Can antihistamines cause SIBO

Irritable Bowel Syndrome and Mast Cells:
Is there a connection? Therapy options?

This interview with Prof. Dr. med. Martin Raithel was kindly made available to us by: My Allergy Portal.

 

The Irritable bowel syndrome (IBS) is pathophysiologically a disease that is difficult to grasp in the individual patient, which manifests itself through a multitude of different symptoms and can be different in each patient. For all the diversity of the trigger mechanisms, however, it appears to be one in many IBS patients common ground to give and thereby play the Mast cells a role. What do mast cells have to do with irritable bowel syndrome and which ones Therapy options result from it? MeinAllergiePortal spoke about this with Prof. Dr. med. Martin Raithel Internist, gastroenterologist, allergist, health economist (EBS), nutritional medicine (BLAEK) and chief physician of the Medical Clinic II of the St. Marien Forest Hospital in Erlangen.

Prof. Raithel, abdominal complaints are often associated with irritable bowel syndrome (IBS), is this actually a new clinical picture?

Irritable bowel syndrome (IBS) is not a new disease, but has been known for a long time. In the last five decades, however, we have observed a certain increase in the disease, which is essentially clinically defined, as there are no laboratory parameters that can be used to prove it. In western countries in particular, complaints that correspond to irritable bowel syndrome and are increasing in a similar way to obesity, allergies and psychosomatic complaints are becoming more and more common.

However, not all complaints and irritations from the gastrointestinal tract (irritable bowel-like symptoms) can actually be assigned to irritable bowel syndrome. Rather, important diseases that can be quickly and objectively understood are ruled out in the clinic, e. B. gastrointestinal ulcers, infections, cancer etc) .. Often the question of z. B. Food intolerances such as lactose intolerance or fructose malabsorption or the presence of a gastrointestinal allergy, all of which can cause similar symptoms. These diseases can be treated well by avoiding the corresponding carbohydrates or the triggering triggers, while in the case of so-called idiopathic IBS, the cause, the trigger and the exact therapy are unclear in individual cases.

It is noticeable that there has also been an increase in the number of cases of other illnesses over the past fifty years, especially in western countries. These include, for example, obesity, food intolerance, allergies and bronchial asthma, so that one already has the impression that many of our current lifestyles, nutritional factors, hygiene, antibiotic consumption and, last but not least, the consumption of alcohol, exotic spices, etc., have an impact on health and the benefit of certain Have illnesses.

Has there actually been more patients with irritable bowel syndrome in the last fifty years, or is IBS just becoming increasingly better diagnosed using exclusion diagnosis?

In the past, irritable bowel complaints, i.e. functional gastrointestinal complaints or dyspepsia, were often classified as being mediated by nervous, neuropsychiatric or neuro-vegetative factors. Today we know that the irritable bowel can have a huge spectrum of different causes and disorders, some of which are localized in the immune system, but also in the intestinal flora or the nervous system. The manifestation of the complaints is of course also linked to neurovegetative and psychosomatic mechanisms, but these are often not the sole cause, but a modulation factor.

This means: While irritable bowel symptoms were seen as an intangible mental illness in the past, an explanation of the symptoms is increasingly found in various sub-areas, e.g. the genetic expression of serotonin transporter proteins, in the breakdown of histamine in certain intestinal segments (keyword histamine-mediated IBS) or differentiated changes in the intestinal flora (microbiota). Further examples of this are, for example, patients with bacterial overgrowth in the small intestine, patients who react to FODMAP components of food, i.e. certain carbohydrates, so-called fructo- and galacto-oligosaccharides, disaccharides, polyols, with flatulence, patients with gastrointestinal food allergies and patients who intensify Ultimately, the symptoms of irritable bowel syndrome are the result of a disturbed intestinal physiology, which manifests itself in the interaction with the environment for a given genetic constitution in a disturbed intestinal immune homeostasis and a disturbed intestinal barrier.

Irritable bowel patients are an extremely heterogeneous group. The spectrum of phenotypes in irritable bowel syndrome is enormous and is extremely difficult to fully clarify medically. In terms of phenotype, there are irritable bowel patients who only have flatulence, others only complain of diarrhea in stressful exam situations and still others cannot go to work due to extreme diarrhea and severe pain. In severe forms, people change psychologically over time due to constant concern for their intestines, diet and life. There is also a high level of comorbidity with other stress disorders, psychological changes and depression.

Can you estimate how often irritable bowel syndrome occurs in Germany?

We know from surveys that between 10 and 15 million people complain of irritable bowel symptoms. Every second patient who visits a clinic for functional gastrointestinal complaints has irritable bowel syndrome. However, one should not overinterpret these figures, because only those patients come to the clinic who have significant symptoms, in which the suffering or fear is stronger than the symptoms experienced. Patients with milder complaints usually do not see a doctor, but make do with home remedies, unconsciously avoiding certain stressors or triggers. Herbal supplements in particular can also be quite effective in light forms, e.g. fennel, ginger, caraway or essential oils such as peppermint can relax the intestine with increased contractions and thus relieve flatulence and abdominal pain.

Is Irritable Bowel Syndrome a "Women's Disease"?

Men can have irritable bowel symptoms too, but women are more likely to be affected. In terms of the frequency of irritable bowel syndrome, a ratio of around two to three women to one man is assumed. Reasons for this could be the different genetic makeup, the hormonal regulation of the histamine breakdown, the different perception of pain, etc. Women seem to be more susceptible to irritable bowel symptoms, depressive illnesses or neurodegenerative disorders than men.

Regarding the symptoms: there doesn't seem to be any typical irritable bowel symptoms ...

There are a great many possible symptoms of irritable bowel syndrome. Possible symptoms begin at the junction between the esophagus and the stomach. They can make themselves felt as a burning sensation, discomfort and sometimes pain, bloating or gas and they can be an indication of irritable stomach syndrome¸ which can occur together with irritable bowel syndrome. Some patients also feel that the stomach is not emptying properly.

Although many patients perceive these symptoms as heartburn or as increased pressure, when the pH value is measured, it is often not possible to determine over-acidity and a manometric disturbance can often not be detected either. That is, the esophagus in these patients is simply hypersensitive and so there is an increased sensation.

A similar phenomenon occurs in irritable bowel patients. Studies in which a balloon was inflated in the rectum showed that irritable bowel patients felt this much earlier than healthy patients. It is therefore a question of visceral hypersensitivity, i.e. the sensation of the mucous membrane with regard to pressure and pain is increased.

Irritable bowel syndrome also has symptoms in the middle abdomen and around the navel. If the small intestine is involved in IBS, gas, bloating or, in some cases, colicky pain can occur. Soft stools, flatulence or watery diarrhea are also possible if the small intestine is involved. In the case of irritable bowel disease in the large intestine, on the other hand, patients report pulling pains in the right or left lower abdomen, as well as flatulence and irregular stool (frequent evacuations with normal consistency) and constipation. In a study on irritable bowel patients, we were able to determine that different IBS people had different activities of the histamine-degrading enzymes in the individual gastrointestinal segments mentioned, which can explain different organ segment-related symptoms.

