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: 05.01.2023

Dieser Artikel auf Deutsch


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

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Willan, 1808

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A multifactorial, chronically persistent or also chronically recurrent, non-contagious, usually considerably pruritic dermatitis of varying acuity belonging to the group of atopic diseases (Greek: atopos = out of place), which develops, is maintained or is activated due to complex interactions of congenital and environmental factors.

The atopic eczema shows a topographically and morphologically different appearance in the different stages of life:

  • in infancy, rather uncharacteristic diffuse eczematous skin manifestations on the face and on the extensor sides of the extremities of varying severity and acuity (see atopic dermatitis in infancy)
  • in infancy , more localized and less diffuse eczema, with a variable and seasonal course (see atopic dermatitis in infancy)
  • inschoolchildren it occurs preferentially as flexural eczema
  • in adulthood there is a great morphological variety. Both localized minus variants of atopic dermatitis (eyelids, genitalia, hands, neck) and extensive eczema variants up to those universally affecting the entire integument (erythrodermic atopic dermatitis) characterize the extremely varied clinical picture.

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Atopic eczema shows different symptoms in different stages of life.

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

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

Furthermore, a number of different variants can be assigned to atopic dermatitis, 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 clinical course (e.g. prurigo form of atopic eczema). Such dermatitis may also be triggered by other factors (e.g. contact allergy).

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Prevalence in industrialized countries: 10-20% of all children, 1-5% of adults (in children, atopic eczema is the most common chronic disease of all).

The incidence peak is in the first two LY.

The prevalence has almost tripled in industrialized countries in the past 3 decades.

In addition, about 40-60% of patients with atopic eczema suffer from respiratory allergies (pollinosis, perennial rhinitis, allergic bronchial asthma).

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It is caused by a combination of genetic and environmental factors that induce skin barrier dysfunction, dysregulation of the cutaneous and systemic immune systems, dysbiosis of the skin microbiota, and a strong genetic influence (Torres T et al. 2019).

From practical clinical considerations, 2 forms with largely identical skin manifestations can be distinguished:

  • Intrinsic (non-allergic) atopic eczema (about 20-30% of patients; non-IgE mediated). At present, it is still unclear whether this clinical picture should be evaluated as a separate entity.
  • Extrinsic (allergic) atopic eczema (60-70% of patients, IgE-mediated).

Notice. Patients with 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 dermatitis should not be assumed to be healthy despite the absence of symptoms. Evidence of increased skin dryness, barrier disruption with increased irritability, subtle perivascular T-cell infiltrates, increased number of Th2 cells with increased IL-4 and IL-13 production.

In diseased skin: due to skin barrier disruption , allergens can penetrate into the deeper layers of the epidermis (Cappello C et al. 2017). Here they are recognized and taken up by Langerhans cells. 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 stream, reducing their dendritic extensions during this passage (so-called veiled cells - see below Langerhans cell). In the lymph node, they present the antigen to naïve lymphocytes and induce a Th2 response.

There is increased expression of IL-16, C-C chemokine ligand 27, RANTES, monocyte chemotactic protein-4, and eotaxin. Activation of eosinophilic leukocytes and macrophages. Expression of IL-4 and IL-13 is decreased. Increased expression of IL-5, GM-CSF, IL-11, IL-12, IL-22, and IFN-gamma continues. Interleukin-22, in turn, is able to downregulate barrier proteins (Brüggen M-C et al. 2016).

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

Genetics: Genetic factors play a significant role in the predisposition of atopic eczema. The risk of a child developing atopic eczema (AE) is 50% if one parent has asthma, atopic eczema or rhinitis allergica, 75% if both parents are affected. Concordance in monozygotic twins is 72%, and 23% in dizygotic twins.

Genome studies revealed several candidate genes predisposing to atopy on chromosomes 1q21, 3q21, 5q32, 6, 11q13, 17q25 (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". 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 significant 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 encodes the protein filaggrin, show a clear association with an early onset and a chronic course of atopic dermatitis.

