Managing Atopic Dermatitis: From Triggers to Targeted Treatment

2026-04-28 |

Introduction

Atopic dermatitis (AD) is an inflammatory skin disease characterized by itching and a chronic or chronically relapsing course. AD is common in families with individuals suffering from other atopic diseases (bronchial asthma, allergic rhinoconjunctivitis), and usually AD is the first atopic disease (the so-called atopic march). It is a common skin disease. Up to 20% of children and 2–8% of adult patients suffer from it. AD usually occurs in childhood, but the disease can develop in patients of any age (about one-third of adults develop AD in adulthood).

AD is diagnosed based on clinical symptoms. The most widely used are the classical diagnostic criteria of John Hanifin and George Rajka (1). There is no pathognomonic laboratory marker for the diagnosis of AD. Some patients may have an increased concentration of total or allergen-specific immunoglobulin E (IgE); positive skin prick tests may be found, but this is not typical for all patients with AD.

In the pathogenesis of AD, besides genetic predisposition, other factors are important: dysregulation of the immune system (activation of T helper 2 cells and IgE production, increased production of various inflammatory mediators), impaired skin barrier function due to filaggrin gene mutation and altered lipid metabolism in the skin, altered normal skin microflora (colonization by Staphylococcus aureus or Malassezia spp.), and a tendency to skin infections. A strong psychosomatic influence is also observed.

After diagnosing AD, the next important step is to assess the severity of the disease—both objective (skin lesions) and subjective symptoms (itching and sleep disturbances) are evaluated (2). The SCORAD index is recommended for assessing the severity of AD (3). If the SCORAD is >50 points, AD is considered severe.

The article further reviews recommendations for AD prevention (avoidance of triggering factors) and local treatment. Systemic treatment options are not discussed in this article.

Non-pharmacological treatment

It is important for each patient to avoid triggering factors that may be nonspecific (general, exacerbating the disease in many patients) and specific.

Non-specific triggering factors of the disease

Many environmental factors (both physical, chemical, and biological irritants) can irritate the skin of individuals with sensitive AD and exacerbate the condition.

Air and indoor air pollution have a negative impact on the skin. It has been observed that formaldehyde increases the risk of skin barrier dysfunction (6). Traffic-related air pollution is associated with an increased risk of AD development in preschool-aged children (7, 8). Exposure to tobacco smoke increases the risk of AD, especially in children whose parents have atopic diseases (9). In the primary prevention recommendations for allergic diseases in Germany, it is suggested to avoid exposure to tobacco smoke and traffic-related air pollution in young children (10).

AD patients are recommended to wear lightweight, breathable clothing and avoid irritating fabrics (e.g., wool).

Avoidance of specific triggers (allergens)

For some patients, inhalant allergens such as house dust mites and pollen can trigger AD exacerbation. Several studies have shown that reducing house dust mite concentrations (especially by using mite-impermeable covers) improves AD control (11, 12), but a meta-analysis conducted in 2015 did not confirm the positive effect of house dust mite avoidance (13). Nevertheless, significant and long-term improvement in AD has been observed in environments without dust mites (e.g., in the Alps) (14). In addition to house dust mites, pollen can also trigger AD exacerbations (15), but it is practically impossible to avoid them (lower pollen concentrations are found in the mountains).

Regarding animals, several aspects are important to mention. Contact with cats is believed to be a risk factor for developing AD, so it should be avoided (primary preventive measure) (16, 17). There is no evidence that dogs increase the risk of AD; on the contrary, studies have shown that contact with dogs prevents the development of AD (due to contact with non-pathogenic microorganisms) (18–20). However, once AD has developed and there is skin damage, the risk of bacterial infections increases with close contact with dogs (21). In any case, if a patient is diagnosed with sensitization and experiences symptoms after contact with an animal, avoiding contact is necessary.

AD patients have a slightly higher risk of sensitization to contact allergens (22). The most common contact allergens in cosmetics are emulsifiers, preservatives, and fragrances (23). If contact allergy is diagnosed, the allergen should be avoided.

