Atopic dermatitis (overview) L20.-

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

Co-Autors: Jeton Luzha, Hadrian Tran

Our authors

Last updated on: 29.10.2020

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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
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Willan, 1808

Definition
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Multifactorial, chronically persistent or chronically recurring non-contact dermatitis of varying acuteity, which belongs to the group of atopic diseases (Greek atopos = out of place), usually clearly itching, which develops, is maintained or activated due to complex interactions of plant and environmental factors.

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

  • diffuse eczematous skin appearancesin infancy rather uncharacteristically diffuse eczematous skin appearances on the face and on the extensor sides of the extremities of varying severity and acuteity (see atopic eczema in infancy)
  • eczemain infants is more localised and less diffuse, with variable and seasonal course (see atopic eczema in children)
  • in schoolchildren preferably occurring as flexural eczema
  • in adulthood there is a great morphological diversity. Localized minus variants of atopic eczema (eyelids, genitals, hands, neck) as well as large-area eczema variants up to eczema that affects the entire integument (erythrodermal atopic eczema) characterize the extremely diverse clinical picture.

Classification
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Atopic eczema shows different disease symptoms in the different phases of life.

An alternative classification distinguishes 4 phenotypes in children (study in 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. Early persistent phen otype (6.5%): HV within the first 2 LJ, healing by the 6th LJ. High risk of developing asthma. High risk of developing food allergies.
  3. Later phen otype (4,8%): HV only after the 2nd LJ. High risk of allergic rhinitis.
  4. Sporadic phenotype (79,5%): only sporadic or missing 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 may also be triggered by other factors (e.g. contact allergies).

Occurrence/Epidemiology
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  • Prevalence in industrialised 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 LJ.
  • The prevalence has almost tripled in industrialised countries over the last 3 decades.
  • In addition, about 40-60% of patients with atopic eczema suffer from respiratory allergies (pollinosis, perennial rhinitis, allergic bronchial asthma)

Etiopathogenesis
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From an etiopathogenetic and practical clinical point of view, one can distinguish 2 forms with largely identical skin symptoms:

  • intrinsic (non-allergic) atopic eczema (about 20-30% of patients; not IgE-mediated). At present it is still unclear whether this clinical picture can be evaluated as a separate entity.
  • Extrinsic (allergic) atopic eczema (60-70% of patients, IgE-mediated).
  • Notice! Patients with intrinsic form do not show elevated IgE levels or sensitization to environmental or food allergens.

Immunological pathogenesis: The initial inflammation of atopic eczema is seen in a Th2 directed immune response. In this context, disturbances of cytokine production play a central role in the pathogenesis, especially an increased expression of IL-4, IL-5, IL-10, IL-13 (see belowinterleukins). This causes an induction of IgE in B-lymphocytes. During the acute phase, high amounts of the chemotactically active cytokines interleukin-16, eotaxin, macrophage-derived-chemokine (MDC), thymus and activation regulated chemokine (TARC), regulated on activation, normal T-cell expressed and secreted(RANTES) as well as the soluble CD30 can be detected in the blood (see below chemokines). An association with functionally relevant gene polymorphisms of the genes for IL-3, TGF-beta1, IL-13 and RANTES is suspected. The thymic stromal lymphopoietin (TSLP) is also attributed an important role in inflammatory skin diseases. TSLP is believed to act via activation of dendritic cells to proliferate naïve CD4-positive T cells and T memory cells. Furthermore, TSLP induces activation of innate lymphoid cells (ILCs) and macrophages, which produce chemokines that attract eosinophil and neutrophil granulocytes and mast cells.

Immune response in atopic skin: Clinically inconspicuous skin in patients with atopic eczema is not considered to be healthy despite the absence of symptoms. Increased skin dryness, a barrier disorder with increased irritability, discreet perivascular T-cell infiltrates, increased number of Th2 cells with increased IL-4 and IL-13 production can be detected.

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 recognised and absorbed by Langerhans cells. The antigen-presenting cells(Langerhans cells, inflammatory dendritic cells and macrophages with IgE molecules) are elevated. Langerhans cells enter the draining lymph nodes with the lymph flow, reducing their dendritic offshoots during this passage (so-called veiled cells - see below Langerhans cell). In the lymph node they present the antigen naive lymphocytes and induce a Th2 response.

There is an increased expression of IL-16, C-C chemokine ligand 27, RANTES, monocyte chemotactic protein-4 and eotaxin. Activation of eosinophilic leukocytes and macrophages. The 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 are also expressed. Interleukin-22 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 lead to changes in the vascular endothelia via activation of NF-κB with subsequent extravasation of proinflammatory cytokines.

