Atopic dermatitis (overview) L20.-

Authors: Prof. Dr. med. Peter Altmeyer, Prof. Dr. med. Martina Bacharach-Buhles

Co-Autors: Dr. med. Jeton Luzha, Hadrian Tran

All authors of this article

Last updated on: 26.02.2024

Dieser Artikel auf Deutsch

Synonym(s)

Asthma eczema (Jadassohn); Asthmaprurigo (Sabouraud); atopic dermatitis; Atopic eczema; Bending eczema; Besnier M.; constitutional eczema (Koch); Dermatitis atopic; Dermatitis lichenoides pruriens (Neisser); Dermatosis neurogenic; Eczema atopic; Eczema constitutional; Eczema disease (Scholl); Eczema endogenous; eczema endogenum; eczema flexuarum; endogenous eczema; exudative eczema (Schreuss); exudative eczematoid; flexular mycosis (Hebra); late exudative eczema (Rost); M. Besnier; neurodermatitis atopica; neurodermatitis constitutionalis; neurodermatitis diffusa; neurodermatitis disseminata; neurodermitic eczematoid (Stümpke); neurogenic dermatosis (Epstein); neuropathic eczema (Brill); Prurigo à forme eccemato-lichénienne (Brocq); prurigo diathésique (Besnier); Prurigo eczema (Kreibich); Prurigo Veneer

History
This section has been translated automatically.

Willan, 1808

Definition
This section has been translated automatically.

A multifactorial, chronically persistent or chronically recurrent, non-contagious, usually very itchy dermatitis of varying acuity, which belongs to the group of atopic diseases (Greek atopos = out of place) and is caused, maintained or activated by complex interactions between constitutional and environmental factors.

Atopic dermatitis shows a topographically and morphologically different appearance in the individual stages of life:

  • in infancy, rather uncharacteristic diffuse eczematous skin symptoms on the face and on the extensor sides of the extremities of varying severity and acuteity (see atopic dermatitis in infancy)
  • in infancy, more localized and less diffuse eczema, with a variable and seasonal course (see atopic dermatitis in infancy)
  • Preferably occurring as flexural eczemain school-age children
  • in adulthood there is a great morphological variety. Both localized minus variants of atopic dermatitis (eyelids, genitals, hands, neck) as well as large-area eczema variants up to universally affecting the entire integument (erythrodermic atopic dermatitis) characterize the extremely diverse clinical picture.

Classification
This section has been translated automatically.

Atopic eczema shows different symptoms at different stages of life.

An alternative classification distinguishes 4 phenotypes in children (study on 1,038 children: Roduit C et al. 2017):

  1. Early transient phenotype (9.2%): HV within the first 2 LJ, healing by the 4th LJ. High risk of developing food allergies.
  2. Earlypersistent phenotype (6.5%): HV within the first 2 LJ, healing by 6 LJ. High risk of developing asthma. High risk of developing food allergies.
  3. Late phenotype (4.8%): HV only after the 2nd year of life. High risk of developing allergic rhinitis.
  4. Sporadic phenotype (79.5%): only occasional or absent HV.

Furthermore, a number of different variants can be assigned to atopic eczema, some of which have historical names (e.g. eccema symmetricum faciale), some of which are named according to topical or seasonal aspects (e.g. atopic hand eczema, genital eczema, dermatitis hiemalis etc.) or differ in their particular clinical course (e.g. prurigo form of atopic eczema). Such dermatitis can also be triggered by other factors (e.g. contact allergies).

Occurrence/Epidemiology
This section has been translated automatically.

Taking primary and secondary data analyses into account, AD has an annual prevalence of around 10% in children and adolescents and 1.7% in adults in Germany. 8-12 This means that around 1.2 million adults and 1.3 million children are affected each year across Germany, corresponding to 2.5 million people per year. The self-reported lifetime prevalence in a larger study was 3.5% (Langen U et al. (2013). According to more recent SHI data from 2021 (Augustin M et al. 2021), the one-year treatment prevalence of atopic dermatitis is around 4.2% overall, including 3.3% in adults and 8.4% in children and adolescents up to the age of 20. This means that around 2.2 million adults and 1.4 million children in Germany have an AD as a treatment diagnosis each year, corresponding to 3.6 million people per year. Of the 2.2 million adults, around 10-15% have a moderate to severe form of AD for which systemic therapy must be considered. The cumulative incidence of AD in children in the first year of life in birth cohort studies from Japan and Denmark was 13% and 11.5% respectively (Sugiyama M et al. 2007). A study from Sweden showed a cumulative incidence of AD of 21% up to school age (Broberg A et al. 2007).

This makes AD one of the most common chronic diseases in children. Various studies have shown a significant increase in the prevalence of AD and other atopic diseases between 1950 and 2000. This is primarily due to changes in environmental conditions and the Western lifestyle. More recent studies indicate that there has been no further increase in the prevalence of the disease in recent years.

Note: Around 40-60% of patients with atopic dermatitis also suffer from respiratory allergies (pollinosis, perennial rhinitis, allergic bronchial asthma).

Etiopathogenesis
This section has been translated automatically.

The cause is a combination of genetic and environmental factors that cause a dysfunction of the skin barrier, a dysregulation of the cutaneous and systemic immune system, a dysbiosis of the skin microbiota and a strong genetic influence (Torres T et al. 2019).

From a practical clinical point of view, a distinction can be made between 2 forms with largely identical skin symptoms:

  • Intrinsic (non-allergic) atopic dermatitis (about 20-30% of patients; not IgE-mediated). It is currently still unclear whether this clinical picture should be evaluated as a separate entity.
  • Extrinsic (allergic) at opic dermatitis (60-70% of patients, IgE-mediated).

Note! Patients with an intrinsic form do not have elevated IgE levels or sensitization to environmental or food allergens.

Immunopathology (see below atopic dermatitis, immunopathology)

Immune response in atopic skin: Clinically inconspicuous skin in patients with atopic eczema cannot be assumed to be healthy despite the absence of symptoms. Increased skin dryness, a barrier disorder with increased irritability, subtle perivascular T-cell infiltrates, increased number of Th2 cells with increased IL-4 and IL-13 production are detectable.

In diseased skin: Due to the barrier disorder of the skin, allergens can penetrate into the deeper layers of the epidermis (Cappello C et al. 2017). Here they are recognized and absorbed by Langerhans cells. The antigen-presenting cells(Langerhans cells, inflammatory dendritic cells and macrophages with IgE molecules) are increased. Langerhans cells enter the draining lymph node with the lymph flow, reducing their dendritic projections during this passage (so-called veiled cells - see Langerhans cell below). In the lymph node, they present the antigen to naive lymphocytes and induce a Th2 response.

This leads to an increased expression of numerous cytokines such as: IL-16, C-C chemokine ligand 27, RANTES(CCL5), monocyte chemotactic protein-4(CCL13) and eotaxin. These cytokine expressions lead to the activation of eosinophilic leukocytes and macrophages. In contrast, the expression of IL-4 and IL-13 is reduced. IL-5, GM-CSF, IL-11, IL-12, IL-22 and IFN-gamma are also increasingly expressed. Interleukin-22 is able to downregulate barrier proteins, which could promote atopic readiness (Brüggen M-C et al. 2016).

Collagen deposition with lichenification is also increasingly observed. The basic mechanism here is the release of TNF-α and IL-1, which lead to changes in the vascular endothelia via activation of NF-κB with subsequent extravasation of proinflammatory cytokines.

Genetics: Genetic factors play a significant role in the predisposition to atopic eczema. The risk of a child developing atopic dermatitis is 50% if one parent suffers from asthma, atopic dermatitis or allergic rhinitis, 75% if both parents are affected. The concordance in homozygotic twins is 72%, in heterozygotic twins 23%.

In genome-wide association studies, > 30 candidate genes predisposing to atopy have been identified on chromosomes 1q21, 3q21, 5q32, 6, 11q13, 17q25 in the last two decades (Castro-Giner F et al. 2009). Some regions correspond closely with the gene loci found for psoriasis (3q21), indicating that these genes have a general influence on "skin inflammation". Chronic inflammatory bowel diseases are found on very similar gene segments.

