Atopic Dermatitis

The words dermatosis, dermatitis and eczema are frequently used and should not be confused with each other.

Dermatosis:

• Refers to any diagnosis of the skin.
• Encompasses congenital, inflammatory, neoplastic, and all other skin conditions.

Dermatitis:

• Indicates inflammation of the skin, presenting as erythema alone, erythema with scaling, or the latter with vesiculation and crusting.

Dermatitis Classification:

• Endogenous (Constitutional) Dermatitis: e.g., atopic dermatitis and seborrhoeic dermatitis.
• Exogenous Dermatitis: e.g., contact dermatitis caused by external factors in contact with the skin.

Eczema (Boiling Over):

Describes various skin conditions characterized by:

1. Erythema and skin swelling.
2. Oozing and/or vesiculation.
3. Crusting and scaling.
4. Lichenification or thickening and evidence of repeated excoriations.
5. Post-inflammatory hyperpigmentation and/or hypopigmentation due to inflammation's effect on melanocytes.

The first 3 stages are of acute eczema, while the latter 2 appear after weeks when the condition becomes chronic.

All changes can co-exist, progressing independently.

Atopic Dermatitis (AD) Definition:

An inherited, chronic, relapsing pruritic skin condition characterized by xerosis and inflammation. It is associated with various pharmacologic and immunologic abnormalities, including overproduction of specific IgE in response to common environmental antigens.

The severity ranges from mild to severe, potentially interfering with growth and development in severe cases.

• A major cause of morbidity in the western world.
• Exact incidence is challenging to determine due to undiagnosed mild cases.
• Incidence seems to be increasing worldwide.
• AD is more common in highly industrialized nations and the western hemisphere compared to Asia.
• Higher incidences found in immigrants from less prevalent areas to more prevalent areas support the strong environmental influence in pathogenesis.

• Unclear Etiology: The exact etiology of AD remains unclear.
• Genetic and Environmental Factors: It is believed to be linked to both genetic causes and environmental agents.
• Family History: There is a strong family history of associated atopic diseases in families of AD patients. Nearly 40% of newly diagnosed patients report a positive family history for AD in at least 1 first-degree relative.
• Prevalence with Affected Parents: The prevalence of AD in children with 1 affected parent is 60%, rising to nearly 80% for children of 2 affected parents.
• Twin Concordance: Much higher concordance of AD exists in monozygotic twins (86%) compared to dizygotic twins (21%).

• Hyperactive T Helper Cell 2 (Th2) Theory: One causative theory is that AD results from a hyperactive T helper cell 2 (Th2) and down-regulation of T helper cell 1 (Th1) activity.
• Role of Cytokines: Th2 cells normally secrete interleukin (IL)-4, IL-5, and IL-13. IL-4 and IL-13 promote immunoglobulin E (IgE) synthesis from B lymphocytes and activate vascular endothelium. IL-5 enhances eosinophil-mediated responses.
• Elevated Serum IgE and Eosinophilia: This theory is supported by elevated serum IgE levels and peripheral blood eosinophilia commonly seen in AD patients.
• Cytokine Administration: Evidence suggests that administration of IL-2 or gamma-interferon, cytokines of the Th1 immune response system, to atopic patients can result in improvement in disease severity.

• Typically, the disease presents in early infancy, usually in the first 6 months of life.
• There may be a positive family history, and a history of exacerbating factors may be elicited.
• History of intense pruritus and a chronic relapsing course of the condition would be prominent.
• The earliest lesions are erythematous, weepy patches on the cheeks, with subsequent extension to the remainder of the face, neck, wrists, hands, abdomen, and extensor aspects of the extremities.
• Typical locations of lesions by age:
• Nonmobile infant - Face and scalp
• Crawling infant - Extensor surfaces of extremities, trunk, face, and neck
• Older child and adolescent - Wrists, ankles, antecubital fossae, popliteal fossae, and neck
• Adult - May be limited to hand and foot eczema

