Dermatitis Pharmacotherapy

Contact Dermatitis

Irritant contact dermatitis results from direct chemical or physical damage to the skin, commonly from soaps, detergents, solvents, and wet work. It is not immunologic and usually appears within minutes to hours of exposure. Allergic contact dermatitis is a type IV delayed hypersensitivity reaction to agents such as poison ivy and related plants, nickel and other metals, latex and rubber, and topical anesthetics such as benzocaine. It appears hours to days after reexposure and can extend beyond the area of contact. Patch testing may be needed to identify the allergen when the history is unclear or the dermatitis recurs (Ernsthausen & Mills, 2026).

Treatment

The first step is identifying and removing the causative agent, including washing skin, clothing, and objects that may still carry it. Cool compresses, tepid soapless showers, colloidal oatmeal baths, and emollients relieve symptoms. Astringent compresses such as aluminum acetate (Burow’s solution), applied for about 30 minutes several times daily, dry weeping lesions (Ernsthausen & Mills, 2026).

Topical corticosteroids are effective for allergic contact dermatitis, which generally responds better than the irritant form. Potency is selected by severity and site: higher potency for thick or poorly penetrated skin such as the hands, elbows, and knees, and lower potency for the face, axillae, and groin. Ointments should be avoided on weeping lesions. Use should be limited once symptoms resolve (Ernsthausen & Mills, 2026).

Extensive or severe allergic contact dermatitis, such as widespread poison ivy or facial involvement, may require an oral corticosteroid. Two to 3 weeks of therapy may be needed because short courses can be followed by rebound (F.A. Davis Company, 2021a).

Sedating oral antihistamines such as diphenhydramine or hydroxyzine can relieve itching, although sedation, dizziness, hypotension, blurred vision, and confusion limit their use. Topical antihistamines are generally avoided because they can cause sensitization. Most contact dermatitis improves within about a week and resolves within 3 weeks. Fever, difficulty breathing, spreading rash, or lack of improvement warrants reassessment (Ernsthausen & Mills, 2026).

Atopic Dermatitis

Atopic dermatitis is a chronic, relapsing inflammatory skin disease marked by pruritus, dry skin, and a characteristic age-related distribution. It reflects epidermal barrier dysfunction, including filaggrin mutations in some patients, together with a predominantly T-helper type 2 immune response driven by cytokines such as interleukin (IL)-4, IL-5, and IL-13 (Ernsthausen & Mills, 2026). Affected skin is frequently colonized by Staphylococcus aureus, and secondary infection with bacteria or herpes simplex virus can complicate flares (Ernsthausen & Mills, 2026; Kapur et al., 2018).

Management combines patient education, trigger avoidance, daily skin care, anti-inflammatory therapy, and management of infection. Allergy testing should follow the clinical history rather than broad screening, because food allergen panels have poor positive predictive value (Kapur et al., 2018).

Bathing and Moisturizers

Daily bathing in warm water for about 10 to 15 minutes with a gentle, fragrance-free cleanser, followed by liberal moisturizer application while the skin is still slightly damp, is the foundation of care. Creams and ointments moisturize more effectively than lotions. Inexpensive products in large containers support the generous, frequent use needed to maintain the barrier (Kapur et al., 2018). The 2023 AAD topical guideline gives moisturizers a strong recommendation (Sidbury et al., 2023).

Topical Corticosteroids

Topical corticosteroids are first-line anti-inflammatory therapy for flares. They are typically applied once or twice daily to active lesions until the flare is controlled. A higher-potency agent may be used briefly to regain control on the trunk or extremities, while low-potency agents are used on the face and skin folds and in young children. Long-term treatment should rely on the lowest effective potency (Ernsthausen & Mills, 2026; Kapur et al., 2018). Once the disease is stable, proactive twice-weekly application to sites that tend to flare reduces the risk of relapse while keeping cumulative corticosteroid exposure low (Kapur et al., 2018).

