|PRACTICE CHANGING CONTINUING EDUCATION: PEDIATRIC DERMATOLOGY
|Year : 2014 | Volume
| Issue : 1 | Page : 33-40
Allergic contact dermatitis in children: Culpable factors, diagnosis and management
Taru Garg, Pravesh Yadav, Surekha Meena, Ram Chander
Department of Dermatology, Lady Hardinge Medical College and Associated Hospitals, New Delhi, India
|Date of Web Publication||3-May-2014|
Prof. Taru Garg
Department of Dermatology, Lady Hardinge Medical College and Associated Hospitals, New Delhi
Source of Support: None, Conflict of Interest: None
Allergic contact dermatitis (ACD) is not uncommon in children. Prevalence of ACD was previously thought to be low in children and adolescents, but of late increased prevalence has been reported. Actual increase in the prevalence could be due to increased recognition of the disease or due to other factors such as changes in lifestyle. Various factors such as age, gender, atopy, social and cultural practices, habits of parents and caregivers, and geographical changes may influence the prevalence and pattern of ACD in children. It can significantly affect the quality of life among children.
ACD can affect various sites, including hands, face, neck, axillae, trunk, anogenital region, thigh, feet, and others, depending on the site of exposure to allergen. Common allergens implicated in childhood ACD include nickel, cobalt, potassium dichromate, mercury, aluminium, skin care products, fragrances, neomycin, dyes, preservatives, rubber, and so on. Identification of the implicated allergen is vital as the patient may experience recurrent episodes of dermatitis in the absence of avoidance of allergen. Patch testing is by far the commonly used method of identification of the causative allergen. The only etiologic treatment is elimination of the contact allergen. The patients/parents should be informed about the identity of the offending agent and the possible sources of the sensitizer.
Topical steroids used in the acute stage and topical calcineurin inhibitors along with oral H1-antihistamines to alleviate itching are the mainstay of treatment. In widespread and severe cases, systemic corticosteroids may be indicated for a short period of time. The prognosis of ACD is dependent on its cause and the feasibility of avoiding repeated or continued exposure to the causative allergen.
Keywords: Allergic contact dermatitis, children, diagnosis, management
|How to cite this article:|
Garg T, Yadav P, Meena S, Chander R. Allergic contact dermatitis in children: Culpable factors, diagnosis and management. Astrocyte 2014;1:33-40
|How to cite this URL:|
Garg T, Yadav P, Meena S, Chander R. Allergic contact dermatitis in children: Culpable factors, diagnosis and management. Astrocyte [serial online] 2014 [cited 2019 Aug 17];1:33-40. Available from: http://www.astrocyte.in/text.asp?2014/1/1/33/131860
| Introduction|| |
Contact dermatitis is a localized or generalized inflammation of the skin, due to extrinsic factors and could be influenced by intrinsic factors. It may be classified as (1) allergic contact dermatitis (ACD) and (2) irritant contact dermatitis (ICD).
ACD is an acquired disease and its development depends on the time and intensity of the exposure to haptens, sensitive and irritant potential of haptens, and also on the functional state of skin protective barrier-both physical and immunological.  ACD is the most common clinical form of contact allergy.  It has been estimated that 20% of pediatric population is affected by ACD. 
In the past, prevalence of ACD was said to be low in children and adolescents but now an increase in the prevalence has been reported. It may be due to rapid urbanization, westernization of lifestyles, poor quality of products available, and extremely relaxed vigilance on adherence to product safety guidelines.  Improved recognition of ACD and increased patch testing in children may also be responsible for the awareness of increased prevalence of ACD. 
ACD acquired in childhood has important repercussions for the patients, and may affect decisions regarding future occupation in adulthood.  Loss of sleep due to uncontrolled itching, absence at school, feeling of inferiority among the peer groups, and irritability can be found in children suffering from chronic severe contact dermatitis.  The patient may experience chronic or recurrent episodes of dermatitis if the source is not correctly identified as early as possible by patch testing. 
| Epidemiology|| |
ACD affects approximately 7% of the general population.  Reported prevalence of ACD in childhood has risen from 13.3% to 67% during the last decade. , This alarming increase in prevalence has been explained due to either a true increase in ACD or an increased rate of diagnosis.  In the perspective of developing countries, like India, westernization of lifestyle has resulted in an increased exposure to cosmetics, hair and other dyes, and packed food.  There are various factors such as age, gender, atopy, social and cultural practices, habits of parents and caregivers, and geographical changes, which can affect the prevalence of ACD in children. 