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

Furthermore, an atopy association involves the claudin I gene, which encodes an important tight junction protein. Polymorphisms of this gene lead to disorders of epidermal integrity, which is substantially disturbed in atopic dermatitis.

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

The following genes have also been evaluated as risk factors for atopic dermatitis:

  • COL29A1 (3q21); encoded protein: collagen type XXIX, alpha1.
  • COL18A1 encoded protein: collagen type XXIX, alpha1
  • EMSY (11q13.5); encoded protein: EMSY
  • FLG (1q21); encoded protein: filaggrin
  • RAD50 (5q23-q32) encoded 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
  • 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: Disorders in filaggrin assembly 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 crosslinks the disulfide bridges between 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 mechanical disruption of the barrier and maintains the cytokine-mediated inflammatory and itch response. Filaggrin mutant patients with AE have a significantly higher propensity to allergic bronchial asthma as well as ichthyosis vulgaris than those without this mutation. It is also possible that the demonstrated increased expression of aquaporin-3 in the keratinocytes of atopic patients plays a significant role in the impaired skin barrier function.

The allergens relevant for the atopic syndrome are grass pollen, house dust mites and animal dander. Because these proteins have a high molecular weight, they cannot penetrate through normal skin (only proteins < 1000 Daltons can). However, in atopic skin, molecules with a higher molecular weight can penetrate due to barrier disruption. They are taken up there by dendritic cells. Concordant to this are clinical observations proving an exacerbation of atopic eczema after local provocation with grass pollen. Local exposure to cat epithelia also leads to an increased tendency to eczema in filaggrin-mutated newborns (!). That this is not only a specific (local) reaction in case of sensitization is shown by the observation that birch pollen can induce eczema reactions, even in non-birch pollen sensitized individuals. Other mechanisms are responsible for this, such as pollen-associated lipid mediators (PALMS), which stimulate an inflammatory reaction even non-specifically. Airborne pollen particles are also able to penetrate the atopic skin.


  • Type I sensit izations: Tree and grass pollen: Apparently, there is an increased sensitizability via the skin in patients with AE. This also correlates with the observation of "flare-up" reactions during increased pollen counts or house dust exposure.
  • Type IV sensitization (see below contact allergy): Patients with atopic eczema seem to have a higher sensitization rate than non-atopics (most frequent contact allergens: nickel(II) sulfate and fragrance mix).

Microbial factors: Of pathophysiological relevance is Staph. aureus (high colonization density (> 80%) in the nasal mucosa and on weeping areas). Staphylococcus aureus produces high amounts of enterotoxins (enterotoxin A-D, toxic-shock-syndrome-toxin-1), which act as superantigens and are thus T-cell proliferative; against which patients continue to form IgE antibodies, 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 et al.). This dermal dysbacteria could thus directly lead to an increase in inflammatory cytokines.

Pityrosporum ovale colonization plays a pathogenetic role in patients with the "head-and-neck" form of atopic dermatitis. Patients affected in this way benefit from antimyotic local therapy.

Furthermore, there is evidence that focal infections (such as dental infections) seem to be involved in triggering or exacerbating atopic eczema. This is surprising in so far as such influences have not been assumed so far!

Hygiene hypothesis: Presumption that the increase of atopic eczema is related to a higher standard of living as well as improved hygienic conditions. A reduction of bacterial or viral infections leads to a decreased production of TH1 cytokines (e.g. interferon gamma) and thus to a decrease of the protective effect of the Th1 immune responses in favor of the Th2 responses characteristic for atopic diseases.

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

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: Reported inverse correlation between severity of atopic eczema and Vit.D level.
  • Climate, stress, post-traumatic stress disorder, pollution exposure may lead to onset or exacerbation of the disease.

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70% of patients with atopic eczema show an initial manifestation in infancy, usually after the 3rd month of life (see atopic eczema in infancy).

Late manifestations in adulthood are possible.

During pregnancy, an exacerbation of a pre-existing atopic eczema occurs in 20% of cases. see also Pregnancy dermatosis, atopic.