Topical Calcineurin Inhibitors

Tacrolimus ointment and pimecrolimus cream are second-line or steroid-sparing agents for atopic dermatitis beginning at age 2. Tacrolimus 0.03% is used in children 2 to 15 years, while either 0.03% or 0.1% may be used from age 16 onward. They are especially useful for the face, eyelids, and skin folds and for patients who need frequent or prolonged anti-inflammatory treatment without corticosteroid atrophy. Transient burning is common. Both carry a boxed warning regarding rare malignancy reports, and patients should limit ultraviolet exposure (Ernsthausen & Mills, 2026; Sidbury et al., 2023).

Nonsteroidal Topical Alternatives

Crisaborole ointment, a phosphodiesterase-4 (PDE4) inhibitor, is approved for mild-to-moderate atopic dermatitis in patients 3 months and older and is generally reserved as an alternative because of cost. Application-site pain is the most common adverse effect. Ruxolitinib cream, a topical Janus kinase (JAK) inhibitor, is approved for short-term and noncontinuous treatment of mild-to-moderate disease covering up to 20% of body surface area; it carries the JAK-inhibitor boxed warnings (Ernsthausen & Mills, 2026). The American Academy of Dermatology’s (AAD’s) 2025 focused update added strong recommendations for roflumilast cream 0.15% for mild-to-moderate atopic dermatitis and tapinarof cream 1% for moderate-to-severe atopic dermatitis in adults (Davis et al., 2025).

Antihistamines, Antimicrobials, and Wet Wraps

Antihistamines do not treat the underlying inflammation of atopic dermatitis. A sedating first-generation antihistamine may be used briefly when severe nocturnal itching prevents sleep, but routine use is discouraged because the benefit is mainly sedation and adverse effects include impaired attention and next-day drowsiness. Second-generation antihistamines are most useful when a concurrent histamine-mediated condition, such as allergic rhinitis or urticaria, is present rather than as primary treatment for eczema itch (Kapur et al., 2018). The 2023 AAD guideline recommends against topical antihistamines (Sidbury et al., 2023).

Clinically infected eczema is treated with short courses of topical or oral antibiotics according to the extent and severity of infection. Oozing, pustules, and yellow crusting increase concern for secondary bacterial infection, while uninfected eczema should not receive routine antibiotics. Dilute bleach baths received a conditional recommendation for selected patients with moderate-to-severe disease and recurrent infection, but the dilution must be calculated from the concentration of the household bleach product rather than relying on a universal cup-based recipe. Routine topical antimicrobials and antiseptics are otherwise discouraged (Kapur et al., 2018; Sidbury et al., 2023).

Wet-wrap therapy applies a topical agent under a damp inner layer and a dry outer layer. It can help severe flares, but high-potency corticosteroids under wet wraps increase absorption and the risk of hypothalamic-pituitary-adrenal axis suppression (Ernsthausen & Mills, 2026; Kapur et al., 2018).

Referral and Systemic Therapy

Patients whose disease remains moderate to severe despite optimized topical therapy should be referred. Specialist options include phototherapy, dupilumab (IL-4 receptor alpha antagonist that blocks IL-4 and IL-13 signaling, approved from 6 months of age), tralokinumab and lebrikizumab (IL-13), nemolizumab (IL-31 receptor), oral JAK inhibitors such as upadacitinib and abrocitinib, and conventional immunosuppressants. Systemic corticosteroids should be avoided except in exceptional circumstances because disease often rebounds when they are stopped (Davis et al., 2025; Ernsthausen & Mills, 2026; Kapur et al., 2018).

Clinical response should be reassessed after treatment begins rather than judged by a fixed two-week expectation. Improvement in pruritus often precedes clearing of the rash; persistent or worsening disease should prompt reassessment of adherence, application technique, diagnosis, infection, and the need to step up therapy. Daily moisturizer use continues during both active treatment and maintenance (Ernsthausen & Mills, 2026).

Diaper Dermatitis

Diaper dermatitis is an irritant dermatitis caused by prolonged contact with urine and feces, friction, and excess moisture. Prevention and treatment start with frequent diaper changes, gentle cleansing with water or fragrance-free wipes, complete drying, and diaper-free time (Ernsthausen & Mills, 2026).

Barrier protectants are applied with every diaper change. Zinc oxide is among the most used and adds astringent and antiseptic effects; white petrolatum, lanolin, vitamin A and D products, and topical cornstarch are alternatives. Pastes provide the thickest barrier for more severe rashes (Ernsthausen & Mills, 2026).