Genetic factors play an important role in the predisposition of atopic eczema. The risk of a child suffering from atopic eczema (AE) is 50% if one parent suffers from asthma, atopic eczema or allergic rhinitis, 75% if both parents are affected. The concordance in monozygotic twins is 72%, in dizygotic twins 23%. Genome studies revealed several atopic predisposing loci on chromosomes 1q21, 3q21, 5q32, 6, 11q13, 17q25 and 20p. Some regions correspond closely with the found gene loci for psoriasis (3q21), an indication that these genes have a general influence on "skin inflammation". Chronic inflammatory bowel diseases are found on very similar gene loci. Further SNP`s (single-nuclide polymorphisms - see pharmacogenetics below) were found in a larger study on OVOL1 transcriptional repressor, which plays a role in epithelial differentiation), ADAMST10 (a disintegrin and metalloproteinase with thrombospondin motifs) and KIF3A (kinesin like protein 3A).

Disturbance of the skin barrier: Disturbances in the filaggrin structure play an important role in the reduction of epidermal integrity. Polymorphisms and loss-of-function mutations in the profile aggrin/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 which cross-links the disulfide bridges between the keratinocytes in the skin barrier and thus has a strengthening function. Due to a mutation this function can no longer be guaranteed and the skin is more susceptible to mechanical irritations. The itch-scratch-cycle ensures the mechanical disruption of the barrier and maintains the cytokine-mediated inflammatory and itching reaction. Filaggrin mutated patients with AE have a significantly higher susceptibility to allergic bronchial asthma and ichthyosis vulgaris than those without this mutation. Possibly, the proven increased expression of aquaporin-3 in the keratinocytes of atopic patients also plays an important role in the disturbed skin barrier function.

The allergens relevant for the atopic syndrome are grass pollen, house dust mites and animal hairs. As these proteins have a high molecular weight, they cannot penetrate normal skin (only proteins < 1000 Dalton can do this). In atopic skin, however, molecules with a higher molecular weight may also penetrate due to the barrier disorder. There they are absorbed by dendritic cells. Concordant to this are clinical observations which prove an exacerbation of the atopical eczema after local provocation with grass pollen. Also the local exposure with cat epithelia leads to an increased tendency to eczema in filaggrin-mutated newborns (!). The fact that these are not only specific (local) reactions in the presence of sensitisation is shown by the observation that birch pollen can induce eczema reactions, even in non-birch pollen-sensitised babies. For this purpose, other mechanisms are veratowrtlich such as pollen-associated lipid mediators (PALMS) which also stimulate an inflammatory reaction in a non-specific way. Airborne particles may also penetrate the atopic skin.

Sensitisation:

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

Microbial factors: Staph. aureus is of pathophysiological relevance (high colonisation 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 therefore T-cell proliferative; against which Pat. aureus also produces IgE antibodies, whereby the degree of sensitization and disease activity correlate. A disorder 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 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 thus directly lead to an increase in inflammatory cytokines.

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

Furthermore, there are indications that apparently also focal infections (such as dental infections) are involved in triggering or exacerbation of the atopical eczema. This is surprising in that such influences have not been assumed so far!

Hygiene hypothesis: It is assumed that the increase in atopic eczema is associated with a higher standard of living and 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 favour of the Th2 responses characteristic for atopic diseases.

Farm animals as risk factors? Remarkable is a study in 5 European countries on 1063 children, in which it could be proven 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 play a role here, but also apparently non-microbial substances such as N-glycolylneuraminic acid (Neu5Gc), a sensitising sialic acid produced by animals, whose degree of sensitisation is 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 peptides (CGRP), proopiomelanocortin-derived-hormones (alpha-MSH) act as anti-inflammatory regulators.

Various triggers:

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

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

Late manifestations in adulthood are possible.

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

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

Childhood, adolescence: elbows, hollow of the knee (sweet itch).

Adulthood: elbows, knees, face, chest, shoulders, back of the hands.

Described as minus variants in different localisations (see above).

Clinical features
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Depending on the age of the patient and the acuteity of the disease, different stages and manifestations of eczema can be observed, ranging from weeping red plaques to pale, dry, possibly scaly, bran-like, mostly scratched skin.

Typical is a seizure-like, tormenting itching, which increases with sweating (especially stress sweating). Furthermore a wool intolerance. The clinical symptoms of atopic eczema vary considerably depending on age. In this respect, clinical subdivisions by age are useful.