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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
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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
    • Shiny nail (fingernails that look polished).
    • Dermopathic lymphadenopathy in generalized affection.

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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).

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

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

Clinical picture, family history, self history (eczema history, rhinitis allergica, bronchial asthma, food allergies, viral and bacterial infection susceptibility).

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

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

Results of an orienting prick and intradermal test

  • Extrinsic form
    • IgE > 150 kU/ml
    • ECP
    • Increased 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 to question contact sensitization (higher rate of contact allergy to topical agents, external ingredients, rubber materials, fragrance mix)

Differential diagnosis
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Increased incidence of (severe) viral and bacterial infections. S.a.u. Eccema herpeticatum; Eccema molluscatum; pyoderma, erythroderma.

Occasionally, in the course of atopic eczema, "light sensitisation" occurs with an intensification of the eczema reaction in light-exposed areas. S.u. Eczema atopic photoaggravated

Other complicated comorbidities are:

General therapy
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Skin dryness: xerosis, depending on the ambient temperature and humidity. Avoid excessive heating of living spaces, increase humidity, optimal ventilation of rooms. Due to the reduced alkaline neutralizing capacity, the use of soaps, detergents and rinsing agents should be reduced to a minimum. Re-greasing 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 accumulation and itching crises due to high outdoor temperatures during physical exertion, but also in stressful situations.

Sun and UV: UV exposure usually has an alleviating effect on eczema. Occasionally, increased UV sensitivity is present. See also photoaggravated endogenous eczema.

Contact allergies: Often 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 are excellent (e.g. Eucerin shower oil, Lipoderm shower gel).
  • As an alternative to bath oils, an O/W emulsion or hydrophilic oils can also be used for cleansing. For very dry skin, after drying, apply an emulsion or cream (e.g. Ungt. emulsif. aq., Eucerin Lotio, Excipial U Lipolotio or Excipial U Hydrolotio, etc.) according to compatibility.

Choice of occupation: Unsuitable are occupations with intensive contact with water, detergents, oils, greases, drilling water, disinfectants, adhesives, leather, chemical products, animals, flour and dusts. Dry, clean occupations are recommended. Cave. Spread of molds through air conditioning systems!

Clothing: Breathable clothing, loosely woven cotton or also textiles made of silk (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 definitely to be expected. In this case, sericin is considered to be the main allergen. The solution to this problem situation is sericin-free silk fabrics, which have been proven to be suitable for atopics (Koller DY et al. 2007).

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

Pollen sensitization: The skin reacts with eczema (type IV reaction) to pollen. It is recommended to apply pollen filters (Tesa Protect) to the windows. Apply a protective cream before leaving the living rooms, shower off after returning.

Dust mite allergy (see also mite allergens): Avoidance of dust catchers (carpet, curtains, soft toys, etc.), encasing with special mite-repellent covers (recommended e.g. Allergocover). When traveling, 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): Regarding type I sensitizations, there is controversy in the literature regarding the implementation of SIT in terms of its efficacy. It is also discussed whether SIT contributes to the improvement of atopic eczema. In this regard, 26 robust randomized trials could be evaluated worldwide, in which no usable benefit for atopic eczema could be demonstrated compared to control collectives (Tam 2016). SIT is not approved in atopic eczema (without allergic asthma or rhinits).

Sports: According to physical capacity, avoiding extreme perspiration, followed by showering with moisturizing shower gels.

Sauna: According to personal tolerance, avoid extreme temperatures.

Climatic therapy: The most effective measure with the fewest side effects to improve the symptoms of the disease is a sea climate (e.g. Borkum, Norderney or Sylt) or a high mountain climate (altitude over 1500 m, e.g. Davos), especially in spring and autumn. For younger children, the somewhat milder stimulating climate of the Baltic Sea is also helpful. Recommended minimum duration: 4 weeks. Application to health insurance companies or pension insurance companies.

