Posts Tagged ‘greek word’

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.

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