In 1999, Mortz et al reported an overall patch test positivity of 14.5%-70.7% in children with suspected ACD. Of the positive tested children, approximately 56-93% had been thought of current relevance. Weston et al estimated that ACD accounts for up to 20% of all dermatitis in childhood. A retrospective study of 500 children tested between 1995 and 2004 in one UK center showed patch test positivity of 27%, with 61% of reactions considered to be of current clinical relevance.  In a Spanish study, patch test was found to be positive in 318 children upto the age of 14 years, out of 1023 patch-tested children. 
In a retrospective epidemiologic study from Singapore involving 2340 children and adolescents, 1063 (583 girls, 480 boys) were found to be positive to one or more allergens. [16 ] Jacob et al in 2010 reported the highest rate of sensitization of 95.6% among 45 children of 0-16 years of age. One Indian study of total 70 children (age range 1-15 years) showed positive allergic reactions in 80% and relevant positive reactions in 48.6% of patients. 
One population-based patch test study of unselected pediatric patients found the prevalence of past or current relevant reactions to be 7%, with a higher risk seen infemales.  This is significantly lower than the prevalence in selected pediatric populations (symptomatic patients). Thus, the real prevalence of ACD, which is defined as a positive patch test with clinical correlation with the dermatitis experienced by a symptomatic individual, ranges from 14% to 77% among children referred for patch testing due to clinical suspicion of contact dermatitis. ,,
| Predisposing Factors|| |
Uhr's study  supported that infants could indeed be sensitized, but the younger the infant, the weaker the response. Two studies have shown that the highest rate of sensitization occurs in children younger than 3 years. , In 2003, Wohrl et al tested 2770 children and adults with suspected disease, finding positive patch tests in 49% of the study participants. The highest rate of sensitization was found in children younger than 10 years at a rate of 62%. 
Women are usually more frequently patch-tested, and have more positivity than men.  ACD to cosmetics is more common in teenage girls.  A large study of 1094 children between 7 months and 12 years of age, did not show significant variations in sensitization according to their gender. 
The relationship of atopy, particularly atopic eczema, to predisposition to ACD is still not clear.  One explanation for increased risk of contact allergy in children with atopic dermatitis is due to their damaged epidermal barrier, with subsequent increased penetration of allergens or, alternatively these children are exposed to more sensitizers as a result of topical treatments that they may be using for their disease. , Atopic eczema may be an important risk factor for development of ACD in children rather than in adults. In an Indian study by Nilendu et al, atopy was present in 25.7% children out of 70. th
ACD is a Th1 cell-mediated delayed hypersensitivity and atopics are known to exhibit down regulation of Th1 cells, which should mean a decreased tendency to develop ACD. , Indeed, patients with severe atopic dermatitis may have a diminished capacity for dinitrochlorobenzene sensitization.  However, clinical studies are conflicting, some showing an increase in the prevalence of contact allergy in atopics, especially to medicaments,  others the same,  and some others a low prevalence. , In a study of 101 sets of twins, no correlation was found between positive patch tests and atopy. 
The key role of filaggrin in maintaining an effective skin barrier against the external environment has been shown.  Lack of expression of filaggrin has been shown to increase the risk of developing allergic sensitization and atopic dermatitis, but the association between mutations in the filaggrin gene and ACD in children remains to be thoroughly explored. 
Percutaneous absorption is facilitated by inflammatory changes in the dermis. Hand eczema predisposes to nickel sensitivity and vice versa. Longer the duration of eczema, the greater is the chance of sensitization. Occlusion greatly promotes percutaneous absorption and probably contributes to the high incidence of medicament dermatitis.  As sensitivity is more easily acquired if an allergen is applied to damaged skin, concomitant ICD will promote sensitization and lower the threshold for elicitation of an ACD in those exposed to associated allergens. 
UVB exposure has shown to diminish the skin's response to contact allergens. Seasonal variation of the dermatitic lesions might also suggest a plant allergen or photo aggravation or photo allergy.th
Socioeconomic and Cultural Factors
Different prevalence and patterns of contact dermatitis have been attributed to various social and cultural practices prevalent in a particular area, for example, nickel allergy due to jewellery that is worn at a young age for religious reasons.  In a German study, higher rates of sensitization have been documented in 13-18 years old adolescents who worked as hair dressers or in the healthcare field. 