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

I. Major criteria:

  1. Itching (intense, unsuppressible itching that is answered with bloody scratching (not rubbing but scratching with the fingernails)
  2. Eczema plaques (on the stretching side in infants and toddlers, on the flexing side in post-pubertal adolescents and adults)
  3. Chronicity (long-term, chronic or chronically recurrent course)
  4. Medical history (positive atopic signs of disease in EA and/or FA - e.g. rhintis allergica, allergic bronchial asthma)

II Minor criteria or optional symptoms:

  1. milkcrust (Crusta lactea)
  2. Xerosis cutis (general sebostasis of the skin, skin feels dry and brittle)
  3. Ichthyosis hand, foot ("I-hand"; hyperlinear pattern of the unusually cotton wool-like soft palms and soles)
  4. Dennie Morgan infraorbital fold (double eyelid crease; Grd 1 to the pupil, Grd 2 including the entire iris, Grd 3 entire eye)
  5. Earlobe rhagade (the so-called stubbornly torn earlobe)
  6. Atopic facial pallor (pale, grey-white facial colour; the halonated dark eyes also belong to the special atopic facial colouring)
  7. Dermographism albus
  8. keratosis pilaris
  9. Hertogesches sign (Rarefication of the lateral eyebrows)
  10. Fur cap-like hairline (the adult atopic patient very rarely suffers from androgenetic alopecia!)
  • Other associated atopy signs:
    • Intolerance to (animal) wool (not cotton)
    • Food intolerances (citrus fruits, strawberries, tomatoes = unspecified histamine liberators which cause itching shortly after ingestion)
    • itching through sweating
    • IgE increased (only for extrinsic type)
    • Positive prick or intradermal test (only for extrinsic type)
    • Detection of specific IgE (only for extrinsic type
      )Perlèche
    • Shiny nail (like polished looking fingernails).
    • Dermopathic lymphadenopathy with generalized infestation

Laboratory
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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).

Histology
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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.

Diagnosis
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  • Clinical picture, family history, personal history (history of eczema, rhinitis allergica, bronchial asthma, food allergies, viral and bacterial infections)
  • Allergy score - varies according to Diepgen - (if atopy is suspected)
    1. White dermographism (line test on the skin turns white)
    2. Hertoghe-signs (thin, light outer eyebrows)
    3. Dennie-Morgan fold (transverse fold (or two) parallel to the lower eyelid)
    4. Pityriasis alba (dry, finely scaled light spots)
    5. Eczema herd
    6. Palmare Hyperlinearity
    7. Pulpitis sicca (dry eczematous fingers/toes)
    8. Dyshidrosis (hands/feet)
    9. Pearl (torn corner of the mouth)
    10. Earrhagades (torn earlobes)

Orientation prick test and intradermal test

  • Extrinsic shape
    • 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
    • Exhaust diet and search diet ( food allergy, food intolerance)
    • Epicutaneous test for the question of contact sensitization (higher rate of contact allergies to topical agents, external ingredients, rubber materials, fragrance mix)

Differential diagnosis
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Complication(s)
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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 in humidity, optimal ventilation of rooms. Due to the reduced alkaline neutralization capacity, the use of soaps, detergents and dishwashing liquids should be reduced to a minimum. Recommended are moisturizing wash lotions (Eucerin 5% Urea wash lotion, Atopicontrol shower and bath oil, Lipoderm shower gel, Cetaphil wash lotion).

Sweating: The reduced sweating leads to heat accumulation and itching crises due to high outside temperatures during physical exertion, but also in stress situations.

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

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

skin cleansing:

  • No commercial 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 excellently suited.
  • As an alternative to bath oils, an O/W emulsion or hydrophilic oils can also be used for cleansing. In case of 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 the skin tolerance.

Career choice: Unsuitable are professions with intensive contact with water, detergents, oils, fats, drilling water, disinfectants, adhesives, leather, chemical products, animals, flour and dust. Dry, clean professions are recommended. Cave! Spread of moulds 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 on their skin pleasant and hardly irritating, cooling. With this clientele the danger of a "silk protein dermatitis" can be expected. Sericin is considered the main allergen. The solution for this problem situation are sericin-free silk materials which are proven to be suitable for atopic persons (Koller DY et al. 2007) are to be preferred.

Avoid animal materials (wool, furs), uneven rough fabrics, but also materials made of breathable synthetic fibres. Silver-coated textiles (e.g. Padycare) seem to have an inhibiting influence on the staphylococcus colonization of the atopic skin.

