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Classification according to ICD-10
T78.4 Allergy, unspecified
ICD-10 online (WHO version 2019)

As an allergy (from ancient Greek ἀλλεργία 'external reaction', from ἄλλος állos 'different', 'strange', 'strange' and ἔργον érgon 'work', 'activity', 'work', 'reaction') there is an excessive, pathological defense reaction of the immune system referred to certain normally harmless environmental substances ( allergens , antigens ).

The allergic reaction is directed against substances coming from outside (through breathing, the gastrointestinal tract, skin, mucous membrane or blood vessels). Autoimmune reactions, i.e. pathological reactions of the immune system against components of the own body, are only counted as allergies if they are triggered by substances and particles entering the body from outside.

In addition to the allergic reactions mediated by antibodies or T cells , there are other intolerance reactions, e.g. B. pseudo-allergy or intolerance , which can be associated with a clinical picture similar to an allergy. Since an allergy, a pseudo-allergy or an intolerance can cause similar symptoms, these terms are undifferentiated in common parlance and are often incorrectly used synonymously.

History and the origin of the term

Descriptions of diseases that would be called allergies today are known from ancient Egypt and ancient Rome.

In 1565 , the Italian surgeon Leonardo Botallo described his observation that some people have colds and narrowed airways when they are near blossoming roses . A nasal disease that depends on the season was described by the London doctor John Bostock in 1819. That grass pollen is the triggering cause of this "hay fever" was recognized in 1870 by Charles Blackley in England and independently of this Morrill Wyman at Harvard University . In 1903, the German Wilhelm P. Dunbar caused hay fever symptoms in test subjects through salt solutions mixed with pollen.

The term allergy was coined in 1906 by Clemens von Pirquet , a Viennese pediatrician who examined symptoms after initial and reinjection of diphtheria sera, in analogy to energy in the sense that “the en - érgeia , a body's own (inner) force, an all - confront érgeia as an expression of reactions to exogenous substances ”. Pirquet defined allergy broadly as "an altered ability of the body to react to a foreign substance". This definition includes both increased ( hyperergy ), decreased ( hypoergy ) and a lack of ( anergy ) reactivities . Pirquet was the first to recognize that antibodies not only mediate protective immune responses, but can also trigger hypersensitivity reactions. He is considered to be the founder of clinical allergy theory .

As early as 1902, Charles Richet and Paul Portier (1866–1962) observed an altered reaction to low-dose toxin administration in dogs after the test animals had survived poisoning with these intravenously administered high-dose toxins. Richet called this hypersensitivity, which occurred after two to three weeks and which led to the death of the animals despite the harmless dose of toxin, anaphylaxis . In 1903, the French physiologist Maurice Arthus was able to observe that even non-toxic substances, namely "foreign proteins", after pretreatment, can cause hypersensitivity after re-injection (re-injection).


Allergies are common illnesses. Inhalation allergies such as hay fever play a particularly prominent role here.

In Germany, at the beginning of the 1990s, 9.6% of those questioned in the national investigation survey stated that they had had hay fever before. There was a significantly higher proportion of those affected in the old federal states (10.6%) than in the new federal states (5.8%). There was hardly any difference between men and women.

At the end of the 1990s, the Federal Health Survey (GNHIES98) affected 14.5% of the population (15.4% of women and 13.5% of men). The prevalence had grown significantly in both the old and the new federal states. This increase was greater for women, so that by 1998 a gender-specific difference had emerged.

Another 10 years later, in the DEGS1 examination and interview survey, which was carried out from 2008 to 2011, the numbers had stabilized at this high level (14.8% overall, 16.5% of women and 13.0% of men) .

The fact that between the beginning and the end of the 1990s not only the response behavior of the respondents changed, but also an actual increase in the frequency of hay fever, could be found out through comparative analyzes and laboratory tests. On the basis of allergen-specific IgE tests, the sensitization to inhalation allergens was randomly checked in the health surveys.

