Atopic Dermatitis

Atopic dermatitis (AD), also called eczema, is a chronic, relapsing inflammatory skin disease driven by a combination of skin-barrier dysfunction and Th2-skewed immune dysregulation, with onset usually in early childhood.^[1] Loss-of-function mutations in the filaggrin (FLG) gene and other structural skin-barrier defects reduce the skin's natural moisturizing factor and its ability to retain water, letting irritants, allergens, and microorganisms penetrate more easily and triggering the itch-scratch cycle that perpetuates flares.^[2] Most affected children improve or clear by adulthood, though a minority have persistent disease, and genuine adult-onset AD also occurs. AD frequently coexists with other atopic conditions (asthma, allergic rhinoconjunctivitis, food allergy) and, particularly in adults, has been associated with alopecia areata, urticaria, anxiety, depression, and reduced bone density — reflecting both the burden of chronic inflammation and the cumulative effects of disrupted sleep and, in some patients, systemic corticosteroid exposure.

AD can present with any combination of itch (which may occur even without a visible or palpable rash), erythema (macular or papular), scale, open erosions, exudate, crusting (dried exudate), and — with chronic rubbing or scratching — lichenification (thickened skin with accentuated skin markings). In patients with darker skin tones, erythema may be subtle and inflammation can appear violaceous, grey, or hyperpigmented rather than classically red; scale is often more visually prominent, and lichenification may appear as hyperpigmentation rather than simple thickening — recognizing these skin-of-colour presentation differences prevents both under- and over-diagnosis.

Distribution varies widely from these classic patterns in an individual patient, and more than one pattern can overlap at once. Poorly controlled AD carries a real functional cost beyond the visible rash: discomfort from itch and pain, sleep disruption from scratching, and downstream effects on mood, concentration, self-esteem, social relationships, school or work performance, and participation in sports and activities.

Active atopic dermatitis with erythema, excoriation, and crusting from scratching. (NIAID, CC BY 2.0, Wikimedia Commons)

Chronic atopic dermatitis on a child's arm, showing lichenification — thickened skin with accentuated markings — from repeated scratching. (Eisfelder, CC BY-SA 3.0, Wikimedia Commons)

• Personal or family history of atopy — asthma, allergic rhinitis, food allergy, or AD itself — the single strongest risk factor.
• Loss-of-function mutations in the filaggrin (FLG) gene or other skin-barrier structural gene variants.
• Early-onset, more severe eczema in infancy, which carries a higher likelihood of persistence and of progression along the "atopic march" toward asthma and allergic rhinitis.
• Low ambient humidity, dry or cold climate, and hard-water exposure.
• Frequent exposure to irritants — harsh soaps and detergents, wool, fragranced products, dry grass and leaves.
• Recurrent skin colonization or infection with Staphylococcus aureus, which can trigger and perpetuate flares.
• Coexisting or prior allergic or irritant contact dermatitis — patients with AD have a higher risk of developing both.
• Psychological stress or anxiety as an individual flare trigger in susceptible patients.

Differentiating atopic dermatitis from its common mimics

Nummular (discoid) eczema — coin-shaped, well-demarcated plaques that can resemble tinea corporis — is considered a pattern of eczema rather than a separate diagnosis. A potassium hydroxide preparation or fungal culture distinguishes it from tinea when the diagnosis is uncertain, since tinea corporis will not respond to, and may worsen with, topical corticosteroid monotherapy.

History

• Onset age, personal and family history of atopy (asthma, allergic rhinitis, food allergy, AD), and the typical distribution pattern for the patient's age.
• Character of the itch, its impact on sleep, and any identifiable triggers (irritants, seasonal patterns, stress, specific products).
• Prior treatments tried, at what potency, frequency, and duration, and the actual response — essential before concluding a treatment has "failed."
• History of recurrent skin infections, and any prior episode concerning for eczema herpeticum.

Physical examination

Diagnosis is clinical, based on the morphology and distribution described in Recognize the Condition together with the history above — there is no confirmatory laboratory test for typical AD.

Investigations

Investigations are rarely required for the work-up of classic AD.

