Atopic eczema

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Classification according to ICD-10
L20 Atopic [endogenous] eczema
L20.0 Prurigo Besnier
L20.8 Other atopic [endogenous] eczema
L20.9 Atopic [endogenous] eczema, unspecified
ICD-10 online (WHO version 2019)
Atopic eczema in a toddler
Atopic eczema on the arm of a 5 year old child

The atopic dermatitis ( Greek ατοπία, ATOPIA - "rootlessness", "not attributable"; Greek έκζεμα, eczema - "leavened") is a chronic, non-contagious skin disease that the atopic belongs diseases.

Other common names are neurodermatitis , atopic dermatitis and endogenous eczema. The disease is also known as chronic constitutional eczema, asthma eczema and prurigo Besnier . The term neurodermatitis comes from the 19th century. At that time it was thought that the cause of the skin disease was an inflammation of the nerves . This view was later refuted, but the name is still common.

The main symptoms are red, flaky, sometimes weeping eczema on the skin and severe itching . The disease progresses in phases and has an individual, age-dependent appearance.

Atopic eczema is considered incurable, but it is treatable. The most common treatment consists mainly of combating the characteristic dryness of the skin and the topical application of anti-inflammatory agents. There are other therapies that not only include external treatments, for example by changing your diet with the use of B vitamins.

Epidemiology

Atopic eczema is a common disease in industrialized countries . The disease affects 5–20% of children and 1–3% of adults. In Germany, 8–16% of all children develop atopic eczema by the time they start school. In around 60% of those affected, the disease occurs in the first year of life, in 90% by the age of five. Symptoms often decrease as you get older and go away with the onset of puberty . Up to 70% of those originally affected are symptom-free in adulthood.

Atopic eczema is observed more and more often. Compared to the middle of the 20th century, it can be assumed to be four to six times more frequent today. The reasons for this are not yet known. More frequent allergies , changed living conditions and increased hygiene ( hygiene hypothesis ) are discussed as possible causes .

root cause

The causes of atopic eczema have not yet been fully clarified. Experts see an interplay of genetic factors, immunological changes and environmental influences in the complex disease process and its very individual course.

Genetic factors

It is assumed that those affected react more strongly to certain influences than others due to their genetic predisposition .

The clear genetic disposition of this disease is difficult to prove. Previous mutation analyzes had drawn attention to around 20 different candidate genes. However, these were not always reproducible in repeat studies. More recent results show that the skin's barrier function to the environment is disturbed because genetic defects mean that important structural proteins are not formed. Mutations in the filaggrin gene were discovered that lead to a reduction in filaggrin in the outer layers of the skin. This filaggrin protein is a key element of the epidermal skin barrier and promotes cornification on the skin surface. In atopic dermatitis, the protective function of the skin is decisively impaired. The weakened barrier could make it easier for allergens to penetrate and make atopic skin more susceptible to inflammation. Other results show that the lack of a collagen variant in the skin is also associated with atopic diseases. Other genetic defects are also known: In order to keep the skin supple, the healthy body produces sebum. This skin oil consists, among other things, of gamma-linolenic acid . To do this, the body needs linoleic acid ingested with food . The enzyme delta-6 desaturase is required for the conversion of linoleic acid into gamma-linolenic acid. In atopic dermatitis, the activity of this enzyme may be reduced or impaired.

Furthermore, it has been shown that there are common candidate genes for the disposition to atopic eczema and the also immunologically caused skin disease psoriasis vulgaris .

An outwardly apparent regression of the symptoms in some patients can be attributed to the fact that the genetic defect is only present in a part of the approximately 2 billion body cells and thus the less or not damaged gene variants can also be used. It has not yet been fully clarified which mechanisms control protein biosynthesis , i.e. when and to what extent which genes are read and proteins are created.

Atopic dermatitis can occur in the context of rare syndromes , such as the Konigsmark-Hollander-Berlin syndrome .

Immunological processes

At the beginning of the development of the disease, there is always a defect in the skin barrier, possibly due to local inflammation or a primary defect in the function of the keratinocytes . As a result of this defect, more cytokines are released that recruit inflammatory cells such as T cells . At the same time, the dendritic cells in the skin , the so-called Langerhans cells of the skin, but also additional inflammatory dendritic epidermal cells , have receptors for the IgE antibody on their surface . Allergens that penetrate the disturbed skin barrier cause IgE antibodies to be produced; these in turn are bound to dendritic cells, which in turn activate the T cells.

The now activated T cells produce a number of cytokines and chemokines , in particular the interleukins IL-4, IL-5 and IL-13, as well as interferons in the further course . This stimulates further T cells and dendritic cells to immigrate. In addition, eosinophilic granulocytes migrate . In general, T helper cells of the Th1 type that stimulate antibody production are more active at the beginning , and Th2 cells are more active later. This T-cell reaction is a Type IV allergic reaction .