Vaccination

It is often believed that children with AD should avoid vaccinations, but there is no evidence that vaccines affect the development of AD or other atopic diseases (24). All children, including those with AD, should be vaccinated according to the schedule. The only exception is the live attenuated intradermal vaccine for measles (due to the risk of eczema vaccinatum) (25). In case of exacerbation of AD, vaccination should be postponed (vaccinated after a 2-week course of local anti-inflammatory treatment) (24). Patients receiving cyclosporine or other systemic immunosuppressive therapy should consult a specialist before receiving live vaccines (24).

Emollients and Skin Care

Bathing. For bathing, it is best to use low-allergen, non-irritating cleansers (bath oils, soap substitutes). Infants and young children should be wiped with a wet soapy cloth before bathing (2), quickly rinsed with lukewarm water (27–30°C), and bathed for up to 5 minutes, with 2 minutes remaining until the end of the procedure to add bath oil. This reduces transepidermal water loss during bathing. Possible additives to the bath:

antiseptics (e.g., 0.005% sodium hypochlorite – improvement in AD observed in children (26, 27), reduced need for local glucocorticosteroids (GCS) and antibiotics (28));
salts, especially in cases of ichthyosis and impetigo (helps remove dead keratinocytes (29));
fragrance-free baby oil can be used instead of soap (30). For children under 2 years old, oils containing peanuts or oats should be avoided.

Emollients. Long-term use of emollients reduces skin dryness associated with AD (31). Daily use of emollients from birth protects high-risk infants from developing AD in the first 6 months of life (32, 33). Additionally, emollients have been observed to reduce the need for GCS in mild to moderate AD (34–36).

Emollients should be applied to damp skin (immediately after bathing) at least 2 times a day and in sufficient quantity (up to 100 g per week for children, at least 250 g per week for adults). Avoid applying emollients to acutely inflamed skin due to poor tolerance (may cause burning or stinging). It is not recommended to use plant oils (e.g., coconut, palm), as they increase transepidermal water loss. Ointments are not recommended for infants due to poor tolerance and potential kidney function impairment, and for young children, smaller amounts should be used than for adults (2). Glycerol is better tolerated than ointments (37). Propylene glycol should not be used in children under 2 years old due to its irritating properties. To avoid sensitization, emollients without protein-derived ingredients (peanuts (38), oats (39), potential contact allergens (lanolin, methylisothiazolinone, etc.)) are recommended for children under 2 years old. Emollients with tannins and ammonium bituminosulfonate (ichthammol) may be beneficial for some patients (40). Some emollients contain active ingredients such as saponins, flavonoids, riboflavins, or bacterial lysates. Several studies have shown a positive effect of lysates on skin rashes and the skin microbiome (41, 42).

Diet and Nutritional Recommendations

Clinically significant food allergy affecting AD progression is detected in one-third of children with moderate to severe AD (43). The most commonly identified allergens are cow’s milk, chicken eggs, nuts, soy, and fish (44). Plant-based foods are associated with AD and pollen allergies in adolescents and adults (45, 46). Adherence to elimination diets worsens patients’ quality of life, so they should only be prescribed after confirming food allergy.

Primary prevention recommendations for food-related AD:

exclusive breastfeeding until 4 months of age;
if breastfeeding is insufficient, low-risk infants are recommended cow’s milk formulas;
if breastfeeding is insufficient, high-risk infants (at least one first-degree relative with a confirmed allergic disease) are recommended hypoallergenic milk formulas;
complementary foods should be introduced from 4–6 months, regardless of atopic history. The diet should be varied.

Topical Anti-Inflammatory Treatment: General Principles

The success of topical treatment depends on three factors—sufficient strength of the medication, proper dosage, and appropriate use (2). AD can be treated with two groups of drugs—topical GCS and topical calcineurin inhibitors (TCIs). Topical treatment should always be applied to moist skin, and the type of medication (ointment, cream, lotion, etc.) should be chosen based on the type and location of skin lesions.

In addition to conventional treatment, where topical anti-inflammatory drugs are used only as long as there is skin inflammation, proactive treatment is also possible. This involves long-term treatment of previously affected skin areas with topical anti-inflammatory drugs (usually two times per week) in low doses, along with continuous use of emollients. This treatment regimen reduces the risk of AD recurrence (47–50).

