ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Contact dermatitis in children

Contact dermatitis in children
Author:
Moise L Levy, MD
Section Editor:
Jeffrey Callen, MD, FACP, FAAD
Deputy Editor:
Rosamaria Corona, MD, DSc
Literature review current through: Sep 2022. | This topic last updated: Sep 16, 2022.

INTRODUCTION — Contact dermatitis refers to inflammation of the dermis and epidermis as a result of direct contact between a substance and the surface of the skin. In fact, almost all dermatitis is the result of skin surface injury from epicutaneous exposures. Contact dermatitis is divided into two broad categories: irritant contact dermatitis and allergic contact dermatitis. Irritants cause immediate inflammation of the skin; allergens cause an inflammatory response that is delayed by days.

This topic will discuss irritant and allergic contact dermatitis in children. Contact dermatitis in adults is discussed separately.

(See "Irritant contact dermatitis in adults".)

(See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

(See "Clinical features and diagnosis of allergic contact dermatitis".)

(See "Management of allergic contact dermatitis".)

(See "Common allergens in allergic contact dermatitis".)

IRRITANT CONTACT DERMATITIS — Irritant contact dermatitis results from exposure to substances that cause physical, mechanical, or chemical irritation of the skin. Diaper dermatitis and dry skin dermatitis are two common forms of irritant contact dermatitis in children.

Diaper dermatitis — Diaper dermatitis is the prototype for irritant contact dermatitis in children. Diaper dermatitis is discussed in detail separately. (See "Diaper dermatitis".)

Dry skin dermatitis — In dry skin dermatitis, also called xerosis, the surface of the skin appears dry and cracked; erythematous areas often appear within the surface cracks. Common causes of dry skin dermatitis in children include frequent soaping of the skin and frequent wet-to-dry episodes (eg, lip licking, thumb sucking, and playing with water).

Pathogenesis — The cells on the surface of the skin, called corneocytes, have the ability to bind three times their weight in water. Water binding involves corneocyte surface lipids, such as ceramides, and the proteins of the outer corneocyte envelope, such as involucrin and filaggrin [1]. In a case-control study, loss-of-function mutations in the filaggrin gene were associated with susceptibility to chronic irritant contact dermatitis [2]. The bound water provides almost all of the skin surface moisture. It is unrelated to the state of internal hydration. Air humidity of 60 percent is ideal for the skin.

Corneocyte disruption occurs when air humidity falls below 15 percent and/or corneocyte surface lipids are removed from the surface of the skin by soap or chemicals that cause the corneocytes to shrink from one another [3]. Disruption of corneocytes causes release of the inflammatory cytokines, tumor necrosis factor (TNF)-alpha, and interleukin (IL) 1, which are stored in corneocytes.

Clinical features — In children with dry skin dermatitis, a history of excessive soaping of the skin, frequent water exposure, or excessive sweating may be obtained. On examination, the skin surface appears dry, cracked, and chapped with a macular erythema. Involvement may be limited to the hands in compulsive hand-washers; to the feet in children who have excessive sweating or water exposure of the feet (juvenile plantar dermatosis (picture 1A-B)); or to the lips and perioral area (lip licking dermatitis (picture 2)) due to contact with saliva, milk/formula, or food. Symptoms include burning, stinging, or discomfort. In contrast to allergic contact dermatitis, itching is usually modest or absent.

Diagnosis and differential diagnosis — The diagnosis of dry skin dermatitis is usually straightforward, based upon the clinical finding of localized areas of dry, cracked, and erythematous skin in children with a history of excessive exposure to water and detergents, or excessive sweating. Patch testing is not routinely performed in children with irritant contact dermatitis.

The differential diagnosis includes allergic contact dermatitis, atopic dermatitis, and the ichthyoses. Patch tests to relevant environmental allergens are typically positive in children with allergic contact dermatitis. In contrast to dry skin dermatitis, which typically affects a localized area, the entire surface of the skin may be affected in atopic dermatitis [4,5]. Atopic dermatitis and the ichthyoses are discussed in detail separately. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Overview and classification of the inherited ichthyoses".)