For the differential diagnosis of food allergies: In contrast to pure irritable bowel patients with symptoms in the gastrointestinal tract, certain patients with real IgE-mediated food allergies often also show symptoms outside of the gastrointestinal tract, such as hay fever, chronic urticaria or migraines. However, there are also food allergies that are only locally restricted to the gastrointestinal tract - these are known as gastrointestinally mediated food allergies. The problem here is that such allergies in the gastrointestinal tract are not noticed in routine diagnostics and can be negative in blood or skin tests, so-called seronegative food allergies. That is why we developed the endoscopically guided segmental lavage test as early as 1996 in order to search for locally formed IgE in the individual segments of the intestine.

You have investigated the role of mast cells in irritable bowel syndrome, what are the connections?

It is interesting that in over 90 percent of the histological studies on irritable bowel patients an increased occurrence of mast cells or an increased activation of mast cells was found in almost all forms of irritable bowel syndrome. Most often, these studies were found in the lower small intestine and large intestine with significant collections of mast cells. This is important insofar as mast cells release their mediators in the tissue, but also at the nerve endings, and can thus influence the nerve cells. The eosinophils were nowhere near as frequently involved. This shows that irritable stomach and irritable bowel syndrome are strongly related to mast cell hyperplasia, i.e. mast cell proliferation. However, the causes that ultimately lead to mast cell activation are very diverse and are not always close to the appearance of the symptoms and they are by no means always an expression of an allergy.

What causes can contribute to mast cell activation in IBS patients?

The causes for the activation of the mast cells or the development of irritable bowel syndrome are multifactorial. A possible cause of mast cell activation are genetic changes, a hidden allergy, previous infections of the gastrointestinal tract, such as Campylobacter or norovirus infections. Sometimes we find that patients don't develop irritable bowel syndrome until many months after becoming infected with Campylobacter. This means that the infection activated the immune system and the mast cells in the intestine. The mast cells then remain in the intestine and become hyperactive for reasons that we do not yet know, or due to a small change in the intestinal microbiota or the immune system, their activity is no longer inhibited. The intestinal barrier plays an important role in the manifestation of IBS, or whether it is more permeable (antigen overload) or tight (antigen exclusion). A permeable intestinal barrier can lead to foreign material getting inside the body, but alcohol can also damage the intestinal barrier and in the further course promote irritable bowel syndrome.

Would that mean that mast cell abnormalities could occur in these patients before irritable bowel symptoms develop?

There is little data available on this issue because patients do not come to the practice at such an early stage of the disease. In the case of many allergy patients whom we have cared for over a longer period of time, however, we were able to see that mast cell accumulations were usually present in advance of the allergic symptoms. If the balance is then disturbed by certain factors, e.g. changes in the breakdown of histamine, changes in the composition of the intestinal flora or antibiotics, food allergies or intolerance can become manifest.

What other factors can lead to irritable bowel syndrome?

In addition to damage to the mucous layer on the intestinal surface due to the aforementioned infections or damage to the intestinal barrier, e.g. alcohol, malnutrition can also contribute to the manifestation of irritable bowel syndrome. Unusual, hot spices, such as those used in Asian cuisine, can change the intestinal permeability, so that more capsaicin, sodium glutamate or other nutritional factors can penetrate the body.

If you look at how people ate in the 18th century, you can see that the menu at that time consisted only of local vegetables and fruits that were just ripe and that the soil and the season gave. In addition, the meat of local animal species was consumed, but no exotic dishes, fewer additives, less industrially produced foods and, above all, less alcohol (in younger years) were consumed. Modern humans, on the other hand, are confronted with an enormous number of unusual dishes that are not typical of the country, highly industrially processed finished products, unconsciously swallow fine dust, cosmetics, environmental toxins, etc. and all these factors can influence the composition of the gastrointestinal mucosa. Medicines such as painkillers or diabetes medication can also change the intestinal permeability. Some people do not develop a food allergy until they take pain medication. Salicylates, which are contained in many painkillers, but also in curry, are also not tolerated by some patients.

Physical activity can also play a role in irritable bowel syndrome. Most people work in sedentary jobs and don't get enough exercise. This increases the intraluminal pressure in the intestine, which can lead to the food allergens being pressed into the intestinal mucosa and thus activating the intestinal immune system and the mast cells. This is one of the reasons why we are seeing an increase in the number of diseases in irritable bowel syndrome, just like in other so-called "affluence or civilization diseases" such as metabolic syndrome or obesity. The increased intraluminal pressure in the entire intestinal tract is an important risk factor here. Therefore, all measures that are suitable to reduce this pressure can significantly alleviate the symptoms.

What measures do you take to reduce intraluminal pressure in irritable bowel syndrome?

Exercise is an important factor. Man is actually made to cover eight km on foot every day. In fact, you mostly sit. A helpful measure for lowering intraluminal pressure is not only bleeding medication, but also daily exercise, e.g. a daily walk of at least 40 minutes. Basically, about 40 minutes of exercise two to three times a week would be very important for maintaining health, including heart health. But even two to three walks a week are helpful, because then the small intestine works much better and the air is transported downwards. In the case of an irritable stomach, we know that there is less heartburn and belching. Regular exercise significantly reduces visceral discomfort, reduces burping, stimulates intestinal peristalsis and thus shortens the contact time of food allergens or incompatible substances with the intestinal mucosa. Together with a typical mixed diet, the metabolism and the intestinal barrier would be optimally regulated. This can be supported by treatment with bleeding drugs, simple measures that can very well help to regain normal physiology in the gastrointestinal tract.

Regarding the diagnosis: Wouldn't the activity level of the mast cells be a way of diagnosing irritable bowel syndrome or irritable stomach syndrome precisely and not just through a diagnosis of exclusion?

It would be a positive way of diagnosing irritable bowel syndrome, but not all pathological institutes count the mast cells in a routine biopsy, and mast cell activation can also be an expression of various triggers. The immunohistochemical mast cell staining must be carried out separately

be requested. In addition, there is the difficulty of correctly interpreting these mast cell findings. Often patients come to our clinic's office hours who already have all the findings without having been properly evaluated.The standards for this are still missing, which is why we have developed a quantification grid for the mast cells that differentiates between a small, moderate or strong increase in mast cells and results in further clinical conclusions. In the case of irritable bowel syndrome with a moderate to severe increase in mast cells and no evidence of allergies, treatment with mast cell stabilizers such as disodium cromoglycic acid can be useful, as studies that are over thirty years old have already shown. In a more recent study, the older histamine antagonist ketotifen was also able to produce beneficial effects in IBS.

How can disodium cromoglycic acid help with irritable bowel syndrome?

In particular, disodium cromoglycic acid for the treatment of food allergies has been known as a topical mast cell stabilizer for decades. However, it was not the focus of inflammatory bowel disease and irritable bowel syndrome because other mechanisms were more important than the importance of mast cells. However, over the past thirty years we have been able to demonstrate, through studies, that patients with food allergies and irritable bowel syndrome respond very well to cromoglycic acid disodium. In 60 to 70 percent of patients, cromoglycic acid disodium can stabilize the mast cells in the gastrointestinal tract, calm the overactivity and lead to fewer mediators being secreted. This lowers the pain intensity, the abdominal contractions decrease and so does the secretion of mucus and water. Especially in IBS with diarrhea, we could see that disodium cromoglycic acid had a positive effect on stool consistency and frequency. In one of our IBS patients, we were even able to achieve this effect with just a 400 mg disodium cromoglycic acid dose once a week. From this we could conclude that the sensitivity of the individual patients and their respective mast cell types are differently sensitive to disodium cromoglycic acid, since not all patients respond to it or require different dosages.