• Various diagnostic criteria have been drawn up to enhance the diagnosis of AD.
• The most prominent is that proposed by Hanifin and Rajka (1980) and largely adopted by the American Academy of Allergy, Asthma, and Immunology.
• At least 3 major and 3 minor criteria must be present to make a diagnosis.
• Major criteria:
  • Pruritus
  • Typical morphology and distribution (i.e. flexural lichenification and linearity in adults, facial and extensor involvement in infants and young children)
  • Chronic or chronically relapsing dermatitis
  • Personal or family history of atopy (e.g. asthma, allergic rhinitis, conjunctivitis, AD)
• Minor criteria:
  • Xerosis (dry skin)
  • Ichthyosis/palmar hyperlinearity/keratosis pilaris
  • Hand and/or foot dermatitis
  • Cheilitis
  • Nipple eczema
  • Susceptibility to cutaneous infection (e.g. with Staphylococcus aureus, herpes simplex virus [HSV], other viruses, warts, molluscum, dermatophytes)
  • Erythroderma
  • Perifollicular accentuation
  • Pityriasis alba
  • Early age of onset
  • Impaired cell-mediated immunity
  • Recurrent conjunctivitis
  • Orbital darkening
  • Infraorbital fold (e.g. Dennie pleat, Morgan fold)
  • Anterior neck folds
  • Keratoconus
  • Anterior subcapsular cataracts
  • Sensitivity to emotional factors
  • Food intolerance
  • Pruritus with sweating
  • Intolerance of wool
  • White dermographism
  • Immediate type I skin test response
  • Elevated total serum IgE
  • Peripheral blood eosinophilia

The U.K. Working Party’s Diagnostic Criteria for Atopic Dermatitis

Individual must have an itchy skin condition plus three or more of the following:

• History of flexural involvement
• History of asthma/hay fever
• History of a generalized dry skin
• Onset of rash under the age of 2 years
• Visible flexural dermatitis

The transverse nasal crease (arrows) characteristic of allergic rhinitis. This linear change results from repetitive rubbing of the nose vertically, pushing the tip of the nose cephalad.

Identifying such a crease in a family member of a patient is a useful feature supporting a positive family history of allergy.

Definitive laboratory tests are lacking for diagnosing AD.

Elevated serum IgE levels and peripheral blood eosinophilia often occur in individuals with AD.

Tests for infections that mimic or complicate AD include:

• Tzanck smear for HSV
• Potassium hydroxide (KOH) preparation for dermatophytes
• Gram stain for bacterial infections

Prick skin testing for common allergens can identify triggers of AD, especially in young children with moderate-to-severe disease, though false-negative and false-positive results are possible in children under 8 years.

AD is often confused with other skin disorders.

Seborrheic dermatitis is the most common condition mistaken for AD.

It typically presents as a yellow greasy scale on an erythematous base. Unlike AD, it is usually not pruritic and has an excellent prognosis.

Distinguishing Features Between Infantile Seborrhoeic Dermatitis and Atopic Dermatitis

Features	Infantine Seborrhoeic Dermatitis	Atopic Dermatitis
Age of Onset	4 – 6 weeks (early)	3 – 6 months (late)
Site involved	Scalp & Skin fold	Face
Pruritus	Absent	Present (notable features)
Morphology	“Benign” looking mildly scaling patches, minimal or no erythema	“Angry” looking, active reddish eruption.
Post infl. Colour	Hypopigmentation	Hyperpigmentation
Prognosis limiting	Good and self-resolving within a few weeks	Poor, often progresses to childhood

Infections

• During early infancy and childhood, secondary infection of the lesions of atopic dermatitis with bacterial, fungal, or viral agents is common.
• Staphylococci and B-hemolytic streptococci are the bacterial agents most often recovered from infected lesions.
• Herpes simplex (Kaposi's varicelliform eruption) is also of particular concern.

Contact dermatitis

• The hands of AD patients are intolerant to irritants like detergents, shampoos, and wet jobs. They are also prone to nickel hand eczemas.

Anaphylactic syndromes

• These patients are prone to IgE mediated urticaria-anaphylactic syndromes. Therefore, various injections, penicillin, chloroquine, and horse sera are best avoided in these patients.

Psychological stress

This usually sets in because of the resentment from school mates and teachers who believe in the contagiousness of all skin diseases.