There are many potential causes of ACD in children, such as nickel in toys, sports gear, and boating shoes. Children are becoming exposed to a wider variety of allergens at a younger age; body piercing among teenagers is increasing in popularity, girls tend to use make-up and beauty products at a younger age, face painting is popular and participation in a wider variety of sports and other hobbies appears to be more widespread among an increasingly affluent society. 
| Histopathology|| |
When the clinical diagnosis of allergic and/or ICD is not clear, skin biopsy is considered as a useful tool for the diagnosis.
The earliest change is the appearance of few perivascular lymphocytes. Focal spongiosis also appears at the same time. Vesiculation occurs when focal areas of spongiosis coalesce. Eosinophils may be present in both dermis and epidermis and are suggestive of ACD. In subacute and chronic dermatitis, inflammation is less prominent and may be absent from the dermis. Mild spongiosis and micro vesicles may be seen, which are absent in long-standing cases. Chronically, acanthosis with hyperkeratosis and some parakeratosis may be seen. Upper dermal fibrosis may occur as result of thickened collagen. 
| Clinical Features|| |
The clinical characteristics of ACD are same in children as in adults.  The classical clinical presentation of ACD is pruritic eczematous dermatitis. The location can be important for identification of the causal allergen because contact dermatitis is generally restricted to the contact site.
In children with hand eczema, the most frequent final diagnoses were ACD, followed by atopic dermatitis, and vesicular (dyshidrotic) hand eczema.  Streaky dermatitis of the fingers, dorsa of the hands and forearms is typically caused by plants.  Allergy to nickel, chromate, and p-tertiary-butylphenolformaldehyde resin (PTBPFR) may develop at the wrists from sensitivity to the metal, leather, and glue, respectively, in watchstraps containing these allergens [Figure 1].
|Figure 1: Nickel dermatitis involving the forearms due to artificial metal bangles.|
Click here to view
The face is a common site of involvement. Facial ACD from fragrances, hair dyes, preservatives, and other constituents of skincare products and cosmetics, including nail varnish are common. Nail varnish allergy often affects the face in well-localized patches, and may be associated with eyelid dermatitis. 
The forehead is affected by allergy to anything applied to the hair and also to chromate in leather hatbands. Spectacle frames containing nickel or plastics may cause dermatitis on areas of contact with the cheeks, nose, eyelids, and ears. 
The skin of eyelid is thin, sensitive, and common sources of eyelid dermatitis are aerosolized, applied, or transferred products: Cosmetics, nail varnish, fragrances, eye drops, metal particles from objects handled, and so on , [Figure 2].
Ear Lobe Dermatitis
Earrings and clips are the common sources of ear lobe dermatitis. Granulomatous contact allergy to nickel, palladium, and gold has been seen after ear piercing. 
Nickel in the clasps of necklaces or zip fasteners produce a small area of dermatitis on the nape of the neck. Textiles and necklaces may cause a collar-like dermatitis, or eruptions on the sides of the neck. Perfume may cause both ACD and phototoxic dermatitis (Berloque dermatitis) on the neck, especially the sides.
In adolescent patients, axillary exan them may indicate a fragrance allergy due to the use of deodorants. The dermatitis produced by textiles tends to be periaxillary.
In both genders, nickel buttons and zip fasteners cause dermatitis localized to where they are worn, but a more widespread secondary spread eruption is often associated [Figure 3]. Textile dermatitis predominantly affects the neck and axillary folds and spares the area covered by undergarments. 
|Figure 3: Allergic contact dermatitis over the abdomen due to nickel present in the button of jeans.|
Click here to view
The anogenital region is a common site for medicament sensitization. 
Textile dermatitis starts at the edge of the underwear, and is usually more pronounced in the popliteal spaces or gluteal folds. Finishes in the material of the pockets or objects kept in the pockets (eg, nickel coins or boxes of matches) may provoke a patch of dermatitis on the underlying skin. 