How exactly do you go about treating irritable bowel syndrome with cromoglycic acid disodium?

The basis of treatment with cromoglycic acid disodium is a clear diagnosis of irritable bowel syndrome. If possible, an interdisciplinary clarification should take place, which is controlled by the family doctor and includes a gastroenterologist, an allergist, a pathologist, a psychologically trained doctor and a nutritionist.

For patients with symptoms that match irritable bowel syndrome and for whom other diseases such as inflammation, intestinal diverticula or intestinal polyps have been excluded, it is possible, for example, to have existing biopsies examined retrospectively for mast cells. To do this, we carry out a special immunohistochemistry for staining the mast cells, the eosinophils and the lymphocytes, as well as a special immunohistochemistry for diamine oxidase (the latter for the question of histamine-mediated IBS). If there is an increased number or activity of mast cells, one can assume irritable bowel syndrome if other cell types are not present.

As the correct interpretation of the laboratory results can be difficult, as I said, close cooperation with the pathologist is highly recommended for the doctor. We are also continuously developing new standards for this purpose, e.g. to better identify histamine-mediated irritable bowel syndrome or mast cell-mediated irritable bowel syndrome and post-infectious or allergic irritable bowel syndrome.

With the Association for the Promotion of Allergy and Endoscopy Research on Humans (VAEM), we inform doctors and patients about new developments and also support colleagues with diagnosis. Here there is also information on colleagues who have specialized in the interpretation of such findings, how and where they can be contacted or when special training courses are held on this topic.

You mentioned a patient who managed to get by with just one dose of cromoglycic acid disodium per week for the treatment of irritable bowel syndrome, how often do you normally take cromoglycic acid disodium?

This is very different, because the individual sensitivity of the respective irritable bowel type differs greatly. Some patients manage with infrequent doses of disodium cromoglycic acid and others cannot control their symptoms until they take 400-500 mg disodium cromoglycic acid at least four times a day.

Are there any side effects with cromoglycic acid disodium?

With disodium cromoglycic acid, only less than 2 percent of the substance gets into the blood. Therefore, there are practically no serious systemic side effects. So it is definitely worth trying the disodium cromoglycic acid treatment. As already mentioned, the prerequisite is the histological findings of a mast cell accumulation and the detection of increased methylhistamine, a degradation product of histamine, in the urine. In this way it can be proven that the patient suffers from histamine-mediated complaints.

Does that mean you can't overdose on disodium cromoglycic acid?

In an adult, cromoglycic acid disodium is assumed to be between 200 mg and 2000 mg per day. We work with a maximum dose of disodium cromoglycic acid of four times 500mg per day, in the form of capsules or granules. In children, the dose is 100 mg to 1000 mg. Which dosage is the right one for which patient has to be agreed individually.

Do I have to take cromoglycic acid disodium permanently to treat irritable bowel syndrome?

If the individually triggering irritable bowel syndrome triggers, e.g. salicylates, certain foods, psychological stress factors, etc. are found and these are eliminated or changed, then there is actually no longer any idiopathic irritable bowel syndrome. Because one then knows the etiology and expresses this in the diagnosis, e.g. allergic and alimentary gastroenteritis, food intolerance, bacterial overgrowth of the small intestine, etc. In IBS with identified triggers, often with mast cell hyperplasia and if after two to three years of treatment with disodium cromoglycic acid, the intestinal barrier again If it is intact, one may not need further treatment.

In the case of allergic irritable bowel syndrome, for example, we can see that the intestinal barrier is intact by the fact that there are fewer inflammatory cells in the intestinal mucosa and by the lower excretion of methylhistamine in the urine or the regression of IgE in the intestine, which we determine through endoscopic lavage. This was the case in 10 to 15 percent of our patients. In these cases it is worthwhile to track down the etiology of IBS, to review the diagnosis critically and to adapt the therapeutic measures to the course and success of the measures.

However, most irritable bowel syndrome patients without an identified trigger will need to take the irritable bowel medication long-term.

Prof. Raithel, thank you very much for this interview!

VAEM would like to thank Mein Allergie Portal and Ms. Sabine Jossé for making the interview available.

Bibliography:

  1. Furlong TJ, DeSimone J, Safe S. Peanut and tree nut allergic reactions in restaurants and other food establishments. J Allergy Clin Immunol 2001; 108: 867-870
  2. Host A, Halken S. Hypoallergenic formulas: when, to whom and how long: after 15 years we know the right indication. Allergy 2004; 59 suppl 78: 45-52
  3. Schwab D, Raithel M, Hahn EG. Enteral nutrition therapy for Crohn's disease. Z Gastroenterol 1998; 36: 983-995

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5. Detailed dietary recommendations

Authors: U. Hetterich, M. Raithel, W. Taumann

In our download area for doctors, members and patients you will find detailed nutritional recommendations for:

  • Lactose malabsorption
  • Fructose malabsorption
  • Sorbitol malabsorption
  • Histamine intolerance
  • Salicylate intolerance

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4. Hypoallergenic Form Diets

Authors: U. Hetterich, M. Raithel, W. Taumann

If the symptoms of a food allergy cannot be fully controlled with specific allergen avoidance, the olioallergenic diet and the control of important accompanying factors, hypoallergenic diets are used as a further therapeutic measure. These include nutrient-defined polymer diets, elementary diets with amino acids or oligopeptide solutions [2, 3]. These are taken either in adjuvant form with approx. 500 - 1500 calories / the tolerated diet or together with a hypoallergenic “potato rice diet”. In severe forms with several allergens, in childhood or in malabsorption syndromes with reduced nutritional status, they are temporarily used for exclusive nutrition (> 1500 - 2500 calories / die) and then administered e.g. via a naso-gastric or jejunal tube (enteral nutrition).

With these diet forms, the avoidance of allergens or foods containing histamine and other biogenic amines (e.g. tyramine, putrescine, etc.) can often be significantly supported. Nutritional deficits are prevented and the hypoallergenic diet leads to a significant reduction in the allergic inflammatory reaction, which can also be well objectified on the basis of the methylhistamine excretion. Overall, the hypoallergenic elementary, oligopeptide and polymer diets are well established, especially for severe polyvalent allergies and in pediatrics.

Various immunological mechanisms such as the reduction of existing nutritive antigens due to the hypoallergenic diet, reduced HLA-DR expression or a decrease in soluble interleukin 2 receptors in the intestinal lavage fluid are discussed for this favorable therapeutic response. In addition, it should also be noted that such hypoallergenic formula diets are completely free of histamine, so that part of these protective effects of nutritional therapy in food allergy sufferers can also be attributed to the histamine abstinence achieved as a result.

In order to be able to record long-term success with such people, the principle of adjuvant nutritional therapy with hypoallergenic diets is sought today. Since the elementary or astronaut diet is not very tasty, it is more difficult to adhere to an exclusive diet with liquid food preparations. In the form of adjuvant nutritional therapy, the patient should add 1 - 2 packs of a hypoallergenic diet (e.g. Nutricia Neocate, Nutricia Elemental 028 amino acid diet, Mead Johson Nutramigen LGG Lipil, Nestlé Modulen IBD polymer diet) to his normal diet in the long term, which he will definitely tolerate, take in. In the long term, this leads to a dilution and reduction of the various food antigens (antigen dilution) and a reduction in intestinal inflammation. Such an adjuvant therapy regime is carried out by the patient for much longer than an exclusive diet with monotonous tasting amino acids or oligopeptides.