• A bacterial swab of a resistant or non-healing patch can help identify secondary infection when moderate-to-heavy growth of an organism is found, but interpretation is complicated by the fact that many patients with AD are asymptomatically colonized with Staphylococcus aureus — light growth on a swab does not, by itself, confirm active infection.
• Routine IgE, skin-prick, or food-specific allergy testing is not indicated for typical AD, since food ingestion is an uncommon cause of AD flares; reserve allergy testing for a patient with a specific, reproducible history suggesting a food or environmental trigger, or with coexisting allergic symptoms warranting evaluation in their own right.
• Skin biopsy is rarely needed and is reserved for atypical presentations or genuinely treatment-resistant disease in an adult, where excluding cutaneous T-cell lymphoma or another mimic is the goal — not for routine confirmation of typical AD.
• Patch testing should be considered when allergic contact dermatitis is suspected to be contributing — for example, a treated area that worsens rather than improves, an atypical or asymmetric distribution, or a reaction to a specific topical product.

• Relieve pruritus and generalized dry skin, particularly where they interfere with activities of daily living or sleep.
• Reduce inflammation in active patches of dermatitis and achieve clearance.
• Reduce the frequency and severity of flares and extend time in remission.
• Restore and maintain skin-barrier function through consistent, adequate moisturizer use.
• Prevent secondary bacterial or viral infection, and treat it promptly when it occurs.
• Use the lowest effective potency and smallest necessary quantity of medication for the shortest duration that achieves control, matched to the affected body site.
• Support overall quality of life — sleep, mood, and school, work, and social participation — not only visible skin clearance.

Skin-barrier repair and moisturizer technique

Regular moisturizer application is foundational, first-line therapy for AD — for preventing new flares and treating minimal irritation or itch, and as an adjunct alongside active medication during a flare. Applying an adequate amount matters more than which specific product is chosen; there is no reliable evidence that one moisturizer is superior to another.

• Choose a product the patient likes the feel and smell of, since this drives actual adherence.
• Prefer a fragrance-free product without added irritants such as salicylic acid.
• Stop any product that stings, burns, or worsens the dermatitis on contact.
• Use a noncomedogenic moisturizer on the face if acne is also a concern.
• Cost and availability matter — plain petrolatum is greasy but highly effective, nonirritating, and inexpensive, and a more expensive product is not necessarily superior or less likely to contain a contact allergen.
• Ointments penetrate best and are generally the least irritating vehicle, but are cosmetically less acceptable, which can reduce adherence — balance efficacy against a formulation the patient will actually use consistently.

A subset of moisturizers marketed as "barrier repair" products contain ceramides intended to restore the skin's disrupted lipid barrier. Evidence for a clinically meaningful advantage over a standard, well-tolerated moisturizer — including plain petrolatum — is mixed, so treat a ceramide-based product as one reasonable option among several rather than a required upgrade.^[5] Prophylactic moisturizer use in an unaffected, at-risk infant (for example, one with a sibling who has AD) to try to prevent AD from developing has not been shown to reduce that risk in larger trials, despite earlier promising smaller studies — moisturizer's proven benefit is in treating and maintaining control of existing AD, not preventing its onset.

"Soak and seal" bathing technique

Bathing itself is not strongly evidence-supported as an independent treatment, but the technique matters when a patient does bathe or shower: keep it brief (5 to 10 minutes) in warm, not hot, water; pat the skin dry rather than rubbing; and apply moisturizer within a few minutes, while the skin is still slightly damp, to help seal in moisture ("soak and seal"). When both a topical medication and a moisturizer are being used, apply the medicated product directly to the affected skin first and the moisturizer over top, unless both are cream-based, in which case the order matters less. Do not add bath oils or emollients to the bathwater — this has not been shown to add clinical benefit, complicates the bathing routine, and creates a real slip-and-fall risk.

Trigger avoidance

Identify and reduce exposure to irritants that consistently trigger flares in an individual patient — common examples include harsh or fragranced soaps, wool, and dry grass or leaves. Other triggers vary by patient and can include temperature extremes, dry climates, skin infection (particularly S. aureus), and allergens such as dust mites or pollen; address these only when a specific trigger is consistently identified for that patient, rather than broadly restricting exposure without evidence of benefit. Stress and anxiety can precipitate flares in some patients — stress-management strategies may help, but a stress-triggered flare should still be treated with standard AD therapy, not left untreated on the assumption that resolving the stressor alone will clear it.