Common sources of allergy are shoes materials, including leather, rubber, glues, nickel, stockings, topical medicaments, antiseptics, and antiperspirants. Shoe dermatitis presents as pruritic papular and oozy rash on the dorsum of toes, extending on to the feet and sparing the toe webs. It should be differentiated from juvenile plantar dermatosis, which is a more common dermatosis in children [Figure 4]. 
| Specific Allergens|| |
Nickel is the most widespread allergen in the general population and is most often identified as the leading allergen in children.  It accounts for up to 14.9% of positive patch test reactions in asymptomatic children and generally more frequent reactions are seen in females. ,
Ear piercing is often considered the major risk factor for sensitization to nickel.  Other sources include everyday items such as jewellery, eyeglass frames, belt buckles, jean snaps, zippers, coins, keys, and even cell phones. Typical locations for nickel dermatitis include the face, earlobes, wrist, neck, and periumblical skin with the last site being most common.  Id eruptions due to nickel may sometimes be confused with atopic dermatitis. They tend to be more persistent than localized contact dermatitis, lasting up to months after localized plaques have cleared. Systemic contact dermatitis has also been reported with nickel. 
This metal often co-sensitizes with other metals, particularly nickel and potassium dichromate.  Yet, cobalt itself remains relevant for ACD. One study attributed 2 of 17 cases of pediatric hand dermatitis to cobalt.
A common source for potassium dichromate exposure in children is its use in tanning leather, particularly in shoes.  Distribution of dermatitis is typically located at the dorsa of feet and occasionally at the plantar surfaces.  Sources of potassium dichromate are shoes, boots, belts, gloves, dental implants, orthopaedic prostheses, suture materials, vitamin supplements, green tattoos, dyes, pigments, paints, ceramic, and antirust products.  Although many of these items are encountered more so in occupational exposures, these items could potentially exist in a child's home environment or relate to adolescent hobbies.
Sensitization to mercury is relatively common. Sources of exposure include shoes in which mercury is used as a preservative, and more classically antiseptic solutions.  Other items that may contain mercurial agents are eye drops, depigmenting creams, pediculosis preparations, vaccines, broken thermometers, amalgam fillings, contact lens solutions, and pesticides. 
Children may develop cutaneous granulomas in relation to immunizations containing aluminum hydroxide; the prognosis is good with spontaneous resolution. These children have a positive patch test to metallic aluminum or aluminum salts. The Finn chambers used for patch testing are of aluminum and similar plastic chambers are required for the testing these children. 
Skin Care Products and Fragrances
In the present day, many cosmetic products are being marketed, especially for children. Kohl et al. patch tested 70 children suspected of having ACD where cosmetics was found to be the most common cause for sensitization.  Most cases of ACD to skin care products are caused by leaveon cosmetics. The risk of developing ACD from rinse-off products such as soaps, shampoos, and shower foams has been less studied; however, they seem to be a rare cause of dermatitis in children. 
Ingredient labeling on cosmetics is very important to help us in identifying the possible allergens in the products. Fragrance are the common sensitizers in the pediatric population and involve the same areas as the adults as face, neck, and axillae.  Balsam of Peru is an excellent allergen for fragrance allergy screening. Sources of balsam of Peru are cosmetic products such as perfumes, lotions, diaper area care products, toothpaste, mouthwashes, pharmaceutical preparations, scents, and flavorings for foods and drinks.  In one Indian study of 70 children, fragrance mix was the third most frequent allergen and second most relevant allergen. 
It is the most sensitizing of all topical antimicrobials.  The patch test positivity with neomycin in children was found to be 6%.  Neomycin was found to cross react with gentamicin (40%-66%), and tobramycin (25%-65%) but not to streptomycin. 
Other Topical Antibiotics
Other common sensitizers among topical antibiotics are nitrofurazone, framycetin, and sodium fusidate. Less common being penicillins, bacitracin, and metronidazole. 
Corticosteroids have been implicated in pediatric ACD. It has been recommended that the standard corticosteroid series as well as any agents being used by the child be patch tested when ACD is suspected in the setting of topical steroid use. 
Preservatives, Antimicrobials, and Vehicles
p-Phenylene Diamine (PPD)
PPD is an oxidizing agent commonly used as a permanent hair dye and as rubber antioxidant.  Semi permanent henna tattoos containing PPD are a well-known cause of severe contact dermatitis, mainly in children. Another relevant exposure source to PPD are hair dyes, which are increasingly being used by the children and have also been reported to cause intense facial and scalp dermatitis.