Liquid food preparations are therefore nowadays considered to be important therapeutic agents for reducing allergic inflammatory activity, for preventing further re-sensitization and for maintaining nutritional requirements.

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3. Oligoallergenic basic diet and addition diet

Authors: U. Hetterich, M. Raithel, W. Taumann

If multiple food allergies or immunological food allergies are suspected, a basic oligoallergenic diet can be used. For example, food intolerances in mast cell activation syndrome (MCAS) and the frequently associated irritable bowel syndrome are very diverse and vary from patient to patient. The basic oligoallergenic diet is supported by a Addition diet Completed step by step with compatible foods.

Oligoallergenic basic diet

The oligoallergenic basic diet is a compilation of a basic diet that is tolerable for the individual patient individually have to be.

Example of a basic oligoallergenic diet:

  • Grains: rice, rice cakes, rice noodles, rice pops, rice bread
  • Vegetables: potatoes, lettuce, broccoli
  • Meat: poultry or lamb
  • Fats: sunflower oil, margarine
  • Other: rice drink, sugar, salt, sugar beet, possibly additional food

 

In the meantime, for example, there is a variety of foods made from rice to put together a varied menu (see Figure 1).

Figure 1: Wide range of foods made from rice

Principles of the addition diet (diet structure)

The diet is built up in different stages, whereby a new stage should only be started if you are symptom-free. To rule out late reactions, you should after three days at the earliest use a new food. If complaints occur in one level, you automatically go back to the last level and start after three days with the next but one level.

The individually determined oligoallergenic diet is considered the basic diet. With a little creativity, the oligoallergenic basic diet can be varied (see Figure 2).

Figure 2: Creative design of the oligoallergenic basic diet

 

Example of a possible daily menu of the oligoallergenic basic food

breakfast
Rice, boiled potatoes or rice porridge made from rice milk (without additives) and short grain rice
Rice bread or rice waffles possibly with caramel syrup / sugar beet cabbage / cold chicken breast
Milk / water with rice flakes
Snack Rice cakes, pita
Having lunch
Cooked rice (basmati, parboiled rice), rice noodles, rice noodles
Boiled potatoes, fried potatoes, potato dumplings, rösti potatoes, mashed potatoes, potato salad, potato pan
Roast chicken, sliced ​​turkey, chicken breast, etc.
Lettuce, broccoli
Snack Rice cakes, pita
Dinner see lunch

Once the symptoms are free, new foods can be gradually added to the basic diet. To the basic diet every three days an allowance of individually specified foodswhich are perceived as tolerable from the experience of the patient. example for one individual Diet structure:

  1. coffee
  2. Beef and veal
  3. Sea bream
  4. egg
  5. spinach
  6. Bread (consisting of wheat, salt and yeast)
  7. pig
  8. carrot
  9. White pepper
  10. Green tea
  11. Apple

It is important for the patient to closely observe the body's reactions to the new food and take a look exact consumption and complaint log (with time) so that intolerance or allergic reactions can be assigned to individual foods.

Important information about the preparation

  • Only salt and sugar may be used for seasoning.
  • Only use sunflower oil to prepare the food.
  • Rice flour or potato starch can be used to bind sauces, for example.
  • Salad dressing made from water, salt, sugar, oil and a little fresh lemon.
  • Manufacture- Alternatively, natural yoghurt or buttermilk.
  • If possible, consume food in cooked form.
  • Pay attention to the note "gluten-free" for products made from rice.

The table salt used should be iodized and fortified with fluorine and folic acid. In order to meet the calcium requirement, you should pay attention to the calcium content of the mineral water (> 400mg / liter). The sodium content is irrelevant.

Recipe examples

Rice porridge: Bring 500 ml of water or rice milk without additives to the boil with 50 - 60 g of rice pudding. Cook slowly or let it soak for 30 minutes. Season to taste with sugar (approx. 2 tablespoons) or caramel syrup.

Pita bread: Knead 100g rice flour with 1 tablespoon rice gruel, ½ teaspoon salt and a little water to form a firm dough. Let the dough rest briefly. Then roll out the dough about ½ cm thick and cut into square pieces. Preheat the deep fryer with sunflower oil to 180 ° C (only foods that are part of the diet may be prepared in the deep fryer). Fry the dough pieces for about 3 minutes. Place on paper towel and let cool. If possible, eat the pita on the same day.

Potato rice waffles: Ingredients: 50g rice flour, 120g potatoes, 10g potato flour, 5g oil, 10g sugar, 90ml water; Press the potatoes through the potato press and mix with the remaining ingredients to form a dough. Bake in the preheated waffle iron until golden brown.

Rösti potatoes: Grate the raw potatoes into coarse sticks. Squeeze out the mixture and season with salt. Add some potato flour. Heat the oil in the pan and fry the potato biscuits until golden.

Potato dumpling: Finely grate raw potatoes and squeeze. Add potato starch to bind. Season to taste with salt. Shape the dumplings and let them steep in boiling salted water. If you like, some of the raw potatoes can be replaced with cooked, squeezed potatoes.

Potato salad: cut the cooked potatoes into slices while they are still warm. Make a marinade from water, salt, sugar, ascorbic acid and oil. Pour the marinade over the still warm potatoes and let them steep.

Analysis of calorie intake and nutrient intake

It is important to ensure that malnutrition does not occur and that sufficient calories and nutrients are consumed during the addition diet. Often the food allergy / intolerance or the underlying gastrointestinal illness make the absorption of nutrients more difficult. A computer-based evaluation of the calorie intake and the intake of essential minerals, trace elements, vitamins and amino acids (see Figure 3) gives an insight into possible deficiencies or excesses.However, the computer-based evaluation does not take into account any absorption difficulties, so that in individual cases a laboratory determination of the most important trace elements, e.g. iron, magnesium, calcium, as well as the most important vitamins, e.g. vitamin D, vitamin C, vitamin B6 / B12, is necessary.

In the case of malnutrition in particular, dietary supplements with hypoallergenic formulas are urgently needed. Hypoallergenic form diets can also be useful with a sufficiently balanced diet, for example to degrade gastrointestinal allergic or inflammatory reactions (see Chapter 4).

Figure 3: Example of a computer-based analysis of the
Absorption of calories and nutrients

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2. Allergen avoidance

Authors: U. Hetterich, M. Raithel, W. Taumann

For all patients with food allergies, an antigen-specific waiting period is the fundamental basis for a successful therapy. For this reason, the reliable diagnosis of a food allergy and the exact Identification of the responsible allergens not only with skin tests (prick, intracutaneous, patch test) and the antigen-specific IgE determination from blood or intestinal lavage, but also clinical confirmation through an oral (in vivo) provocation or an (ex vivo) biopsy test extremely important role (see diagnostic link install). Exact allergen avoidance shows the best remission rate, is the cheapest form of therapy and is the least burdened with side effects compared to other therapies. It should be noted that a strict elimination diet should not lead to deficiencies, which is why structured diet advice is always necessary today and the diagnosis - as described above - should be precisely secured.