Treatment — Restoration of water and lipid to the skin surface and prevention of transepidermal water loss are essential to the treatment of dry skin dermatitis. This is best accomplished with application of moisturizers at least twice per day (table 1) [4,6,7]. In one randomized trial, the use of moisturizing cream reduced transepidermal water loss, normalized skin Corneometer values, and decreased irritant reactions [8]. The use of nanoemulsions of lipids improves skin hydration, elasticity, and erythema [9]. Overall, preparations that restore moisture to the skin surface also enhance delivery of steroids and other active topical medications into the skin [10].

In addition, elimination of factors that may predispose to dryness, such as excessive washing of the skin with soap, is critical to the success of therapy. Moisturizers that are accidentally ingested cause no problem other than greasy stools.

ALLERGIC CONTACT DERMATITIS — Allergic contact dermatitis (ACD) is an acquired, inflammatory reaction of the skin that requires absorption of antigen from the skin surface and recruitment of previously sensitized, antigen-specific T lymphocytes into the skin. (See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

Epidemiology — The exact incidence and prevalence of ACD in children are not known [5,9]. Incidence and prevalence of ACD depend upon exposure to contact allergens, which varies according to geography (eg, poison ivy) and cultural practices (eg, jewelry wearing, use of fragrances) [11]. It has been estimated that ACD accounts for at least 20 percent of all cases of childhood dermatitis [12,13].

Although as many as 25 percent of randomly selected asymptomatic children who undergo epicutaneous patch testing react to one or more antigens, the true prevalence of ACD is not known [11,14-16]. A positive patch test reaction that is not found to be clinically relevant is termed "contact allergy" rather than ACD [17]. One specific example of an allergen that induces contact sensitization that is rarely clinically relevant is thimerosal.

The North American Contact Dermatitis Group reported that of 883 children tested from 2005 to 2012, 62 percent had ≥1 positive patch test and 57 percent had ≥1 relevant positive patch test [18]. In a single institution study of 2614 children under 10 years of age who underwent patch testing for suspected allergic contact dermatitis, 1220 (47 percent) developed at least one positive reaction, which was deemed to be relevant in approximately 50 percent of cases [19]. The frequency of positive reaction was similar among children with or without a history of atopic dermatitis. The most common allergens were nickel sulfate (23 percent), cobalt chloride (11 percent), and potassium dichromate (10 percent). A study of 343 Israeli children confirmed these results, with nickel ACD more common in girls than in boys (38 versus 16 percent) [20].

ACD has been reported in one-week-old infants [21,22], and sensitization often begins as early as six months of age [15]. By two years of age, many children are already sensitized to at least one common allergen (eg, nickel) [15].

Pathogenesis — An intact immune system is required for the development of ACD, which occurs in two phases: the sensitization phase and the elicitation phase [23] (see "Basic mechanisms and pathophysiology of allergic contact dermatitis"):

The sensitization phase begins with initial exposure to the antigen and may begin in infancy [15]. Contact antigens are usually low-molecular-weight substances that penetrate the outer layer of the skin and are taken up by Langerhans cells (LC). Sweating may enhance this process [23]. After processing the antigen and migrating to regional lymph nodes, LC present the antigen to T lymphocytes. These antigen-specific T lymphocytes undergo clonal expansion, creating a pool of cells with immune memory that can generate an immune response upon re-exposure to the allergen (the elicitation phase). Preliminary studies indicate that macrophages and neutrophils are also important in the pathophysiology of contact allergy [24]. Antigen-presenting cells and the cellular immune response are discussed in detail separately. (See "Antigen-presenting cells" and "The adaptive cellular immune response: T cells and cytokines".)

In the elicitation phase, the sensitized T lymphocytes proliferate and release inflammatory mediators, producing a localized dermatitis. The resulting dermatitis begins 12 to 24 hours after allergen exposure, peaks in three to five days, and may last three to four weeks if untreated [23,25,26]. The potency of the allergen determines the number of exposures necessary for this process to occur. A strong antigen, such as poison ivy, requires only one exposure, while weaker antigens require numerous exposures over weeks to years. Once sensitization occurs, however, it is thought to be long-lived [9,23,25,26].