The genes localized on chromosome 1q21, which in their entirety as an epidermal differentiation complex are important for the regulation of epidermal homeostasis, play a special role in the pathogenesis of atopic dermatitis (see below). Loss-of-function mutations in the FLG gene (1q21), which codes for the protein filaggrin, show a clear association with the early onset and chronic course of atopic dermatitis.

The SPINK5 gene (5q31-5q32) codes for LEKTI , a serine protease. Germline mutations in the SPINK5 gene result in an enzyme defect that is phenotypically associated with Netherton syndrome, which is characterized by a pronounced atopic diathesis. However, polymorphisms in this gene are also associated with atopic dermatitis.

Furthermore, an atopy association affects the claudin I gene, which codes for the important tight junction protein of the same name. Polymorphisms of this gene lead to disorders of the epidermal integrity of AD.

The following other genes have been identified as risk factors that may play a role in the initiation, maintenance or exacerbation of atopic inflammation. Their knowledge and the encoded gene products provide information about the interaction of the inflammatory components (Castro-Giner F et al. 2009):

  • COL29A1 (3q21); encoded protein: collagen type XXIX, alpha1
  • COL18A1 encoded protein: collagen type XXIX, alpha1
  • EMSY (11q13.5); coded protein: EMSY
  • FLG (1q21); encoded protein: filaggrin
  • RAD50 (5q23-q32) coded protein: RAD50
  • IL4 (5q31.1) Interleukin-4
  • IL4R (16p12.1-p1.2) Interleukin-4 receptor
  • IL5 (5q31.1) Interleukin-5
  • Il13 (5q31) Interleukin-13
  • IL18 (11q22.2-q22.3) Interleukin-18
  • IL31 (12q24.31) Interleukin-31
  • CSF2 (5q31.1) Granulocyte-macrophage colony stimulating factor
  • CCL5 (17q11.2-q12) CCL5/RANTES
  • FcεRI (1q32) High affinity IgE receptor

Disruption of the skin barrier: Disruptions in filaggrin structure play an important role in the reduction of epidermal integrity. Polymorphisms and loss-of-function mutations in the profilaggrin/filaggrin gene (FLG - this is located in the so-called epidermal differentiation complex - EDC - on chromosome 1q12.3) are observed 2-3 times more frequently in patients with atopic eczema (AE) than in healthy individuals. Filaggrin is a structural protein that cross-links the disulfide bridges between the keratinocytes in the skin barrier and thus has a reinforcing function. Due to a mutation, this function can no longer be guaranteed and the skin is more susceptible to mechanical stimuli. Theitch-scratch cycle ensures the mechanical disruption of the barrier and maintains the cytokine-mediated inflammatory and itch reaction. Filaggrin mutated patients with AD have a significantly higher tendency to allergic bronchial asthma and ichthyosis vulgaris than those without this mutation. It is also possible that the proven increased expression of aquaporin-3 in the keratinocytes of atopic patients plays a significant role in the impaired skin barrier function.

The allergens relevant to atopic syndrome are grass pollen, house dust mites and animal dander. As these proteins have a high molecular weight, they cannot penetrate through normal skin (only proteins < 1000 Daltons can do this). In atopic skin, however, molecules with a higher molecular weight can also penetrate due to the barrier disorder. They are absorbed by dendritic cells. Clinical observations confirming an exacerbation of AD after local provocation with grass pollen are consistent with this. Local exposure to cat epithelia also leads to an increased tendency to eczema (!) in filaggrin-mutated newborns. The fact that birch pollen can induce local eczema reactions, even in non-birch pollen-sensitized individuals, shows that this is not just a matter of specific (local) reactions in the presence of sensitization. Other mechanisms are responsible for this, such as pollen-associated lipid mediators (PALMS), which also stimulate an inflammatory reaction non-specifically. Airborne pollutants are also able to penetrate the atopic skin.

Sensitizations:

  • Type I sensitizations: Tree and grass pollen: Apparently, patients with AE have an increased sensitizability via the skin. This also correlates with the observation of "flare-up" reactions with increased pollen count or house dust exposure.
  • Type IV sensitization (see contact allergy below): Patients with AD seem to have a higher sensitization rate than non-atopic patients (most common contact allergens: nickel(II) sulphate and fragrance mix).

Microbial factors: Staph. aureus is of pathophysiological relevance (high colonization density (> 80%) in the nasal mucosa and on weeping areas). Staphylococcus aureus forms high amounts of enterotoxins (enterotoxin A-D, toxic-shock-syndrome-toxin-1), which act as superantigens and are therefore T-cell proliferative; patients continue to form IgE antibodies against them, whereby the degree of sensitization and disease activity correlate. A disturbance of antimicrobial lipids and peptides is involved in the pathological colonization of the skin (reduction of the antimicrobial peptides (AMP) cathelicidin LL-37, dermcidin (occurring in sweat) and beta-defensin-2), which are transported in the so-called "lamellar bodies" into the intercellular space of the str. corneum. This results in a reduction of antimicrobially active free sphingosines: a 2-fold reduction in the str. corneum correlates with a > 100-fold increase in the colonization of Staph. aureus. There is evidence that Staph. aureus penetrates the atopic epidermis with subsequent expression of AE-related cytokines (IL-4, IL-13, IL-22, etc.). This dermal dysbacteria could therefore lead directly to an increase in inflammatory cytokines.

Colonization with Pityrosporum ovale plays a pathogenetic role in patients with the clinical "head-and-neck" variant of atopic dermatitis. Patients affected in this way benefit from antimycotic local therapy.

Furthermore, there are indications that focal infections (such as dental infections) are apparently also involved in the triggering or exacerbation of atopic dermatitis. This is surprising, as such influences were not previously assumed!

Hygiene hypothesis: It is assumed that the increase in AD is linked to a higher standard of living and improved hygiene conditions. A reduction in bacterial or viral infections leads to a reduced production of TH1 cytokines (e.g. interferon gamma) and thus to a decrease in the protective effect of the Th1 immune response in favor of the Th2 response characteristic of atopic diseases.

Farm animals as risk factors? Remarkably, a study of 1063 children in 5 European countries showed that children of mothers who spent their pregnancy in the environment of farm animals had a lower risk of developing atopic dermatitis in the first two years of life. Not only immunostimulatory microbial factors play a role here, but apparently also non-microbial substances such as animal-produced N-glycolylneuraminic acid (Neu5Gc), a sensitizing sialic acid whose degree of sensitization is, however, inversely associated with wheezing and bronchial asthma.

Neuroimmunological factors: Stress and other emotional factors are often blamed as triggers. Neuropeptides such as calcium-gene-related peptide (CGRP), proopiomelanocortin-derived hormone (alpha-MSH) act as anti-inflammatory regulators.

Various triggers:

  • Vitamin D correlation: An inverse correlation between the severity of AD and the level of vitamin D has been reported.
  • Climate, stress, post-traumatic stress disorders, exposure to pollutants can lead to the onset or exacerbation of the disease.

Manifestation
This section has been translated automatically.

Natural course of the disease According to birth cohort studies, AD manifests itself in around half of patients in the first six months of life, in 60% of cases in the first year of life and in over 70 to 85% of cases before the age of five (see atopic dermatitis in infancy). By early adulthood, around 60% of affected children are symptom-free.

Late manifestations in adulthood are possible.

Early onset, comorbidity with other atopic diseases, severe course of the disease in childhood and positive family history of atopy are predictors for the persistence of AD into adulthood (Williams HC et al. 2000).

During pregnancy, an exacerbation of pre-existing atopic dermatitis occurs in 20% of cases (see also pregnancy dermatosis, atopic).

Localization
This section has been translated automatically.

Infancy: face, trunk, extensor sides (!) of the extremities, diaper area remains free.

Childhood, adolescence: crook of the elbow, back of the knee (flexural eczema!).

Adulthood: crook of the elbow, back of the knee, face, chest and shoulder area, back of the hand.

Circumscribed: as minus variants in various localizations (see above).

Clinical features
This section has been translated automatically.

Depending on the age of the patient and the acuity of the disease, different stages and manifestations of eczema appear, from weeping red plaques to pale, dry, possibly small-shaped scaling, usually scratched skin.

A typical feature is an attack-like, agonizing itching, which is intensified during sweating (especially during stress sweating). Furthermore, there is an intolerance to wool. The clinical symptoms of atopic eczema vary considerably depending on age. In this respect, clinical subdivisions according to age groups are useful.