Another factor in the development of symptoms is that additional T cells cause the keratinocytes to apoptosis via Fas receptors . This causes skin defects and the skin's barrier function is further disturbed. In addition, autoallergens are released from inside the cell , the atopy-associated autoantigens (ARA), which often react in a cross-reaction with exogenous allergens. These are also recognized as IgE-mediated and could be the reason why the inflammatory reaction can persist even if contact with exogenous allergens is avoided. In the further course this can come to the fore so far that atopic eczema can be understood as a kind of autoimmune disease with chronic inflammatory allergy symptoms.

Another hypothesis about the development of the disease even states that atopic eczema in toddlers begins as an inflammation caused by the autoallergens, later on due to the defect in the skin barrier caused by exogenous allergens.

Another disease mechanism is the colonization of the skin and mucous membranes by microorganisms. On the skin and in the nasal cavities of sick people there is often a heavy colonization with bacteria of the Staphylococcus aureus species . Due to the skin defects that are already present, they penetrate the skin and produce enterotoxins , against which IgE antibodies are also formed and thus intensify the inflammatory reaction. Fungi such as Pityrosporum ovale or Candida albicans, as well as viruses, can cause similar amplification reactions.

Symptoms and ailments

Sensitive skin

The skin of the person affected differs from healthy skin in that it has an impaired barrier function. Therefore, atopic eczema manifests itself in particular through very sensitive and dry skin, which is often reddened. It is particularly susceptible to external stimuli that can lead to itching. Typical areas ( predilection sites ) for the affected skin are in particular the crooks of the arms, the hollows of the knees, and the neck and face areas.

itching

The main problem for those affected is the severe itching , which is made easier by the sensitive, often injured skin. It can be triggered, for example, by irritation on sensitive skin. Those affected react by scratching, which leads to further skin irritation. This vicious circle helps maintain symptoms. The itching is particularly severe at night, which is why there is often a lack of sleep. The resulting overtiredness and reduced performance often represent a strong psychological burden for those affected.

Provocation factors

The skin of those affected is very sensitive to internal and external irritations, which are known as provocation factors or triggers. In connection with severe itching, they can trigger reddening of the skin , which quickly develops into eczema.

Provocation factors (according to Fischer, Ring, Abeck)
irritating (pseudo) allergic microbial mentally other
textiles Stress (positive / negative) UV light
food Staphylococcus aureus climatic
Washing habits Food additives Malassezia species hormonal
Sweat Aeroallergens Infections
Water hardness

Possible provocation factors are, for example, mechanical stimuli on the skin, sweating , food, alcohol and psychological stress .

Allergies also have a negative impact on the clinical picture. A large number of patients with atopic eczema also suffer from allergies. Adults mostly have allergies to aeroallergens such as house dust , pollen or animal hair , while food allergies particularly affect patients in infancy and young children . The most common food allergies are to milk, eggs, nuts, fish, soy and wheat.

In contrast to this, a distinction must be made between pseudo-allergic reactions to food in which mediators such as histamine are released without an IgE -mediated reaction. Food additives can trigger or worsen itching or skin irritation. Foods containing histamines can make itching worse. Spicy or acidic foods can cause skin irritation to worsen eczema.

The clothes of the person affected can affect the skin condition in different ways. The focus is on unspecific mechanical irritation, which can be seen, for example, in the incompatibility of wool and some synthetic fabrics . In principle, the coarser the fibers of the textiles, the stronger the irritation. Allergic reactions to clothing are comparatively rare. Furthermore, the type of clothing should be adapted to the ambient temperature. Clothing that is too warm means that the build-up of heat causes increased sweat to occur, which can worsen atopic dermatitis.

Complications

Bacterial skin infection

The very sensitive and often cracked skin of those affected is often associated with a disturbed balance of the natural skin flora . The sometimes massive colonization with Staphylococcus aureus is characteristic . By triggering weeping skin reactions, these bacteria lead to improved environmental conditions for staphylococci with further bacterial growth and thus to an increasing deterioration in the condition of the skin due to the mutual reinforcement of both diseases, a so-called vicious circle , i.e. a self-sustaining or reinforcing process.

The defective skin barrier also makes it easier for yeasts to penetrate the skin. Yeasts are a natural part of the skin flora. Healthy people usually have formed immunoglobulin G antibodies against yeasts. Studies show that the lipophilic yeast fungus Malassezia increasingly colonizes the skin of patients. Malassezia-specific IgE antibodies are detected in 30–80% of patients. These keep the inflammation going.

In rare cases, it may be related to the herpes simplex virus to a Eczema Herpeticatum come, which in many cases only stationary with infusions should be treated.

course

Cradle cap in a two-month-old infant

The symptoms of the disease manifest themselves in different ways and in different places in each person affected. They depend on the age. The disease usually occurs in bouts of varying duration and severity - often for no directly identifiable reason. Just as often they end without a direct trigger (e.g. a specific treatment) being able to be identified. This often creates great uncertainty about the ultimately successful treatment method.

In the acute development phase, the focus is on inflammatory changes such as reddening, swelling of the skin, oozing and crust formation due to the secretion drying up. If this acute inflammatory reaction is not treated in time, secondary bacterial infections can occur.