Allergens — Contact allergens are found in both the natural and man-made environment (table 2) [27]. The most common plant contact allergen is urushiol, a pentadecylcatechol found in plants of the Toxicodendron species, such as poison ivy, poison oak, and poison sumac (figure 1 and picture 3A-C). (See "Poison ivy (Toxicodendron) dermatitis".)

Other common childhood contact allergens in the United States and Europe include metals such as nickel [28], cobalt, and potassium dichromate (also tanning agent in leather); topical antimicrobials such as neomycin and bacitracin; fragrances (fragrance mix and Myroxylon pereirae [balsam of Peru]), preservatives (formaldehyde and formaldehyde-releasing preservatives, methylchloroisothiazolinone [MCI] and methylisothiazolinone [MI]), colophony (rosin from wood), wool alcohol (lanolin), and several others [14,17,29-31]. MCI and MI are preservatives found in infant products such as wet wipes, protective creams, liquid soaps, and shampoos (a fixed 3:1 combination of MCI/MI is known as Kathon CG). In an analysis of 1100 positive patch tests in children, 96 (9 percent) were positive to MCI/MI or MI alone [32]. (See "Common allergens in allergic contact dermatitis".)

Additional allergens of potential importance in the pediatric population are cocamidopropyl betaine, a non-ionic surfactant used in cleansing products for children and disperse dyes that are found in diaper material and colored garments [17]. The active ingredients of chemical sunscreens (eg, oxybenzone, octocrylene), although uncommon causes of childhood ACD, are increasingly reported causes of ACD [33-35]. Despite the widespread use of personal care products, such as diaper wipes in infants and cosmetics in teens, adverse skin reaction reports to the US Food and Drug Administration (FDA) are infrequent (166 reports from 2004 to 2016) [36].

Clinical findings — ACD presents as pruritic dermatitis most commonly localized to the site of allergen contact with the skin, but can also present as a generalized dermatitis (see 'Autoeczematization ('id' reaction)' below). The configuration and location of the dermatitis often is a clue to the offending allergen (table 2 and picture 4A-B) [37]. Regional lymph nodes may be enlarged but are not tender [23].

ACD may be acute, subacute, or chronic:

Acute ACD to potent allergens (eg, poison ivy, poison oak, poison sumac, nickel) is characterized by erythema and edema with vesicles or bullae (picture 5) that often rupture, leaving a crust.

Subacute and chronic ACD, which are more common, are characterized by lichenification, erythema, and scaling (picture 6), and are produced by less potent antigens.

Autoeczematization ('id' reaction) — A more generalized dermatitis, termed autoeczematization, may develop distal to the original site of contact one or more weeks after the appearance of the initial localized dermatitis. This secondary dermatitis is also called autosensitization dermatitis or an "id" reaction. Autoeczematization is particularly common among children with nickel dermatitis who have subacute dermatitis at the initial site for several weeks before appearance of a more widespread dermatitis [37]. Autoeczematization is treated in the same manner as widespread ACD. (See 'Management' below.)

Diagnosis

Clinical — A history of allergen exposure and the pattern of the eruption are important factors in making the correct diagnosis. Patterns of dermatitis that are suggestive of ACD include persistent, localized dermatitis that has not responded as expected to therapy, and dermatitis in an unusual pattern or distribution (picture 4A-B) [37]. In contrast with ACD, which often has a bizarre or asymmetrical distribution, atopic dermatitis is typically symmetric. ACD also should be considered in any child who has a persistent dermatitis regardless of the pattern, as well as facial, eyelid, or palmo-plantar dermatitis [29].

Considering the child's hobbies, activities, occupation, and other exposures is important in assessing and diagnosing allergic contact dermatitis.