The common sources are cosmetics, textile resins, paints/lacquers, printing inks, cleaning products, tanning agents for leather, preservatives, coloring agents, filling agents, and glues. 
Paraben is the most widely used preservative in cosmetics, drugs, and foods.  Relevant allergy to this is considered to be rare. The reported range of allergy is remarkably constant, within 0.5%-1.7% of the patch-tested patients in many studies.  Paraben was the most common allergen tested positive among all other allergens of Indian Standard Series (ISS) in an Indian study of 70 children. 
It is a rare allergen, found in corticosteroids creams. It has a very low patch test positivity ranging from 0.4% to 0.6%. 
Lanolin, containing wool alcohols is found in many skin care products. A few large scale epidemiologic studies list wool alcohols as one of the most common allergens in children. ,
It can cause ICD, ACD, and nonimmunologic contact urticaria. It should not be used in children younger than 2 years.
Thimerosal is composed of two allergenic compounds, mercury and thiosalicylic acid. It is among one of the most common causes for positive patch testing in pediatric studies. ,
It is used as a preservative in vaccines, antitoxins, ophthalmic preparations, contact lens solutions, and eardrops. High rates of sensitization were likely due to the presence of this compound in mandatory vaccines used in the past.
Relevance of rubber allergy to current dermatitis was found in 50% of patients, which was highest for thiuram mix and lowest for black rubber mix and 80% of these allergens originated from footwear.  Other common sources of hapten exposure in children are synthetic fibers and dyes used in their clothing, toys, and toys cosmetics.
| Diagnosis|| |
The site and clinical appearance of the lesions frequently suggest the etiologic factor when the patient is first seen.  If the dermatitis has taken a chronic course, the patient's observations about factors causing relapses may be helpful. Patch testing is the universally accepted method for the detection of the causative contact allergens.  A proper patch test uses a specific substance that produces the disease, contact dermatitis; it is the purified etiologic agent reproducing the clinical disease in a susceptible host and causing no disease outside the proper clinical settings  [Figure 5].
Special Consideration in Pediatric Patch Testing
It is now generally accepted that dilution of allergens used when patch testing children should be the same as those for adults.  Several types of chambers are available for the application of allergens to the skin. The most widely used and, often taken as the "standard" is the Finn chamber. One of the intrinsic challenges of pediatric patch testing is the child's anatomical small back size. As children are active, special attention should be paid in properly securing the patches with rolled gauze, Hypafix, or special garments. ,
The patch test should be applied to the upper quadrants of the back [Figure 6]. Other sites for patch test application are front of the trunk, upper arms, or thighs; these are not, however, standard sites and anatomical variations in skin thickness, and degree of occlusion will alter allergen penetration and elicitation responses. 
|Figure 6: Patch test strip with labelled antigens applied over the upper back.|
Click here to view
Under ideal circumstances, allergens are applied for 2 days and site of the application is kept dry. Readings should be made at 2 days after application with a second reading at 4 days. A single reading is unsatisfactory as it may not be possible to distinguish an irritant reaction from an allergic one. Doubtful reactions may be further evaluated by a repeat open application test. This requires application of an agent or a product several times daily for 2-3 days to the skin of upper arm or other suitable sites. A papular response indicates a positive reaction. 
A positive patch test reaction does not always mean that the cause of presenting dermatitis has been found, likewise a negative patch test result does not fully exclude ACD. Standard screening series include only statistically common allergens; we must remain alert to the possibility of rare, exotic, or new sensitizers. 
Other tests for diagnosis of ACD include true test, open test, usage test, repeat open application tests, and so on.
| Treatment|| |
The only available etiologic treatment of ACD is elimination of the contact allergen. The patients should be informed about the identity of the offending agent and the possible sources of the sensitizer. Cross reacting substances should be listed.
Topical steroids are used in the acute stage and are gradually replaced by cold creams as the skin lesions withdraw. Topical calcineurin inhibitors are another therapeutic option and should be considered when steroid-sparing agents are required. These agents can be used for certain areas, such as the face, axilla, and groin, which are more susceptible to steroid-induced atrophy.  If ACD is widespread and severe, systemic corticosteroids may be indicated for a short period of time. [ 61] Oral H1-antihistamines are widely used as an adjuvant treatment for pruritus in infants and children. 
| Prognosis|| |
The prognosis of ACD depends on its cause and the feasibility of avoiding repeated or continued exposure to the causative allergen.  In Sweden, skin atopy was the factor that carried the worst outlook, followed by contact allergy, especially to nickel, and female gender. 