In infants, the appearance of cradle cap on the head is an early form of atopic eczema. This usually occurs in the third month of life, rarely earlier. Erythema with papulovesicles develops, especially on the cheeks, sometimes all over the face and also on the hairy head . Scratching leads to weeping and crusty areas, the typical cradle cap. Sometimes the skin appearance spreads all over the body. The extensor sides of the arms and knees in particular are often affected. Secondary bacterial infections often occur.

From the age of two, however, the skin changes tend to be dry and to be found on the flexors of the extremities. Typical areas from this age on are the bends of the joints, neck, side face and hands. These parts of the body can also be affected in adulthood.

From puberty onwards, skin changes are mainly found in the forehead and eyelids , neck, large bends of the joints and the back of the hand. Characteristic at this age is a coarsening of the skin folds in combination with a visible thickening of the epidermis ( lichenification ) in the affected areas.

Special and minimal forms

Dyshidrotic eczema

Apart from the typical symptoms, special forms of atopic eczema can occur. Especially in adulthood, after the main symptoms have disappeared, these can be the only signs of atopic eczema. They are then referred to as minimal variants.

The special forms include:

  • exclusive infestation of the head and neck ( head-and-neck variant)
  • Nipple eczema
  • Dyshidrotic eczema (small, itchy blisters on the palms of the hands or the soles of the feet)
  • Tears ( rhagades ) of the earlobes
  • Eczema of the eyelids - especially on the lower eyelid - as an allergic reaction to pollen or food, but also irritative from rubbing
  • light, scaly patches of skin on otherwise tanned skin ( pityriasis alba )
  • isolated chronic eczema on the external genitals
  • Itchy, inflamed lips ( cheilitis sicca) , which can lead to inflammation of the corner of the mouth due to frequent licking
  • Pinhead-sized, bloody crusts on the scalp with severe itching
  • dry, flaky skin on the palms of the hands and soles of the feet
  • dry fingertip or toe tip eczema ( pulpitis sicca , common in young children and in winter)

Psychological consequences

Psychosomatic relationships play a major role in atopic eczema. On the one hand, the clinical picture can worsen through psychological stress; on the other hand, the skin complaints have a negative impact on the patient's psyche.

Nocturnal itching and scratching attacks can lead to a sleep deficit and thus also to concentration problems or irritability. In addition, those affected can suffer from their appearance being impaired . The cosmetically disturbing rashes can lead to social exclusion and a reduction in self-esteem. It is also possible that scratching as a behavioral pattern in conflict and stress reactions. In this context, the family situation can also play a role in children, if behavior patterns are reinforced by increased attention from the parents.

Comorbidities

diagnosis

criteria

Various main and secondary criteria were established for the diagnosis of atopic eczema. The main criteria include the typical appearance of the skin, the itching and a detailed personal and family anamnesis .

In addition to the actual symptoms of the disease, characteristic external features usually indicate the disease. These so-called atopiestigmata include dry skin ( sebostasis ), a thinner lateral eyebrow area ( Hertoghe sign ), a double crease in the eyelid ( Dennie-Morgan crease ) and the "paradoxical vascular reaction": In contrast to healthy skin, scratching does not cause red but white stripes on the skin (white dermographism ).

Determination of provocation factors

An attempt is made to determine possible trigger factors on the basis of the medical history . Allergy tests may be carried out for this purpose . The prick test serves to detect allergens of the immediate type. Contact allergies can be detected with the patch test .

Differential diagnosis

In the differential diagnosis , other inflammatory skin diseases in particular must be differentiated. These include in particular allergic contact eczema , toxic contact eczema , pyoderma and, in infants, seborrheic eczema . Various metabolic and immune diseases can also lead to symptoms that are confusingly similar to atopic eczema. In children, scabies is rarely an option . In some cases it is difficult to differentiate it from psoriasis , especially if both diseases are present at the same time.

Severity

Various scores have been developed to quantify the extent and intensity of atopic eczema . They document the disease and its course. In Europe, the SCORAD (Scoring Atopic Dermatitis) is mainly used.

treatment

Just like the causes, the forms of treatment used are very diverse. Since different factors appear to play a role, the parallel application should be considered and individually tailored to the needs of the patient. Not all treatment approaches work the same for all; some methods that have a soothing effect in one person may worsen the disease in others. Treatment methods may have to be combined or changed several times, as it can happen that the skin reacts differently to a previously well-accepted type of treatment than expected. It may be necessary to discontinue treatment and replace it.

The therapy of atopic eczema depends on the course of the disease and is adapted to the severity of the symptoms. The following step-by-step scheme can serve as a guide, which must be adjusted individually, for example to age, disease progression and localization of the skin changes. The treatment options of the lowest level are gradually expanded to include additional options as the degree of severity increases.

Step therapy for atopic eczema
step 1 Level 2 level 3 Level 4
dry skin mild eczema moderate eczema persistent, severe eczema
  • External treatment with glucocorticoids of class 2 and 3 and / or calcineurin inhibitors
  • antiseptic agents
  • Treatment of itching
  • external treatment with glucocorticoids of class 1 and 2 (external) and / or calcineurin inhibitors
  • Basic skin care
  • Avoidance and reduction of provocation factors

Basic care

The focus of symptomatic therapy is topical treatment of the skin. This is what ointments , creams and lotions available. Different preparations are used depending on the severity and type of symptoms.