In the National Research Survey 1990–1992, the rate of sensitization to inhalation allergens - just like the prevalence of hay fever - was higher in the old federal states (27.4%) than in the new federal states (24.1%). The overall rate was 26.7%. According to the Federal Health Survey (BGS98), there was a nationwide increase in the awareness rate to 31.2% by the end of the 1990s . This increase was somewhat less pronounced than that of the self-reported hay fever. The increase in West (to 31.9%) and East (to 28.5%) was similar.

Theses on the causes of the increase in allergic diseases

There is no satisfactory explanation for the increase in allergic diseases in recent decades - as well as for the increase in autoimmune diseases - but there are some theses:

Hygiene hypothesis

Some researchers attribute the observed increase in allergic diseases in western industrialized countries to the so-called “dirt and jungle hypothesis”. This is based on a lack of activation (“insufficient demand”) of the immune system - especially in childhood and early adolescence - due to excessive hygiene measures. It is assumed that contact with certain bacteria is important, especially in the first months of life, in order to steer the immune system, which tends to be more type 2 T helper cells during pregnancy , back towards a type 1 T helper cell response, which is less associated with allergic reactions. A prominent study on the subject is the ALEX study.

Decrease in parasitic diseases

The physiological function of IgE - antibodies , which play an essential role in allergies, is the defense of worms and other parasites . The decline in parasitic diseases could lead to the immune system being redirected to other, harmless structures. This is supported by the lower incidence of allergies in countries with lower hygiene standards. Since parasite infestation is virtually non-existent in western industrial nations, but there is increased IgE antibody formation in allergic reactions, it is being examined whether there could be a connection here. A study of 1,600 children in Vietnam showed that children with intestinal worm infestation compared to children with no worms decreased by sixty percent chance of an allergy to dust mites had. However, there are currently contradicting research results, so that this hypothesis cannot yet be conclusively assessed.

environmental pollution

Allergens such as the main allergen of the birch, Bet v 1 , can adhere to diesel soot particles (including fine dust ) and can thus reach deeper lungs when inhaled. It is possible that the diesel soot particles as "carriers" of the allergens also have an adjuvant (supporting) effect and thus promote sensitization.

The environmental pollution also causes stress in hazel bushes and changes the protein formation in such a way that the people affected react more and more violently to it.

Scientists at the Helmholtz Center in Munich have found that the allergic reactions of ragweed (Ambrosia artemisiifolia) increase when they come into contact with nitrogen dioxide . This increases the number of allergens and makes them more aggressive. Ambrosia pollen is one of the strongest allergy triggers.

Vaccinations and other medical measures

A connection between allergies and vaccinations could not be proven. In the GDR , the vaccination coverage rate was significantly higher (close to 100%), while the allergy rates were lower than in the FRG (until 1989). New to the discussion are studies on early vitamin D prophylaxis , on paracetamol and on antibiotic therapy .

Increased allergen exposure

This consideration relates to the fact that increased allergen exposure could lead to increased sensitization. Reasons for increased exposure could be: the increase in pollen as a result of a stress reaction of trees to global warming or pollution, the increase in mite exposure due to improved insulation of the houses, the increased consumption of exotic foods such as kiwi.

Changes in the commensal flora

Changes in the commensal flora could also affect the immune system and be related to the increased incidence of allergies. Changes in the intestinal flora can be triggered by the use of antibiotics and modern eating habits. The skin's bacterial flora may have been altered by the introduction of diapers.

It is debated whether probiotics could have a beneficial effect on the development of allergies.

Changed lifestyle

There are a number of other factors that are also believed to promote the development of allergic diseases. These are smoking, car exhaust fumes, stress, smaller families, a changed diet, but also a changed individual lifestyle, which could affect the development of atopy and allergies, such as the shorter breastfeeding period for young mothers and the resulting higher risk of allergies for the child. Children of women who have had contact with animals, grain or hay during pregnancy are less likely to develop allergic respiratory and skin diseases later in life. For optimal protection, however, constant contact with farm animals or grain is necessary.