With allergen avoidance, those affected should also pay attention to the so-called hidden allergens in food. It could be shown that the majority of serious allergic reactions were caused by foods that were not prepared in-house. Such meals represent an incalculable risk for allergy sufferers. A survey of 156 food allergy sufferers in the USA showed that in about 50% of cases an allergic reaction was triggered by hidden allergens. In almost 1/3 of those affected, the allergic reaction occurred within 5 minutes of unintentional ingestion (immediate reaction type I allergy) and had to be treated pharmacologically in 86% of cases (antihistamines, epinephrine). The allergic reactions occurred most frequently in Asian restaurants (19%), ice cream parlors (14%) and bakeries (13%). The main risk with the courses served in the restaurant is primarily the dessert [1]. These observations suggest that it is mostly hidden allergens rather than diet errors that are the cause of the most violent allergic reactions. Since December 13, 2014, the Food Information Regulation (LMIV) (Regulation (EU) No. 1169/2011) has also been mandatory in Germany and the 14 most common triggers of allergies and intolerances must always be indicated. The use of the relevant ingredients must result from either the list of ingredients or the name of the food. This guideline also applies to the catering trade, which must note relevant information on the menu. These are the following substances and products made from them:

  • Cereals containing gluten, to be mentioned by name: wheat (such as spelled and khorasan wheat), rye, barley, oats or hybrid strains thereof
  • Crustaceans
  • Eggs
  • fishes
  • peanuts
  • Soybeans
  • Milk (including lactose)
  • Nuts, to be mentioned by name: almonds, hazelnuts, walnuts, cashew nuts, pecans, Brazil nuts, pistachios, macadamia or Queensland nuts
  • celery
  • mustard
  • Sesame seeds
  • Sulfur dioxide and sulphites (from 10 milligrams per kilogram or liter)
  • Lupins
  • Mollusks

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Bibliography:

  1. Stein J, Kist M, Raithel M: Diseases caused by food. Scientific Publishing Company Stuttgart 2011
  2. Tsar S, Kumar D, Benson MJ. Review article: Food hypersensitivity and irritable bowel syndrome. Aliment Pharmacol Ther 2001; 15: 439-449
  3. Osterballe M et al. The prevalence of food hypersensitivity in young adults. Pediatr Allergy Immunol 2009; 20: 686-692
  4. Raithel M, Hahn EG. Allergic enteropathy. In: Hahn EG, Riemann JF. Clinical gastroenterology. Thieme Verlag 1996; 3rd edition: 960-965
  5. Raithel M, Hahn EG, Baenkler HW. Clinic and diagnosis of food allergies (gastrointestinal mediated allergies grade I - IV). English: Gastrointestinal allergies. Dtsch Ärzteblatt Int 2002; 99: A780-786 [issue 12]
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  18. Raithel M et al. Colorectal mucosal histamine release by mucosa oxygenation in comparison with other established clinical tests in patients with gastrointestinally mediated allergy (GMA). W J Gastroenterol 2006 Aug 7; 12 (29): 4699-4705
  19. Moneret Vautrin DA, Sainte-Laudy J, Kanny G. Ulcerative colitis possibly due to hypersensitivity to wheat and egg. Allergy 2001; 56: 458-459
  20. Pietzak M. Celiac disease, wheat allergy, and gluten sensitivity: When gluten free is not a fad. J Parenter Enteral Nutr 2012; 36: 68S-75S
  21. Born P et al. Carbohydrate malabsorption in clinical routine: a prospective observational study. Hepatogastroenterology 2006; 71: 673-677
  22. Lomer MCE, Parkes GC, Sanderson JD. Review article: lactose intolerance in clinical practice - myths and realities. Aliment Pharmacol 2008; 27: 93-103
  23. Fernandez-Banares F et al. Sugar malabsorption in functional abdominal bloating: A pilot study on the long-term effect of dietary treatment. Clinical Nutrition 2006; 25: 824-831
  24. Keller J et al. Clinically relevant breath tests in gastroenterological diagnostics, recommendations of the German Society for Neurogastroenterology and Motility and the German Society for Digestive and Metabolic Diseases. Z Gastroenterol 2005; 43: 1071-1090
  25. Posserud I et al. Small intestinal bacterial overgrowth in patients with irritable bowel syndrome. GUT 2007; 56: 802-808
  26. Jarisch R et al. Histamine intolerance: histamine and seasickness. Thieme Verlag 2013; 3rd edition: 1–175
  27. Reese I, Ballmer-Weber B, Beyer K, Erdmann S, Fuchs T, Kleinetebbe J, Klimek L, Lepp U, Henzgen M, Niggemann B, Saloga J, Schäfer C, Werfel T, Zuberbier T, Worm M. Procedure in case of suspicion for intolerance to orally ingested histamine. Allergo J 2012; 21 (1): 22-28
  28. Küfner MA, Schwelberger HG, Ulrich P, Hahn EG, Raithel M. Total histamine degradation capacity (THDC) as an important biological marker of histamine metabolism in human colonic mucosa. Inflamm Res 2002; 51: S87-S88
  29. Niec AM, Frankum B, Talley NJ. Are adverse food reactions linked to irritable bowel syndrome? Am J Gastroenterol 1998; 93: 2184-2190
  30. Schafer D et al. Dynamics of eicosanoids in peripheral blood cells during bronchial provocation in aspirin-intolerant asthmatics. Eur Respir J 1999 Mar; 13 (3): 638-46
  31. Raithel M, Baenkler HW, Naegel A et al. Significance of salicylate intolerance in diseases of the lower gastrointestinal tract. J Physiol Pharmacol 2005 Sep; 56 Suppl 5: 89-102
  32. Ford AC et al. Yield of diagnostic tests for celiac disease in individuals with symptoms suggestive of irritable bowel syndrome: systematic review and meta-analysis. Arch Intern Med 2009; 169: 651-658.
  33. Wong BS, Camilleri M, Carlson P, McKinzie S, Busciglio I, Bondar O, Dyer RB, Lamsam J, Zinsmeister AR. Increased bile acid biosynthesis is associated with irritable bowel syndrome with diarrhea. Clin Gastroenterol Hepatol 2012; 10: 1009-1019
  34. Raithel M et al. Combination therapy using fexofenadine, disodium cromoglycate, and a hypoallergenic amino acid - based formula induced remission in a patient with steroid - dependent, chronically active ulcerative colitis. Int J Colorectal Dis 2007; 22 (7): 833-839
  35. Rajendran N, Kumar D. Role of Diet in the Management of Inflammatory Bowel Disease. World J Gastroenterol 2010 Mar 28; 16 (12): 1442-1448
  36. Sánchez-Fayos Calabuig P, Martín Relloso MJ, Porres Cubero JC. Multifactorial etiology and pathogenic factors in inflammatory bowel disease. Gastroenterol Hepatol. 2009 Nov; 32 (9): 633-52
  37. Raithel M. Therapy and prophylaxis of food allergies (gastrointestinal mediated allergies grade I – IV). Falk Titisee Congress Volume 2012; 1-10
  38. Eigenmann PhA. Mechanisms of food allergy. Pediatr Allergy immunol 2009; 20: 5-11
  39. Heymann M, Darmon N, Dupont C, Dugas B, Hirribaren A, Blaton MA, Desjeux JF. Mononuclear cells from infants allergic to cow’s milk secrete tumor necrosis factor alpha, altering intestinal function. Gastroenterology 1994; 106: 1514-1523
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  42. Konturek PC, Rienecker H, Hahn EG, Raithel M. Helicobacter pylori as protective factor against food allergy. Med Science Mon 2008; 14 (9): CR453 - CR458
  43. Majamaa H, Miettinen A, Laine S, Ilsolauri E. Intestinal inflammation in children with atopic eczema: faecal eosinophilic cationic protein and tumor necrosis factor alpha as non-invasive indicators of food allergy. Clin Exp Allergy 1995; 26: 181-187
  44. Kleine-Tebbe J, Ballmer-Weber B, Beyer K, Erdmann S, Fuchs T, Henzgen M, Huttegger I, Jappe U, Jäger L, Lepp U, Niggemann B, Raithel M, Reese I, Saloga J, Szepfalusi Z, Vieths S, Worm M, Zuberbier T, Werfel T. In-vitro diagnostics of IgE-mediated food allergies. Guideline of DGAKI, ÄDA and GPA, Allergo J 2010 and Allergology 2010 (in press)
  45. Arslan G, Lillestol K, Mulahasanovic A, Florvaag E, Berstad A. Food hypersensitivity reactions visualized by ultrasonography and magnetic resonance imaging in a patient lacking systemic food specific IgE. Digestion 2006; 73: 111-115
  46. Lacono G, Ravelli A, Di Prima L, Scalici C, Bolognini St, Chiappa S, Pirrone G, Licastri G, Carroccio A. Colonic lymphoid nodular hyperplasia in children: Relationship to food hypersensitivity. Clin Gastroenterology and Hepatol 2007; 5: 361-366
  47. Kokkonen J, Holm K, Kartunnen TJ, Mäki M. Children with untreated food allergy express a relative increment in the density of duodenal gamma / delta T cells. Scand J Gastroenterol 2000; 35: 1137-1142
  48. Frieling1, K. Meis2, U. W. Kolck2, J. Homann2, A. Hülsdonk1, U. Haars1, H.-J. Hertfelder3, J. Oldenburg3, H. Seidel3, G. J. Molderings. Evidence for Mast Cell Activation in Patients with Therapy-Resistant Irritable Bowel Syndrome. Z Gastroenterol 2011; 49 (2): 191-194
  49. J. Molderings, J. Homann, S. Brettner, M. Raithel, T. Frieling. Systemic Mast Cell Activation Disease: A Practice-Oriented Guide to Diagnostics and Therapy. CME Review article, 05/2014, Dtsch Med Wochenschr, Georg Thieme Verlag
  50. Homann, G.J. Molderings. Histamine Intolerance and Mastocytosis: How to Recognize, How to Treat ?. Lecture on May 8th, 2014 at the University Hospital Bonn
  51. Gerhard J. Molderings1 *, Britta Haenisch1,2,3,4, Manuela Bogdanow5, Rolf Fimmers5, Markus M. Nöthen. Familial Occurrence of Systemic Mast Cell Activation Disease. PLoS ONE 8 (9): e76241. September 30, 2013
  52. Britta Haenisch, Markus M. Nöthen and Gerhard J. Molderings. Systemic mast cell activation disease: the role of molecular genetic alterations in pathogenesis, heritability and diagnostics. Immunology 2012 Blackwell Publishing Ltd, Immunology, 137, 197-205