It is clear from a number of studies that poor compliance and higher rate of ongoing exposure to the causative allergen is associated with a worse prognosis.  Once the culpable allergens are identified by patch testing and if the patient can take steps to evade them, improvement of dermatitis is the rule. 
The prognosis of ACD is worse than that of ICD.  Studies show that the most common cause of persistence of contact dermatitis in female is nickel and in male is chromate.  Age was not found to influence the prognosis in most of the studies. 
| References|| |
Czarnobilska E, Dyga W, Krzystyniak D, Czarnobilski K, Myszkowska D, Obtu³owicz K. Influence of environment exposures on the frequency of contact allergies in children and adolescents. Ann Agric Environ Med 2012;19:11-6.
Thyssen JP, Uter W, McFadden J, Menné T, Spiewak R, Vigan M, et al
. The EU Nickel Directive revisited: Future steps towards better protection against nickel allergy. Contact Dermatitis 2011;64:121-5.
Hammonds LM, Hall VC, Yiannias JA. Allergic contact dermatitis in 136 children patch tested between 2000 and 2006. Int J Dermatol 2009;48:271-4.
Sarma N, Ghosh S. Clinico-allergological pattern of allergic contact dermatitis among 70 Indian children. Indian J Dermatol Venereol Leprol 2010;76:38-44.
Hogeling M, Pratt M. Allergic contact dermatitis in children: The Ottawa hospital patch-testing clinic experience, 1996 to 2006. Dermatitis 2008;19:86-9.
Clayton TH, Wilkinson SM, Rawcliffe C, Pollock B, Clark SM. Allergic contact dermatitis in children: Should pattern of dermatitis determine referral? A retrospective study of 500 children tested between 1995 and 2004 in one UK centre. Br J Dermatol 2006;154:114-7.
Jacob SE, Bruk CJ, Connely EA. Patch testing: Another steroid-sparing agent to consider in children. Pediatr Dermatol 2008;25:81-7.
Lee PW, Elsaie ML, Jacob SE. Allergic contact dermatitis in children: Common allergens and treatment: A review. Curr Opin Pediatr 2009;21:491-8.
Heine G, Schnuch A, Uter W, Worm M. Frequency of contact allergy in German children and adolescents patch tested between 1995 and 2002: Results from the Information Network of Departments of Dermatology and the German Contact Dermatitis Research Group. Contact Dermatitis 2004;51:111-7.
Mortz CG, Andersen KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis 1999;41:121-30.
Roul S, Ducombs G, Taieb A. Usefulness of the European standard series for patch testing in children. A 3 year single centre study of 337 patients. Contact Dermatitis1999;40:232-5.
Beattie PE, Green C, Lowe G, Lewis-Jones MS. Which children should we patch test? Clin Exp Dermatol 2007;32:6-11.
Sharma VK, Asati DP. Pediatric contact dermatitis. Indian J Dermatol Venereol Leprol 2010;76:514-20.
Weston WL, Weston JA. Allergic contact dermatitis in children. Am J Dis Child 1984;138: 932-6.
Romagluerac C, Aumor A, Camarasa JM, Garcia Bravo B, Garcia Perez A, Grimalt F, et al
. Contact dermatitis in children. Contact Dermatitis 1985;12:283-4.
Goon AT, Goh CL. Patch testing of Singapore children and adolescents: Our experience over 18 years.Pediatr Dermatol 2006;23:117-20.
Jacob SE, Yang A, Herro E, Zhang C. Contact allergens in a pediatric population: Association with atopic dermatitis and comparison with other North American referral centers. J Clin Aesthet Dermatol 2010;3:29-35.
Mortz CG, Lauritsen JM, Bindslev-Jensen C, Andersen KE. Contact allergy and allergic contact dermatitis in adolescents: Prevalence measures and associations. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS). Acta Derm Venereol 2002;82:352-8.
Seidenari S, Giusti F, Pepe P, Mantovani L. Contact sensitization in 1094 children undergoing patch testing over a 7-year period. Pediatr Dermatol 2005;22:1-5.