Causes of Allergic Diseases

The causes of allergies can be divided into genetic and non-genetic factors.

Genetic factors

The genetic factors include: Disposition to the excessive formation of total IgE and allergen-specific IgE antibodies, as well as their fixation especially on mast cells and basophilic granulocytes of the skin and mucous membranes ( atopy ). The genetic factors also include a reduced activity of regulatory T cells , whose task it is to limit the activation of the immune system and thereby regulate the immune system's self-tolerance . The allergic responsiveness is associated with the HLA genes.

There is clear evidence of an increased risk of allergies for children in whom either one or both parents are allergic. Obviously, several genetic factors play together, so there is no such thing as one “allergy gene”. There are a variety of candidate genes that may or are likely to be involved in the development of allergic diseases. Different allergic predispositions (e.g. allergic asthma , atopic dermatitis ) also seem to be genetically determined differently.

Not genetic factors

Impaired barrier function of the skin

An allergy can also be caused by a disturbed barrier function and an associated increased permeability of the skin and mucous membrane, e.g. B. by bacterial or viral infections or by chemical irritation.

Intensive allergen exposure

Increased allergen exposure can also lead to allergies if predisposed. This form of allergy is particularly important in the case of work-related allergies.


Physical or psycho-social stress is not the cause of an allergy. But stress affects the immune system. Physical and / or psycho-social stress can therefore intensify an existing allergy or, if there is an existing sensitization, it can be the trigger for the allergic disease.



Allergens are the trigger for allergies . Allergens are antigens , i.e. substances that are recognized by the body as foreign and trigger a specific immune response . In the case of an allergy, this normal physical reaction is misdirected, so that actually harmless antigens become allergens. There are a variety of allergens. Most allergens are polypeptides or proteins .

Allergens can be classified according to different aspects:

  • according to the allergen source (e.g. animal allergens, see in particular allergy to cat epithelia , pollen allergens, house dust mite allergens)
  • according to the type of contact with the allergens (e.g. inhalation allergens, food allergens)
  • according to the pathomechanism by which the allergens trigger an allergic reaction (e.g. IgE -reactive allergens, contact allergens )
  • according to their allergenic potency into major and minor allergens
  • according to their amino acid sequence into certain allergen groups (e.g. group 5 grass pollen allergens) or into certain protein families (e.g. lipocalins , profilins ).

Allergens can be absorbed by the body through inhalation , through ingestion , through skin contact or through injection (this also includes insect bites).

Non-immunogenic substances

Allergies to water and sugar are by definition not possible because an allergy is based on an inappropriate immune response to an allergen. However, water and sugar are not immunogenic and therefore not “allergic”. A condition sometimes referred to as a water allergy is the extremely rare aquagenic urticaria ( water urticaria ). An immune response to substances dissolved in tap water is sometimes referred to as a water allergy.


An allergy requires sensitization. Sensitization is understood to mean the first contact with the allergen and the body's specific immune response to this allergen. This sensitization does not cause symptoms of the disease, but it can be detected in the blood. Symptoms of the allergic illness only appear in allergy sufferers when they come into contact with the allergen again after the sensitization phase has ended (5 days to several years).

Prophylaxis of sensitization

The best prophylaxis against an allergy is to avoid sensitization. The complete avoidance of all allergens is impossible. However, in certain cases it is possible and sensible to avoid or reduce exposure to potential allergens:

Avoiding latex

Children born with an open back ( spina bifida ) are at a very high risk of sensitization to latex. It is therefore now the clinical standard to protect these children from any contact with latex (for example with latex surgical gloves) from birth.


The optimal nutrition for newborns is exclusive breastfeeding for at least the first 4 months of life. There are retrospective studies that have observed that breast-fed children suffer from allergies less than those who are not.

dogs and cats

There are also studies showing that domestic dogs and domestic cats can protect against allergies. These collect allergens in the open air, which are later given to the child at home. Its immune system is then trained to recognize the foreign body, but to classify it as harmless. At least in one animal study on mice, this worked.