Daily basic care is intended to stabilize the skin's barrier function in order to reduce the skin's sensitivity to irritation and the penetration of allergens. Ointments and lotions are usually used, depending on the condition of the skin. Their composition depends on the current skin condition: Oil-in-water emulsions are usually used, and water-in-oil emulsions are also used for very dry skin. Oil baths are another way of re-oiling the skin. Both warm and cold wet compresses can also be used for healing and relief.

Specific active ingredients for external use

Ointments containing active ingredients are often used, e.g. B. to improve the moisture retention or the healing of the skin. The skin of those affected has a significantly lower concentration of urea , which acts as the most important moisturizing factor. For example, preparations containing urea help to reduce the characteristic dryness of the skin. The urea, which briefly gets into the skin as a result of the application, holds more water and thus binds it in the skin. However, therapeutically applied urea on and in the skin can lead to further irritation if the skin is already irritated or cracked. Other frequently used ointment additives are z. B. hemp oil , evening primrose oil , St. John's wort extract , zinc or dexpanthenol .

If the skin is overly colonized with bacteria or fungi, anti-infection ointments are used. In the event of excessive colonization by Staphylococcus aureus , triclosan , chlorhexidine , but also antibiotics (e.g. fusidic acid ) are preferred . In this situation, additional treatment with dilute chlorine bleach (sodium hypochlorite solution) can significantly improve the condition of the skin.

In the event of excessive yeast colonization, antifungal agents are used.

For the treatment of weeping eczema, tannin preparations are available that have a drying, itch-relieving and slightly anti-inflammatory effect.

Anti-inflammatory agents

To treat more pronounced inflammatory symptoms, ointments with immunosuppressants are used. Glucocorticoids are most commonly used. They work against itching and inflammation of the skin and can relieve severe relapses or, if used in good time, prevent them. Different active ingredients and ointment bases are used depending on the severity and type of symptoms. Strongly effective glucocorticoids (class 3) are only used for severe attacks. Normally, weakly or moderately effective preparations (class 1 and 2) are sufficient. The preparations have been continuously developed since the 1950s. Newer active ingredients (e.g. prednisolone and methylprednisolone preparations) have a lower risk of side effects than older active ingredients if they are highly effective. Hydrocortisone preparations are often sufficient on the face or with milder symptoms .

Side effects can occur, particularly when glucocorticoids are used over a large area. These include skin thinning ( atrophy ), pigmentation disorders, heavy hair ( hypertrichosis ), stretch marks and partial suppression of the local immune system . Therefore, treatment with glucocorticoids should only be short-term. Strongly effective glucocorticoids should not be used in the area of ​​the genitals , face or on contacting ( intertriginous ) skin areas.

To prevent relapse, topical glucocorticoids must not be stopped suddenly. One possibility is interval therapy, in which the treatment alternates with active ingredient-free basic care and then slowly reduced. Alternatively, the potency can be reduced in stages.

In addition to the anti-inflammatory effect, treatment with glucocorticoids can also reduce the colonization with Staphylococcus aureus .

The locally applicable immunosuppressants tacrolimus and pimecrolimus come from transplant medicine . The two substances have a similar chemical structure and belong to the group of macrolides . Pimecrolimus and tacrolimus act as calcineurin inhibitors and thus suppress the local immune system of the skin, in addition they prevent the release of the inflammatory substances histamine and arachidonic acid metabolites . They have the advantage over glucocorticoids that they do not cause atrophy of the skin.

A common side effect of tacrolimus and pimecrolimus is a short-term burning sensation on the skin. So far there is no long-term experience as to whether these active ingredients contribute to the formation of tumors . Therefore, the US FDA issued a warning in 2005. The European Medicines Agency is following relevant information and is now restricting its use to cases in which adequate therapeutic success with glucocorticoids cannot be achieved or the side effects do not allow glucocorticoid therapy.

Other, rarely used anti-inflammatory agents include tar , sulfonated shale oil preparations ( ammonium bituminosulfonate ) and oak bark.

Findings from a mouse model published in 2010 suggest that the natural flavonoid taxifolin is effective when used externally and internally by preventing the production of inflammatory cytokines and reducing skin inflammation.

In September 2017, the monoclonal antibody dupilumab was approved in the EU for the treatment of atopic eczema ( neurodermatitis ) by the European Commission .

Medicines for internal use

Antihistamines can relieve itching. Often the drowsy effect ( sedation ) of earlier antihistamines is in the foreground, which is the case with more modern preparations, e.g. B. with desloratadine , no longer occurs. One likes to use this with children so that they can fall asleep more easily and thus have less scratching. A sensible treatment is the combined intake of a non-sedating antihistamine in the morning, e.g. B. fexofenadine or desloratadine, and a sedating antihistamine in the evening, e.g. B. Hydroxyzine .

In the case of particularly severe attacks with a large extent of the eczema, internal use of cortisone is possible.

The cyclosporin A is the metabolite of a fungus; As a systemically used drug, it is reserved for the most severe forms of atopic eczema, which often quickly regress to therapy with cyclosporine A. The most important side effects of this therapy correspond to those from transplant medicine , in which it is also used: increase in blood pressure, kidney damage, induction of malignancies , but also gum growths.