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7. Clinical confirmation of the diagnosis

Authors: M. Raithel, A. Hagel, W. Taumann, P.Konturek, G.J. Molderings, U. Hetterich

According to the results from the spectrum of diagnostics, the suspected allergy type (IgE vs. non-IgE), a potential allergen spectrum of approx. 5–15 (basic) foods has been compiled, which are then checked for clinical relevance in the provocation test (1, 3, 14, 17, 18, 42–45). If there are only individual sensitizations for simple mono- or oligovalent IgE-mediated food allergies, the provocation can be dispensed with initially if the corresponding diet attempt is clinically strictly monitored over a defined point in time.

If there are multiple sensitizations and the trigger spectrum is unclear, standardized provocation testing of the foods in question is required. The number of foods to be provoked is much smaller than the number of foods initially checked in the skin, blood test or endoscopic lavage, i.e. a careful selection must be made by an experienced doctor. To carry out a single or double-blind, placebo-controlled provocation test, the patient should be referred to an experienced allergist or center, because oral provocation can only take place under standardized conditions, requires continuous clinical observation (score), and certain safety measures in the With regard to severe allergic reactions and should be provided with placebo tests in order to detect psychological reactions (3, 5, 15, 38, 40, 44). The informative value of oral provocation testing can be improved if objective immune mediators are determined at the same time during the test period (e.g. methylhistamine in the urine, ECP in the serum [5, 7]).

Another possibility of allergen identification at the GIT is the functional testing of living intestinal biopsies with food allergens (mucosal oxygenation) (18). Although this method is now fully developed for clinical routine and the provocation reaction takes place outside the patient, a special letter of indication is often required for the costs to be covered by the health insurances, which increases the risk of testing on the patient for dangerous allergy symptoms (previous history) and the need for a local one Allergy diagnostics are explained [5, 18]. This method was evaluated for IgE- and non-IgE-mediated allergies in comparison to double-blind, placebo-controlled oral provocation testing and to change the transepithelial resistance at the intestinal epithelium and can achieve correct allergen identification in approx. 70-76% of patients (18 ). Since multiple determinations of the allergy mediators are required during cultivation, there is a corresponding expense that has not been generally covered by the health insurances so far, although good therapy results could be achieved with certain individual constellations (irritable bowel, GI bleeding, chronic diarrhea). The allergen correctly identified by provocation, endoscopic lavage or biopsy testing is the best therapy basis (link to therapy chapter) for NMA.

 

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6. Major diseases with associated food intolerance

Authors: M. Raithel, A. Hagel, W. Taumann, P.Konturek, G.J. Molderings, U. Hetterich

6.1 Irritable bowel syndrome

In the case of irritable stomach or irritable bowel syndrome, feeding problems, postprandial symptoms, or post-meal body observations are commonly reported. Therefore, the presence of NMU or NMA is often suspected in this patient group (1–3).It is known that the diagnosis of irritable bowel syndrome often includes patients who have one of the diseases listed above but have not yet been recognized because they may have a clinically inapparent, asymptomatic or atypical course. This applies in particular to the relatively high coincidence of irritable bowel syndrome with, for example, carbohydrate malassimilation, NMA, NMU and celiac disease (1–3, 11, 20–25).

On the other hand, there are also irritable bowel patients in whom the genesis of the symptoms cannot yet be clarified despite extensive differential diagnostics and who have so far been classified as idiopathic, neurovegetative or psychosomatic. Therefore, a corresponding psychosomatic consultation examination must be carried out at least once in a patient's career.

With the diagnostic modalities shown in Figure 3, an attempt should therefore always be made to clarify the differential diagnosis of irritable bowel syndrome as far as possible or to provide evidence of another disease if recurrent NMU is sued.

Interestingly, a study on irritable bowel patients showed that in the majority of patients there are clearly overactivated mast cells, which can be caused by secondary intolerance reactions or primary genetic mutations (48).