The exogenous allergic alveolitis is usually an occupational disease caused by the inhalation of certain dusts (e.g. flour in the baker's lungs). Appropriate occupational health and safety measures, such as wearing fine dust masks or the use of extractor hoods, can reduce allergen contact and thus protect employees from sensitization.


The risk of developing an allergy is determined by genetically determined predisposition , by the current defenses of the body's interfaces, by the frequency and intensity of allergen exposure and by the allergenic potency of the substance in question. The symptoms of an allergy can be mild to severe and in some cases even acutely life-threatening. Due to exposure , the symptoms may only appear seasonally, for example at the time of the corresponding pollen count, or that the symptoms appear all year round, as in the case of an allergy to house dust mite excrement.

Depending on the organ with which the allergens are absorbed by the body, the allergy can have different symptoms. Allergy sufferers can suffer from one form of the disease, but also from mixed forms. Organ manifestations can affect the respiratory tract, digestive tract, heart and circulation, blood-forming organs, skin, kidneys, joints and the nervous system.

Symptoms from inhalation allergens

Inhalation allergies belong to the type 1 allergies of the immediate type. Inhalation allergens are absorbed through the respiratory system and / or enter the body through the mucous membranes of the nose and eyes. The inhalation allergens include e.g. B. allergens from pollen, fungal spores, animal epithelia , feather dust, saliva, sweat, urine and feces, mite feces, insect scales, wood and flour dust, formaldehyde and resins.

Inhalationsallerge solve primarily respiratory symptoms from, can secondary but also trigger skin and bowel symptoms and circulatory and nervous reactions. Typical allergic diseases caused by inhalation allergens are allergic rhinitis (hay fever), conjunctivitis (conjunctivitis), coughing, bronchial hyperreactivity , bronchial asthma .

Symptoms from ingestion allergens

Ingestion allergens are absorbed through the mouth or the digestive tract. Some ingestion allergens are only released and absorbed by the body during the digestive process. The symptoms of an allergy to food or to orally ingested medication can therefore appear within a few minutes or even several hours after the ingestion of food / medication, although the food allergy is a type I immediate type allergy. The drug allergy can also occur as a type IV late reaction in the form of a drug eruption .

Ingestion allergens can primarily cause constipation, vomiting, diarrhea or abdominal colic in appropriately predisposed and sensitized people, and skin and / or respiratory symptoms via the absorption of the allergens into the blood.

Symptoms from contact allergens

Allergic rash

Contact allergens are absorbed through the skin. They overcome the skin's barrier function. Contact allergens can trigger immediate skin reactions, e.g. B. contact urticaria or a late reaction (type IV late-type allergy) that only occurs after 12 to 72 hours, e.g. B. allergic contact eczema .

Injection allergenic symptoms

Injection allergens are introduced into the body by injection or infusion . This bypasses the barrier function of the skin and mucous membrane. Injection allergens include animal poisons (e.g. from bees, wasps, fire ants, jellyfish, sea anemones, fire corals) and drugs (e.g. penicillin).

Typical allergic reactions from injection allergens include an increased local reaction and / or anaphylactic reaction.

Systemic reactions

Regardless of which organ is used to absorb allergens into the body, an allergy can also cause systemic reactions that affect the entire body, e.g. B. Urticaria and anaphylactic reactions.

Cross allergy

A cross allergy is a sensitization to biologically or chemically related substances. The structure of these substances is partially identical, so that the immune system can recognize several different substances as allergens, although there is only one sensitization to one of the substances. For example, people who are allergic to birch pollen can also have an allergic reaction to apples. In the case of cross allergy, the allergic reaction can already take place at the first contact if there was previously sensitization with a similar substance.