Nutrition: Blanket diets are to be condemned. Avoidance of allergologically relevant allergens after appropriate testing (rubbing, pricking and resting test), omission and provocation diet. Review the relevance of test results every 2 years.

Notice. The most important thing for the diet is the patient's self-awareness of his disease!

  • In case of cow's milk allergy, use cow's milk substitutes.
  • Caution! Deficiency symptoms due to iodine deficiency, bone decalcification, rickets, furthermore iron, vitamin and protein deficiency. Substitution may be necessary.
  • Remark. 20-30% of infants who are allergic to cow's milk are also allergic to soy milk!
  • The therapeutic effect of probiotics remains questionable according to recent findings.

External therapy
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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. Use only individually tested ointment bases, especially hydrophilic ointments, hydrophilic creams and hydrophilic emulsions. Hydrophobic o intments tend to be less well tolerated due to their occlusive effect! Consumption of cream/ointment see under fingertip unit

  • Glucocorticoids: The use of topical glucocorticoids under consideration of the benefit/side-effect profile is recommended in the guidelines. For acute exacerbation: Initial 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. In case of superinfection, antiseptic measures, e.g., dressings with octenidine (Octenisept).
  • Education about short-term steroid use is urgently needed. 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).
  • Pimecrolimus, Tacrolimus (calcineurin inhibitors): Tacrolimus (Protopic 0.03% for children and 0.1% for adults; Takrozem® 1 mg/g ointment 16 years and older) and pimecrolimus (e.g., Elidel or Douglan) can be used as cell-selective immunomodulators/suppressors. Indication: acute, especially subacute eczema. Therapy over a longer period is possible, but often not necessary. Several long-term studies in children and adults demonstrate significant efficacy (pimecrolimus) even after 6 and 12 months (no tachyphylaxis). Skin atrophy is not observed. Due to the galenics, Protopic is more suitable for the treatment of dry skin conditions, Elidel or Douglan can also be used for still weeping eczema. Effects: calcineurin inhibition; selective inhibition of T cells & mast cells; eosinophils. Under pimecrolimus, itching subsides significantly within the first three days of treatment; under 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. Caveat. Because of carcinogenicity of pimecrolimus in animal studies, calcineurin inhibitors can no longer be used safely, but only as second-line therapy in case of failure of other therapeutic options, since there are insufficient data on long-term effects in humans. Combinations with UV therapies as well as continuous therapies are also not recommended for the reasons mentioned above. Dosage: Elidel 2 times/day; Protopic 2 times/day within the first three weeks, then 1 time/day. Pay attention to light protection especially after application on the face. Caution. Treat possible infections (herpes, pyoderma)! Caution! After market introduction of the drugs, the occurrence of lymphoma 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 long-term safety of topical calcineurin inhibitors, see there). After healing of the acute episode, proactive therapy is recommended: 1-3 x / week continue to cream the healed skin with Pimecrolimus resp. Tacrolimus.
  • Ruxolitinib: So far, topical approaches with a 1.5% ruxolitinib cream have been experimentally successful (Gong X et al. 2021).
  • Polidocanol: Polidocanol is well tolerated and has anesthetic and antipruritic effects. Major clinical studies are not available for this indication.
  • Tannins: The effect of tannins is based on their astringent action. Both synthetic (tamol-containing) and natural tanning agents (e.g., tea compresses) are available for use appropriate to the stage.
  • Zinc: Zinc-containing externals have an anti-inflammatory and astringent effect with good tolerability and are widely used. Controlled studies are not available for this indication (and will not be available in the future).
  • Vegetable oil additives: Good success under 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 oily 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 urea-containing topical preparations may cause burning in highly inflamed skin.
  • Basic therapy, possible up to 12 years of age via health insurance prescription: SanaCutan basic cream (with 20% glycerine), Optiderm basic cream, Allergica basic cream, Linola fett
  • 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 inhibition of the enzyme phosphodiesterase-4, leading to an increase in cAMP and inhibition of inflammatory cytokines. Approved since 2020 from 3 months of life, dosage 2 x / day.
  • Experimental: Ruxolitinib (JAK inhibitor) shows promising results in 3 phase study in children from 12 years of age, dosage 2dd. Other JAK inhibitors in the pipeline are delgocitinib (already approved in Japan from age 16) and tofacitinib (currently testing positive in 2 phase trials).
  • Balneotherapy:
    • Bathing in cool, salty seawater with the skin surface intact is beneficial. Afterwards, shower off and apply cream. Water with added chlorine dries out strongly; in swimming pools there is a risk of infection with Molluscum contagiosum viruses (see also Molluscum contagiosum) and HPV viruses (see also Papillomaviruses, human).
    • Baths with added polidocanol (Balneum Hermal Plus). Severe itching crises can sometimes be intercepted with potassium permanganate baths (light pink). Caveat. Undiluted potassium permanganate is toxic and does not belong in children's hands.
  • Balneophototherapy (see below Radiation therapy)
  • Silver textiles:
    • The efficacy of silver-coated underwear (see also Silver textiles) in atopic eczema has been proven in various studies.