The management of atopic patients is aimed at:

1. Suppressing the urge to scratch
2. Suppressing inflammation
3. Preventing infections and prompt treatment of infections.
4. Avoiding other exacerbating factors.
5. Avoiding the complications of treatment.
6. Correcting misconceptions about the disease.

Treatment consists of:

• Adequate skin hydration.
• Avoidance of allergenic precipitants.
• Topical anti-inflammatory medications.
• Systemic antihistamines.
• Antibiotic coverage of secondary infections.

One of the most important aspects of therapy is establishing an honest relationship with the parents, explaining the nature of the disease, and stressing the fact that there is no cure.

Topical corticosteroids are the mainstay of treatment of AD.

Topical steroids should be applied only to areas of acute exacerbations, whereas emollients should be used over the remainder of the skin.

Formulations of steroids in ascending order of occlusiveness are lotions, creams, gels, and ointments.

Systemic corticosteroids have been used in severe chronic AD, but usage has been limited in the pediatric population because of the risk of severe adverse effects.

In older children and adolescents, treat mild cases of AD with a low-potency (class VI or VII) topical steroid twice a day to decrease inflammation. Examples include hydrocortisone cream or ointment, 1% and 2.5%.

For moderate cases of AD, intermediate-potency steroids (class III, IV, V) may be used for brief periods (<2 wk).

Class VII steroids on the face, axillae, groin, and intertriginous areas because of increased absorption.

For mild AD in infants, class VI or VII topical steroids should be effective. If the infant has more severe AD, a moderate-potency steroid can be prescribed for up to 1 week and then tapered down to a lower-potency medication for maintenance therapy.

In general, infants should not be treated with topical steroids in the high-potency classes.

Antihistamines are used to reduce pruritus and serve as sedatives, and mild anxiolytics, e.g. diphenhydramine, hydroxyzine, or doxepin.

Oral antibiotics are useful in treating recalcitrant lesions and secondarily infected ones, e.g. Erythromycin.

Coal tar topical preparations have antipruritic and anti-inflammatory effects. They are effective as second-line agents for subacute, chronic, and lichenified AD, e.g. PsoriGel, and Neutrogena T/Derm Tar Emollient.

Topically applied tacrolimus has proven to be an effective new therapy for AD. It is a nonsteroidal alternative that is especially useful when treating facial and intertriginous dermatitis.

Systemic cyclosporine can dramatically reverse severe flares of AD.

Ultraviolet radiation - Ultraviolet light may benefit some patients. Ultraviolet light in the UVB range may provide control and eliminate or markedly reduce the need for steroids.

Adequate rehydration preserves the stratum corneum barrier, minimizing the direct effects of irritants and allergens on the skin.

Lukewarm soaking baths lasting 20-30 minutes are ideal. Small amounts of bath oils or emulsification agents may be used for added hydration benefits.

Recommended soaps are mild and unscented with a neutral pH. Examples include Dove, Oil of Olay, Caress, Camay, Aveeno, and Purpose.

Baths should be followed by the immediate application of an occlusive emollient over the entire skin surface to retain moisture in the epidermis.

Urea, alpha-hydroxy acid, and lactic acid preparations have also been shown to soften and moisturize dry skin.

Wet dressings are very useful for diverse types of atopic dermatitic flares and can be used on dry lichenified lesions to improve hydration and increase the penetration of topical corticosteroids.

There may be some benefit in eliminating some common allergenic foods in the diet until after acute flares or introduce them at about 1 -2 yrs when reactivity would have reduced.

Implement dust mite and mold control measures for allergic children.

Wear loose fitting open-weave cotton or cotton-blend clothing; avoid wool.

Use a humidifier in the winter to prevent excessive skin dryness and an air conditioner in the summer to prevent sweating and associated macerative effects on the skin.

• Sixty percent of affected individuals manifest characteristic lesions during the first year of life. Ninety percent of individuals will be affected by age 5 yr.
• The remaining individuals will typically manifest disease during late childhood or adolescence. It is rare for symptoms to begin during adulthood and should be a clue to question the accuracy of diagnosis.
• The clinical course is variable and unpredictable. Some infants and children will have a mild course with spontaneous remission by 2–3 yr of age. Others will have more persistent disease with a chronic unremitting course throughout childhood.