Systematics of allergies according to pathomechanism

In 1963, Coombs and Gell were the first people to classify allergies according to their pathophysiological mechanisms into four types, which can overlap:

Early types

The early types (type I to type III allergies), also called immediate allergic reactions, are mediated by antibodies ( humoral allergy).

Type I allergy (immediate type, anaphylactic type)

Type 1 response

Type I allergy is the most common type of allergy.

In type I allergies, there is a malfunction in the regulation of IgE antibodies . Through several mediators, IgE antibodies cause the blood vessels to expand even in small quantities and increase their permeability for white blood cells. T cells , which normally limit IgE activity to a reasonable level, are absent in type I allergies or are not active enough. In type I allergy, mediators of inflammation , e.g. B. histamine , leukotrienes , prostaglandins , kallikrein , released from basophils granulocytes and mast cells . This causes inflammation of the skin, mucous membranes, or systemic inflammation.

The allergic reaction in type I allergy occurs within seconds to minutes. A second reaction may be possible after 4 to 6 hours (delayed immediate reaction). This second reaction must not be confused with the late-type reaction of type IV allergy.

Typical diseases of type I allergy:

Type II allergy (cytotoxic type)

In type II allergies, immune complexes are formed from membrane antigens (e.g. drugs, blood group antigens ) with circulating IgG or IgM antibodies. This activates the complement system or cytotoxic killer cells and cytolysis (destruction) of the body's own cells occurs.

The allergic reaction in type II allergies occurs after 6 to 12 hours.

Typical diseases for type II allergies:

Type III allergy (immune complex type, Arthus type)

In type III allergies, immune complexes are formed from precipitating IgG and IgM antibodies and allergens. This activates complement factors, especially C3a and C5a . These special parts of the complement system lead to phagocytosis (active uptake) of the immune complexes by granulocytes with the release of tissue-damaging enzymes , e.g. B. elastase , collagenase , myeloperoxidase .

The allergic reaction in type III allergy occurs after 6 to 12 hours.

Typical diseases for type III allergy:

Late type

The late type (type IV allergy), also called delayed allergic reaction, is mediated by specifically sensitized T cells ( cell-mediated allergy).

Type IV allergy (delayed type)

Type IV allergy is the most common form of allergy after type I allergy.

In type IV allergies, lymphokines are released from specifically sensitized T lymphocytes . These lymphokines cause the activation or reproduction of macrophages and mononuclear cells and their migration to the location of the allergen exposure. This causes local infiltration and inflammation.

The allergic reaction in type IV allergy occurs after 12 to 72 hours.

Typical diseases of type IV allergy:

Allergy tests

Even a positive allergy test alone is not proof of an allergy. The diagnosis of allergy can only be made in connection with the allergy test and the clinical symptoms . The skin test and the blood test only detect sensitization to a certain substance. These tests say little about whether symptoms exist at all or about the type or severity of the symptoms. The provocation tests show an intolerance and the symptoms of this intolerance, but not whether this intolerance is actually an allergy.

Skin tests

Prick test

Skin tests are done as a standard exam when a patient is suspected of having an allergic reaction to a substance. In the skin test, allergen extracts or allergen-containing material are brought into contact with the skin in various ways. Sensitized affected persons show local reactions of the immediate type or the late type after defined times. They can be used to read off which allergens or allergen sources the patient is sensitized to. This test may also provide information about the severity of the allergic reaction.