Avoidance of provocation factors and supportive measures

An important part of therapy is reducing or avoiding known provocation factors. The experience of the patient is also important.

If there are food allergies or intolerances, corresponding foods should be avoided. There are also a variety of nutrition tips and diets for the treatment of atopic eczema. There is no evidence that general diets are effective. In addition, especially in children, there is a risk of deficiency symptoms and developmental disorders.

In the case of existing allergies, it can make sense to ensure a low-allergen environment in living rooms. For example, mite-proof mattress and duvet covers can reduce the exposure to house dust mites.

The typical dry skin requires a correspondingly gentle skin care . This includes only short, not too frequent, lukewarm showers or baths . Water that is too hot or too warm can make symptoms worse. Alkaline cleaning products should not be used.

To avoid external stimuli, soft and smooth materials such as cotton should be used. Wool should be avoided because of the severe skin irritation. Duvet covers should be smooth, towels are often perceived as uncomfortable. Special overalls are offered especially for (small) children , which prevent unconscious scratching of the skin, especially at night. Cotton gloves are also helpful here. Due to its anti-inflammatory and antiseptic effects, some people affected by wearing silver-containing textiles help .

When washing laundry, a mild detergent should be used, if possible without odorous substances . Many patients are sensitive to laundry that has been washed with fabric softener . On the other hand, fabric softener can be beneficial for some people, as the softer laundry is gentle on the skin.

Light therapy and climate treatment

Irradiation with high-dose UV light can provide relief due to its anti-inflammatory effect and allow temporary healing. Nowadays, the narrow spectrum UVB light (311 nm) is mainly used, possibly in combination with UVA lamps.

UVA1 light therapy (340–400 nm) has proven itself particularly in severe forms of atopic eczema; Particularly in high-dose therapy (up to 130 J / cm²), significant advantages over conventional therapies such as corticoids could be demonstrated. The UVA1 radiation penetrates deeper into the tissue with its longer wavelengths and has a strong anti-inflammatory effect by inhibiting the Langerhans cells and the mast cells . The setback known from cortisone (stronger disease flare-up after discontinuation of therapy) does not occur with UVA1 high-dose therapy. However, for prophylactic reasons (all UV rays accelerate skin aging ), children should only be treated with high-dose therapy in exceptional cases.

Treatment with pulsed blue light (400–500 nm, 29 J / cm²) led in a study with 36 patients with severe neurodermatitis after 6 months to a 50% decrease in the inflammatory score (EASI) and the consumption of external corticosteroids. In atopic hand eczema, a single-blind side-by-side comparison study with 10 patients described the inflammation as inhibited 6 months after the end of treatment. In contrast to UV radiation, there was not a decrease, but an increase in lymphocytes and Langerhans cells. The anti-inflammatory mechanism of action of this treatment is new and fundamentally differs from UV therapies in that there is no direct immunosuppression of the skin. There are no controlled studies on the treatment of neurodermatitis with such long-wave light (" light vaccination ").

Because of the low air pollution with allergens, spa stays by the sea or in the high mountains , then at the mite-free altitude of 1000 m in winter and 2000 m in summer , often help .

Vitamin D

Atopic dermatitis and vitamin D deficiency have been linked in some studies. Vitamin D deficiency in the mother during pregnancy is considered a possible trigger of atopic dermatitis in the child. Atopic dermatitis could possibly be treated with vitamin D administration.

Vitamin E.

In a single-blind , placebo-controlled study, symptoms improved in 40 of 50 people (10 moderate, 23 greater, 7 remission ) after supplementing with 268 mg (400 IU ) of vitamin E daily for a period of eight months . In the control group (n = 46) a clinical improvement could be seen in 5 persons (4 moderate, 1 stronger, 0 remission). Furthermore, there was a decrease in serum IgE by 62% in patients in the verum group with a strong improvement in symptoms and only by 34.4% in the control group.

Patient information and self-management

In general, it is recommended to avoid stress (positive and negative, acute and latent). Stress can also arise from the nightly itching attacks in children, which can sometimes be an enormous burden for parents. This often creates a vicious circle. Dealing with stress and itching, for example in the form of relaxation techniques, is therefore important . It is important to acquire scratch alternatives (e.g. distraction, rubbing).

Since the disease is complex in its causes, manifestations and treatment methods, great attention must be paid to the self-competence of those affected. This need is compounded by the fact that many of those affected are children and their parents have to carry out the daily treatment. This is where patient training comes in, the content of which includes conveying medical information, treatment options, nutrition, coping with everyday life, relaxation techniques and dealing with itching. As part of an interdisciplinary model project in Germany, the effectiveness of outpatient neurodermatitis training was confirmed. In this model, the training of doctors, psychologists / psychotherapists and dieticians is carried out. The central associations of the German health insurances have recommended that the costs for this training be covered since 2007.

If there are psychological provocation factors or to cope with the psychological stress, psychotherapy can be used as a complementary therapy. Depending on the personality of the person concerned, it is helpful to exchange experiences with fellow sufferers in self-help groups . The Gelsenkirchen treatment process , which is primarily based on complex psychotherapy and behavioral therapy , is not scientifically recognized.