Diet

Food ingestion is an uncommon cause of AD flares, and elimination diets are not recommended as a general management strategy.^[2] Current guidance favours introducing common allergenic foods early (between 4 and 6 months of age) to promote tolerance, rather than avoidance. A specific, targeted elimination — for example, of egg in a patient with confirmed egg sensitization and suspected clinical relevance — may be considered case by case, but broad, undirected food elimination is not supported and carries real nutritional risk, particularly in children.

Patient education

Structured, disease-specific patient and caregiver education programs improve treatment outcomes in both children and adults and should be considered a standard part of management, not an optional add-on. A written action plan that specifies which product to use where, and when to step therapy up or down, supports this.

Wet-wrap therapy

Wet-wrap therapy — damp bandages or clothing applied over moisturizer, or over a topical medication, for a defined period — can be a useful adjunct for a severe or difficult-to-control flare, but should be supervised by a clinician experienced in the technique, since several different approaches are used in practice and genuine complications can occur: hypothermia, skin maceration, secondary infection, and increased systemic absorption of any topical medication applied underneath the wrap. Favour a lower-potency corticosteroid, or a diluted higher-potency product, when combining with wet wraps, and limit the duration of use. Occlusion is not needed routinely outside this specific, supervised scenario — appropriately-selected topical therapy on its own leads to timely healing without needing to occlude every lesion.

Bleach baths

Diluted bleach baths are sometimes used to reduce bacterial skin counts in patients with frequent secondary infections. Evidence for benefit over plain water baths is inconsistent, so this should be positioned as an option to discuss with a dermatologist for a patient with recurrent infection, not a routine recommendation for all AD patients.

Natural health products

Evidence for probiotics in either preventing or treating established AD is inconsistent, though studies have not shown an increased risk of adverse events with their use — further research is needed before a specific product, dose, or duration can be recommended. Dietary supplements such as vitamin D, selenium, fish oil, and zinc, and herbal products such as borage oil or evening primrose oil, have not shown convincing evidence of benefit in AD and are not recommended as routine therapy.

Pregnancy

AD is the most common skin condition in pregnancy; many patients develop symptoms for the first time during pregnancy, most often in the first two trimesters, and pre-existing AD is more likely to worsen than to improve. Untreated AD is genuinely uncomfortable and carries a real risk of secondary infection, so undertreatment is not a safer default. Maximize nonpharmacologic measures (moisturizers, trigger avoidance). Topical corticosteroids remain the mainstay throughout pregnancy — prefer low- and mid-potency agents over potent or very potent ones where control allows. If further treatment is needed, second-line options include UVB phototherapy and topical calcineurin inhibitors (very low systemic bioavailability). There is no safety data on topical crisaborole, delgocitinib, lebrikizumab, or tralokinumab in human pregnancy; animal studies have not shown adverse effects. Systemic azathioprine or cyclosporine is reserved for the most severe cases, with close monitoring of both patient and fetus. Abrocitinib, methotrexate, mycophenolate mofetil, ruxolitinib (including topical, out of caution), and upadacitinib are contraindicated in pregnancy. Dupilumab has limited human pregnancy data, but case reports and animal studies to date have not shown an increased risk of birth defects.

Breastfeeding

Moisturizers and topical corticosteroids remain the main treatment options — use the lowest effective potency, over the smallest area, for the shortest time. Topical calcineurin inhibitors are poorly absorbed and are second-line. There is no data on transfer of topical crisaborole into breast milk. For all topical medications, avoid direct infant contact with treated skin. UVB phototherapy is considered safe during breastfeeding. Dupilumab, lebrikizumab, and tralokinumab are unlikely to transfer into breast milk in significant amounts given their large molecular weight, but caution is advised when breastfeeding a newborn or premature infant. Avoid abrocitinib, cyclosporine, delgocitinib, methotrexate, mycophenolate mofetil, ruxolitinib, and upadacitinib during breastfeeding. Azathioprine metabolites appear in breast milk only at low or immeasurable levels, with no adverse effects reported in exposed infants. A meaningful proportion of breastfeeding patients develop AD of the nipple or areola — moisturizers and low-potency corticosteroids can be applied and gently but thoroughly wiped off before nursing; do not apply a topical calcineurin inhibitor to the nipple/areola given ingestion risk.