Patch testing — Although the offending allergen may be suspected through history, epicutaneous patch testing may be necessary to identify specific antigens or, in some cases, to make the diagnosis of ACD [17,30,33,37-42]. The most common allergens in children in North America are nickel, cobalt, neomycin, Myroxylon pereirae (balsam of Peru), lanolin, fragrance, bacitracin, carmine, p-phenylenediamine, quaternium 15, propolis, and formaldehyde [16,17]. A pediatric baseline series was proposed by the Pediatric Contact Dermatitis Workgroup in 2018 [43].

Identifying the offending allergen is important, since allergen avoidance is the key to preventing recurrence. However, we recommend not patch testing for poison ivy or poison oak (urushiol) because the reaction can be extreme and someone who is not sensitive may be sensitized by the testing.

Epicutaneous patch testing involves placement of suspected and standard allergens on the skin surface for 48 hours. The patches are then removed and the skin evaluated for irritant or early positive reactions. The final read at 72 to 96 hours is important to document positive reactions (picture 7). Reevaluation is recommended after four to five days to detect reactions to weaker antigens and to permit irritant reactions to clear [23]. Children should avoid bathing and strenuous activity while the patches are in place. (See "Patch testing".)

Because of the potential pitfalls in interpretation of patch tests, epicutaneous patch testing should only be performed by clinicians who are experienced in the procedure and interpretation of the test, and knowledgeable about the relevance of the antigens [44,45]. In a retrospective case series, 80 percent of positive patch test reactions in children were relevant (with relevance determined by the presence of the allergen in the child's environment and/or improvement on allergen avoidance or exacerbation upon re-challenge) [41].

Differential diagnosis — The clinical morphology of ACD is identical to other forms of dermatitis (eg, irritant dermatitis and atopic dermatitis). Other conditions that may be considered in the differential diagnosis of ACD include [23]:

Cellulitis, an infection of the deep dermis and subcutaneous tissue that manifests as skin areas of erythema, edema, and warmth, often accompanied by lymphangitis and inflammation of regional lymph nodes. Fever and leukocytosis, common in cellulitis, are not features of ACD. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Herpes simplex virus, herpes zoster, impetigo (if blistering lesions are present). (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection" and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster" and "Impetigo".)

Fixed drug eruption, which typically recurs in the same location. (See "Fixed drug eruption".)

Management — The treatment of ACD involves two main principles:

The allergen must be identified and avoided to prevent recurrence.

The dermatitis must be treated for at least 14 to 21 days.

Allergen avoidance — Identifying the offending allergen is important, since allergen avoidance is the key to preventing recurrence. Although the offending allergen may be suspected through history, epicutaneous "patch" testing may be necessary to identify specific antigens [40]. (See 'Patch testing' above.)

Once the allergen is known, the patient should be educated about potential sources and avoidance of the antigen. Complete avoidance is possible in many circumstances once the source of the allergen is known. Avoidance may involve placing a barrier between the allergen and the skin. Examples include wearing long pants when out in the woods to prevent poison ivy dermatitis and using a cloth patch or nail enamel to cover the exposed portions of metal snaps or fasteners in a child allergic to nickel. After a known exposure to poison ivy, it is important to remove all clothing and wash the whole body with mild soap as soon as possible. (See "Management of allergic contact dermatitis", section on 'Allergen avoidance'.)

Therapeutic options — Although avoidance of the offending allergen is the mainstay of management of ACD, treatment is required in most cases to achieve rapid control of symptoms. The treatment of ACD follows the general principles of eczema treatment and includes:

Topical corticosteroids – Topical corticosteroids are the mainstay of treatment of ACD. Through various mechanisms, corticosteroids decrease the production of cytokines and halt lymphocyte proliferation, limiting the inflammatory response to contact allergens [46]. In two small trials, the application of topical corticosteroids resulted in decreased transepidermal water loss, clinical improvement, and suppression of allergic reaction compared with the application of placebo in patients with ACD [47,48].