  • Prick test: The most commonly used method is the skin prick test (also skin prick test (SPT) ), are applied to the forearm or the back in which individual droplets of glyzerinisierten allergen extracts and histamine and isotonic saline (as references). A special needle (lancet) is used to pierce about 1 mm of the skin through the drops. The immediate reaction can be read after approx. 15 minutes.
  • Prick-to-prick test: In the prick-to-prick test , the lancet is first used to pierce the suspected allergen source (fruit) and then into the patient's skin.
  • Intracutaneous test: In the intracutaneous test , approx. 20 microliters of aqueous allergen extracts are injected superficially into the skin with a tuberculin syringe.
  • Rub test: The rub test is used on particularly sensitive people. The doctor rubs the suspected allergy trigger on the inside of the forearm. If the reaction is positive, extensive redness or wheals appear.
  • Scratch test: In the scratch test , allergen extracts are placed on the flexor side of the forearm and the skin is scratched on the surface with a lancet 5 mm long. However, this test is rarely used because of its inaccuracy.
  • Patch test: A patch test , the patch test or atopy patch test, is used for contact dermatitis . The suspected allergens are incorporated into petroleum jelly. The allergen-Vaseline mixtures are placed on aluminum disks with a diameter of around 1.5 centimeters and a depth of around two millimeters. These aluminum chambers are then stuck to the skin on the patient's back or upper arms with a plaster in such a way that the allergen-Vaseline mixtures are fixed on the skin. Because contact dermatitis is a late-type reaction, the patch must remain on the skin for two to three days before a result can be read. The problem with this test is the low sensitivity and the poor reproducibility. The atopy patch test is therefore no longer recommended for food.

Provocation tests

In provocation tests, the suspected allergen is not supplied to the patient through the skin, but in a different form. The main advantage of the provocation tests is that the triggering of a complaint can be detected and not just a sensitization, as is the case with a blood test by detecting IgE antibodies. Since provocation tests can lead to unexpectedly severe signs of illness up to life-threatening anaphylactic shock, they should only be carried out by a doctor experienced in allergology , who can also take the appropriate emergency measures if necessary.


In the case of allergic rhinoconjunctivitis (hay fever), an allergen extract can be sprayed into the nose as a provocation and the allergic reaction can then be measured by measuring the swelling of the nasal mucosa using so-called rhinomanometry or the tryptase level in the blood.

Pulmonary function test

In allergic asthma, the provocation is carried out by inhaling an allergen extract with subsequent recording of the allergic reaction with a lung function test . Since asthma is usually associated with bronchial hyperregibility , it can also be provoked unspecifically with increasing concentrations of a methacholine solution ( methacholine test ).

Double-blind placebo-controlled oral food challenge

The double blind placebo controlled food challenge (DBPCFC) can be used for severe food allergies . Various foods are gradually added to a hypoallergenic basic food in such a way that neither the patient nor the doctor can recognize the food. The compatibility is observed. In this way it can be determined which foods trigger allergic reactions and, conversely, foods can also be identified that can be safely consumed. However, this procedure is very time-consuming and can i. d. Usually only be carried out in a stationary manner.

Blood tests

IgE antibodies

IgE antibodies can be measured in blood samples. On the one hand, the total IgE level can be measured, which includes all free IgE antibodies. This value enables a statement to be made as to whether more IgE antibodies are generally formed. Elevated total IgE values ​​do not only occur in allergic diseases, but also in parasitic infestation and certain haematological diseases .

On the other hand, allergen-specific IgE antibodies can also be detected. The IgE levels that are specifically directed against an allergen source are determined here.

However, the quantitative measurement of IgE antibodies in the blood correlates only poorly with the clinical picture. This means that the measurement of IgE antibodies in the blood allows a statement to be made about the sensitizations of an allergy sufferer, but only to a limited extent an assessment of the severity of the symptoms and no statement at all about the type of symptoms. It is also possible that allergen-specific IgE antibodies cannot be detected despite sensitization.


Another parameter that can be measured in blood samples is eosinophil cationic protein (ECP) . ECP is secreted by activated eosinophils . ECP is an inflammation parameter and is used to monitor the progress of allergic asthma or atopic dermatitis.


Tryptase can also be detected in blood samples. Tryptase is released by activated mast cells and is a highly specific parameter for activated mast cells. The tryptase level is also determined for the diagnosis of anaphylactic shock, for the post-mortem diagnosis of asthma, for the diagnosis of mastocytosis and for provocationtestingin allergic rhinitis.


