using the third definition, and just mean IgE-mediated allergy. They may not be conscious of the fact that they are switching from one definition to another. This is not an ideal situation but, generally speaking, it does not create too many problems.
This book deals with ‘allergy’ in the very broadest sense of the word - all kinds of sensitivity. However -and this is purely for the purposes of clarity - where the word allergy is used in the text it always means IgE-mediated allergy (definition 3).
Other immune-mediated problems are called non-IgE immune sensitivity in this book.
Finally, any reaction where the immune system has no proven central role is called an intolerance. (As for other technical words, if you want to find the full definition, look in the index and turn to the page number shown in bold type.)
If you are reading widely on this topic, you may come across sensitivity used either according to definition 1 above, or as another name for intolerance. You may also encounter the word hypersensitivity. This is actually a precise medical term,
but be warned that some writers use ‘hypersensitivity’ very loosely to mean just ’sensitivity’ (definition 1).
Remember that medical politics and economics are powerful forces in all this debate over meanings. Words are quite often redefined by medical interest
groups (such as professional associations) with the clear intention of staking out territory and claiming sole access to medical truth. What is at stake, ultimately, is the right of different doctors to treat patients with certain conditions - and the right of patients to choose for themselves. To add to the longstanding battle over ‘allergy’, there are now rival claims about the meaning of intolerance (74) which have distinctly political overtones.
When you talk with doctors, using the most appropriate terms will help enormously. Talking to a mainstream doctor about ‘food allergy’ when the symptoms suggest food intolerance, for example, is very likely to cause annoyance. This is not unreasonable because IgE-mediated food allergy, unlike food intolerance, is a disease that can very suddenly kill an otherwise healthy person. Using the term `food allergy’ for a headache or mild bowel symptoms is, doctors feel, trivialising a potentially fatal condition.
The important thing is to get along well and communicate clearly with doctors, not to get into a battle about what words mean (in that sense, words don’t matter - they are just labels). Avoid using the word ‘allergy’ unless you are sure it fits in with your doctor’s perception of what is wrong. Just describing how you react - the actual symptoms - is usually the best approach. If you need a general word for your condition, ’sensitive’ is usually a much more diplomatic choice than ‘allergic’.