Topical corticosteroids are classified according to strength, with group 1 corticosteroids being the strongest and group 7 the least strong (table 3). Examples of moderate-potency topical corticosteroids include fluocinolone acetonide 0.025% (group 4), triamcinolone acetonide 0.1% (group 4), and mometasone furoate 0.1% (group 3). Side effects of topical corticosteroid therapy are reviewed in detail separately. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Topical calcineurin inhibitors – Topical tacrolimus and topical pimecrolimus are potential alternatives to corticosteroids in the treatment of subacute and chronic ACD involving areas at high risk for skin atrophy. Topical tacrolimus is available in two concentrations, 0.03% and 0.1%, but only the 0.03% formulation is indicated for use in children aged 2 to 15 years. Topical calcineurin inhibitors should not be used in children younger than two years of age or in immunocompromised individuals.

There is limited evidence from poor-quality randomized studies for efficacy of topical tacrolimus, but not pimecrolimus, in the treatment of ACD [49-51]. Tacrolimus appears to be as effective as mid-potency corticosteroid ointments (eg, triamcinolone acetonide 0.1% or fluocinolone acetonide 0.025%) for the treatment of ACD in adults [50].

Other therapies – Adjunctive treatments that may be beneficial in alleviating the symptoms associated with ACD, such as burning or pruritus, include:

Sedating antihistamines, such as diphenhydramine or hydroxyzine, decrease itching and allow the patient to sleep through the night. As an alternative to standard dosing, we have found a single dose of hydroxyzine 1 to 2 mg/kg, given 30 minutes to 1 hour before bedtime, to be effective in this regard.

Wet dressings are also soothing and help relieve itching, reduce redness, debride crusts, and limit access to the skin. Dampened cotton garments are worn over the affected area and covered with a dry garment. The patient may use these dressings overnight or change them every eight hours during the day. The author prefers wet dressings to topical agents such as calamine or colloidal oatmeal baths because wet dressings limit access to the skin and are more soothing, hydrating, and antipruritic.

Children with acute allergic contact dermatitis

Localized allergic contact dermatitis — For localized eruptions, we suggest mid-potency topical corticosteroids. Corticosteroid ointments (not creams) are applied two times daily for two to three weeks. As with systemic therapy, the topical therapy must be continued for two to three weeks, since stopping the therapy too quickly may cause rebound dermatitis.

Widespread allergic contact dermatitis or allergic contact dermatitis involving the face — When the dermatitis involves 20 percent or more of the skin surface, systemic corticosteroids are indicated. A single morning dose of prednisone (1 to 2 mg/kg, up to a maximum dose of 60 mg) for 7 to 10 days, followed by a taper over the next 7 to 10 days, is usually sufficient. Systemic corticosteroids may be preferred to topical corticosteroids for patients with acute ACD involving the face to achieve a rapid relief of symptoms.

Children with subacute and chronic allergic contact dermatitis — Subacute and chronic ACD is often the result of repeated exposures to modest or weak contact allergens, making treatment challenging. Depending upon the part of the body affected, low- or mid-potency topical corticosteroids (groups 4 to 7 (table 3)) can be applied twice daily for two to three weeks. Intermittent, twice-daily application of topical corticosteroids (eg, during the weekends) may be helpful to maintain long-term remission. Emollients can be liberally used in conjunction with topical corticosteroids.

Appropriate long-term use of low- or mid-potency topical corticosteroids does not cause hypothalamic-pituitary-adrenal suppression in infants and children [52], although localized side effects such as atrophy are possible. Allergic contact dermatitis to topical corticosteroids is also a possible complication of therapy and, if suspected, may be evaluated with patch testing to identify the culprit preparation, as well as other corticosteroids that the patient can tolerate [53]. The classification of topical corticosteroids in cross-reacting groups is also useful in the choice of the preparation the patient may tolerate (figure 2).

Second-line therapy for subacute and chronic ACD involving the face or intertriginous areas may include topical calcineurin inhibitors.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Diaper rash (The Basics)" and "Patient education: Poison ivy (The Basics)" and "Patient education: Eczema (atopic dermatitis) (The Basics)")

Beyond the Basics topics (see "Patient education: Contact dermatitis (including latex dermatitis) (Beyond the Basics)" and "Patient education: Diaper rash in infants and children (Beyond the Basics)" and "Patient education: Poison ivy (Beyond the Basics)" and "Patient education: Eczema (atopic dermatitis) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Irritant contact dermatitis:

Clinical presentation and diagnosis – A diagnosis of irritant contact dermatitis should be considered in children who have localized, macular, erythematous rashes in which the skin is dry, cracked, and chapped. (See 'Irritant contact dermatitis' above and 'Dry skin dermatitis' above.)

