Posts Tagged ‘prick’

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

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

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

Cross Reactions in Allergy

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