Alternative forms of therapy

The alternative medicine has produced some methods which are applied in the treatment of atopic dermatitis.

Most of the procedures (e.g. acupuncture , homeopathy , bioresonance ) could not be proven to be effective.

The oral intake of gamma-linolenic acid is controversial. This fatty acid is found in borage seed oil and evening primrose oil , among others . Most clinical studies have found no effect of gamma-linolenic acid intake in atopic eczema. The black cumin oil is often attributed to a stabilizing, anti-inflammatory, antimicrobial and juckreizmildernde effect. In scientific studies, however, there was no demonstrable improvement in symptoms in a placebo comparison .

Cyanocobalamin (vitamin B12) as an ointment is used in alternative medicine to treat neurodermatitis. The effect was investigated in smaller studies.

There are first indications from laboratory tests that lidocaine could be a promising active ingredient in the event of an infestation with staphylococci , as it can specifically inhibit the inflammation triggered by the toxin . The company Micreos also sells gels and ointments with an enzyme obtained from phages , which specifically destroys the cell wall of staphylococci and is supposed to help with neurodermatitis.

history

This engraving from a book by Robert Willan and Thomas Bateman (1817) is one of the earliest illustrations of the disease .

The first references to descriptions of atopic eczema can be found in antiquity. The Roman biographer Suetonius described typical symptoms of the disease in Emperor Augustus . Descriptions of symptoms that could correspond to atopic eczema can also be found in the first dermatology book De morbis cutaneis , which was written by the Italian doctor Girolamo Mercuriale in 1572. Corresponding descriptions can also be found in the 18th century.

Since it was common until the 19th century to differentiate skin diseases according to their localization, atopic eczema was not yet recognized as an independent disease. At the beginning of the 19th century, a distinction was made based on the type of skin changes. The clinical appearance of atopic eczema was then described in detail for the first time in 1808 by the English doctor Robert Willan . He is considered the founder of dermatology as a medical specialty. This was followed by publications by various authors.

The term neurodermatitis or neurodermatitis was coined by French doctors (L. Brocq and L. Jacquet) from 1891. The French Ernest Henri Besnier described the disease in 1892 as an itchy eczema (dermatitis multiformis prurignosa) . He first recognized the connection with asthma and hay fever, described itching as the main symptom and recognized the variety of skin changes.

At the beginning of the 20th century, the connection with allergies was the focus of publications. In the 1920s and 1930s the terms atopy, atopic dermatitis and atopic eczema were established. The discovery of immunoglobulin E (IgE) and its role in allergies helped to understand the immunopathological relationships of atopic eczema in the second half of the 20th century.

Atopic eczema in animals

Atopic diseases occur mainly in domestic dogs (→ atopic dermatitis of the dog ) and domestic cats .

literature

  • Johannes Ring: Neurodermatitis - Atopic Eczema . Thieme, 2001.
  • Otto Braun-Falco , Gerd Plewig , Helmut H. Wolff: Dermatology and Venereology . Springer, Berlin 2005, ISBN 3-540-43556-5 , pp. 377-395 .
  • Peter Fritsch: Dermatology and Venereology . Springer Verlag, Berlin 2004, ISBN 3-540-00332-0 , pp. 190-196 .
  • Dietrich Abeck: Atopic eczema in childhood - neurodermatitis. The contemporary management . Steinkopff Verlag, Darmstadt 2001, ISBN 3-7985-1307-4 .
  • S2- guideline for neurodermatitis of the German Dermatological Society, the German Society for Allergology and Clinical Immunology and the German Society for Pediatric and Adolescent Medicine. In: AWMF online (as of 2008).

Web links

Wiktionary: Neurodermatitis  - explanations of meanings, word origins, synonyms, translations
Commons : Atopic Eczema  - Collection of images, videos and audio files