The determination of sensitized lymphocytes can be detected and quantified by a lymphocyte transformation test (LTT) . This can be useful for certain type IV (late) allergies.


Allergen avoidance

The allergen avoidance, d. H. Allergen avoidance is the optimal therapy for sensitized people to avoid an allergy, as an allergy can only occur when there is contact with the corresponding allergen. Continued allergen exposure increases the immune response to the allergen, while permanent allergen avoidance does not remove the sensitization, but weakens the specific immune response. If the strict avoidance of an allergen is not possible, the allergen exposure should be reduced as far as possible, since an allergy also depends on the intensity of the allergen exposure.

Certain products, such as mite-proof mattress covers for house dust mite allergies or pollen filters in air conditioning systems for pollen allergies, help to reduce allergen contact. Even if, in the case of animal hair allergies, not using pets greatly reduces allergen contact, animal hair allergens are very stable, are carried around and can also be detected in places such as schools where animals are normally not kept. Food allergens, on the other hand, can usually be avoided very well.

Medical therapy

Most allergies are treated with medications that reduce or prevent the occurrence of allergic symptoms, but cannot cure the allergic disease. These antiallergic drugs are used in different dosage forms (tablets, nasal sprays, asthma sprays, eye drops, creams, ointments and injections) and at different intervals (in acute need, prophylactic, permanent) depending on the form and severity of the disease.

Active ingredients used for allergy treatment are

Patients who are known to be at risk of anaphylactic shock (e.g. with insect venom allergies) are prescribed an emergency kit with an antihistamine, glucocorticoid, possibly an inhalation preparation and an auto-injector with adrenaline ( adrenaline pen ), which they should always be with you.


Various active ingredients, especially those used to dampen the immune response, are currently being tested for their suitability as drugs.

Active ingredient (brand name) Working principle status swell
CYT003-QbG10 Immune modulator ( T cells Th2 -> Th1 Shift) Phase II studies successful Q1 ( Memento from May 13, 2012 in the Internet Archive ) Q2 Q3 ( Memento from May 13, 2012 in the Internet Archive )
TOLAMBA Immune modulator ( T cells Th2 -> Th1 Shift) Phase II / III study successful Q4
AIC Immunomodulator (histamine reduction) Phase III study is ongoing Q5


Desensitization, also known as specific immunotherapy (SIT) , is the only available causal therapy for type I allergies. In the case of desensitization, the allergen- specific IgE- mediated reactivity of the immune system (allergy of the immediate type, type I allergy) is reduced by the regular supply of the allergen over a longer period in subliminal, slowly increasing concentrations. The allergen or the modified allergen ( allergoid ) is either injected under the skin ( subcutaneous immunotherapy (SCIT)) or absorbed as drops or tablets sublingually (sublingual immunotherapy (SLIT)).

The prerequisite for successful desensitization is the willingness and ability of the allergy sufferer to carry out the therapy regularly over a period of three years, as well as the subsequent maintenance therapy. The indication for a desensitization exists for people from 5 years if the causative allergen cannot be avoided, the effect of the desensitization for the treating illness is proven and a suitable allergen extract is available. The effectiveness of the desensitization has been proven by several studies for rhinoconjunctivitis in pollen allergy, for allergic bronchial asthma , for house dust mite allergy , for mold allergy , for animal hair allergy and for insect venom allergy .

Corresponding studies for some products have also shown that desensitization reduces the risk of asthma and new sensitization to other allergens is reduced. For this reason, children and adolescents should be desensitized at an early stage and those products should be selected for which this effect has been proven.


Food allergies in children

Children's immune systems are not yet fully developed. Children therefore have an increased tendency towards allergies. Even and especially in children, one form of allergy can therefore be replaced by another in the course of the disease, or another can be added to one allergy. With consistent avoidance of the triggering allergen, a food allergy usually disappears with maturation of the immune system by the age of 5, especially cow's milk and chicken egg allergies. Other food allergies, e.g. B. the peanut allergy, however, have only a slight tendency to improve.

