Red, itchy scaling plaques on a toddler


  • CA0711DermClinic1

A girl aged 2 years presented to the dermatology clinc with a pruritic rash. The rash began on the toddler’s cheeks when she was just a few months old but has since spread to involve her wrists, elbows, knees, and abdomen.

The girl’s mother reported that the rash comes and goes and is associated with pruritus. No medications are applied to the area because the mother is afraid of irritating the skin. On physical examination, erythematous scaling plaques with scattered excoriations are noted to involve bilateral elbows, knees, wrists, and neck.

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Atopic dermatitis Atopic dermatitis (AD), more commonly referred to as eczema, was first described in 1892. At that time, it was determined that an association existed between allergic rhinitis and asthma. The term "atopy" was chosen to describe the condition...

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Atopic dermatitis

Atopic dermatitis (AD), more commonly referred to as eczema, was first described in 1892. At that time, it was determined that an association existed between allergic rhinitis and asthma. The term “atopy” was chosen to describe the condition because it was derived from the Greek word “atopos,” meaning abnormal. In the 1930s, researchers focused on the cutaneous aspects of the triad and named it atopic dermatitis. In the 1980s, a catalog of distinctive clinical aspects for AD was established.1

AD has an early onset, usually before age 5 years. The condition has been increasing in prevalence since the end of World War II. Children from the United States, Northwest Europe, South America, and Australia show prevalence between 10% and 20%.2 Countries in the Mediterranean, eastern Europe, and Africa have a lower prevalence of AD. Combinations of environmental, immunologic, and genetic factors are believed to be the main drivers contributing to the onset of AD. Genetics is believed to be the highest risk factor, while the environment is thought to be the causal factor for the severity of the disease.

Although the fact that atopy is inherited is widely recognized, a clear mode of transmission has not yet been identified. Various chromosomal regions—which encode for such products as co-stimulatory molecules involved in T-cell activation and Th2 cytokines, the high-affinity immunoglobulin (Ig)E receptor, and mast cell chymase—have been linked to AD. Other gene polymorphisms, loss-of-function mutations, and toll-like receptors are also associated with AD. Chromosome loci 1q21 contains the filaggrin gene, which is part of the epidermal differentiation complex.3 A defect here causes the individual to be filaggrin-deficient, creating an abnormal epidermal barrier that compromises the individual. This abnormal barrier may lead to cutaneous sensitization and a Th2 response in the skin, resulting in AD. However, it may also prime the immune system and set up a systemic Th2 environment that may later lead to asthma and allergic rhinitis.

Immunology also plays a leading role in the development of AD as evidenced by the occurrence of serum IgE elevation and eosinophilia in approximately 70%-80% of patients.4 Acute lesions of AD are Th2-predominant, but as the lesions evolve, there is a predominance of IFN-gamma-producing T-cells.

The environment also contributes to the development of AD. Air temperature, humidity, hygiene, and degree of urbanization are all factors. In winter, when temperatures and humidity are lower, 40% to 60% of patients experience deterioration.4 Others may complain of a flare during the summer months, when perspiration may irritate the skin. Chemicals and perfumes in soaps, detergents, cleaning products, and disinfectants also contribute to skin irritation. Pollution caused by urbanization and such dietary allergens as egg whites, cow’s milk, peanuts, wheat, soy, shellfish, and flour may contribute to the severity of AD.2 Other irritants include tobacco smoke, dyed fabrics, and wool.

Clinical features depend on age, race, severity, aggravating factors, and duration of disease. The three stages of AD are infantile, childhood, and adulthood, all of which are associated with pruritus. In the infantile stage, dry, erythematous, scaly plaques and follicular papules are localized to the scalp, face, and extensor surfaces of the extremities.4 When the infant becomes mobile, extensor regions—especially the knees—become affected. During the childhood phase, the clinical features begin to mimic those seen in adulthood. Lesions predominate such areas as the antecubital and popliteal fossae and posterior neck.2 Adults may also have disease that is localized to the hands or head and neck.