 

6.2 Mast cell diseases

"Systemic mast cell activation disease" (MCAD for mast cell activation disease) is the umbrella term for a group of diseases, namely systemic mastocytosis (SM) with its subtypes, mast cell activation syndrome (MCAS, mast cell activation syndrome) and mast cell leukemia (MCL) (see Figure 5). The molecular cause of the disease is multiple genetic changes in kinases, receptors and other proteins involved in intracellular signal processing (so-called signal transduction chain) in some of the mast cells, which lead to a constitutive increase in the activity of the affected mast cells (49). The unregulated increased level of activity is associated with a disturbed apoptosis and - with certain mutations - also increased proliferation behavior with a slow accumulation of these pathologically altered overactive mast cells in organs and tissues. The uncontrolled released mediators from the pathological mast cells present in the organs and tissues, and above all from healthy mast cells that are activated in a cascade-like manner, get into the tissue and cause tissue-typical changes and local symptoms that are often not initially recognized because such increases in the tissue mediators are usually not recorded in routine clinical practice. When mediators enter the bloodstream or are transported via the lymph, systemic complaints can be induced directly by stimulating success cells and probably indirectly by stimulating resident mast cells in other tissues and organs (49). Depending on the affected tissues and organs and the resulting symptoms that dominate the patient, the disease can present itself in different clinical variants, e.g. irritable bowel symptoms (diarrhea / constipation, abdominal cramps, gastritis, enteritis, colitis, rather underweight, episodic or permanently hypotonic), Fibromyalgia symptoms (rheumatoid joint and muscle pain, burning pain in varying skin areas, paresthesias), cardiac phenotype (tachyarrhythmias with / without palpitations, non-cardiac thoracic pain, dyspnea sensation), CNS phenotype (dizziness, episodic or permanently hypertonic, more likely overweight) , Word finding disorders, concentration disorders, insomnia, panic attacks, depressive states, chronic symptoms of tiredness, hyperventilation-tetany-like states), "idiopathic" anaphylaxis (dermal, respiratory, cardiovascular, intestinal symptoms) (49).

Until recently, it was widely believed that MCAD was a rare disease. However, this only applies to two subclasses: systemic mastocytosis and mast cell leukemia, the prevalence of which was calculated to be 1: 364,000 or at least 2 orders of magnitude lower (49). In contrast, the prevalence of MCAD in the German population was up to 17% in a recent first study (49). This high prevalence has yet to be confirmed in further large epidemiological studies, but an average prevalence of 5 - 10% is estimated. This high prevalence is not surprising, however, because primary and secondary processes (other disease mechanisms) can also contribute to the activation of the mast cells, genetically predisposing situations are increasingly recognized and, last but not least, the occurrence of the mast cell activation syndrome is also found in various clinical pictures such as certain forms of Fibromyalgia, subgroups of irritable bowel syndrome, rheumatic diseases, and autism (49, 50) were observed.

Figure 8: Systemic mast cell activation disease

Unlike previously assumed in the WHO criteria for mastocytosis, for which the presence of the C-KIT point mutation KIT point mutation in codon 816 in mast cells from the bone marrow or from another extracutaneous organ is a main criterion, there are already a large number of other mutations in the C-KIT gene and in a large number of other genes, e.g. PDGFR, CBL, TET2, ASXL1, JAK2, U2AF1, SETBP1, RUNX1, DNMT3, have been identified as causally involved in mast cell disease (50, 52). Due to the strong familial accumulation of mast cell diseases, an epi-genetic component is still suspected (51). In summary, systemic mast cell disease is a polygenic and epi-genetic disease, the basic cause of which is presumably in individually different combinations of, in particular, somatic and germline mutations in the protein-coding genes of the RNA splicing mechanism, the protein-coding genes of the transcript control and in the epigenetics-regulating genes (50, 52).

For complex diagnosis, e.g. anamnesis regarding a mast cell mediator syndrome with the help of a standardized validated questionnaire, mediator determination (tryptase, heparin in the blood, methylhistamine in the urine) or gastro- / colonoscopy with biopsies and mast cell-specific immunohistochemical examination of the tissue sample, as well as the therapy, e.g. beginning With basic therapy (H1 antihistamine, cromoglicic acid, ranitidine, vitamin C 500 mg retard capsules), newly revised CME-certified guidelines are available (49).

Mast cell diseases lead to numerous food intolerances and allergies, which can vary greatly depending on the patient. Therefore, it is difficult to make a general dietary recommendation, and for patients with mast cell disease, a tiered or exclusion diet is recommended in order to work out the optimal nutrition plan. The effects of the mediators and cytokines released by activated mast cells on the central nervous system (CNS) are often underestimated, with the frequent consequence of somatoform disorders, which are usually misinterpreted as purely exogenous psychological disorders (see Figure 9).

Figure 9: Secondary involvement of the CNS in mast cell diseases

Due to the central role of mast cells in NMA and NMU, it can be expected that the increasingly intensive research into the functioning of the mast cell will lead to improved diagnostic and therapeutic options for NMA and NMU.

 

6.3 Inflammatory bowel disease and microscopic enterocolitis

Other organic diseases of GIT that are associated with a disturbance of food absorption or food tolerance and play a role in the diagnosis of NMU and NMA are the chronic inflammatory bowel diseases Crohn's disease and ulcerative colitis as well as microscopic enterocolitides. In the manifest stage of the disease, chronic inflammatory bowel diseases can usually be recognized with simple measures by their systemic and endoscopic-histological inflammatory activity (BKS, CRP, alpha-1 and alpha-2 glycoprotein increase, thrombocytosis) (1, 15, 17 , 19, 25, 29, 33–37), while microscopic enterocolitis (collagenous or lymphocytic enteritis or colitis) can only be identified histologically with certainty due to the lack of systemic signs of inflammation.

It is therefore mandatory to use transabdominal ultrasound, endoscopy and histology, possibly also MRI Sellink of the small intestine, to be infected by Crohn's disease or ulcerative colitis or exclude microscopic enterocolitis. In the last two decades, microscopic enterocolitis in particular, as well as allergic diseases or eosinophilic esophagitis, have experienced a significant increase in incidence and frequency, so that today differential diagnosis it has to be looked for because there are good therapeutic options (for example mesalazine, budesonide [35, 37]).

 

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5. Non-immunological food intolerance (NMU)

Authors: M. Raithel, A. Hagel, W. Taumann, P.Konturek, G.J. Molderings, U. Hetterich

In addition to a simple intolerance to certain NMs (e.g. biogenic amines, histamine, sulfites etc.), NMU without specific involvement of the immune system can be caused by defined organic and functional diseases (e.g. infections, irritable bowel syndrome, chronic pancreatitis etc.), enzyme deficiency (lactase), toxic reactions and disturbances of the transport system, eg fructose, can be caused (1, 2, 19–21).

 

5.1 Carbohydrate malassimilation and bacterial overgrowth of the small intestine

5.1.1 Lactose intolerance

The most common NMU is lactose intolerance (lactose hemaldigestion) with a frequency of around 10–15% in the population. This leads to uncharacteristic abdominal symptoms such as gas, flatulence, pain and changing stool behavior (diarrhea) after the intake of lactose (from approx.> 10 g). Due to the genetic regression of lactase in the brush border of the small intestine, lactose can no longer be broken down into its components glucose and galactose in the small intestine (11, 21, 22). The unabsorbed, osmotically effective lactose reaches the deeper sections of the small and large intestines and is metabolized by bacteria there. The resulting products induce the clinical symptoms. Since diagnosis using the H2 breath test or blood test is very simple, lactose malodigestion can now be diagnosed very quickly as the cause of lactose intolerance.