____________________________________________________________________________________________

According to Hanifin and Rajka, the following symptoms are defined as major and minor criteria. The advantage is high sensitivity and low specificity (80%).

I. Major criteria:

  1. Pruritus (intense non-suppressible itching that is answered by bloody scratching (not rubbing but scratching with fingernails).
  2. eczema plaques (extensor in infants and young children, flexor in post-pubertal adolescents and adults)
  3. chronicity (chronic or chronic recurrent course over many years)
  4. medical history (positive atopic disease signs in EA and/or FA - e.g. rhintis allergica, allergic bronchial asthma)

II. minor criteria or optional symptoms:

  1. Cradle cap(Crusta lactea).
  2. Xerosis cutis (general sebostasis of the skin. Skin feels dry and brittle)
  3. Ichthyosis hand, foot ("I-hand"; hyperlinear pattern of unusually cotton-soft palms and soles).
  4. Dennie-Morgan infraorbital fold (double eyelid fold; Grd 1 up to pupil, Grd 2 including entire iris, Grd 3 entire eye)
  5. Earlobe rhagade (the so-called persistently torn earlobe)
  6. Atopic facial pallor (pale, grayish-white complexion; haloed dark eyes are also part of the special atopic facial coloration)
  7. Dermographism albus
  8. Keratosis pilaris
  9. Hertoghe's sign (rarefaction of the lateral eyebrows)
  10. Fur cap-like hairline (the adult atopic patient very rarely suffers from androgenetic alopecia!)
  • Other associated signs of atopy:
    • Intolerance to (animal) wool (not cotton)
    • food intolerances (citrus fruits, strawberries, tomatoes = unspecific histamine liberators which cause itching shortly after ingestion)
    • Itching due to sweating
    • IgE elevated (only with extrinsic type)
    • Positive prick or intradermal test (only with extrinsic type)
    • Detection of specific IgE (only with extrinsic type
      )Perlèche
    • Shiny nail (fingernails that look polished).
    • Dermopathic lymphadenopathy in generalized affection.

Laboratory
This section has been translated automatically.

IgE increase(IgE > 150 kU/l) in > 25% of patients, specific IgE antibodies, frequent eosinophilia, disturbance of the cellular mediated immunity. IL-16 and ECP can be regarded as good serological parameters (good correlation to SCORAD).

Histology
This section has been translated automatically.

Picture of allergic contact dermatitis with superficial perivascular and interstitial lympho-histiocytic-mastocytic dermatitis with mild spongiosis up to spongiotic blister formation, varying degrees of acanthosis with parakeratosis (in chronic foci, acanthosis with accompanying parakeratosis may be markedly pronounced) and (rather) low eosinophilia.

Diagnosis
This section has been translated automatically.

The diagnosis is based on specific criteria that take into account the patient and family history as well as the clinical manifestations. The overall severity of the disease must be determined by evaluating the objective signs and subjective symptoms.

Clinical picture, family history, personal history (eczema history, allergic rhinitis, bronchial asthma, food allergies, viral and bacterial infection tendency)

Allergy score - varies according to Diepgen - (if atopy is suspected)

  1. White dermographism (line test on the skin turns white)
  2. Hertoghe's sign (thin, light outer eyebrows)
  3. Dennie-Morgan infraorbital fold (transverse fold (or two) parallel to the lower eyelid)
  4. Pityriasis alba (dry, finely scaly light patches)
  5. Eczema foci
  6. Palmar hyperlinearity
  7. Pulpitis sicca (dry, eczematous fingers/toe tips)
  8. Dyshidrosis (hands/feet)
  9. Perlèche (torn corners of the mouth)
  10. Earlobe rhagades (torn earlobes)

Results of an orienting prick and intradermal test

  • Extrinsic form
    • IgE > 150 kU/ml
    • ECP
    • Elevated levels of TH2 cytokines (IL-4, IL-5, IL-13)
    • Specific IgE (food allergens, inhalation allergens, Pityrosporon ovale)
    • Atopy patch test
    • Omission diet and search diet ( food allergy, food intolerance)
    • Epicutaneous test for the question of contact sensitization (higher rate of contact allergies to topical active ingredients, external ingredients, rubber materials, fragrance mix)

Differential diagnosis
This section has been translated automatically.

"Eczema diseases" of a different origin

Furthermore

Ectodermal dysplasia

Syndromes with concomitant atopic dermatitis:

Complication(s)
This section has been translated automatically.

Frequent (severe) viral and bacterial infections. See also Eccema herpeticatum; Eccema molluscatum; Eczema coxsackium; pronounced verrucae vulgares, pyoderma, erythroderma.

Occasionally, "light sensitization" occurs in the course of atopic eczema with intensification of the eczema reaction in light-exposed areas. See below Eczema atopic photoaggravated

Fungal infections: Tinea (especially Trichophyton rubrum, Malassezia species)

Associations with coeliac disease: Patients with AD have a 2-fold increased risk of developing coeliac disease and a 1.8-fold and 1.5-fold increased risk of developing Crohn's disease and ulcerative colitis respectively. Based on a coeliac disease collective, atopic dermatitis was around three times as common (prevalence rate of 3.8 percent) in relatives compared to healthy life partners (Shalom G et al. 2020).

Other complicating comorbidities are:

General therapy
This section has been translated automatically.

Skin dryness: Xerosis, depending on the ambient temperature and humidity. Avoid excessive heating of living spaces, increase humidity, optimize ventilation of rooms. Due to the reduced alkaline neutralization capacity, the use of soaps, detergents and washing-up liquids should be reduced to a minimum. Lubricating wash lotions are recommended (Eucerin 5% Urea Wash Lotion, Atopicontrol Shower and Bath Oil, Lipoderm Shower Gel, Cetaphil Wash Lotion).

Sweating: Reduced perspiration leads to heat build-up and itching crises due to high outside temperatures during physical exertion, but also in stressful situations.

Sun and UV: UV exposure generally has a soothing effect on eczema. Occasionally there is an increased UV sensitivity. See also photoaggravated endogenous eczema.

Contact allergies: Frequently grafted contact allergy, especially to nickel. Caution! Fashion jewelry!

Skin cleansing:

  • No commercially available perfumed soaps, bubble baths and syndets. Use of oils (Linola Fat Oil Bath, Balneum Hermal Oil Bath).
  • Oil/surfactant combinations (e.g. Eucerin Shower Oil, Lipoderm Shower Gel) are excellent.
  • As an alternative to bath oils, an O/W emulsion or hydrophilic oils can also be used for cleansing. For very dry skin, apply an emulsion or cream (e.g. Ungt. emulsif. aq., Eucerin Lotio, Excipial U Lipolotio or Excipial U Hydrolotio etc.) after drying, depending on tolerance.

Choice of occupation: Occupations with intensive contact with water, detergents, oils, greases, drilling water, disinfectants, adhesives, leather, chemical products, animals, flour and dust are unsuitable. Dry, clean occupations are recommended. Caution! Spread of mold via air conditioning systems!

Clothing: Breathable clothing, loosely woven cotton or silk textiles (e.g. Dermsilk with an antimicrobial component: patients with atopic dermatitis find silk fabrics pleasant on their skin and hardly irritating, cooling. In this clientele, the risk of "silk protein dermatitis" is to be expected. Sericin is regarded as the main allergen here. The solution to this problem is sericin-free silk fabrics, which have been proven to be suitable for atopic patients (Koller DY et al. 2007).

Avoid animal materials (wool, furs), uneven rough fabrics, but also materials made of breathable synthetic fibers. Silver-coated textiles (e.g. Padycare) appear to have an inhibitory effect on staphylococcal colonization of atopic skin.

Pollen sensitization: The skin reacts with eczema (type IV reaction) to the pollen. We recommend attaching pollen filters (Tesa Protect) to the windows. Apply a protective cream before leaving the house and shower off after returning home.

House dust mite allergy (see also mite allergens): Avoid dust catchers (carpet, curtains, soft toys, etc.), encasing with special mite-repellent covers (recommended e.g. Allergocover). When traveling, use a mite-repellent sleeping bag.

Indoor allergen reduction: use of air purifiers (e.g. Lifelight or Aclimat Silence A50 or Aclimat Air-Center C50).