Changed responsiveness of cells

The reactivity of mast cells , monocytes , as well as basophils and eosinophils, increases particularly in the chronic course of type I allergies . This can aggravate the symptoms of an existing allergy and / or add new allergies.

Change of floor

In the case of an inhalation allergy, a change of floor is understood as the spread of IgE-mediated allergy symptoms (type 1 immediate allergy) from the conjunctiva (conjunctiva of the eye) to the nasal and bronchial mucosa or from the upper respiratory tract to the lower respiratory tract, causing hay fever to allergic asthma. The occurrence of further inhalation allergies and / or the occurrence of cross allergies is also referred to as a change of floor.

If left untreated, 30–40% of all allergies to inhalation allergens lead to a change of floor.

Pseudo allergies and intolerances

Allergy and pseudo-allergy

There are diseases whose symptoms are similar to an allergy, but which are not immunological. These diseases are known as pseudo-allergy or intolerance .

In the case of pseudoallergy, the allergy-like symptoms are triggered by non-specific activation of mast cells . When mast cells are activated and degranulate , they release a number of inflammatory mediators (e.g. histamine ). An inflammatory reaction develops, which manifests itself in allergy-like symptoms.

While the mast cells are activated specifically in allergies, namely by the fact that certain allergens can bind to surface-bound antibodies , mast cell activation in pseudoallergies is non-specific, i.e. without the involvement of the surface-bound antibodies.

Pseudoallergy and allergy must be differentiated from intolerance , which can also cause allergy-like symptoms. Intolerance is a metabolic disorder. The body cannot metabolize certain substances or cannot metabolize them sufficiently, mostly due to an enzyme defect .


The training to become an allergist is additional training for specialists. This specialist doctor is only responsible for allergies in his specialty. The dermatologist with additional training in allergology is responsible for skin tests. There are no special specialists for pseudo-allergies and intolerances with similar symptoms.

However, since the symptoms of allergy sufferers are only rarely limited to one organ, and the patient cannot even recognize whether his symptoms are due to an allergy, a pseudoallergy or an intolerance and what special diagnostics he needs, the diagnosis of intolerance is often lengthy and difficult, as several doctors often have to be consulted for the diagnosis.

See also


  • Clemens von Pirquet : Allergy. In: Munich Medical Weekly . Volume 30, 1906, pp. 1457-1458 (first mention of the term "allergy").
  • Björn M. Hausen, Ines K. Vieluf: Allergy Plants - Handbook and Atlas. Contact allergens - early allergic reactions . 2nd extended edition, Nikol Verlagsgesellschaft, Hamburg 1997, ISBN 3-933203-48-1 .
  • Claus Bachert, Bernd Kardorff : Allergic diseases in practice , 2nd edition, Uni-Med Verlag, Bremen 2001, ISBN 3-89599-505-3 .
  • Lothar Jäger: allergies. Causes, therapies, prevention . Beck, Munich 2000, ISBN 3-406-44740-6 .
  • Jörg Rinne, Jens Becker: The 1x1 of allergies. Synergia Verlag, Darmstadt 2007, ISBN 978-3-9810894-8-6 .
  • Cathleen Muche-Borowski et al .: Clinical guideline: Allergy prevention . In: Dtsch Arztebl Int . No. 106 (39) , 2009, pp. 625-631 ( Article ).
  • Reto Coutalides: indoor climate . No pollutants in living and working rooms. Werd Verlag, Zurich 2002, ISBN 3-85932-419-5 .
  • Michael Wullinger, Agnes Fatrai (ed.): Allergy treatment with Chinese medicine. Munich, Elsevier, 2007, ISBN 978-3-437-57440-5 .
  • Bärbel Häcker: Allergy. In: Werner E. Gerabek , Bernhard D. Haage, Gundolf Keil , Wolfgang Wegner (eds.): Enzyklopädie Medizingeschichte. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , p. 40 f.

Web links

Individual evidence

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