Topical anti-inflammatory drugs should be prescribed based on the fingertip unit (FTU) rule. FTU is the amount of cream or ointment squeezed from the tube onto the distal phalanx of the index finger (from the fingertip to the crease of the phalanx).

For an area of the forearm the size of the palm, 0.5 fingertip units (FTUs) are enough to cover.

Topical Corticosteroids (TCS)

These are the first-line anti-inflammatory topical medications prescribed based on their potency, formulation, patient’s age, and affected area. In Europe, TCS are classified into four classes based on potency: from class I (weakest) to class IV (strongest). Class IV TCS are not recommended for treating AD.

For rashes on the face, especially around the eyelids, neck, and folds, class I–II TCS should be prescribed. Children are usually given milder TCS than adults. Early application of topical TCS when acute skin damage appears, along with frequent use of emollients, are crucial steps to stabilize AD. Topical TCS can be safely used for proactive treatment for up to 20 weeks.

The most common side effects of topical TCS are usually related to improper drug use. The most frequent side effects occur on the skin: skin thinning, telangiectasia, spontaneous scars, bruising, stretch marks, darkening of the skin, and increased hair growth. Improper use of TCS in the genital area in infants can lead to diaper granuloma or even iatrogenic Cushing’s syndrome. Prolonged use of strong topical TCS on the face can cause rosacea-like perioral dermatitis (known as red face syndrome).

Topical Calcineurin Inhibitors (TCIs)

For AD treatment, two preparations are available: tacrolimus ointment and pimecrolimus cream. Both products are effective for both short-term and long-term AD treatment. TCIs for children with AD in Europe are approved from 2 years of age.

Compared to topical TCS, 0.1% tacrolimus ointment has an anti-inflammatory effect equivalent to medium-potency topical corticosteroids, while the effect of 1.0% pimecrolimus cream is weaker. Studies have shown that proactive treatment with tacrolimus ointment for AD is safe and effective for both children and adults up to 1 year of age.

The most common side effect of topical TCIs is a transient sensation of warmth or burning at the application site during the first days of use. Initial treatment of acute inflammation with topical TCS followed by switching to topical TCIs reduces these unpleasant sensations.

Topical TCIs do not cause skin atrophy, so they can be used in areas of thin skin (e.g., face, neck, folds). Increased risk of systemic viral infections, skin cancer, lymphoma, and photocarcinogenic effects with the use of topical TCIs has not been established. However, it is recommended to use creams with UV filters when prescribing treatment with topical TCIs.

Phototherapy

For most AD patients, symptoms improve in the summer, making phototherapy a possible treatment option. Ultraviolet rays have immunosuppressive, immunomodulatory, and anti-inflammatory effects, reducing skin itching and S. aureus colonization.

Phototherapy is less effective for treating acute AD inflammation and is recommended for chronic, itchy, lichenified skin lesions. Various phototherapy methods are available for AD treatment: broad-spectrum UVB (280–315 nm), narrowband UVB (311–313 nm), broadband UVA (315–400 nm), UVA1 (340–400 nm), UVA with psoralens (PUVA, photochemotherapy), and short-wave visible light therapy.

Medium-dose UVA1 and narrowband UVB are commonly recommended for treating AD. High-dose UVA1 may be more effective for severe AD cases. PUVA is less frequently used due to the higher risk of skin cancer.

Summary

AD is one of the most common non-communicable skin diseases. Various measures are needed to stabilize the course of the disease and reduce the frequency of exacerbations: avoiding triggering factors, proper skin care, regular use of emollients, and timely treatment with topical anti-inflammatory medications. In severe cases and when local treatment measures are insufficient, phototherapy may help some patients.

Eglė Žilėnaitė, Assoc. Prof. Laura Malinauskienė

Clinic of Chest Diseases, Immunology and Allergology, Institute of Clinical Medicine, Faculty of Medicine, Vilnius University

Prepared according to the Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I JEADV 2018;32:657-682.