Hyposensitization (SIT): With regard to type I sensitization, the effectiveness of SIT is controversially discussed in the literature. It is also debated whether SIT contributes to the improvement of atopic eczema. To this end, 26 reliable, randomized studies were evaluated worldwide, in which no usable benefit for atopic eczema could be demonstrated compared to control collectives (Tam 2016). SIT is not approved for atopic eczema (without allergic asthma or rhinitis).

Vaccinations (see below Atopic dermatitis, vaccinations): The period during which many patients develop atopic dermatitis (AD) often coincides with the time of the first vaccinations. This implies a causal relationship between vaccination and the onset of AD (AWMF Guideline 2023). However, current meta-analyses do not indicate an increased risk of AD due to vaccinations, but even a protective effect of some vaccinations (BCG, measles) (Navaratna S et al. 2021).

Sport: According to physical capacity, avoid extreme perspiration, then shower with moisturizing shower gels.

Sauna: According to personal tolerance, avoid extreme temperatures.

Climatotherapy: The most effective measure to improve the symptoms of the disease with the fewest side effects, especially on the high seas (e.g. Borkum, Norderney or Sylt) or in high mountain climates (altitudes above 1500 m, e.g. Davos), especially in spring and fall. The somewhat milder stimulating climate of the Baltic Sea is also helpful for younger children. Recommended minimum duration: 4 weeks. Application to health insurance companies or pension funds.

Diet: All-inclusive diets are to be condemned. Avoid allergologically relevant allergens after appropriate testing (rub, prick and rest test), omission and provocation diet. Review the relevance of the test results every 2 years.

Active probiotics with live bacteria to restore the balance of the skin microbiome (e.g. AktivaDerm®ND)

Remember! The most important thing for nutrition is the patient's self-awareness of their illness!

  • In case of cow's milk allergy, switch to cow's milk substitutes.
  • Caution! Deficiency symptoms due to iodine deficiency, bone decalcification, rickets, as well as iron, vitamin and protein deficiency. Substitution may be necessary.
  • Note! 20-30% of infants with cow's milk allergy also have an allergy to soy milk!
  • The therapeutic effect of probiotics remains questionable according to recent findings.

External therapy
This section has been translated automatically.

Stage-appropriate treatment of eczema, see below. Eczema. In milder forms with circumscribed foci, external therapy is usually sufficient. In severe forms, it should be used in addition to internal therapy. Only use individually tested ointment bases, especially hydrophilic ointments, hydrophilic creams and hydrophilic emulsions. Hydrophobic ointments tend to be less well tolerated due to their occlusive effect! Cream/ointment consumption see under fingertip unit

Currently used therapies

  • Glucocorticoids: The use of topical glucocorticoids is recommended in the guidelines, taking into account the benefit/side-effect profile. In acute exacerbation: Initially 1% hydrocortisone cream or hydrocortisone butyrate (e.g. Laticort cream or Crelo) in combination with moist compresses, e.g. cold black tea or physiological saline solution. In case of superinfection, antiseptic measures, e.g. compresses with octenidine (Octenisept). Education about the short-term use of steroids is urgently required. Recent studies suggest that patients with severe skin lesions in the acute stage benefit better from topical combination therapy (steroids with antibiotics) than from monotherapy (steroids).
  • Calcineurin inhibitors(pimecrolimus, tacrolimus): Tacrolimus (Protopic 0.03% for children and 0.1% for adults; Takrozem® 1 mg/g ointment from 16 years) and pimecrolimus (e.g. Elidel®) can be used as cell-selective immunomodulators/suppressors. Indication: acute, especially subacute eczema. Therapy over a longer period is possible. Several long-term studies in children and adults confirm the significant efficacy (Pimecrolimus) even after 6 and 12 months (no tachyphylaxis). Skin atrophy has not been observed. Due to the galenics, Protopic is more suitable for the treatment of dry skin conditions, Elidel can also be used for eczema that is still weeping. With pimecrolimus, the itching decreases significantly within the first three days of treatment, with tacrolimus, slight irritation of the skin may occur during the first two days of treatment. Pimecrolimus and tacrolimus are approved from 2 years of age. Caution! Due to the carcinogenicity of Pimecrolimus in animal experiments, calcineurin inhibitors can no longer be used safely, but only as a second-line therapy if other therapy options fail, as there is insufficient data on long-term effects in humans. Combinations with UV therapies and long-term therapies are also not recommended for the above reasons. Dosage: Elidel 2 times/day; Protopic within the first three weeks 2 times/day, thereafter 1 time/day. Ensure sun protection, especially after application to the face. Caution! Treat any infections that may occur (herpes, pyoderma)! Caution! Following the market launch of the medication, the occurrence of lymphomas was observed in patients treated topically with calcineurin inhibitors and steroids. However, this could not be confirmed in a study with more than 290,000 cases (for the long-term safety of topical calcineurin inhibitors, see there). After the acute relapse has healed, proactive therapy is recommended: continue to apply pimecrolimus or tacrolimus to the healed skin 1-3 times a week.
  • JAK inhibitors (Ruxolitinib/Opzelura®): Topical approaches with a 1.5% ruxolitinib cream have been experimentally successful to date (Gong X et al. 2021). In the meantime, a 1.5% ruxolitinib cream may be used for the short-term and non-continuous chronic treatment of mild to moderate atopic dermatitis in non-immunosuppressed patients aged twelve years and older if their disease cannot be adequately controlled with topical prescription therapies or if these therapies are not advisable.
  • Polidocanol: Polidocanol is well tolerated and has an anesthetic and antipruritic effect. Larger clinical studies are not available for this indication.
  • Topical antihistamines: These have been used for more than 40 years to treat pruritus despite a lack of evidence of their sufficient efficacy. New topical application methods for cetirizine are still being tested (Kassem MA et al. 2020; Goindi S et al. 2013). A meta-analysis of four studies on the treatment of itching in patients with atopic dermatitis from 2012 showed that the use of topical agents with histamine-reducing effects can moderately reduce itching in AD patients compared to vehicle treatment.

  • Tanning agents: The effect of tanning agents is based on their astringent effect. Both synthetic tanning agents (containing tamol) and natural tanning agents (e.g. tea compresses) are available for use in appropriate stages.
  • Zinc: Zinc-containing topicals have an anti-inflammatory and astringent effect and are well tolerated and widely used. There are no controlled studies available for this indication (nor will there be in the future).

Experimental:

  • Capsaicin: Significant itching relief has been reported in experimental studies and case series. However, practical implementation in treatment and top-up dosing are difficult due to the initially high release of neuropeptides that trigger discomfort. No controlled study has been published to date (Reimann S et al. 2000; Weisshaar E et al. 1998).
  • Crisaborol (trade name: Staquis®), a phosphodiesterase 4 inhibitor, which was tested positively in a 2% ointment form in 3 phase III studies. The effect is based on an inhibition of the enzyme phosphodiesterase-4, which leads to an increase in cAMP and an inhibition of inflammatory cytokines. Approved since 2020 from 3 months of age, dosage 2 x / day.
  • Other JAK inhibitors in the pipeline are delgocitinib (already approved in Japan from the age of 16) and tofacitinib (currently tested positive in 2 phase studies).

Other additive external therapies and measures:

  • Vegetable oil supplements: Good results with 15-20% evening primrose oil creams(e.g. Eucerin 12% Omega, Lipoderm Omega, Linola gamma, R177 ).
  • Urea: Application of hydrating additives such as 2-10% urea (e.g. R102 R104 R113, Basodexan lipid cream/ointment, Excipial U Lipolotio or Hydrolotio; Eucerin 5-10% urea cream/lotion) or 5% dexpanthenol) in combination with moist compresses, e.g. cold black tea or physiological saline solution. It should be noted that topicals containing urea can cause a burning sensation in highly inflamed skin.
  • Basic therapy, possible up to the age of 12 via health insurance prescription: SanaCutan base cream (with 20% glycerine), Optiderm base cream, Allergica base cream, Linola fat
  • Balneotherapy:
    • Bathing in cool, salty sea water is beneficial if the skin surface is intact. Then shower off and apply cream. Water with added chlorine dries out the skin considerably, in swimming pools there is a risk of infection with molluscum contagiosum viruses (see below molluscum contagiosum) and HPV viruses (see below papilloma viruses, human).
    • Baths with added polidocanol (Balneum Hermal Plus). Severe itching crises can sometimes be relieved with potassium permanganate baths (light pink). Caution! Undiluted potassium permanganate is toxic and should not be handled by children.
  • Balneophototherapy (see below radiation therapy)
  • Silver textiles:
    • The effectiveness of silver-coated underwear (see silver textiles below) for atopic eczema has been proven in various studies.