      Notice. Prescription at the expense of the GKV is mostly not possible!

  • In case of superinfection, quinolinol (e.g. quinosol 1:1000), R042 or potassium permanganate or octenidine can be used as supportive agents.
  • active probiotics with living bacteria to restore the balance of the skin microbiome (e.g. AktivaDerm®ND)

Radiation therapy
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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
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In acute extensive exacerbation, sub-/or erythroderma:

Chronic lichenified stage:

  • I.d.R., systemic therapy is not required. In cases of marked pruritus that cannot be controlled by external measures, antihistamines such as desloratadine (e.g., Aerius) 1-4 tbl/day or levocetirizine (e.g., Xusal) 1 film tbl/day may be given. If necessary, the dose can also be set much higher than required according to the manufacturer's instructions.

Severe atopic eczema that cannot be adequately treated topically:

  • Ciclosporin: (approved for atopic dermatitis from 16 years of age) Numerous studies have shown good therapeutic success with ciclosporin (5 mg/kg bw/day for the first 2 weeks). The efficacy of ciclosporin (2.5-5 mg/kg bw/day) in severe atopic dermatitis has been demonstrated several times based on studies with good evidence. Creatinine increase and arterial hypertension have been reported as major adverse drug reactions. Recurrence (or rebound) in severe atopic eczema should be expected 4-5 months after ciclosporin discontinuation. Ciclosporin A is suggested for the treatment of atopic eczema for a maximum of 2 years according to guidelines.
  • Dupilumab, trade name Dupixent ®: IL-4/13-R antibody (approved since 2017 for moderate to severe atopic eczema aged 12 years and older, or since December 2020 for children aged 6 to 11 years with severe atopic dermatitis). By blocking the IL-4 or IL-13 receptor, the initial response during the early phase of atopic inflammation (suppression of Th-2 dominant development) is blocked. The Federal Joint Committee sees an additional benefit under the endpoint categories quality of life, itching, sleep disturbances, patient-reported symptomatology and improvement of the EASI score, compared to standard therapy (consisting of: top. glucocorticoids, tacrolimus, ciclosporin). Adverse outcome was the development of ocular disease, including conjunctivitis. The additional benefit assessment and extension was based in part on data from the AD-1526, CHRONOS, LIBERTY AD PEDS study.
  • Baricitinib, trade name Olumiant®2 mg/4 mg Filmtbl.: Jak inhibitor, indication: treatment of moderate to severe atopic dermatitis, adults eligible for systemic therapy with indication. Dosage 4 mg / day, from the age of 75 years 2 mg / day, also in chronic infections 2 mg / day. Control: if no response after 8 weeks, discontinue therapy.