Pediatrics

Onset is most common in early childhood. Match potency and quantity to age and body site using fingertip-unit dosing (see Drug Tables), and monitor growth in a child on long-term or extensive topical corticosteroid therapy. Approved ages vary by agent: pimecrolimus and crisaborole from 3 months; tacrolimus 0.03% from 2 years (0.1% restricted to 16 years and older); ruxolitinib (topical) from 2 years; roflumilast (topical) from 6 years; dupilumab from 6 months (weight-based dosing); abrocitinib, upadacitinib, tralokinumab, and lebrikizumab from 12 years; delgocitinib is restricted to adults 18 years and older for hand AD.

Older adults

Adult-onset AD occurs and should not be dismissed as an unlikely diagnosis. Thinner, more fragile skin increases the visible risk of atrophy and purpura at a given topical corticosteroid potency, so reassess more frequently. Before starting a biologic or JAK inhibitor, weigh comorbidity and polypharmacy — the class-wide infection/malignancy/MACE/thrombosis precautions for JAK inhibitors carry particular relevance in older patients or those with cardiovascular risk factors.

Renal and hepatic impairment

Not a major factor for topical therapy. It is directly relevant to the traditional systemic immunosuppressants (azathioprine, cyclosporine, methotrexate, mycophenolate mofetil), which require dose adjustment or avoidance based on organ function, and to the JAK inhibitors, which require renal/hepatic-function-based dosing consideration and periodic liver-enzyme monitoring — see Drug Tables for agent-specific detail.

Teach patients and caregivers to recognize an active flare — visible or palpable rash, and/or itch — and to start treatment promptly at the first sign, continuing it at the prescribed frequency until the flare has fully resolved (no rash and no itch; residual skin discoloration alone does not require continued treatment and will self-resolve over time). Reassess any flare that has not resolved within 2 weeks of appropriately intensified treatment — reconsider the diagnosis, adherence and technique, and possible secondary infection, before assuming a stronger agent is needed. For proactive (maintenance) topical corticosteroid or calcineurin-inhibitor therapy, apply 2-3 times weekly to previously affected sites and reassess ongoing need at each follow-up. Monitor growth parameters in a child on long-term or extensive topical corticosteroid therapy. For systemic therapy, follow dermatology-directed reassessment intervals — most biologics are assessed for response at around 16 weeks, and JAK inhibitors follow their own defined laboratory-monitoring schedule (see Drug Tables). Track sleep quality and mood/anxiety/depression symptoms, since these correlate with disease control and often improve alongside the skin. Reinforce moisturizer adherence at every visit — it is the single most consistent flare-prevention measure, regardless of what active therapy is layered on top.

1. Confirm the diagnosis is still AD — reconsider the differential (allergic contact dermatitis overlay, scabies, tinea, psoriasis) if the presentation or distribution is atypical.
2. Confirm adherence and correct technique — quantity (fingertip-unit based), frequency, and the correct potency for the body site, plus continued moisturizer use alongside active treatment; under-treatment or incorrect technique is a far more common cause of apparent "failure" than true tachyphylaxis.
3. Screen for secondary infection — impetiginized eczema, or eczema herpeticum if vesicular or punched-out lesions are present — masquerading as treatment failure, and treat the infection before concluding the anti-inflammatory regimen has failed.
4. Screen for allergic contact dermatitis to a component of the treatment itself (vehicle, fragrance, preservative, or the corticosteroid molecule) if a treated area worsens rather than improves; consider a patch-testing referral.
5. Step up therapy in a stepwise fashion — increase potency or change formulation, add or switch to a steroid-sparing topical (calcineurin inhibitor or PDE4 inhibitor), or move to a topical JAK inhibitor if the patient is still topical-eligible.
6. If genuinely refractory despite steps 1-5, refer to dermatology for consideration of phototherapy or systemic therapy (biologic, oral JAK inhibitor, or, less commonly today, a traditional immunosuppressant).