Management – We recommend the use of moisturizers (table 1) for the treatment of dry skin dermatitis (Grade 1B). Moisturizers should be applied at least twice per day. Avoidance of the irritant (eg, frequent bathing, lip licking, soaps, etc) is essential in the treatment of dry skin dermatitis. (See 'Treatment' above.)

Allergic contact dermatitis:

Clinical presentation – Allergic contact dermatitis (ACD) presents as pruritic dermatitis localized to the site of allergen contact with the skin. The configuration and location of the dermatitis often is a clue to the offending allergen (picture 4A-B). (See 'Clinical findings' above.)

Diagnosis – The diagnosis of ACD should be considered in children who have localized pruritic dermatitis 12 to 24 hours after exposure to a contact allergen to which they have been sensitized. Epicutaneous patch testing may be necessary to make the diagnosis of ACD or to identify specific antigens. Patch testing should be performed by clinicians with experience in its performance and interpretation. (See 'Diagnosis' above.)

Management of acute allergic contact dermatitis – Avoidance of the allergen is essential in the treatment of ACD. We recommend topical corticosteroids as the first-line therapy for acute localized ACD (Grade 1B). Mid-potency corticosteroids (group 4 (table 3)) are applied twice daily for a minimum of 14 to 21 days. For patients with widespread acute ACD or acute ACD involving the face, we suggest systemic corticosteroids (Grade 2C). A single morning dose of prednisone (1 to 2 mg/kg, up to a maximum dose of 60 mg) for 7 to 10 days is usually sufficient. (See 'Management' above and 'Children with acute allergic contact dermatitis' above.)

Management of subacute or chronic allergic contact dermatitis – We suggest topical therapy with a mid-potency corticosteroid ointment (group 4 (table 3)) for subacute or chronic ACD (Grade 2C). Topical corticosteroids are applied twice daily for two to three weeks. Intermittent, twice-daily application of topical corticosteroids (eg, during the weekends) may be helpful to maintain long-term remission. (See 'Children with subacute and chronic allergic contact dermatitis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges William L Weston, MD, who contributed to earlier versions of this topic review.