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

  • Alternative: Methotrexate can be used as an alternative to ciclosporin(off-label use). The folic acid antagonist has not been studied at all in placebo-controlled trials so far! The efficacy of MTX was confirmed in 2018 in a smaller study (Gerbens et al. 2018). An analogous good clinical effect could also be demonstrated for azathioprine .
  • Alternative: mycophenolate mofetil (off-label use): Several authors report good treatment success in severe and refractory atopic eczema with the drug mycophenolate mofetil.
  • Alternative: In a smaller multicenter study (n=167), good clinical effects were obtained 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 refractory cases. The clinical effects can be considered good. The data situation is still unsatisfactory.
  • Experimental:
    • Anti-interleukin-5 therapy: Previous studies on this form of therapy in atopic eczema with monoclonal antibodies were unsatisfactory.
    • Omalizumab: Casuistic successes have been reported with the human anti-IgE antibody omalizumab(off-label use; so far approved only for the indication bronchial asthma), which could not be confirmed in a randomized, placebo-controlled double-blind pilot study.
    • Nemolizumab: A humanized interleukin-31 receptor antibody (nemolizumab) targeting IL-31 receptors (see below Interleukin-31), including IL-31 receptors on neurons, was shown to significantly reduce itch and eczema severity with monthly administrations (Ruzicka T et al. (2017).
    • Experimental: other inerleukin antibodies are expected in the therapy of atopic dermatitis or there are already fully published studies: lebrikizumab, tralokinumab, fezakinumab, ustekinumab, baricitinib there are already fully published studies.

  • Experimental:
    • IVIG: The approaches to treat therapy-resistant atopic eczema with high-dose intravenous immunoglobulins (IVIG: doses 2.0/kgKG) must still be considered experimental. This is especially true for patients with severe atopic eczema in whom immunosuppressive therapy is not possible for various reasons. There are a number of studies on this subject in both adults and children dating back to 1996. Turner PJ and co-workers describe in a restrospective study of 10 children with severe therapy-resistant atopic eczema significant positive effects of IVIG therapy. Side effects were not observed. The treatment was administered once a month over a period of 1 year. At the same time, a previously necessary immunosuppressive therapy could be reduced. A research group was able to demonstrate a decrease in IgE levels in 50% of the patients. In a direct comparison in patients with severe atopic eczema between ciclosporin (4mg/kgKG) and IVIG (2g/kgKG) positive effects could be demonstrated in both groups with a superiority of ciclosporin. It is noted that both adults and children respond to IVG therapy, with a more pronounced positive effect in children than in adults. Of note is the statement that combination therapy works better than monotherapy in adults, whereas children are more likely to benefit from a monotherapeutic approach.
  • Outlook: further innovative therapeutic options for systemic treatment could bring compounds whose development is at different stages. A monoclonal antibody that specifically targets TH2 inflammation, dupilumab, is already approved for the treatment of atopic dermatitis (see above). There are already fully published studies on 7 other compounds for the treatment of atopic dermatitis: Lebrikizumab, Tralokinumab, Nemolizumab, Fezakinumab, Ustekinumab, Baricitinib and ZPL3893787.

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

Important: the disease can be significantly improved by therapeutic measures, but not cured! Promises of healing by miracle healers are charlatanism.

As a rule of thumb the third rule can be applied:

  • 1/3 loses the disease
  • 1/3 must reckon with the persistence of the disease
  • 1/3 must reckon with aggravations.

An improvement of the skin symptoms with increasing age is to be expected. 75% of patients with atopic eczema, show remissions at puberty. There is an increased susceptibility to viral, bacterial and mycotic infections due to impaired cellular immunity.

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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.).

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Naturopathic treatment is suitable in the subacute and chronic stages.

Order therapy: The adequate lifestyle is essential, avoidance of allergens, extreme stress situations, see also therapy in general.

Climatic therapy: Allergen-poor stimulating climate (high sea climate, high mountain climate), long-wave UVA 1 irradiation, baths with locally disinfecting, skin-soothing additives such as lavender oil, alleviate the skin irritation. Caution: rare allergic reaction to lavender, especially linalool. Due to the disinfecting effect of lavender oil also suitable in case of superinfection. 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 substance to the skin first.