      Please note! Prescription at the expense of the SHI is usually not possible!

Complications:

Radiation therapy
This section has been translated automatically.

Phototherapy (UV therapy):

UVA/UVB (see below UV rays) combinations or low-dose UVA1 therapy have proven effective, with higher doses in exacerbations.

Photosol therapy (hypertonic salt baths plus UVB). Caveat. Possible risk of photoaggravated atopic eczema!

Photosol therapy vs. narrow band UVB: In a larger prospective randomized study with 160 patients a superiority of balneophototherapy could be shown in patients with severe to moderate atopic eczema. 10% brine solution!

PUVA bath therapy: In case of therapy resistance, treatment with PUVA bath therapy or PUVA therapy, systemic.

Narrowband UVB: According to a Brazilian study, narrowband UVB therapy should significantly reduce Staphylococcus aureus colonization on exacerbated skin.

Internal therapy
This section has been translated automatically.

For acute large-area exacerbation, sub- or erythroderma:

Chronic lichenified stage:

  • As a rule, no systemic therapy is required. In the case of pronounced itching that cannot be controlled by external measures, antihistamines such as desloratadine (e.g. Aerius) 1-4 tbl/day or levocetirizine (e.g. Xusal) 1 filmtbl/day can be given. If necessary, the dose can be set much higher than the manufacturer's instructions.

Severe atopic eczema that cannot be adequately treated topically:

  • Ciclosporin: (approved for atopic dermatitis from the age of 16) Numerous studies have shown good therapeutic success with the administration of ciclosporin (5 mg/kg bw/day in the first 2 weeks). The effectiveness of ciclosporin (2.5-5 mg/kg bw/day) in severe atopic eczema has been proven several times on the basis of studies with good evidence. An increase in creatinine and arterial hypertension were reported as significant adverse drug reactions. It must be expected that a relapse (or rebound) will occur in severe atopic eczema 4-5 months after discontinuation of Ciclosporin. According to the guidelines, Ciclosporin A is recommended for the treatment of atopic eczema for a maximum duration of 2 years.
  • Dupilumab, trade name Dupixent ®: IL-4/13-R antibody (approved since 2017 for moderate to severe atopic eczema from 12 years of age, and since December 2020 also for children aged 6 to 11 years with severe atopic dermatitis). By blocking the IL-4 or IL-13 receptor, the initial reaction during the early phase of atopic inflammation (suppression of Th-2-dominant development) is blocked. The Joint Federal Committee sees an additional benefit in the endpoint categories of quality of life, itching, sleep disorders, patient-reported symptoms and improvement in the EASI score compared to standard therapy (consisting of: top glucocorticoids, tacrolimus, ciclosporin). A disadvantage was the development of eye diseases, including conjunctivitis. The added benefit assessment and extension were based, among other things, on the data from the AD-1526, CHRONOS, LIBERTY AD PEDS study.
  • Baricitinib, trade name Olumiant®2mg/4 mg Filmtbl.: Jak inhibitor, indication: treatment of moderate to severe atopic dermatitis, adults with indication for systemic therapy are eligible. Dosage 4 mg/day, from the age of 75 2 mg/day, also for chronic infections 2 mg/day. Control: if there is no response after 8 weeks, discontinue therapy.

  • Tralokinumab (Adtralza®) is a human monoclonal IgG4 antibody which, unlike dupilumab, binds specifically to the interleukin-13 cytokine(IL-13). IL-13 plays a key role in the pathogenesis of atopic dermatitis and bronchial asthma. Blocking IL-13 prevents the interaction with the IL-13 receptor (for details see Interleukin-13) and prevents the subsequent downstream IL-13 signaling. Tralokinumab has been approved since 2022 for patients aged 12 and over with moderate to severe atopic dermatitis (AD). Even in adults, Adtralza® shows impressive efficacy, which continues to improve and persist over the course of therapy. After 16 weeks, 56 % of patients achieved an almost appearance-free skin appearance (EASI-75), after 32 weeks it was 70 %.3 After one year of treatment, Adtralza® achieved an EASI-75 for 83 % of patients - a noticeable and visible success that remained constant even after 2 years. The pivotal study for adolescents confirms the strong efficacy and good safety profile of Adtralza®. The safety profile is at placebo level.

  • Lebrikizumab (preparation Ebglyss®) is a high-affinity monoclonal antibody that selectively binds to soluble interleukin-13 (IL-13). It thereby prevents the formation of the heterodimer complex IL-13Rα1/IL-4Rα and thus the subsequent signal transmission. Lebrikizumab is indicated for the treatment of moderate to severe atopic dermatitis in adults and adolescents aged 12 years and older weighing at least 40 kg who are eligible for systemic therapy. Acute flare-up, short-term, long-term treatment: dosage of 500 mg at the beginning and after week 2 and thereafter every 2 weeks of 250 mg as optimal. The antibody was generally well tolerated. The most common side effects were (allergic) conjunctivitis, injection site reactions and dry eye (Silverberg JI et al. 2023).

  • Baricitinib, an oral selective JAK1 and JAK2 inhibitor, can be used in a dosage of 1 mg, 2 mg and 4 mg once daily in adults with moderate to severe AD. Clinical studies have shown a significant improvement in EASI scores from baseline to 16 weeks, especially at the two higher doses, 2 mg daily and 4 mg daily (Drucker AM et al. (2020). After a response to therapy, a dose reduction can be considered according to the individual benefit/risk assessment and the clinical course. Like all JAK inhibitors, baricitinib is a fast-acting drug. The most common side effects of baricitinib observed in clinical trials include an increase in LDL cholesterol, upper respiratory tract infections, acne and headaches.

    Alternative: Methotrexate can be used as an alternative to ciclosporin in both adults and children(off-label use). Methotrexate is considered an effective, relatively safe and well-tolerated treatment for severe AD - results that are confirmed by recent retrospective studies. The efficacy of MTX was confirmed in a smaller study in 2018 (Gerbens et al. 2018). According to the TREATgermany Register, methotrexate is practically no longer prescribed for adults with AD in Germany, at least since the approval of dupilumab.

  • Alternative: Azathioprine can be considered for the treatment of chronic, severe AD in adults if drugs approved for AD are ineffective or contraindicated (off-label). Azathioprine should not be used in combination with UV therapies. The efficacy of azathioprine in AD is comparable to that of methotrexate, but lower than that of dupilumab and ciclosporin A (Drucker AM et al. (2020)

  • Alternative: mycophenolate mofetil (off-label use): Several authors report good treatment success with the preparation mycophenolate mofetil in severe and therapy-resistant atopic eczema. Mycophenolate mofetil can be considered in patients with AD for whom systemic treatment is an option if substances approved for AD are ineffective or contraindicated (offlabel). Study results show a significant reduction in SCORAD scores, with 77.6% of patients reporting partial or complete remission. Dosage: acute relapse, short-term, long-term treatment: adults: 1-3 g per day, usual dose 2 g per day; children: 30-50 mg/kg per day, usually administered in two divided doses
  • Alternative: In a smaller multicenter study (n=167), good clinical effects were achieved with the JAK inhibitor upadacitinib in atopic dermatitis (Guttman-Yassky E et al. 2019)
  • Alternative: Extracorporeal photopheresis: This treatment option is reserved for severe, otherwise therapy-resistant cases. The clinical effects can be described as good. The data situation is still unsatisfactory.
  • Experimental:
    • Anti-interleukin-5 therapy: Previous studies on this form of therapy for atopic eczema with monoclonal antibodies have been unsatisfactory.
    • Omalizumab: Casuistic successes have been reported with the human anti-IgE antibody omalizumab(off-label use; so far only approved for the indication bronchial asthma), which could not be confirmed in a randomized, placebo-controlled double-blind pilot study. There is now a broad consensus that omalizumab should not be used for the treatment of AD.
    • Nemolizumab: With a humanized interleukin-31 receptor antibody (nemolizumab) that targets IL-31 receptors (see interleukin-31 below), including the IL-31 receptors on neurons, a significant reduction in itching and eczema severity was achieved with monthly doses (Ruzicka T et al. (2017). As of February 2024, no approval has yet been granted.
    • Experimental: Further interleukin antibodies are expected in the treatment of atopic dermatitis or there are already fully published studies on: Fezakinumab (fully humanized monoclonal antibody against IL-22) and ustekinumab.