 

5.1.2 Fructose and sorbitol intolerance

Symptoms similar to those of lactose intolerance can also arise with fructose and sorbitol malabsorption (23, 24). This results in an overload or disruption of the fructose transporter in the small intestinal mucosa (GLUT-5 and -2). This can occur either primarily when high amounts of fructose overwhelm the transporter quantitatively (limited absorption capacity), so that the monosaccharide fructose is metabolized in the colon by bacteria, or secondarily in certain diseases of the small intestine (23, 24). Since sorbitol is converted intestinally into fructose, inhibits the GLUT-5 transporter and is also osmotically effective, sorbitol intolerance or sorbitol malabsorption is pathophysiologically similar to that of fructose malabsorption (21, 23). The clinical symptoms are often unspecific, as is the case with irritable bowel syndrome. There is no relevant systemic or histological inflammatory activity.

Lactose, fructose and sorbitol malabsorption often occur together, which is why it is advisable to clarify all three in the event of symptoms and to look for a common cause of brush border damage to the small intestine (e.g. bacterial overgrowth of the small intestine, gastrointestinal allergy, infection, celiac disease).

 

5.1.3 Bacterial overgrowth of the small intestine

Incorrect colonization of the small intestine by bacteria from the oral flora or the large intestine can trigger similar unspecific symptoms of NMU and manifest themselves as irritable bowel characteristics. It is therefore an important differential diagnosis to the KH malassimilation listed above, and like this, it shows no increased inflammatory activity and mostly normal endoscopic findings (1, 21, 25). In some cases, bacterial overgrowth in the small intestine could also be detected in irritable bowel patients with KH malassimilation, so that in the case of such symptoms, the suspicion of bacterial overgrowth should be clarified using an H2 breath test. People with diverticula, interenteric fistulas, ileocecal resection, postoperative conditions, peristalsis disorders (e.g. collagenosis, intestinal pseudo-obstruction), diabetes mellitus or who are taking immunosuppressants or proton pump inhibitors are particularly at risk (21, 23, 25). The H2 breath test is carried out with 50 g glucose for three to four hours and, if carried out in a standardized manner, is currently the most practicable method for detecting bacterial overgrowth in the small intestine (Fig. 4). An increased fasting H2 concentration prior to performing the test (H2 gas> 20 ppm) can be an indication of the presence of this clinical picture (21, 25).

 

5.2 Intolerance to histamine and other biogenic amines

Intolerance reactions to biogenic amines such as histamine, tyramine, serotonin etc. are based either on high concentrations of these substances (intoxication) or, in predisposed persons, on pharmacological, pseudoallergic and idiosyncratic mechanisms (intolerance) (1, 10, 13).

The amine histamine formed from the amino acid histidine can lead to asthma, diarrhea, flushing symptoms, migraines, nausea, restlessness, edema and atrial fibrillation. A systemic or local increase in histamine can occur on the one hand through a reduction in the breakdown of histamine by the enzymes diamine oxidase (DAO) and / or histamine-N-methyltransferase (HNMT). Medicines and alcohol can also inhibit these enzymes (including amoxycillin, diclofenac, metoclopramide, etc.). On the other hand, an increased release of histamine in the body, such as in the case of undetected allergies, mastocytosis, neoplasia, etc., can also cause symptoms of the histamine effect (10, 13). The symptomatology of histamine intolerance ("so-called histaminosis") is correspondingly varied, which can manifest itself in various organ systems and has therefore recently been summarized under the term "histamine intolerance syndrome (HIS)" (13, 26).

Attempts are often made to diagnose HIS using only the DAO detection in the plasma. Unfortunately, this cannot be achieved without adding further clinical factors, a diet change to a low-histamine diet, a determination of methylhistamine in the urine and a correlation to plasma histamine, because the DAO concentration in the plasma is far too low compared to the GIT (1, 10, 13, 26).

Since the effects of histamine in type I – IV allergies are by definition not considered to be histamine intolerance, it is necessary to carry out immunological diagnostic measures to rule out NMA before diagnosing HIS. Anamnestically, certain foods such as aged cheese, tuna, red wine, sauerkraut probably indicate an intolerance to histamine and / or other biogenic amines. However, since this is not conclusive, different clinical strategies are used to diagnose HIS. Targeted oral provocation with 75–150 mg histamine or the suspected biogenic amine (e.g. tyramine) while monitoring vital parameters (1, 13, 26, 27) is still the gold standard.

 

5.3 Alcohol intolerance

Alcohol inhibits DAO so that exogenously absorbed or endogenously released histamine is no longer broken down quantitatively enough, which can promote symptoms of histamine intolerance (10, 13, 26–28). It is also known that acetaldehyde can release histamine as a breakdown product of the alcohol. If one takes into account that many alcoholic beverages contain histamine, this explains the fact that histamine intolerance often manifests itself first when drinking alcohol. This applies to complaints such as headaches, migraines, abdominal pain, diarrhea, flushing, pruritus and even induction of cardio-circulatory disorders (hypotension, tachycardia) up to atrial fibrillation (26–28).

In addition to histamine, alcoholic beverages can also contain other factors that can cause intolerance reactions, such as sulfites, salicylates, sorbic acid (e.g. wine, beer, etc.), other biogenic amines or certain allergens (barley, yeast, mold, etc.) (11, 23).

Regardless of the histamine intolerance mechanisms, which can be increased by alcohol, it should be noted from an allergological point of view that even after the smallest amount of alcohol consumption, reactions with real food allergens can occur more intensely, as alcohol changes the permeability of the mucosa and increases the local blood flow in the intestine, so that Allergens can be better absorbed. In further diagnostics, provocations of the allergen in combination with a small amount of alcohol or aspirin will be necessary in order to definitely secure the disease mechanism (9, 13, 26). In the differential diagnosis of NMU, the toxic effects associated with increased alcohol consumption (> 40–60 g / day) should always be taken into account (e.g. chronic pancreatitis - fat intolerance).

 

5.4 Salicylate intolerance (NSAID intolerance)

The classic symptoms of salicylate intolerance or intolerance to non-steroidal anti-inflammatory drugs are respiratory complaints (misplaced or runny nose, sinusitis, nasal polyposis, bronchial asthma; so-called Samter's triad), but it can also lead to gastrointestinal complaints with meteorism, Abdominal pain, flatulence, diarrhea and, rarely, colitis with strictures and ulcers (1, 29, 30). Skin changes such as chronic urticaria, pruritus and skin sensations can also occur, which must be differentiated in the differential diagnosis from allergies or the HIS.

The pathogenesis is based on an inhibition of cyclooxygenase-1 by salicylates and other non-steroidal pain medication, but also by salicylate-containing NMs and other acids (e.g. benzoic acid, dyes, etc.) with the result of reduced synthesis of prostaglandins (29–31). In intolerant people, this leads to an increased formation of leukotrienes. This form of NMU can occur in different patient groups such as atopics, but also in irritable bowel patients, chronic inflammatory bowel diseases and people with persistent eosinophils.

Diagnostically helpful for stratifying patients is often the question of intolerance to aspirin, non-steroidal anti-inflammatory drugs, salicylate-containing foods such as curry, other spices, peppers, berries, raisins and organic potatoes (high salicylate content, as the plant is thus resistant to pests, insects, etc. fights back if no crop protection is administered) or after reactions to preservatives and dyes. A diagnostic clue is the presence of nasal polyposis or non-allergic asthma (29–31). Evidence is provided by a blood cell test (heparin blood) with incubation of 5-ASA and arachidonic acid or by a provocation test with aspirin or salicylic acid (nasal, bronchial, oral [1, 29–31]).

 

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