Individual evidence

  1. ↑ a b c Peter Fritsch: Dermatology and Venereology . Springer Verlag, Berlin 2004, ISBN 3-540-00332-0 , pp. 190 .
  2. ↑ a b Barbara Fröschl u. a .: Topical anti-inflammatory treatment of neurodermatitis in childhood . In: German Institute for Medical Documentation and Information [DIMDI] (Ed.): Health Technology Assessment series . tape 60 , 2007, ISSN  1864-9645 , p. 21st f . ( portal.dimdi.de [PDF]).
  3. ↑ Thomas Werfel u. a .: Therapy of neurodermatitis . In: German Institute for Medical Documentation and Information [DIMDI] (Ed.): Health Technology Assessment series . tape 46 , 2006, ISSN  1864-9645 , p. 16 ( portal.dimdi.de [PDF]).
  4. ↑ Colin NA Palmer, Alan D. Irvine, Ana Terron-Kwiatkowski, Yiwei Zhao, Haihui Liao, Simon P. Lee, David R. Goudie, Aileen Sandilands, Linda E. Campbell, Frances JD Smith, Gráinne M. O'Regan, Rosemarie M. Watson, Jo E. Cecil, Sherri J. Bale, John G. Compton, John J. DiGiovanna, Philip Fleckman, Sue Lewis-Jones, Gehan Arseculeratne, Ann Sergeant, Colin S. Munro, Brahim El Houate, Ken McElreavey , Liselotte B. Halkjaer, Hans Bisgaard, Somnath Mukhopadhyay, WH Irwin McLean: Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis . In: Nature Genetics . tape 38 , no. 4 , 2006, p. 441-446 , doi : 10.1038 / ng1767 .
  5. ↑ a b c Natalija Novak, Thomas Bieber: Pathophysiology of atopic dermatitis. In: Deutsches Ärzteblatt. Issue 3, year 101, January 2004, pp. 108–120.
  6. ↑ G. Rassner: Dermatology. Elsevier, Munich 2007, p. 146 ff.
  7. ↑ Otto Braun-Falco , Gerd Plewig, Helmut H. Wolff: Dermatology and Venerology . Springer, Berlin 2005, ISBN 3-540-43556-5 , pp.  383 .
  8. ^ A b Otto Braun-Falco, Gerd Plewig, Helmut H. Wolff: Dermatology and Venereology . Springer, Berlin 2005, ISBN 3-540-43556-5 , pp. 385 .
  9. ↑ a b c d e f g h i j S. Fischer, J. Ring, D. Abeck: Atopisches Ekzem. Provocation factors and possibilities for their effective reduction or elimination. In: The dermatologist . Volume 54, Number 10, October 2003, doi: 10.1007 / s00105-003-0557-7 .
  10. ↑ Peter Fritsch: Dermatology and Venereology . Springer Verlag, Berlin 2004, ISBN 3-540-00332-0 , pp. 195 .
  11. ^ A b Dietrich Abeck, Kerstin Strom: Atopic eczema . In: Henning Hamm (Ed.): Pediatric Dermatology . 2nd Edition. Springer, Heidelberg 2006, ISBN 3-540-25646-6 , chapter 22, p. 357-370 , doi : 10.1007 / 3-540-31259-5_22 .
  12. ↑ Practical everyday tips - clothing, relaxation techniques and exercise for atopic dermatitis. In: neurodermitistherapie.info. medical project design GmbH, July 27, 2010, accessed on August 3, 2010 .
  13. ↑ BS Baker: The role of microorganisms in atopic dermatitis. In: Clin Exp Immunol. 144 (1), April 2006, pp. 1-9, doi: 10.1111 / j.1365-2249.2005.02980.x .
  14. ↑ Peter Fritsch: Dermatology and Venereology . Springer Verlag, Berlin 2004, ISBN 3-540-00332-0 , pp. 192 .
  15. ^ Traupe, Hamm: Pediatric Dermatology . 2005, p. 357 ff.
  16. ↑ Atopic dermatitis - causes and symptoms of this skin disease . experto.de
  17. ^ A b Otto Braun-Falco, Gerd Plewig, Helmut H. Wolff: Dermatology and Venereology . Springer, Berlin 2005, ISBN 3-540-43556-5 , pp. 384 .
  18. ^ A b Otto Braun-Falco, Gerd Plewig, Helmut H. Wolff: Dermatology and Venereology . Springer, Berlin 2005, ISBN 3-540-43556-5 , pp. 388 f .
  19. ↑ a b c d e f g h i j S2 guideline atopic dermatitis of the German Dermatological Society (DDG), the Austrian Society for Dermatology and Venereology, the Working Group Pharmaceutical Economics in Dermatology, the Working Group Dermatological Research, the Working Group Pediatric Dermatology in the German Dermatological Society, the Professional Association of Pediatricians, the Psycho-Dermatology Working Group of the German Society for Allergology and Clinical Immunology, the Society for Pediatric Allergology, the Professional Association of German Dermatologists, the Swiss Society for Dermatology and Venereology, the Swiss Society for Allergology and clinical immunology, the Neurodermatitis Training Working Group, the German Society for Pediatric and Adolescent Medicine, the Dermatological Rehabilitation Working Group, the German Allergy and Asthma Association and the German Cont actallergy group. In: AWMF online (as of 4/2008).
  20. ↑ a b c d CA Akdis, M. Akdis, T. Bieber, C. Bindslev-Jensen, M. Boguniewicz, P. Eigenmann, Q. Hamid, A. Kapp, DYM Leung, J. Lipozencic, TA Luger, A. Muraro, N. Novak, TAE Platts-Mills, L. Rosenwasser, A. Scheynius, FER Simons, J. Spergel, K. Turjanmaa, U. Wahn, S. Weidinger, T. Werfel, T. Zuberbier: Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology / American Academy of Allergy, Asthma and Immunology / PRACTALL Consensus Report. In: Allergy. Volume 61, Issue 8, 2006, pp. 969-987, doi: 10.1111 / j.1398-9995.2006.01153.x .