• Under-dosing topical corticosteroid out of "steroid phobia," resulting in chronically undertreated, active dermatitis — the risk of undertreatment usually exceeds the risk of appropriately-used corticosteroid therapy.
• Using a high- or ultra-high-potency corticosteroid on the face, eyelids, or skin folds — these thin-skin sites need a low-potency agent or a steroid-sparing alternative.
• Recommending sedating or nonsedating antihistamines for AD-related itch — AD pruritus is not histamine-mediated, so antihistamines do not meaningfully improve it (a nonsedating agent may still help a coexisting allergic symptom, such as allergic rhinitis or conjunctivitis).
• Recommending elimination diets or food avoidance without a specific, clinically supported indication — not supported by evidence, and can create unnecessary nutritional risk in a child.
• Attributing apparent treatment failure to tachyphylaxis without first confirming correct technique, adherence, and the absence of secondary infection.
• Applying moisturizer to open, actively inflamed, or weeping skin without first treating the active dermatitis — can cause stinging or irritation and reinforces the misconception that "moisturizer doesn't work."
• Adding bath oils or emollients to bathwater — no proven added benefit, and a real slip-and-fall risk.
• Missing eczema herpeticum by treating rapidly-spreading, punched-out vesicular lesions as a routine bacterial flare.
• Continuing a topical or oral JAK inhibitor without the required baseline and periodic monitoring (infection screening including TB, lipid panel, CBC/LFTs as applicable to the specific agent).

How to use this table: doses are adult doses unless a pediatric line is given, and require patient-specific confirmation. Select any drug name to open its complete Pharmasist Drug Database page.

Estimating quantity: the fingertip unit (FTU)

One FTU is approximately 0.5 g — the amount of ointment or cream expressed from a tube with a standard 5 mm nozzle, from the fingertip to the first crease of an adult finger. One FTU covers approximately 250 cm² of skin (about 2 adult handprints with fingers together). To calculate the quantity to prescribe: (FTU for the body area x 0.5 g/FTU) x (number of applications per day) x (number of days of treatment).

FTU values are the number of fingertip units needed per single application to the stated body area, by age group.

Topical corticosteroids — low potency

Preferred for the face, eyelids, skin folds, and young children.

Topical corticosteroids — medium potency

Good for body/trunk areas of moderate disease.

Topical corticosteroids — high and ultra-high potency

Reserve for thick, lichenified, or resistant plaques on the trunk and limbs, and for the palms/soles — never the face or skin folds.

Topical calcineurin inhibitors

Second-line, steroid-sparing option, particularly for the face and folds. A boxed warning regarding a theoretical malignancy risk exists on the product label; a dedicated systematic review and meta-analysis found no increased malignancy risk with labelled use.^[6]

Topical phosphodiesterase-4 (PDE4) inhibitors

Nonsteroidal options with no potency-based site restriction.

Topical Janus kinase (JAK) inhibitors

No bloodwork monitoring is required for the topical formulations, unlike their oral counterparts, but the boxed warning (serious infection, malignancy, MACE, thrombosis) is retained on the label, extrapolated from oral JAK inhibitor safety data.

Topical antibiotic/corticosteroid combinations and topical antibiotics

For localized, mild-to-moderate impetiginized eczema — not a substitute for oral therapy when infection is widespread or the patient is systemically unwell.

Oral antibiotics for widespread or systemic secondary bacterial infection

Antivirals for eczema herpeticum

Start immediately on clinical suspicion — do not wait for viral culture or PCR confirmation.

Systemic monoclonal antibodies (biologics)

For moderate-severe AD inadequately controlled by topical therapy. Screen for active infection and latent/active TB before starting; avoid live vaccines during therapy. Referral to dermatology is recommended before initiating any of these agents.^[5]

Systemic Janus kinase (JAK) inhibitors

Require baseline and periodic laboratory monitoring; screen for latent/active TB before starting; avoid live vaccines during therapy.

Traditional systemic immunosuppressants (off-label)

Long history of use; may be the best option for some patients but require close laboratory monitoring. Consult a clinician experienced with these agents before prescribing.

Phototherapy

Ultraviolet (UV) phototherapy — narrowband UVB or, less commonly, psoralen plus UVA (PUVA) — is a second-line physical treatment typically given several times per week for a period of months, requiring dedicated equipment and repeated in-person visits. It should not be used in patients with a photosensitive comorbidity, such as a history of skin cancer or a photodermatosis.