Pollen sensitization: The skin reacts to pollen with eczema (type IV reaction). It is advisable to attach pollen protection filters (Tesa Protect) to the windows. Apply a protective cream before leaving the living quarters, shower on return.

House dust mite allergy (see also mite allergens): Avoid dust traps (carpets, curtains, soft toys, etc.), encasing with special mite-repellent covers (recommended e.g. Allergocover). When travelling, 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 sensitizations, the implementation of an SIT is controversially discussed in the literature with regard to its effectiveness. It is also discussed whether SIT contributes to the improvement of atopic eczema. For this purpose, 26 robust randomized studies were evaluated worldwide, in which no usable benefit for atopic eczema could be proven compared to control collectives (Tam 2016). SIT is not approved for atopic eczema (without allergic asthma or rhinitis).

Sports: According to physical fitness, avoidance of extreme sweating, followed by showering with moisturising shower gels.

Sauna: According to personal tolerance, avoid extreme temperatures.

Climatotherapy: The most effective and least side-effect measure to improve the symptoms of the disease, especially in the high seas (e.g. Borkum, Norderney or Sylt) or in the high mountains (altitudes above 1500 m, e.g. Davos), especially in spring and autumn. Recommended minimum duration: 4 weeks. Application to the health or pension insurance companies.

Nutrition: flat-rate diets are to be condemned. Avoid allergologically relevant allergens after appropriate testing (rubbing, pricking and resting test), outlet and provocation diet. Check the relevance of the test results every 2 years.

Notice! The most important aspect of nutrition is the patient's self-awareness of his or her illness!

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

External therapy
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Treatment of eczema according to its stage, see below Eczema. For milder forms with circumscribed foci, external therapy is usually sufficient. In severe forms, it should be used in addition to the internal therapy. Only use individually tested ointment bases, especially hydrophilic ointments, hydrophilic creams and hydrophilic emulsions. Due to their occlusive effect hydrophobic ointments are rather less tolerated!

  • 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 solution. In case of superinfection, antiseptic measures, e.g. compresses with octenidine (Octenisept).
  • Information on short-term use of the steroids is urgently required. Recent studies suggest that patients with severe acute stage skin lesions benefit more from topical combination therapy (steroids with antibiotics) than from monotherapy (steroids).
  • Pimecrolimus, Tacrolimus (calcineurin inhibitors): As cell-selectively acting immune modulators/suppressors Tacrolimus (protopic 0,03% for children and 0,1% for adults) and Pimecrolimus (e.g. Elidel or Douglan) can be applied. Indication: acute, especially subacute eczema. Therapy over a longer period of time is possible, but often not necessary. Several long-term studies with children and adults prove the significant effectiveness (Pimecrolimus) also after 6 and 12 months (no tachyphylaxis). Skin atrophies are not observed.
  • Due to the galenics, Protopic is more suitable for the treatment of dry skin conditions, Elidel or Douglan can also be used in case of still weeping eczema. Effects: Calcineurin inhibition; selective inhibition of T cells and mast cells; eosinophils. Under Pimecrolimus the itching clearly decreases within the first three days of treatment, under Tacrolimus a slight irritation of the skin may occur during the first two days of treatment. Pimecrolimus and Tacrolimus are admitted from the age of 2 years. Caution! Because of the carcinogenicity of Pimecrolimus in animal experiments, calcineurin inhibitors cannot be used without risk anymore, but only as a second-line therapy in case of failure of other therapy options, because there are not sufficient data about long-term effects in humans. Combinations with UV-therapies as well as long-term therapies are also not recommended for the reasons mentioned above. Dosage: Elidel 2 times/day; Protopic within the first three weeks 2 times/day, afterwards 1 time / day. Pay attention to light protection, especially after use on the face. Caution! Treat any infections that may occur (herpes, pyoderma)! Cave! After the market launch of the drugs, the occurrence of lymphomas was observed in patients who were treated topically with calcineurin inhibitors and steroids. In a study with more than 290,000 cases, however, this could not be confirmed (for the long-term safety of topical calcineurin inhibitors see there).
  • Polidocanol: Polidocanol is well tolerated and has an anaesthetic and anti-pruritic effect. Larger clinical studies are not available for this indication.
  • Tanning agents: The effect of tanning agents is based on their astringent action. Both synthetic tanning agents (containing tamol) and natural tanning agents (e.g. tea envelopes) are available in the appropriate stages of application.
  • Zinc: Zinc-containing external agents have an anti-inflammatory and astringent effect with good tolerance and are widely used. Controlled studies are not available for this indication (they will not be available in the future).
  • Vegetable oil additives: Good results under 15-20% evening primrose oil creams(e.g. Eucerin 12% Omega, Lipoderm Omega, Linola gamma, R177 ).
  • Urea: Application of hydrating additives like 2-10% urea (e.g. R102 R104 R113, Basodexan fat 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 topicals may cause a burning sensation in highly inflammatory skin.
  • Basic therapy, available until the age of 12 years via cash prescription: SanaCutan Base Cream (with 20% glycerin), Optiderm Base Cream, Allergica Base Cream, Linola fat
  • Experimental: Crisaborol, a phosphodiesterase 4 inhibitor, tested positive in a 2% ointment form in 2 phase III studies. The effect is based on an inhibition of the enzyme phosphodiesterase-4, which leads to an increase in cAMP and to an inhibition of inflammatory cytokines.
  • Balneotherapy:
    • Bathing in cool, salty seawater is beneficial if the skin surface is intact. Then rinse 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 below Molluscum contagiosum) and HPV viruses (see below Papilloma viruses, human).
    • Baths with Polidocanol addition (Balneum Hermal Plus). Severe itching crises can sometimes be intercepted with potassium permanganate baths (light pink). Cave! 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 below silver textiles) in atopic eczema has been proven in various studies.