Intestinal rehabilitation is becoming increasingly important in atopic eczema. Patients with atopic eczema tend to have a reduction of protective germs in the intestine, in particular enterococci. Frequently, especially after antibiotic therapies, Candida albicans overgrowth occurs and reactively triggers the atopic eczema. In addition to the reduction of Candida colonisation(Nystatin), the correction of the bacterial overgrowth should be carried out by means of symbiosis control after differentiation of the missing protective germ.

Locally, probiotic bacterial strains (bacterial complex Baplexin 621, which is
composedof lactobacilli, namely Lactobacillus gasseri, L. paracasei, L. plantarum, L. rhamnosus, L. reuteriL.
johnsonii, as well as bifidobacteria: Bifidobacterium lactis and B. longum, and streptococci: Streptococcus thermophilus)can be used.
Prebiotic ingredients inulin and maltodextrin are included with the bacteria, these are optimal nutrients for the probiotic bacterial strains.

Phytotherapy: Phytotherapeutically, especially the rational phytotherapeutics have proven to be effective, while the effect of some traditional plants could not be proven in studies.

Note: always test ointment compatibility! Caution: Wool wax alcohols

Traditional phytotherapy:

Dulcamaris (bittersweet stalk, Solanum dulcamara) from the nightshade family, positive monograph for supportive treatment of eczema, no confirmed 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 fortified wine). Extracts of the drug contain steroid saponins, which have steroid-like effects, tannins, and steroid alkaloid glycosides.

Hamamelis (witch hazel), positive Commission E/ESCOP monograph for use in skin lesions, mild inflammation, of skin and mucous membranes, haemorrhoids and varicose vein complaints
, in studies no superiority over placebo. Topically 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. To date no systematic studies in eczema, in prophylaxis of radiodermatitis superior to placebo. Topically as ointment (e.g. Calendumed ointment) or essence for the preparation of baths and compresses. Caution: Allergic potency, daisy!

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

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 smaller positive application study is available on Tormentillae rhizoma (2% ) in a good spreadable oil/w base (Hoffmann 2015).

Ice Plant Ointment: A positive application study is available on a paraffin-based base care with the juice of the "edible ice plant (see below Mesembryanthemum edule)". The atopic children treated in this way had a significantly increased hydration of the str. corneum and a lower transpepidermal water loss after 16 weeks (Schario 2014).

Seed Oats (Medicinal Plant of the Year 2017): Extracts of oat herb (containing 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, shows antibacterial, antipruritic, anti-inflammatory, wound-healing and antitumor activity. In local application 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 significant reduction of transepidermal water loss (Laszczyk 2009).

Hypericum (St. John's wort): A positive, randomized, placebo-controlled study 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 fungus of the larkspur family) have antieczematous effects 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 in cases of atopic eczema.

Liquiritiae radix (liquorice root) the 1% and 2% gel shows significant improvement of erythema, oedema and pruritus (improvement of 80%) in a double-blind placebo-controlled study. Trade name: Atopiclair, applicable from 6 months of age (Abramovits 2006).

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

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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!