  • Experimental:
    • IVIG: The approaches to treat therapy-resistant atopic eczema with high-dose intravenous immunoglobulins (IVIG: dosages 2.0/kgKG) must still be regarded as experimental. This applies in particular to patients with severe atopic eczema in whom immunosuppressive therapy is not possible for various reasons. There are a number of studies on this in both adults and children dating back to 1996. However, IVIG is unlikely to be used in the future, as numerous newer, proven effective therapies are available.

Progression/forecast
This section has been translated automatically.

An individual prediction of the course of the disease is not possible due to the high clinical variability. A chronic, intermittent course with relapses of varying duration and severity is to be expected.

Important: although the disease can be significantly improved by therapeutic measures, it cannot be cured! Promises of cures by miracle healers are charlatanry.

As a rule of thumb, the rule of thirds can be applied:

  • 1/3 loses the disease
  • 1/3 must expect the disease to persist
  • 1/3 must expect aggravations.

An improvement in skin symptoms can be expected with increasing age. 75% of patients with AD show remissions during puberty. Around 30% of all children suffering from AD continue to develop eczema, at least temporarily, into adulthood.

Due to impaired cellular immunity, there is an increased susceptibility to viral, bacterial and mycotic infections.

Prophylaxis
This section has been translated automatically.

Preventive measures in case of known atopic diathesis, see also Allergy prevention.

  • Breastfeeding (previously accepted position): Full breastfeeding of infants for at least 4 months, supplementary feeding of porridge before 5 months of age. According to various meta-analyses, the "Breast is best! Meta-analyses a 30% significant risk reduction! These results are now being called into question by the results of a large Canadian study (final evaluation in 11,000 children), which found a higher sensitization rate in the breastfed children than in the control group. A larger study (n=335) also failed to demonstrate a risk reduction for allergic bronchial asthma. An Italian study came to similar results.
  • Complementary feeding: For years it was recommended to introduce potent food allergens as late as possible in infant feeding. This can no longer be deduced from the relevant studies on this topic. Rather, delayed introduction of complementary foods seems to increase the risk for later sensitization to aero- and food allergens at 5 years of age.
  • Maternal diet during breastfeeding: The evidence base is relatively weak. Avoidance of potent allergens (milk, egg, fish, nut, wheat, soy) appears to have a beneficial effect on eczema prevention.
  • Food supplements ( probiotics ): The preventive effect of probiotics is controversially discussed and completely negated by several research groups due to insufficient studies, current studies confirm the preventive effect. Proponents of probiotics have the following hypothesis: The intestine of allergic persons seems to be poorly colonized by lactobacilli. The addition of LGG (Lactobacillus Goldin and Gorbach = Lactobacillus rhamnosus GG) is said to lead to a significant reduction (68%) of the atopy rate in at-risk children, but has since been relativized to 21%. In a Dutch study of 138 children, hydrolyzed protein formulations with indigestible oligosacchrids were shown to have a formulation of intestinal flora comparable to that of breastfed children (Wopereis H et al. 2018).
  • Vitamin D (high dose): High-dose supplementation of vitamin D (4,400IU/day versus the current recommendation of 400IU/day) resulted in neonatal immunomodulation in a randomized trial that may provide protection against wheezing and bronchial asthma (Hornsby E et al 2018).
  • Pet ownership: Individual epidemiological studies have found a significant association between the ownership of small rodents (rabbits, guinea pigs) and the prevalence of atopic eczema. Keeping these animals (including cats) should be avoided in children at risk. There are no restrictive recommendations regarding the keeping of dogs. In case of sensitization and clinical symptoms ( rhinitis/conjunctivitis/asthma), direct contact should be avoided, also via contact persons.
  • Smoking: Do not smoke at home! Atopy stigma is significantly more frequent in children whose mothers smoked during pregnancy (52.2% in the verum group vs 37.7% in the control group). Maternal smoking doubles the risk of developing atopic eczema.
  • Mold (see mold illnesses below): Remediate living spaces from mold! Moisture and mold exposure indoors seems to be associated with an increased risk of eczema!
  • House dust mites: For children at risk, it is necessary to minimize house dust mite exposure:
    • Remove dust traps from living rooms and bedrooms.
    • Keep bedrooms cool and clean. Do not carpet but prefer smooth surfaces that can be mopped with a damp cloth.
    • Toys: Prefer washable toys (e.g., washable stuffed animals).
    • Bedding: Use washable bedding, remove bedsprings. Frequent airing and cleaning of mattresses. The mite-proof mattress cover (see Encasing below) is an effective measure for mite minimization in bedrooms. Alternatively, bedding made of microfiber can be used.

Occupations to avoid in atopic dermatitis(see Occupational dermatoses below):

  • Hairdresser, nursing professions, photographer, painter, machining professions (lathe operator/miller), manual professions in the metal and car industries, carpenter, bricklayer professions, work underground (miner), employment in leather tanning and processing, baker, confectioner, cook (food professions), professions with constant damp work (room attendant; window cleaner, etc.).

Naturopathy
This section has been translated automatically.

Naturopathic treatment is suitable in the subacute and chronic stages.

Order therapy: Adequate lifestyle, avoidance of allergens, extreme stress situations is essential, see also general therapy

Climatotherapy: Low-allergen stimulating climate (high sea climate, high mountain climate), long-wave UVA 1 radiation, baths with local disinfectant, skin-soothing additives such as lavender oil, alleviate skin irritation. Cave: rare allergic reaction to lavender, especially linalool. Also suitable for superinfections due to the disinfectant effect of lavender oil. In the acute stage of eczema, cool, moist compresses with black tea or oak bark extract (see tannins below) relieve the itching and inflammation; to prevent the skin from drying out, always apply the cream or care cream containing the active ingredient to the skin first.

Intestinal cleansing is becoming increasingly important in atopic eczema. Patients with atopic eczema tend to have a reduction in protective bacteria in the intestine, in particular enterococci. Frequently, especially after antibiotic therapy, this leads to overgrowth with Candida albicans and reactively triggers atopic eczema. In addition to the reduction of Candida colonization(nystatin), the correction of bacterial overgrowth should be carried out by means of symbiosis reduction after differentiation of the missing protective germ. see also microbial therapy.

Probiotic bacterial strains (bacterial complex Baplexin 621, which consists of lactobacilli, namely Lactobacillus gasseri, L. paracasei, L. plantarum, L. rhamnosus, L. reuteri
L. johnsonii, as well as bifidobacteria: Bifidobacterium lactis and B. longum, and streptococci: Streptococcus thermophilus) can be used locally. The bacteria are accompanied by the prebiotic ingredients inulin and maltodextrin, which are optimal nutrients for the probiotic bacterial strains.

Phytotherapy: Phytotherapeutically, rational phytotherapy in particular has proven itself, while the effect of some traditional plants could not be proven in studies. see also under section Phytotherapy external/internal below.

Note: always test ointment tolerance! Cave: Wool wax alcohols

Traditional phytotherapy:

Dulcamaris (bittersweet stem, Solanum dulcamara) from the nightshade family, positive monograph for the supportive treatment of eczema, no reliable studies to date, can be used locally (Cefabene ointment and gel, Dulcamaris ointment) as well as systemically (e.g. in Cefabene drops, Cave contains ethanol and liqueur wine). The extracts of the drug contain steroid saponins, which have steroid-like effects, tannins and steroid alkaloid glycosides.

Witch hazel (witch hazel), positive monograph of Commission E/ESCOP for use in skin injuries, mild inflammation of the skin and mucous membranes, haemorrhoids and
varicose vein complaints, no superiority over placebo in studies. Locally as ointments (e.g. Hametum® wound and healing ointment, Hamasana®, Hamadest®).