      Notice!

      The prescription at the expense of the GKV is usually not possible!
  • In case of superinfection, quinolinol (e.g. Chinosol 1:1000), R042 or potassium permanganate or octenidine can be used as a supporting agent.

Radiation therapy
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Phototherapy (UV-Therapy):
  • UVA/UVB (see below UV rays) combinations or low-dose UVA1 therapy have proven to be effective, in the case of exacerbations also in higher doses.
  • Photosol therapy (hypertonic salt baths plus UVB). Cave! Possible danger of photoaggravated atopic eczema!
  • Photosoletherapy 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 resistance to therapy, treatment with PUVA Bath Therapy or PUVA Therapy, systemic.
  • Narrowband UVB: According to a Brazilian study, narrowband UVB therapy is said to significantly reduce Staphylococcus aureus colonization on exacerbated skin.

Internal therapy
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For acute large-scale exacerbation, sub and/or erythroderma:

  • Short-term glucocorticoids 100-150 mg prednisolone equivalent(e.g. Solu Decortin H) and antihistamines such as dimetinden (e.g. Fenistil 0.1 ml/kg bw/day) i.v., if necessary fluid and protein balancing. Rapid reduction of the steroid 75-50-25-15 mg/day and then reduce or discontinue in steps of 5 every 2nd day.

Chronic lichenified stage:

  • Usually no systemic therapy is required. If the itching is severe and 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. The dose may also be set much higher than required by the manufacturer.

Severe atopic eczema which cannot be treated adequately topically:

  • Ciclosporin: 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 by studies with good evidence based. The main adverse drug reactions reported were creatinine increase and arterial hypertension. It must be expected that in severe atopic eczema a relapse (or rebound) occurs 4-5 months after discontinuation of the Ciclosporin. Ciclosporin A is proposed according to the guidelines for the treatment of atopic eczema for a maximum period of 2 years.
  • Alternative: Methotrexate can be used as an alternative to Ciclosporin(off-label use). The folic acid antagonist has not yet been investigated at all in placebo-controlled studies! The effectiveness of MTX was confirmed in a smaller study in 2018 (Gerbens et al. 2018). An analogously good clinical effect could also be proven for azathioprine .
  • Alternative: Mycophenolatmofetil (Off-Label-Use): Several authors report good treatment success with the preparation Mycophenolatmofetil in severe and therapy-resistant atopic eczema.
  • Alternative: Dupilumab: IL-4/13-R antibody (approved since September 2017 for moderate to severe atopic eczema) By blocking the IL-4 or IL-13 receptor, the initial reaction is blocked during the early phase of atopic inflammation (suppression of a Th-2-dominant development). Dupilumab, an IL-4/13-R antibody that has already been shown to be effective in allergic bronchial asthma, has been the subject of several clinical phase II studies and 2 phase III studies (n=1379 Pat.) in atopic eczema with good results. In the phase III studies, at least 75% improvement (pacebo 14%) in the EASI score was achieved in slightly more than half of the patients.
  • Alternative: Extracorporeal photopheresis: This treatment option is reserved for severe, otherwise refractory 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 in atopic eczema with monoclonal antibodies were unsatisfactory.
    • Omalizumab: Casuistic success has 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.
    • Nemolizumab: With a humanized interleukin-31 receptor antibody (nemolizumab), which is applied to IL-31 receptors (see below interleukin-31), including IL-31 receptors on neurons, a significant reduction of itching and eczema severity could be achieved by monthly administration (Ruzicka T et al. (2017).
    • Experimental: further 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 treat refractory atopic eczema with high-dose intravenous immunoglobulins (IVIG: dosages 2.0/kgKG) must be considered experimental. This is especially true for patients with severe atopic eczema where immunosuppressive therapy is not possible for various reasons. There is a series of studies on this subject in adults and children dating back to 1996. Turner PJ and collaborators describe in a restrospective study in 10 children with severe therapy-resistant atopic eczema the clear positive effects of IVIG therapy. No side effects were observed. The treatment was administered once a month for a period of 1 year. At the same time a previously necessary immunosuppressive therapy was reduced. A working group was able to demonstrate a decrease in IgE levels in 50% of the patients. In a direct comparison of patients with severe atopic eczema between Ciclosporin (4mg/kgkgKG) and IVIG (2g/kgKG) positive effects could be demonstrated in both groups with a superiority of Ciclosporin. It should be noted that both adults and children respond to IVG therapy, with the positive effect being more pronounced in children than in adults. Remarkable is the statement that in adults a combination therapy works better than a monotherapy, whereas children are more likely to benefit from a monotherapeutic approach.
  • Outlook: further innovative therapeutic options for systemic treatment could lead to substances at different stages of development. A monoclonal antibody that specifically targets TH2 inflammation, Dupilumab, is already approved for the treatment of neurodermatitis (see above). There are already fully published studies on 7 further substances for the treatment of neurodermatitis: lebrikizumab, tralokinumab, nemolizumab, fezakinumab, ustekinumab, baricitinib and ZPL3893787.

Progression/forecast
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Due to the high clinical variability, it is not possible to make an individual prediction about the course of the disease pattern. A chronic, intermittent course with relapses of varying duration and severity is to be expected.

Important: the disease can be significantly improved by therapeutic measures but not cured! Healing promises of miracle healers are charlatanry.

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

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

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

Prophylaxis
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Preventive measures for known atopic diathesis:

  • Breastfeeding (previously accepted position): Infants over 6 months of age should be fully breastfed and then fed. The procedure "Breast is best! According to various meta-analyses, the procedure "Breast is best!" should result in a 30% significant risk reduction! These results are now called into question by the results of a large Canadian study (final evaluation in 11,000 children), which found a higher sensitisation rate in the breastfed children than in the control group. Also for the allergic bronchial asthma no risk reduction could be proven in a larger study (n=335). An Italian study comes to similar results.
  • Supplementary food: For years it was recommended to include potent food allergens as late as possible in the infant diet. This can no longer be deduced from the relevant studies on this subject. Rather, the delayed introduction of complementary foods seems to increase the risk of later sensitisation to aero- and food allergens at the age of 5 years.
  • Maternal diet during lactation: The evidence base is relatively weak. Avoiding potent allergens (milk, egg, fish, nut, wheat, soya) seems to have a beneficial effect on eczema prevention.
  • Food supplements ( probiotics ): The preventive effect of probiotics is controversially discussed and completely negated by several working groups due to the insufficient number of studies. The following hypothesis is put forward by supporters: The intestines of allergy sufferers seem to show a low colonisation by lactobacilli. The addition of LGG (Lactobacillus Goldin and Gorbach = Lactobacillus rhamnosus GG) should lead to a significant reduction (68%) of the atopy rate in children at risk. Therapeutic approach: In the last two months of pregnancy, the mother takes 2 cps LGG daily. The infant receives one capsule daily for at least 2 years. In a Dutch study with 138 children using hydrolysed protein formulations with indigestible oligosacchrides, a formulation of intestinal flora comparable to that of breastfed children was found (Wopereis H et al. 2018).
  • Vitamin D (high-dose): A high-dose supplementation of vitamin D (4,400 IU/day compared to the current 400 IU/day recommendation) resulted in a randomized study of immune modulation in newborns that may provide protection against wheezing and bronchial asthma (Hornsby E et al. 2018).
  • Household pets: Individual epidemiological studies have shown a significant association between the keeping of small rodents (rabbits, guinea pigs) and the prevalence of atopic eczema. The keeping of these animals (including cats) should be avoided in children at risk. There are no restrictive recommendations regarding the keeping of dogs. If sensitisation and clinical symptoms ( rhinitis/conjunctivitis/asthma) have occurred, direct contact, including through contact persons, should be avoided.
  • Smoking: Do not smoke at home! In children whose mothers smoked during pregnancy, atopic stigmas occur significantly more frequently (52.2% in the verum group vs. 37.7% in the control group). Maternal smoking doubles the risk of developing atopic eczema.
  • Mould (see mould diseases below): Renovate living spaces from mould! Moisture and mould indoors seems to be associated with an increased risk of eczema!
  • House dust mites: For children at risk, the exposure to house dust mites should be as low as possible:
    • Remove dust traps from the living rooms and bedrooms.
    • Keep bedrooms cool and clean. Do not lay carpeting but prefer smooth, damp wipeable surfaces.
    • Toys: Prefer washable toys (e.g. washable soft toys).
    • Bedding: Use washable bed material, remove bed springs. Ventilate and clean mattresses frequently. The mite-proof mattress cover (see encasing below) is an effective measure to minimize mites in bedrooms. Alternatively, bedding made of microfibre can be used.