Histologically, eczema is characterized by focal parakeratosis, spongiosis, and superficial perivascular lymphocytes.3 Neutrophils may be seen in the stratum corneum if it is secondarily impetiginized. Acanthosis or hyperkeratosis may be seen in cases that are associated with chronic irritation and rubbing. In acute cases, spongiosis may be marked, and spongiotic vesicles may be seen in the epidermis. Occasionally, eosinophils also may be seen in a perivascular distribution.3

Skin biopsies are not essential for the diagnosis but may be useful in difficult cases or in those recalcitrant to therapy. The list of differential diagnoses is fairly extensive and includes such other chronic dermatoses as psoriasis, contact dermatitis, and seborrheic dermatitis. Common infections and infestations that may mimic AD include scabies, dermatophytoses, and HIV-associated dermatoses. Immunodeficiencies associated with pruritic dermatitis include Wiskott-Aldrich and hyper-IgE syndrome. Such malignancies as mycosis fungoides and Langerhans cell histiocytosis are also possibilities.3 Many other autoimmune, drug, metabolic, and genetic disorders should always be considered in the differential diagnosis.

Treatment of this condition requires a combination of dry- and sensitive-skin care, identification and elimination of triggers, and anti-inflammatory and antipruritic medications. The frequent use of topical emollients represents a mainstay of AD treatment. Patients should avoid perfumes, dyes, or other chemicals that may be irritating to the skin. Pharmacologic therapy includes topical and systemic medications. Topical treatments are most effective when applied within three minutes after bathing, as there is greater absorption during this time. Topical corticosteroids are the first-line therapy, and potency depends on the severity of the disease. A general rule is to apply the topical corticosteroid b.i.d. during flares and discontinue use when the skin is clear. Corticosteroid-induced cutaneous atrophy is a risk, especially on the face or in intertriginous sites. Monotherapy for these areas often includes a mild-strength topical corticosteroid or topical calcineurin inhibitors. Sedating antihistamines may help to break the “itch-scratch cycle.” Antimicrobials and the use of bleach baths are important for those who develop infections frequently. Other systemic therapies include cyclosporine, azathioprine, mycophenolate mofetil, methotrexate, interferon therapy, IV immunoglobulin, and biologics.2

AD can have a significant impact on patients’ lives. Therapy alone is exhausting and causes disruption of normal life. Severe AD hits families financially as well as psychologically. Medications tend to be expensive, and parents often have to take time off from work to take their children to the doctor or care for their skin. However, in approximately 40% to 60% of patients, AD is completely cleared at puberty or shortly thereafter.5 For those who do not improve with time, education regarding dry- and sensitive-skin care and proper use of medications is key to improving the patient’s quality of life.

In this case, dry- and sensitive-skin care—including the application of a heavy bland emollient at least three times daily—was discussed. The patient was treated with tacrolimus (Protopic) 0.1% ointment b.i.d. to the face as needed and triamcinolone 0.1% ointment b.i.d. to affected areas on the body as needed. Hydroxyzine (Atarax, Vistaril) was used as needed for severe pruritus.

Dr. Robbins is a resident in the department of dermatology at Baylor College of Medicine in Houston. The author has no relationships to disclose relating to the content of this article.

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1. Hanifin JM, Rajka G. Diagnostic features of atopic eczema. Acta Derm Venereol Suppl (Stockh). 1980;92:44-47.

2. Paller AS, Mancini AJ. Hurwitz Clinical Pediatric Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2006:49-64.

3. RP Rapini. Practical Dermatopathology. Philadelphia, Pa.: Elsevier-Mosby; 2005:51-53:45.

4. JL Bolognia, JL Jorizzo, RP Rapini, eds. Dermatology, 2nd ed., St. Louis, Mo.: Mosby-Elsevier; 2008:181-195.

5. Wüthrich B. Clinical aspects, epidemiology, and prognosis of atopic dermatitis. Ann Allergy Asthma Immunol. 1999;83:464-470.

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