Calendula (marigold), composite plant, positive monograph of Commission E/ESCOP for use in inflammatory changes of the oral and pharyngeal mucosa, poorly healing wounds, ulcus cruris. No systematic studies on eczema to date, superior to placebo in the prophylaxis of radiodermatitis. Locally as an ointment (e.g. Calendumed ointment) or essence for the preparation of baths and compresses. Cave: Allergy potency, composite plant!

Evening primrose oil: Seeds of Oenothera biennis (common evening primrose; see evening primrose oil below), which consists of 60-80% linoleic acid and 8-14% gamma-linolenic acid, an omega-6 fatty acid, no positive monograph as not processed. Recognized by the WHO for the indication atopic eczema, diabetic neuropathy, mastodynia. Efficacy not yet sufficiently proven in studies. Locally as a cream (e.g. Eucerin Omega®, Allergika Night Seed Oil Cream®), systemically in capsule form (e.g. Epogam®, dosage: 2-3 g/day = 4-6 capsules).

Borage seed oil is also rich in gamma-linolenic acid and can be applied internally (e.g. Glandol®, borage oil capsules) or externally as a formulation.

Tormentillae rhizoma: A small positive application study is available on Tormentillae rhizoma (2% ) in an easily spreadable oil/w base (Hoffmann 2015).

Midday flower ointment: A positive application study is available on a paraffin-based basic care with the juice of the edible midday flower (see below Mesembryanthemum edule)". The atopic children treated in this way had significantly increased hydration of the str. corneum and reduced transpepidermal water loss after 16 weeks (Schario 2014).

Seed oats (medicinal plant of the year 2017): Extracts of the oat herb (contain flavonoids and saponins) are used in medicinal baths with good success in atopic eczema.

Rational phytopharmaceuticals (placebo-controlled, partly double-blind studies):

Betulin, found in birch bark, has antibacterial, antipruritic, anti-inflammatory, wound-healing and antitumor effects. When applied locally as a cream (Imlan® Creme pur and plus), it leads to a statistically significant rehydration of the horny layer, improvement of the skin barrier and a significant reduction in transepidermal water loss (Laszczyk 2009).

Hypericum (St. John's wort): A positive, randomized, placebo-controlled, half-side comparison study is available on atopic eczema with a 1.5% cream application (Schempp 2003) with significant superiority compared to placebo. Local application (e.g. Bedan® cream), approved from the 6th month of life.

Cardiospermum halicacabum leaves (balloon vine leaves) Extracts from the monk's head plant (not to be confused with the "monk's head" Infundibilicybe geotropa - an edible mushroom from the chivalrous family) have an anti-eczematous effect due to their content of saponins, tannins, flavonoids and traces of alkaloids. Clinical studies with Cardiospermum halicacabum showed good anti-inflammatory effects comparable to the active ingredient bufexamac. Preparations: Dermaplant® ointment, Halicar® cream or Halicar ointment. Dermaplant can be prescribed and reimbursed for children up to the age of 12 for atopic eczema

Liquiritiae radix (licorice root) the 1% and 2% gel shows a significant improvement in erythema, edema and itching (improvement of 80%) in a double-blind placebo-controlled study. Trade name: Atopiclair, applicable from the 6th month of life (Abramovits 2006).

Mahonia+pansy+waterpennywort as a fixed combination in Ekzevowen® derma cream showed statistically significant superiority to placebo only in winter.

Internal phytotherapeutics:

see under Cannabidiol, Dulcamaris

Regulative therapy
This section has been translated automatically.

AD is associated with a considerable burden of disease. This affects all areas of quality of life, which are significantly impaired in the majority of those affected. The loss of quality of life is on average higher for those affected than for most other skin diseases, as well as for many other chronic internal diseases such as type 2 diabetes, rheumatoid arthritis, heart disease or hypertension. Significant clinical predictors of impaired quality of life include severe itching, infestation of visible areas of the body such as the face and hands, pronounced skin dryness, the extent of the lesions and sleep disturbances.

Furthermore, increased comorbidity, especially for atopic diseases, mental illnesses, somatic stress disorder or depression, as well as the significantly higher frequency of skin infections also contribute to the reduction in quality of life (Zander N et al. 2020). This comorbidity can already be found in children with atopic dermatitis. A serious complication is eczema herpeticatum.

Phytotherapy external
This section has been translated automatically.

see also under section Naturopathy -

Rational phytotherapeutics

Betulin, Glycyrrhiza glabra, Hypericum perforatum, Hyperici herba, Balloon vine, Avena herba

___________________________________

Positively monographed phytotherapeutics

Dulcamarae stipites, calendula, witch hazel, evening primrose, cod liver oil

_______________________________________

Hydrotherapy with

Tea, black; lavender oil, Quercus cortex, camomile, tea tree oil, sandalwood

Note(s)
This section has been translated automatically.

Atopy is derived from the Greek word "atopos" (= in the wrong place).

The importance of atopic eczema in everyday life is illustrated by the world's largest study of the impact of the disease on the lives of sufferers and relatives ( ISOLATE study).

Evaluation of the clinical course is possible using the SASSAD score.

The frequency of sensitisation to food allergens (see below food allergy) is particularly high in atopic children who have already developed atopic eczema in the first three months of life and lowest in children who do not show symptoms of atopic eczema until after the first year of life.

Specific immunotherapy: Specific immunotherapy should be discussed only in the presence of appropriate pulmo-conjunctival or bronchial symptoms. Caution. Worsening of the eczema. Possibly danger of floor change!

Literature
This section has been translated automatically.

  1. Abramovits W et al. (2006) A multicenter , randomized, vehicle-controlled clinical study to examine the efficacy and safety of MAS 063 DP (Atopiclair) in the management of mild to moderate atopic dermatitis in adults. J Drugs Dermatol 5: 236-244
  2. Ambros-Rudolph CM (2006) Dermatoses of pregnancy. J Dtsch Dermatol Ges 4: 748-759
  3. Angelova-Fischer UC et al. (2006) Significance of interleukin-16, macrophage-derived chemokine, eosinophil cationic protein and soluble E-selectin in reflecting disease activity of atopic dermatitis-from laboratory parameters to clinical scores. Br J Dermatol 154: 1112-1117
  4. Augustin M et al (2012) Atopic dermatitis report. Prevention, care and innovation. Analysis of data from the Techniker Krankenversicherung. Accessed 30.04.2022; www.cvderm.de)
  5. Brenninkmeijer EE et al. (2007) Clinical differences between atopic and atopiform dermatitis. J Am Acad Dermatol 58: 407-414
  6. Broberg A et al. (2007) Atopic dermatitis in 5-6-year-old Swedish children: cumulative incidence, point prevalence, and severity scoring. Allergy 55:1025-1029)
  7. Brüggen M-C et al. (2016) Antigen or allergen presentation. In: T. Biedermann et al. (Eds.) Allergology. Springer-Verlag Berlin-Heidelberg p 63
  8. Bussmann C et al. (2006) Does allergen-specific immunotherapy represent a therapeutic option for patients with atopic dermatitis? J Allergy Clin Immunol 118: 1292-1298
  9. Bussmann C et al. (2009) Which systemic therapy options are available for severe forms of atopic dermatitis? JDDG 7: 205-221
  10. Capello C et al. (2017) Investigation of the protective effect of a basic therapy with multiple protection against the penetration of aeroallergens into the skin of atopic dermatitis. Allergo J Int 26: 70
  11. Charman CR et al. (2002) Reliability testing of the Six Area, Six Sign Atopic Dermatitis severity score. Br J Dermatol 146: 1057-1060.
  12. Drucker AM et al. (2020) Systemic Immunomodulatory Treatments for Patients With Atopic Dermatitis: A Systematic Review and Network Meta-analysis. JAMA Dermatol 156:659-667.