Low-potency hydrocortisone (0.5% to 1%) applied twice daily may be used briefly for inflammation, but infants absorb topical corticosteroids readily, so higher potencies, longer courses, and any use in children younger than 2 years require prescriber direction. Recommended limits range from 2 to 3 days (F.A. Davis Company, 2021a) to no more than 2 weeks (Ernsthausen & Mills, 2026).

Persistent diaper dermatitis should be reassessed for Candida, especially when there is beefy erythema involving the skin folds with satellite papules or pustules; duration alone does not establish candidiasis. Candidal diaper dermatitis is treated with topical nystatin, clotrimazole, or miconazole, with frequency based on the selected product and diaper-care plan. Secondary bacterial infection may require topical or systemic antibiotics. Referral is indicated for bullae, ulceration, extensive spread, fever, systemic illness, or failure to improve after an appropriate treatment trial (Ernsthausen & Mills, 2026).

Seborrheic Dermatitis

Seborrheic dermatitis produces greasy scale on the scalp, face, and other sebaceous areas. First-line treatment is a medicated shampoo containing selenium sulfide, ketoconazole, or pyrithione zinc, used about twice weekly and left on the scalp briefly before rinsing. Low-potency topical corticosteroids are added for inflammation that does not respond to shampoo (F.A. Davis Company, 2021b, 2021a).

High-Yield Distinctions

• Remove the offending agent first in contact dermatitis.
• Allergic contact dermatitis responds better to topical corticosteroids than irritant contact dermatitis.
• Avoid ointments on weeping lesions; use astringent compresses instead.
• In atopic dermatitis, moisturizers and daily skin care are part of treatment.
• Use proactive twice-weekly topical corticosteroid application to prevent atopic flares.
• Topical calcineurin inhibitors are steroid sparing for the face and folds beginning at age 2; tacrolimus 0.1% is reserved for patients 16 years and older.
• Treat infected eczema with antibiotics, not uninfected eczema.
• Topical antihistamines are not recommended.
• Persistent diaper dermatitis with fold involvement and satellite papules or pustules raises concern for Candida; duration alone is not diagnostic.
• Seborrheic dermatitis starts with antifungal or cytostatic shampoos.

Related YourDNP Resources

• Topical Dermatologic Pharmacology Foundations
• Superficial Fungal Infections and Topical Antifungals
• Allergic Contact Dermatitis

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References

Davis, D. M. R., Frazer-Green, L., Alikhan, A., Bercovitch, L., Cohen, D. E., Darr, J. M., Drucker, A. M., Eichenfield, L. F., Paller, A. S., Schwarzenberger, K., Silverberg, J. I., Singh, A. M., Wu, P. A., & Sidbury, R. (2025). Focused update: Guidelines of care for the management of atopic dermatitis in adults. Journal of the American Academy of Dermatology, 93(3), 745.e1–745.e7. https://doi.org/10.1016/j.jaad.2025.05.1386

Ernsthausen, L., & Mills, J. M. (2026). Dermatitis. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed., pp. 480–507). McGraw Hill.

F.A. Davis Company. (2021a). Dermatological conditions [PowerPoint slides].

F.A. Davis Company. (2021b). Drugs affecting the integumentary system [PowerPoint slides].

Kapur, S., Watson, W., & Carr, S. (2018). Atopic dermatitis. Allergy, Asthma & Clinical Immunology, 14(Suppl. 2), Article 52. https://doi.org/10.1186/s13223-018-0281-6

Sidbury, R., Alikhan, A., Bercovitch, L., Cohen, D. E., Darr, J. M., Drucker, A. M., Eichenfield, L. F., Frazer-Green, L., Paller, A. S., Schwarzenberger, K., Silverberg, J. I., Singh, A. M., Wu, P. A., & Davis, D. M. R. (2023). Guidelines of care for the management of atopic dermatitis in adults with topical therapies. Journal of the American Academy of Dermatology, 89(1), e1–e20. https://doi.org/10.1016/j.jaad.2022.12.029