  21. ↑ The Hemp Product Line Project. Nova Institute, 1996, ISBN 3-9805840-1-1 .
  22. ↑ JT Huang, M. Abrams, B. Tlougan, A. Rademaker, AS Paller: Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity . In: Pediatrics . tape 123 , no. 5 , May 2009, p. e808-14 , doi : 10.1542 / peds.2008-2217 , PMID 19403473 ( aappublications.org ).
  23. ^ Atopic dermatitis: Household bleaching relieves eczema ( Memento from April 29, 2009 in the Internet Archive ). German-language summary of the "Huang 2009" study at Ärzteblatt Online.
  24. ↑ JY Ahn et al .: Effect of taxifolin glycoside on atopic dermatitis-like skin lesions in NC / Nga mice. In: Phytotherapy research. 24 (7), Jul 2010, pp. 1071-1077. PMID 0041431
  25. ↑ Dupixent / dupilumab , PM EMA: Dupixent - dupilumab Authorization details of September 27, 2017, accessed on October 26, 2017.
  26. ↑ D. Becker, E. Langer, M. Seemann, G. Seemann, I. Fell et al .: Clinical Efficacy of Blue Light Full Body Irradiation as Treatment Option for Severe Atopic Dermatitis. In: PLoS ONE . 2011, 6 (6), e20566. PMID 21687679 , doi: 10.1371 / journal.pone.0020566 .
  27. ^ J. Krutmann, K. Medve-Koenigs, T. Ruzicka, U. Ranft, JH Wilkens: Ultraviolet-free phototherapy. In: Photodermatology, Photoimmunology & Photomedicine . Volume 21, No. 2, 2005, p. 59.
  28. ↑ MM Kleinpenning, T. Smits, MH Frun, PE van Erp, PC van de Kerkhof, RM Gerritsen: Clinical and histological effects of blue light on normal skin. In: Photodermatology, Photoimmunology & Photomedicine. 2010, Volume 26, No. 1, p. 16.
  29. ^ A. Schwarz, M. Noordegraaf, A. Maeda, K. Torii, BE Clausen, T. Schwarz: Langerhans cells are required for UVR-induced immunosuppression. In: Journal of Investigative Dermatology . 130 (5), 2010, pp. 1419-1427.
  30. ↑ Clinical Efficacy of Blue Light Full Body Irradiation as Treatment Option for Severe Atopic Dermatitis .
  31. ↑ Z. Samochocki, J. Bogaczewicz, R. Jeziorkowska, A. Sysa-Jędrzejowska, O. Glińska, E. Karczmarewicz, DP McCauliffe, A. Woźniacka: Vitamin D effects in atopic dermatitis . PMID 23643343 .
  32. ↑ A. Borzutzky, CA Camargo Jr .: Role of vitamin D in the pathogenesis and treatment of atopic dermatitis . PMID 23971753 .
  33. ^ Daniel A Searing, Donald YM Leung: Vitamin D in Atopic Dermatitis, Asthma and Allergic Diseases . PMC 2914320 (free full text)
  34. ↑ LB Bacharian: Vitamin D status at birth: An important and potentially modifiable determinant of atopic disease in childhood? PMID 24001801 .
  35. ^ DG Peroni, GL Piacentini, E. Cametti, I. Chinellato, AL Boner: Correlation between serum 25-hydroxyvitamin D levels and severity of atopic dermatitis in children . doi: 10.1111 / j.1365-2133.2010.10147.x
  36. ↑ E. Tsoureli-Nikita, J. Hercogova, T. Lotti, G. Menchini: Evaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels. In: International Journal of Dermatology . 41 (3), 2002, pp. 146-150. PMID 12010339 , doi: 10.1046 / j.1365-4362.2002.01423.x .
  37. ^ Colette Hoare, Alain Li Wan Po, Hywel Williams: Systematic review of treatments for atopic eczema. In: Health Technol Assess. 4 (37), 2000, pp. 1-191. PMID 11134919
  38. ^ T. Stern, C. Bayerl: Black seed oil ointment - A new approach for the treatment of atopic dermatitis? In: Current Dermatology. 28 (3), 2002, pp. 47-79.
  39. ^ Evaluation of topical vitamin B (12) for the treatment of childhood eczema . PMID 19368512
  40. ↑ Jiao, Qingqing et al .: Lidocaine inhibits staphylococcal enterotoxin-stimulated activation of peripheral blood mononuclear cells from patients with atopic dermatitis. In: Archives of dermatological research. 2013, pp. 1–8.
  41. ↑ L. Gravitz: Turning a new phage. In: Nature medicine. Volume 18, Number 9, September 2012, pp. 1318-1320, ISSN  1546-170X . doi: 10.1038 / nm0912-1318 . PMID 22961150 .
  42. ↑ a b c d e f Johannes Ring : Handbook of atopic eczema. Chapter 2: The History of Atopic Eczema / Dermatitis . Springer, Berlin / Heidelberg / New York 2006, ISBN 3-540-23133-1 .
  43. ^ Robert Willan, Thomas Bateman: Delineations of Cutaneous Diseases . Oxford University, 1817. (books.google.de)
  44. ↑ Chiara Noli, Fabia Scarampella: Atopic Dermatitis. In: Practical Dermatology in Dogs and Cats. 2nd Edition. Schlütersche Verlagsanstalt, 2005, ISBN 3-87706-713-1 , pp. 252-259.
This version was added to the list of articles worth reading on April 22, 2005 .