  13. Gauger A et al. (2006) Efficacy and functionality of silver-coated textiles in patients with atopic eczema. J Eur Acad Dermatol Venereol 20: 534-541
  14. Gerbens LAA et al.(2018) Methotrexate and azathioprine for severe atopic dermatitis: a 5-year follow-up study of a randomized controlled trial. Br J Dermatol 178:1288-1296.
  15. Griffiths CE (2006) Update on the use of ciclosporin in immune-mediated dermatoses. Br J Dermatol 155: 1-16
  16. Gong JQ et al. (2006) Skin colonization by Staphylococcus aureus in patients with eczema and atopic dermatitis and relevant combined topical therapy: a double-blind multicentre randomized controlled trial. Br J Dermatol 155: 680-687
  17. Gong X et al. (2021) Pharmacokinetics of Ruxolitinib in Patients with Atopic Dermatitis Treated With Ruxolitinib Cream: Data from Phase II and III Studies. Am J Clin Dermatol 22:555-566.
  18. Guttman-Yassky E et al. (2019) Upadacitinib in adults with moderate to severe atopic dermatitis: 16-week results from a randomized, placebo-controlled trial. J Allergy Clin Immunol 145:877-884.
  19. Heil PM et al. (2010) Omalizumab therapy of atopic dermatitis: IgE depletion does not lead to clinical improvement - a randomized, placebo-controlled, double-blind pilot study. JDDG 8: 990-999
  20. Heinlin J et al.(2011) A first prospective randomized controlled trial on the efficacy and safety of synchronous balneophototherapy vs. narrow-band UVB monotherapy for atopic dermatitis.J Eur Acad Dermatol Venereol 25:765-773
  21. Hijnen DJ et al. (2007) Efficacy and safety of long-term treatment with cyclosporin A for atopic dermatitis. J Eur Acad Dermatol Venereol 21: 85-89
  22. Hornsby E et al. (2018) Vitamin D supplementation during pregnancy: Effect on the neonatal immune system in a randomized controlled trial. J Allergy Clin Immunol 141:269-278
  23. Igaawa K et al.(2007) Odontogenic focal infection could be partly involved in the pathogenesis of atopic dermatitis as exacerbation factor. Int J Dermatol 46: 376-379
  24. Jelding-Dannemand E et al. (2015) Breast-feeding does not protect against allergic sensitization in early childhood and allergy-associated disease at age 7 years. J Allergy Clin Immunol 136: 1302-1308
  25. Kalliomäki M et al. (2001) Probiotics in primary prevention of atopic disease: a randomized placebo-controlled trial. Lancet 357: 1076-1079
  26. Landeck L et al. (2011) Contact sensitization pattern in 172 atopic subjects. Int J Dermatol 50:806-810
  27. Lane JE et al. (2005) Treatment of recalcitrant atopic dermatitis with omalizumab. J Am Acad Dermatol 54: 68-72
  28. Langen U et al. (2013) Prevalence of allergic diseases in Germany: results of the German Health Interview and Examination Survey for Adults (DEGS1)]. Federal Health Gazette Health Research Health Protection. 56:698-706.
  29. Laszczyk MN et al. (2009) Regenerative and anti-inflammatory effects of betulin emulsions in impaired epidermal barrier function. Act Dermatol 35: 1-5
  30. Nakatsuji T et al. (2016) Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression.J Invest Dermatol 136:2192-2200.
  31. Navaratna S et al. (2021) Childhood vaccination and allergy: A systematic review andmeta-analysis. Allergy 76:2135-2152.

  32. Niebuhr M et al (2011) Contact allergy and atopy. Dermatology 62: 744-750
  33. Novak N et al.(2011) Specific immunotherapy and atopic dermatitis. Dermatologist 62: 650-656
  34. Nwaru BI et al. (2010) Age at the introduction of solid foods during the first year and allergic sensitization at age 5 years. Pediatrics 125: 50-59
  35. Ownby DR et al. (2002) Exposure to dogs and cats in the first year of life and risk of allergic sensitization at 6 to 7 years of age. JAMA 288: 963-972
  36. Paller AS et al. (2016) Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol 75:494-503.
  37. Peroni DG et al.(2011) Correlation between serum 25-hydroxyvitamin D levels and severity of atopic dermatitis in children. Br J Dermatol 164:1078-1082.
  38. Proksch E et al.(2016) Epidermal barrier dysfunction in dermatoses. Dermatologist 67: 907-921
  39. Reimann S et al. (2000) Topical administration of capsaicin in dermatology for treatment of itching and pain. Dermatologist 51:164-172.

  40. Riedler J et al. (2001) Exposure to farming in early life and development of asthma and allergy: a cross-sectional survey. Lancet 358: 1129-1133

  41. Roduit C et al. (2011) Prenatal animal contact and gene expression of innate immunity receptors at birth are associated with atopic dermatitis. J Allergy Clin Immunol 127:179-185
  42. Roduit C et al. (2017) Phenotypes of Atopic Dermatitis Depending on the Timing of Onset and Progression in Childhood. JAMA Pediatr 171:655-662.
  43. Ruzicka T et al. (2017) Anti-Interleukin-31 Receptor A Antibody for Atopic Dermatitis. N Engl J Med 376:826-835.
  44. Sand M et al. (2007) Extracorporeal photopheresis as a treatment for patients with severe refractory atopic dermatitis. Dermatology 215: 134-138
  45. Schario M et al.(2014) Children with dry skin and atopic predisposition: daily use of emollients in a participant-blinded, randomized, prospective trial. Skin Pharmacol Physiol 27:208.
  46. Schmitt J (2018) Increased attention-deficit/hyperactivity symptoms in atopic dermatitis are associated with history of antihistamine use. Allergy 73: 615-626.
  47. Schram ME (2011) A randomized trial of methotrexate versus azathioprine for severe atopic eczema. J Allergy Clin Immunol 128:353-359
  48. Shalom G et al. (2020) Atopic dermatitis and celiac disease: a cross-sectional study of 116,816 patients. Am J Clin Dermatol 21:133-138.

  49. Sic Haw et al. (2010) The Efficacy and Safety of Long-term Oral Cyclosporine Treatment for Patients with Atopic Dermatitis. Ann Dermatol 22: 9-15
  50. Silva SH et al. (2006) Influence of narrow-band UVB phototherapy on cutaneous microbiota of children with atopic dermatitis. J Eur Acad Dermatol Venereol 20: 1114-1120
  51. Silverberg JI et al. (2023) Two Phase 3 Trials of Lebrikizumab for Moderate-toSevere Atopic Dermatitis. N Engl J Med 388:1080-1091.

  52. Sugiyama M et al. (2007) Early-life risk factors for occurrence of atopic dermatitis during the first year. Pediatrics. 119:E716-E723
  53. Tam HH et al. (2016) Specific allergen immunotherapy for the treatment of atopic eczema: a Cochrane systematic review. Allergy 71:1345-1356.
  54. Torres T et al (2019) Update on Atopic Dermatitis. Acta Med Port 32:606-613.
  55. Turati F et al. (2016) Early weaning is beneficial to prevent atopic dermatitis occurrence in young children. Allergy 71:878-888
  56. Viljanen M et al. (2005) Probiotics in the treatment of atopic eczema/dermatitis syndrome in infants: a double-blind placebo-controlled trial. Allergy 60: 494-500
  57. Weatherhead SC et al. (2007) An open-label, dose-ranging study of methotrexate for moderate-to-severe adult atopic eczema. Br J Dermatol 156: 346-351
  58. Weisshaar E et al. (1998) Effect of topical capsaicin on the cutaneous reactions and itching to histamine in atopic eczema compared to healthy skin. Arch Dermatol Res 290:306-311.

  59. Werfel T et al. (2016) S2k guideline atopic dermatitis (atopic eczema, atopic dermatitis) - short version. Allergo J 25: 36-49

  60. Wollenberg A. et al. (2018) Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I. J Eur Acad Dermatol Venereol 32:657-668
  61. Wopereis H et al. (2018) Intestinal microbiota in infants at high risk for allergy: Effects of prebiotics and role in eczema development. J Allergy Clin Immunol 141:1334-1342
  62. Willan R (1808) On Cutaneous Diseases. Johnson, London
  63. Williams HC et al. (2000) The natural history of atopic dermatitis. In: Williams HC, ed. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge University Press;2000:41-59.24
  64. Yagis S et al. (2004) presence of staphylococcal exfoliative toxin A in sera of patients with atopic dermatitis. Clin Exper Allergy 34: 984-993
  65. Yazdi AS (2012) Genetic risk of atopic dermatitis. Dermatologist 63: 161-163
  66. Zander N et al. (2020) Atopic dermatitis shows significant cutaneous comorbidity:results from large-scale investigations in the working population. J Eur Acad Dermatol Venereol 34:135-141

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.