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  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
  2. of mld to moderate atopic dermatitis in adults. J Drugs Dermatol 5: 236-244
  3. Ambros-Rudolph CM (2006) Dermatoses of pregnancy. J Dtsch Dermatol Ges 4: 748-759
  4. 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
  5. Brenninkmeijer EE et al (2007) Clinical differences between atopic and atopiform dermatitis. J Am Acad Dermatol 58: 407-414
  6. Brüggen M-C et al (2016) Antigen or allergen presentation. In: T. Biedermann et al (eds) Allergology. Springer-Verlag Berlin-Heidelberg p 63
  7. 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
  8. Bussmann C et al (2009) What are the systemic therapeutic options in severe forms of atopic dermatitis. JDDG 7: 205-221
  9. Capello C et al (2017) Studies of the protective effect of a basic therapy with multiple protection against ds penetration of aero-allergens into the skin of atopic dermatitis. Allergo J Int 26: 70
  10. Charman CR et al (2002) Reliability testing of the Six Area, Six Sign Atopic Dermatitis severity score. Br J Dermatol 146: 1057-1060.
  11. 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.
  12. 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.
  13. Griffiths CE (2006) Update on the use of ciclosporin in immune-mediated dermatoses. Br J Dermatol 155: 1-16
  14. 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
  15. 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.
  16. 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.
  17. 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
  18. 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.
  19. 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
  20. 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
  21. Igaawa K et al.(2007) Odontogenic focal infection could be partly involved in the pathogenesis of atopic dermatitis as an exacerbation factor. Int J Dermatol 46: 376-379
  22. 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
  23. Kalliomäki M et al. (2001) Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet 357: 1076-1079
  24. Landeck L et al (2011) Contact sensitization pattern in 172 atopic subjects. Int J Dermatol 50:806-810
  25. Lane JE et al (2005) Treatment of recalcitrant atopic dermatitis with omalizumab. J Am Acad Dermatol 54: 68-72
  26. Laszczyk MN et al (2009) Regenerative and anti-inflammatory effects of betulin emulsions in impaired epidermal barrier function. Act Dermatol 35: 1-5
  27. Nakatsuji T et al (2016) Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression.J Invest Dermatol 136:2192-2200.
  28. Niebuhr M et al (2011) Contact allergy and atopy. Dermatologist 62: 744-750
  29. Novak N et al.(2011) Specific immunotherapy and atopic dermatitis. Dermatologist 62: 650-656
  30. 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
  31. 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
  32. 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.
  33. 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.
  34. Proksch E et al.(2016) Epidermal barrier disruption in dermatoses. Dermatologist 67: 907-921
  35. 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
  36. 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
  37. Roduit C et al (2017) Phenotypes of Atopic Dermatitis Depending on the Timing of Onset and Progression in Childhood. JAMA Pediatr 171:655-662.
  38. Ruzicka T et al (2017) Anti-Interleukin-31 Receptor A Antibody for Atopic Dermatitis. N Engl J Med 376:826-835.
  39. Sand M et al (2007) Extracorporal photopheresis as a treatment for patients with severe refractory atopic dermatitis. Dermatology 215: 134-138
  40. Schario M et al.(2014) Children with dry skin and atopic predisposition: daily use of emollients in a
  41. participant-blinded, randomized, prospective trial. Skin Pharmacol Physiol 27:208.
  42. Schmitt J (2018) Increased attention-deficit/hyperactivity symptoms in atopic dermatitis are
  43. associated with history of antihistamine use. Allergy 73: 615-626.
  44. Schram ME (2011) A randomized trial of methotrexate versus azathioprine for severe atopic eczema. J Allergy Clin Immunol 128:353-359
  45. 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
  46. 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.
  47. Tam HH et al. (2016) Specific allergen immunotherapy for the treatment of atopic eczema: a Cochrane
  48. systematic review. Allergy 71:1345-1356.
  49. Torres T et al (2019) Update on atopic dermatitis. Acta Med Port 32:606-613.
  50. Turati F et al. (2016) Early weaning is beneficial to prevent atopic dermatitis occurrence in young
  51. children. Allergy 71:878-888
  52. 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
  53. 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
  54. Werfel T et al (2016) S2k guideline neurodermatitis (atopic eczema, atopic dermatitis) - abridged version. Allergo J 25: 36-49
  55. 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.
  56. Wopereis H et al. (2018) Intestinal microbiota in infants at high risk for allergy: effects of prebiotics
  57. and role in eczema development. J Allergy Clin Immunol 141:1334-1342
  58. Willan R (1808) On Cutaneous Diseases. Johnson, London
  59. Yagis S et al (2004) Presence of staphylococcal exfoliative toxin A in sera of patients with atopic dermatitis. Clin Exper Allergy 34: 984-993
  60. Yazdi AS (2012) Genetic risk of atopic dermatitis. Dermatologist 63: 161-163


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