Occupations to be avoided in case of atopic dermatitis (see below occupational dermatoses):

  • Hairdresser, nursing professions, photographer, painter, machining professions (lathe operator/milling cutter), craft professions in the metal and car industry, carpenter, bricklayer professions, working underground (miner), employment in leather tanning and processing, baker, confectioner, cook (food professions), professions with permanent wet work (room attendant; window cleaner etc.).

Naturopathy
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Naturopathic treatment is suitable in the subacute and chronic stages.

Order therapy: Essential is an adequate lifestyle, avoidance of allergens, extreme stress situations, see also general therapy

Climatotherapy: Low-allergen stimulating climate (ocean climate, high mountain climate), long-wave UVA 1 irradiation, baths with locally disinfecting, skin-soothing additives such as lavender oil, soothe skin irritation. Cave: rarely allergic reaction to lavender, especially linalool. Due to the disinfecting effect of lavender oil, also suitable for superinfection. In the acute stage of eczema, cool moist compresses with black tea or oak bark extract (see tanning agents below) alleviate itching and inflammation. To prevent the skin from drying out, always apply the active substance-containing cream or skin care cream to the skin first.

Intestinal cleansing is becoming increasingly important in atopic eczema. Patients with atopic eczema tend to have a reduced tendency to the protective germs in the intestine, in particular the enterococci. Frequently, especially after antibiotic therapy, an overgrowth of Candida albicans occurs and reacts to trigger atopic eczema. In addition to the reduction of Candida colonisation(Nystatin), the correction of the bacterial false colonisation should be carried out by symbiosis control after differentiation of the missing protective germ.

Phytotherapy: Phytotherapeutically, rational phytotherapeutics in particular have proved their worth, whereas the effect of some traditional plants could not be proven in studies.

Remember! Always test ointment compatibility! Cave: Wool wax alcohols

Traditional Phytotherapy:

Dulcamaris (bitter-sweet stem, Solanum dulcamara) from the nightshade family, positive monograph for the 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 liqueur wine). The extracts of the drug contain steroid saponins, which have steroid-like effects, tannins and steroid alkaloid glycosides.

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

Calendula(marigold), composite plant, positive monograph of the Commission E/ESCOP for use in inflammatory changes of the mucous membranes of the mouth and throat, poorly healing wounds, ulcus cruris. So far no systematic studies on eczema, in the prophylaxis of radiodermatitis superior to placebo. Locally as ointment (e.g. Calendumed ointment) or essence for the production of baths and compresses. Cave: Allergenic potency, composite!

Evening primrose oil: Seeds of the Oenothera biennis (common evening primrose; see below evening primrose oil), which consists of 60-80% linoleic acid and 8-14% gamma-linolenic acid, an omega-6 fatty acid. Recognized by the WHO for the indication atopic eczema, diabetic neuropathy, mastodynia. Efficacy not sufficiently proven in studies to date. Locally as cream (e.g. Eucerin Omega®, Allergic 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 small positive application study is available for Tormentillae rhizoma (2% ) in a well spreadable Ö/W base (Hoffmann 2015).

Ice Plant Ointment: A positive application study is available on a paraffin-based basic care with the juice of the edible ice plant (see Mesembryanthemum edule below)". 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 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, has an antibacterial, anti-itching, anti-inflammatory, wound healing and anti-tumour effect. When applied locally as a cream (Imlan® cream pure 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, half-side comparative study is available for atopic eczema with a 1.5% cream application (Schempp 2003) with significant superiority over placebo. Local application (e.g. Bedan® cream), approved from 6 months of age.