Lewis VJ, Statham BN, Chowdhury MM. Allergic contact dermatitis in 191 consecutively patch tested children. Contact Dermatitis 2004;51:155-6.
Fernández Vozmediano JM, Armario Hita JC. Allergic contact dermatitis in children. J Eur Acad Dermatol Venereol 2005;19:42-6.
Uhr J, Dancis J, Newmann CG. Delayed-type hypersensitivity in premature neonatal humans. Nature 1960;187:1130-1.
Manzini BM, Ferdani G, Simonetti V, Donini M, Seidenari S. Contact sensitization in children.PediatrDermatol 1998;15:12-7.
Wohrl S, Hemmer W, Focke M, Gotz M, Jarisch R. Patch testing in children, adults, and the elderly: Influence of age and sex on sensitization patterns. Pediatr Dermatol 2003;20:119-23.
García-Gavín J, Armario-Hita JC, Fernández-Redondo V, Fernández-Vozmediano JM, Sánchez-Pérez J, Silvestre JF, et al
. Epidemiology of contact dermatitis in Spain. Results of the Spanish surveillance system on contact allergies for the year 2008. Actas Dermosifiliogr 2011;102:98-105.
Krafchik BR. Eczematous dermatitis. In: Schaner LA, Hansen RC, editors. Pediatric Dermatology. 2nd ed. Edinburgh: Churchill Livingstone; 1995. p. 710-3.
Jacob SE, Bruk CJ, Connely EA. Patch testing: Another steroid-sparing agent to consider in children. Pediatr Dermatol 2008;25:81-7.
Clark RA. Cell-mediated and IgE-mediated responses in atopic dermatitis. Arch Dermatol 1989;125:413-6.
Bos JD, Wierenga EA, Sillevis Smitt JH, van der Heijden FL, Kapsenberg ML. Immune dysregulation in atopic eczema. Arch Dermatol 1992;128:1509-12.
Uehara M, Sawai T. A longitudinal study of contact sensitivity in patients with atopic dermatitis. Arch Dermatol 1989;125:366-8.
Bandmann HJ, Breit R, Leutgeb C. Contact allergy and atopic dermatitis. Arch Dermatol Forsch 1972;244:332-4.
Cronin E, Bandmann HJ, Calnan CD, Fregert S, Hjorth N, Magnusson B, et al
. Contact dermatitis in the atopic. Acta Derm Venereol (Stockh) 1970;50:183-7.
De Groot AC. The frequency of contact allergy in atopic patients with dermatitis. Contact Dermatitis 1990;22:273-7.
Hanifin JM. Atopic dermatitis. J Am Acad Dermatol 1982;6:1-13.
Frsbeck M, Skog E, Ytterborn KH. Delayed type of allergy and atopic disease among twins. Acta Derm Venereol (Stockh) 1968;48:192-7.
McGrath JA, Uitto J. The flaggrin story: Novel insights into skin barrier function and disease. Trends Mol Med 2008;14:20-7.
Novak N, Baurecht H, Schafer T, Rodriguez E, Wagenpfeil S, Klopp N, et al
. Loss-of-function mutations in the flaggrin gene and allergic contact sensitization to nickel. J Invest Dermatol 2008:128;1430-5.
Menné T, Borgan O, Green A. Nickel allergy and hand dermatitis in a stratified sample of the Danish female population: An epidemiological study including a statistic appendix. Acta DermVenereol (Stockh) 1982;62:35-41.
Beck MH, Wilkinson BM. Allergic contact Dermatitis. In: Burns T, Breathnach SM, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8th ed. Oxford: Blackwell; 2010. p. 26.1-26.106.
Pedersen LK, Johansen JD, Held E, Agner T. Augmentation of skin response by exposure to a combination of allergens and irritants-a review. Contact Dermatitis 2004;50:265-73.
Histiology of contact dermatitis. In: Rietschel RL, Fowler JF, editors. Fisher's contact Dermatitis, 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 31-2.
Militello G, Jacob SE, Crawford GH. Allergic contact dermatitis in children. Curr Opin Pediatr 2006;18:385-90.
Toledo F, García-Bravo B, Fernández-Redondo V, De la Cuadra J, Giménez-Arnau AM, Borrego L, et al
. Patch testing in children with hand eczema. A 5-year multicentre study in Spain. Contact Dermatitis 2011;65:213-9.
