creation date: 2025-06-25 01:55
tags: Pathologies
Atopic Dermatitis
Background
Definitions
Atopic dermatitis (AD), also known as eczema, is a chronic, pruritic, inflammatory skin condition.
There is an association with elevated serum levels of immunoglobulin E (igE) and personal and/or family history of atopy.
Atopy refers to a predisposition to a group of disorders that includes:
- Eczema
- Asthma
- Allergic rhinitis
Etiology and Pathogenesis
While the exactly initiation of atopic dermatitis is still debated, several mechanisms are involved in the pathogenesis.
Epidermal barrier dysfunction
- Function primarily in stratum corneum and is the first line of defence against the environment and controls water homeostasis.
- Altered stratum corneum causes transepidermal water loss, increased permeability, reduced water retention, and altered lipid composition
- Caused by reduced filaggrin production, imbalance of stratum corneum protease and antiprotease activity, tight junction abrnoamlities, altered epidermal lipids, microbial colonization, itch-scratch cycle, and release of proinflammatory cytokines.
Genetic factors - Number of loci associated with skin barrier abnormalities
- Association with specific phenotypes such as early-onset and persistent, increased risk of other allergies, etc.
T helper type 2 (Th2) cell-skewed immune dysregulation - Tissue damage or microorganisms can result in release of alarmins by keratinocytes and antigen-presenting cells in the skin.
- Alarmins activate a number of immune cells, of which Th2 cells promote further inflammation via the production of IgE as well as affect epidermal barrier function by promoting epidermal hyperplasia.
Altered skin microbiome - Reduced diversity of bacterial community and overgrowth of Staphylococcus aureus is common
- Bacterial proteins can act as virulence factors that contribute to inflammation
Environmental triggers of inflammation - With defects in skin barrier function, triggers such as detergents, soaps, solvents, and allergens can result in flare ups
- Stress, temperature, humidity, and infections can also exacerbate symptoms
Clinical Presentation
Signs & Symptoms
The cardinal signs are:
- Dry skin
- Pruritus
Clinical manifestations can vary based on age, ethnicity, and severity. And may present as some of the following:
- Erythematous papules and vesicles with exudation and crusting (acute)
- Dry, scaly, or excoriated, erythematous papules (more chronic)
- Skin thickening (lichenification) and fissuring from chronic scratching
- Erythema may appear dark brown or violaceous in darkly pigmented skin
- Postinflammatory hyper- and hypopigmentation
Findings can generally be seen anywhere on the body but axillary, gluteal, and groin areas are uncommon.
Infants and young children: extensor surfaces, cheeks, scalp but diaper sparing
Older children and adolescents: flexural distribution such as the antecubital and politeal fossae, volar aspects of the wrists, ankle, and neck.
Adults: skin flexures but less than younger, often face, neck, hands.
Other features are included in as part of the “atopic stigmata”:
- Centrofacial pallor
- White dermographism
- Keratosis pilaris
- Palmer hyperlinearity
- Pityriasis alba
- Periorbital darkening and Dennie-Morgan intraorbital folds
- Thinning or absence of lateral portion of eyebrows
- Infra-auricular and retroauricular fissuring
- Nipple eczema
There are also variants of AD that have been described:
- Atopic hand eczema - volar wrist and dorsum hands, concurrent foot sometimes
- Eyelid eczema
- Atopic cheilitis - lip eczema characterized by dryness, peeling, and fissuring of the lips
History & Physical Exam
History and physical exam should assess for features of atopic dermatitis. Morphology and distribution of skin lesions should be evaluated.
Note the variations that may exist.
Risk factors
Genetic
- Family history of atopy is strongest risk factor
- 70% of patients with AD has a positive family history
Environmental exposures - Climate, urban environment, air pollution, early exposure to nonpathogen microorganisms, and high levels of calcium carbonate in water (hard water) may increase risk
Diagnosis
Criteria
Diagnosis is made clinically although some criteria have been proposed.
The American Academy of Dermatology suggests the following criteria:
Essential features (all of the following):
- Mild to severe pruritus
- Eczematous dermatitis with typical morphology and age specific pattern
- Chronic or relapsing course
Important features (≥2 required):
- Onset before two years of age
- Personal and/or family history of allergic rhinitis, asthma, food allergies, or atopic dermatitis
- Dry skin within the last year
Associated features (≥1 required):
- Atypical, vascular response (eg. facial pallor)
- Keratosis pilaris, pityriasis alba, hyperlinear palms, ichthyosis
- Periocular changes
- Perioral eczema, bitlateral periauricular eczema lesions, prurigo nodules or papules
- Perifollicular accentuation or lichenification
- Sparing of groin or axilla
Work-up
There is no routine workup for atopic dermatitis.