  1. Abe T. Studies on skin surface barrier functions. Transepidermal water loss and skin surface lipids during childhood. Chem Pharm Bull (Tokyo) 1978; 26:1659.
  2. de Jongh CM, Khrenova L, Verberk MM, et al. Loss-of-function polymorphisms in the filaggrin gene are associated with an increased susceptibility to chronic irritant contact dermatitis: a case-control study. Br J Dermatol 2008; 159:621.
  3. Seidenari S, Giusti G. Objective assessment of the skin of children affected by atopic dermatitis: a study of pH, capacitance and TEWL in eczematous and clinically uninvolved skin. Acta Derm Venereol 1995; 75:429.
  4. Chamlin SL, Kao J, Frieden IJ, et al. Ceramide-dominant barrier repair lipids alleviate childhood atopic dermatitis: changes in barrier function provide a sensitive indicator of disease activity. J Am Acad Dermatol 2002; 47:198.
  5. Williams HC, Burney PG, Strachan D, Hay RJ. The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. II. Observer variation of clinical diagnosis and signs of atopic dermatitis. Br J Dermatol 1994; 131:397.
  6. Lynde CW. Moisturizers: what they are and how they work. Skin Therapy Lett 2001; 6:3.
  7. Lodén M. Role of topical emollients and moisturizers in the treatment of dry skin barrier disorders. Am J Clin Dermatol 2003; 4:771.
  8. Lodén M. Barrier recovery and influence of irritant stimuli in skin treated with a moisturizing cream. Contact Dermatitis 1997; 36:256.
  9. Yilmaz E, Borchert HH. Effect of lipid-containing, positively charged nanoemulsions on skin hydration, elasticity and erythema--an in vivo study. Int J Pharm 2006; 307:232.
  10. Orchard D, Weston WL. The importance of vehicle in pediatric topical therapy. Pediatr Ann 2001; 30:208.
  11. Militello G, Jacob SE, Crawford GH. Allergic contact dermatitis in children. Curr Opin Pediatr 2006; 18:385.
  12. Weston WL, Weston JA, Kinoshita J, et al. Prevalence of positive epicutaneous tests among infants, children, and adolescents. Pediatrics 1986; 78:1070.
  13. Jacob SE, Steele T, Brod B, Crawford GH. Dispelling the myths behind pediatric patch testing-experience from our tertiary care patch testing centers. Pediatr Dermatol 2008; 25:296.
  14. Mortz CG, Lauritsen JM, Bindslev-Jensen C, Andersen KE. Prevalence of atopic dermatitis, asthma, allergic rhinitis, and hand and contact dermatitis in adolescents. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis. Br J Dermatol 2001; 144:523.
  15. Silverberg NB, Licht J, Friedler S, et al. Nickel contact hypersensitivity in children. Pediatr Dermatol 2002; 19:110.
  16. Neale H, Garza-Mayers AC, Tam I, Yu J. Pediatric allergic contact dermatitis. Part I: Clinical features and common contact allergens in children. J Am Acad Dermatol 2021; 84:235.
  17. Admani S, Jacob SE. Allergic contact dermatitis in children: review of the past decade. Curr Allergy Asthma Rep 2014; 14:421.
  18. Zug KA, Pham AK, Belsito DV, et al. Patch testing in children from 2005 to 2012: results from the North American contact dermatitis group. Dermatitis 2014; 25:345.
  19. Belloni Fortina A, Fontana E, Peserico A. Contact Sensitization in Children: A Retrospective Study of 2,614 Children from a Single Center. Pediatr Dermatol 2016; 33:399.
  20. Zafrir Y, Trattner A, Hodak E, et al. Patch testing in Israeli children with suspected allergic contact dermatitis: A retrospective study and literature review. Pediatr Dermatol 2018; 35:76.
  21. Bruckner AL, Weston WL, Morelli JG. Does sensitization to contact allergens begin in infancy? Pediatrics 2000; 105:e3.
  22. Seidenari S, Manzini BM, Motolese A. Contact sensitization in infants: report of 3 cases. Contact Dermatitis 1992; 27:319.
  23. Weston WL, Bruckner A. Allergic contact dermatitis. Pediatr Clin North Am 2000; 47:897.
  24. Tuckermann JP, Kleiman A, Moriggl R, et al. Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy. J Clin Invest 2007; 117:1381.
  25. Bruckner AL, Weston WL. Beyond poison ivy: understanding allergic contact dermatitis in children. Pediatr Ann 2001; 30:203.
  26. Hogan PA, Weston WL. Allergic contact dermatitis in children. Pediatr Rev 1993; 14:240.