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 from the family of the knight's head) 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 in children up to the age of 12 years prescription and reimbursable for atopic eczema

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

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

Note(s)
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Ovenbar is used to detect ADHD symptoms (attention hyperactivity disorder) in school-aged children with early atopic dermatitis (Schmitt J et al. 2018).

Various syndromes are associated with skin changes which can be diagnosed as atopic dermatitis:

Literature
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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 managementof
    mld 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. Brenninkmeijer EE et al (2007) Clinical differences between atopic and atopiform dermatitis. J Am Acad Dermatol 58: 407-414
  5. Brüggen M-C et al (2016) Antigen or allergen presentation. In: T. Biedermann et al. (eds.) Allergology. Springer-Verlag Berlin-Heidelberg S 63
  6. 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
  7. Bussmann C et al. (2009) Which systemic therapy options exist for severe forms of atopic dermatitis. JDDG 7: 205-221
  8. Capello C et al (2017) Investigations 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
  9. Charman CR et al (2002) Reliability testing of the Six Area, Six Sign Atopic Dermatitis severity score. Br J Dermatol 146: 1057-1060.
  10. 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
  11. 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.
  12. Griffiths CE (2006) Update on the use of ciclosporin in immune-mediated dermatoses. Br J Dermatol 155: 1-16
  13. 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
  14. 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
  15. 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
  16. 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
  17. 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
  18. 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
  19. 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
  20. Kalliomäki M et al (2001) Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet 357: 1076-1079
  21. Landeck L et al (2011) Contact sensitization pattern in 172 atopic subjects. Int J Dermatol 50:806-810
  22. Lane JE et al (2005) Treatment of recalcitrant atopic dermatitis with omalizumab. J Am Acad Dermatol 54: 68-72
  23. Laszczyk MN et al. (2009) Regenerative and anti-inflammatory effects of betulin emulsions in cases of impaired epidermal barrier function. Act Dermatol 35: 1-5
  24. Nakatsuji T et al (2016) Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression.J Invest Dermatol 136:2192-2200.
  25. Niebuhr M et al (2011) Contact allergy and atopy. Dermatologist 62: 744-750
  26. Novak N et al(2011) Specific immunotherapy and atopic dermatitis. Dermatologist 62: 650-656
  27. 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
  28. 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
  29. 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.
  30. 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.
  31. Proksch E et al.(2016) Epidermal barrier disorder in dermatoses. Dermatologist 67: 907-921
  32. 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
  33. 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
  34. Roduit C et al (2017) Phenotypes of Atopic Dermatitis Depending on the Timing of Onset and Progression in Childhood. JAMA Pediatr 171:655-662.
  35. Ruzicka T et al. (2017) Anti-Interleukin-31 Receptor A Antibody for Atopic Dermatitis. N Engl J Med 376:826-835.
  36. Sand M et al (2007) Extracorporeal photopheresis as a treatment for patients with severe refractory atopic dermatitis. Dermatology 215: 134-138
  37. Schario M et al(2014) Children with dry skin and atopic predisposition: daily use of emollients in
    aparticipant-blinded, randomized, prospective trial. Skin Pharmacol Physiol 27:208.
  38. Schmitt J (2018) Increased attention-deficit/hyperactivity symptoms in atopic dermatitis
    areassociated with history of antihistamine use. Allergy 73:615-626.
  39. Schram ME (2011) A randomized trial of methotrexate versus azathioprine for severe atopic eczema. J Allergy Clin Immunol 128:353-359
  40. 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
  41. 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
  42. Tam HH et al (2016) Specific allergen immunotherapy for the treatment of atopic eczema: a Cochranesystematic
    review. Allergy 71:1345-1356.
  43. Turati F et al (2016) Early weaning is beneficial to prevent atopic dermatitis occurrence in youngchildren
    . Allergy 71:878-888
  44. 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
  45. 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
  46. Werfel T et al. (2016) S2k guideline neurodermatitis (atopic eczema, atopic dermatitis) - short version. Allergo J 25: 36-49
  47. Wopereis H et al (2018) Intestinal microbiota in infants at high risk for allergy: Effects of prebioticsand
    role in eczema development. J Allergy Clin Immunol 141:1334-1342
  48. Willan R (1808) On Cutaneous Diseases. Johnson, London
  49. Yagis S et al (2004) presence of staphylococcal exfoliative toxin A in sera of patients with atopic dermatitis. Clin Exper Allergy 34: 984-993
  50. Yazdi AS (2012) Genetic risk of atopic dermatitis. Dermatologist 63: 161-163

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