In select patients, histological examination of a skin biopsy or other laboratory tests (eg. serum IgE) may be helpful for ruling out other skin conditions.
In cases where affected skin doesn’t resolve with treatment, use skin shaving to rule out tinea corporis (Ringworm) - especially with annular eczema.
Differential
Allergic or irritant contact dermatitis:
- Difficult to differentiate from AD (even with histology) and can also coexist
- Typically more localized and exposure may be found in history
Seborrheic dermatitis: - Common differential diagnosis in infant and can also coexist
- Presence of salmon-red, erythematous skin patches with greasy scale
- Often scalp involvement with little or no pruritus
Psoriasis: - Often involves diaper area
- Well-demarcated, erythematous patches with little scale
Scabies: - Demonstration of mites or eggs by skin scraping, demoscopy, or adhesive tape test can differentiate
Other conditions include:
- Drug reactions
- Primary immunodeficiencies
- Nutritional deficiencies
- Netherton syndrome
- Cutaneous T cell lymphoma
Red Flags / Complications
Infectious complications:
- Because of S. aureus colonization of lesions, impetiginization is frequent
- Eczema herpeticum is herpes seimplex viral infection of affected skin
Risk of cancer: - Controversial association between AD and skin cancer/lymphoma
Management
Lifestyle / Social
Bathing practices:
- Less frequent bathing for infants and up to daily showering in older children/adults
- Use of a mild or soap-free cleansers
- Additives such as bath emollients may improve skin hydration
- Consider dilute bleach bath (low evidence, but low harm)
Use of emollients and moisturizers:
- Skin hydration is a key component of management
- Should be used at least twice daily and preferably immediately after bathing or hand washing
- Thick creams or ointments (with low water content) are preferred; avoid fragranced emollients
Consider elimination of exacerbating factors which can disrupt the skin barrier such as:
- Excessive bathing without subsequent moisturization
- Low-humidity environments
- Emotional stress
- Xerosis
- Overheating and sweating
- Use of hard water
- Exposure to solvents and detergents
Other measures may include:
- Avoiding irritants such as rough wool, fragranced soaps, perfumes etc.
- Treating skin infections
- Managing stress and anxiety
Pharmacological / Interventional
Mild to moderate disease
Topical corticosteroids as monotherapy in addition to liberal emollient use are the first-line treatment.
Selection of corticosteroid potency and formulation should be based on patient age, body area involved, and degree of skin inflammation.
Types and potencies are discussed separately.
Ointment formulations tend to be superior in terms of potency and emollient properties. Oil formulations are easier to spread and are useful for scalp or large body surfaces. Creams contain more additives and are more likely to burn or sting.
Instruction for patient to apply to affected area once or twice daily for up to two weeks. Note that 30g is needed to cover an adult body once in its entirety.
Some topical corticosteroid options are:
- Mild - low potency ointment (eg. hydrocortisone 2.5%) once to twice daily until 3-5 days following clearance
- Moderate - medium to high potency ointment (eg. mometasone furoate 0.1%). With acute flare-ups, can use high potency for 2 weeks before replacement with lower-potency options.
- Face and skin folds (area at risk of atrophy) - low potency ointment (eg. desonide 0.05%). Can consider high potency very briefly (eg. 4-5 days) for a more rapid response.
- Ear canal - fluocinolone 0.01% oil or topical corticosteroid-based ophthalmic solution (eg. prednisolone 1% ophthal. sol).
Other treatments should first-line not work include:
- Topical calcineurin inhibitors
- Topic PDE4 inhibitors
- Topical ruxolitinib
- Topical delgocitinib
- Tapinarof
For acute exacerbations, systemic corticosteroids may be considered but is not recommended due to adverse effects and rebound on discontinuation. Prednisone can be prescribed as follows:
- 40-60 mg/day for 3-4 days
- then, 20-30 mg/day for 3-4 days
- then, 10 mg/day for 4 days
Moderate to severe disease
For patients with persistent moderate to severe disease despite optimized topical therapy, systemic treatment is indicated.
First-line biologic agent options include:
- Dupilumab
- Tralokinumab
- Lebrikizumab
Oral Janus kinase inhibitors may also be considered for short term control.
Narrowband ultraviolet B phototherapy may also be acceptable for first-line therapy in conjunction with topical corticosteroids for adults and adolescents.