  27. Brasch J, Geier J. Patch test results in schoolchildren. Results from the Information Network of Departments of Dermatology (IVDK) and the German Contact Dermatitis Research Group (DKG). Contact Dermatitis 1997; 37:286.
  28. Silverberg NB, Pelletier JL, Jacob SE, et al. Nickel Allergic Contact Dermatitis: Identification, Treatment, and Prevention. Pediatrics 2020; 145.
  29. Clayton TH, Wilkinson SM, Rawcliffe C, et al. Allergic contact dermatitis in children: should pattern of dermatitis determine referral? A retrospective study of 500 children tested between 1995 and 2004 in one U.K. centre. Br J Dermatol 2006; 154:114.
  30. Seidenari S, Giusti F, Pepe P, Mantovani L. Contact sensitization in 1094 children undergoing patch testing over a 7-year period. Pediatr Dermatol 2005; 22:1.
  31. Belloni Fortina A, Cooper SM, Spiewak R, et al. Patch test results in children and adolescents across Europe. Analysis of the ESSCA Network 2002-2010. Pediatr Allergy Immunol 2015; 26:446.
  32. Goldenberg A, Lipp M, Jacob SE. Appropriate Testing of Isothiazolinones in Children. Pediatr Dermatol 2017; 34:138.
  33. Bryden AM, Moseley H, Ibbotson SH, et al. Photopatch testing of 1155 patients: results of the U.K. multicentre photopatch study group. Br J Dermatol 2006; 155:737.
  34. Avenel-Audran M, Dutartre H, Goossens A, et al. Octocrylene, an emerging photoallergen. Arch Dermatol 2010; 146:753.
  35. Haylett AK, Chiang YZ, Nie Z, et al. Sunscreen photopatch testing: a series of 157 children. Br J Dermatol 2014; 171:370.
  36. Cornell E, Kwa M, Paller AS, Xu S. Adverse events reported to the Food and Drug Administration from 2004 to 2016 for cosmetics and personal care products marketed to newborns and infants. Pediatr Dermatol 2018; 35:225.
  37. Sharma V, Beyer DJ, Paruthi S, Nopper AJ. Prominent pruritic periumbilical papules: allergic contact dermatitis to nickel. Pediatr Dermatol 2002; 19:106.
  38. Wöhrl S, Hemmer W, Focke M, et al. Patch testing in children, adults, and the elderly: influence of age and sex on sensitization patterns. Pediatr Dermatol 2003; 20:119.
  39. Jacob SE, Burk CJ, Connelly EA. Patch testing: another steroid-sparing agent to consider in children. Pediatr Dermatol 2008; 25:81.
  40. Bruckner AL, Weston WL. Allergic contact dermatitis in children: a practical approach to management. Skin Therapy Lett 2002; 7:3.
  41. Jacob SE, Brod B, Crawford GH. Clinically relevant patch test reactions in children--a United States based study. Pediatr Dermatol 2008; 25:520.
  42. Neale H, Garza-Mayers AC, Tam I, Yu J. Pediatric allergic contact dermatitis. Part 2: Patch testing series, procedure, and unique scenarios. J Am Acad Dermatol 2021; 84:247.
  43. Yu J, Atwater AR, Brod B, et al. Pediatric Baseline Patch Test Series: Pediatric Contact Dermatitis Workgroup. Dermatitis 2018; 29:206.
  44. Stables GI, Forsyth A, Lever RS. Patch testing in children. Contact Dermatitis 1996; 34:341.
  45. Sherertz EF. Patch testing children. Pediatr Dermatol 1998; 15:68.
  46. Weston WL, Lane AT, Morelli JG. Color Textbook of Pediatric Dermatology, 4th ed, Mosby-Elsevier, 2007.
  47. Hachem JP, De Paepe K, Vanpée E, et al. Efficacy of topical corticosteroids in nickel-induced contact allergy. Clin Exp Dermatol 2002; 27:47.
  48. Green C. The effect of topically applied corticosteroid on irritant and allergic patch test reactions. Contact Dermatitis 1996; 35:331.
  49. Amrol D, Keitel D, Hagaman D, Murray J. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol 2003; 91:563.
  50. Katsarou A, Makris M, Papagiannaki K, et al. Tacrolimus 0.1% vs mometasone furoate topical treatment in allergic contact hand eczema: a prospective randomized clinical study. Eur J Dermatol 2012; 22:192.
  51. Saripalli YV, Gadzia JE, Belsito DV. Tacrolimus ointment 0.1% in the treatment of nickel-induced allergic contact dermatitis. J Am Acad Dermatol 2003; 49:477.
  52. Ellison JA, Patel L, Ray DW, et al. Hypothalamic-pituitary-adrenal function and glucocorticoid sensitivity in atopic dermatitis. Pediatrics 2000; 105:794.
  53. Davis MD, el-Azhary RA, Farmer SA. Results of patch testing to a corticosteroid series: a retrospective review of 1188 patients during 6 years at Mayo Clinic. J Am Acad Dermatol 2007; 56:921.
Topic 1731 Version 27.0

References