Lidén C, Berg M, Farm G, Wrangsjö K. Nail varnish allergy with far-reaching consequences. Br J Dermatol 1993;128:57-62.
Heim KE, McKean BA. Children's clothing fasteners as a potential source of exposure to releasable nickel ions. Contact Dermatitis 2009;60:100-5.
Dotterud LK, Falk ES. Contact allergy in relation to hand eczema and atopic diseases in north Norwegian school children. Acta Paediatr 1995;84:402-6.
Smith-Sivertsen T, Dotterud LK, Lung E. Nickel allergy and its relationship with local nickel pollution, ear piercing, and atopic dermatitis: A population-based study from Norway. J Am Acad Dermatol 1999;40:726-35.
Hsu JW, Matiz C, Jacob SE. Nickel Allergy: Localized, id, and systemic manifestations in children. Pediatr Dermatol 2011;28:276-80.
Castanedo-Tardan MP, Jacob SE. Potassium dichromate. Dermatitis 2008;19:e24-5.
Goossens A. The allergens in children. Contact Dermatitis 2008;58Suppl 1:9-30.
White IR. Allergic contact dermatitis. In: Harper J, Oranje A, Prose N. editors. Textbook of pediatric dermatology. Oxford: Blackwell Sciences; 2002. p. 287-94.
Kohl L, Blondeel A, Song M. Allergic contact dermatitis from cosmetics. Retrospective analysis of 819 patch-tested patients. Dermatology 2002;204:334-7.
Uter W, Balzer C, Geier J, Frosch PJ, Schnuch A. Patch testing with patient's own cosmetics and toiletries: Results of the IVDK, 1998-2002. Contact Dermatitis 2005;53:226-33.
Tomar J, Jain VK, Aggarwal K, Dayal S, Gupta S. Contact allergies to cosmetics: Testing with 52 cosmetic ingredients and personal products. J Dermatol 2005;32:951-5.
Veien NK, Halter T, Justesen O, Nørholm N. Oral challenge with balsam of Peru. Contact Dermatitis 1985;12:104-7.
Topical antimicrobial. In: Rietschel RL, Fowler JF, editors. Fischer's contact dermatitis. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 167-83.
Fisher AA. Prevention of contact dermatitis. N Y State J Med 1978;78:1739-41.
Auricchio L, Nino M, Suppa F. Contact sensitivity to budesonide in a child. Contact Dermatitis 2000;42:359.
Flyvholm MA. Preservatives in registered chemical products. Contact Dermatitis 2005;53:27-32.
Britton JE, Wilkinson SM, English JS, Gawkrodger DJ, Ormerod AD, Sansom JE, et al
. The British standard series of contact dermatitis allergens: Validation in clinical practice and value for clinical governance. Br J Dermatol 2003;148:259-64.
Saint-Mezard P, Rosieres A, Krasteva M, Berard F, Dubois B, Kaiserlian D, et al
. Allergic contact dermatitis. Eur J Dermatol 2004;14:284-95.
Practical aspects of Patch testing. In: Rietschel RL, Fowler JF, editors. Fischer's contact dermatitis. 5th ed. Baltimore: Lippincott Williams and Wilkins; 2001. p. 9-33.
McAlwany JP, Sheretz EF. Contact dermatitis in infants, children and adolescents. Adv Dermatol 1994;9:205-23.
Meding B, Lantto R, Lindahl G, Wrangsjö K, Bengtsson B. Occupational skin disease in Sweden-a 12-year follow-up. Contact Dermatitis 2005;53:308-13.
Agner T, Flyvholm MA, Menné T. Formaldehyde allergy: A follow-up study. Am J Contact Dermatitis 1999;10:12-7.
Khan SA, Rani Z, Ahmed KM, Hussain I, Kazmi AH. Evaluation and pattern of nickel dermatitis in patients with allergic contact dermatitis. J Pak Assoc Dermatol 2005;15:136-9.
Meding B, Swanbeck G. Consequences of having hand eczema. Contact Dermatitis 1990;23:6-14.
Rosen RH, Freeman S. Prognosis of occupational contact dermatitis in New South Wales, Australia. Contact Dermatitis 1993;29:88-93.
Burrows D. Prognosis in industrial dermatitis. Br J Dermatol 1972;87:145-8.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]