Clinical Commentary Review

Pediatric Allergic Contact Dermatitis: Lessons for

Better Care
Alina Goldenberg, MASa, Nanette Silverberg, MDb, Jonathan I. Silverberg, MD, PhD, MPHc, James Treat, MDd,e, and
Sharon E. Jacob, MDf La Jolla and Loma Linda, Calif; New York, NY; Chicago, IL; Philadelphia, Pa

INFORMATION FOR CATEGORY 1 CME CREDIT

Credit can now be obtained, free for a limited time, by reading the
review articles in this issue. Please note the following instructions.
Method of Physician Participation in Learning Process: The core
material for these activities can be read in this issue of the Journal or online
at the JACI: In Practice Web site: www.jaci-inpractice.org/. The accompanying tests may only be submitted online at www.jaci-inpractice.org/.
Fax or other copies will not be accepted.
Date of Original Release: September 1, 2015. Credit may be obtained
for these courses until August 31, 2016.
Copyright Statement: Copyright 2015-2017. All rights reserved.
Overall Purpose/Goal: To provide excellent reviews on key aspects of
allergic disease to those who research, treat, or manage allergic disease.
Target Audience: Physicians and researchers within the eld of
allergic disease.
Accreditation/Provider Statements and Credit Designation: The
American Academy of Allergy, Asthma & Immunology (AAAAI) is
accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The AAAAI designates these educational activities for a maximum
of 1 AMA PRA Category 1 Credit. Physicians should only claim credit
commensurate with the extent of their participation in the activity.

List of Design Committee Members: Alina Goldenberg, MAS,

Nanette Silverberg, MD, Jonathan I. Silverberg, MD, PhD, MPH, James
Treat, MD, and Sharon E. Jacob, MD
Activity Objectives
1. To understand the risk factors for nickel sensitization.
2. To recognize the uses and pitfalls of epicutaneous patch testing.
3. To understand the physiology of the elicitation phase of allergic
contact dermatitis.
Recognition of Commercial Support: This CME has not received
external commercial support.
Disclosure of Signicant Relationships with Relevant Commercial
Companies/Organizations: S. E. Jacob has received research support
from the Society for Pediatric Dermatology; has served as an independent investigator on the safety and efcacy of the Thin-Layer
Rapid Use Epicutaneous Patch Test (Smart Practice; Phoenix,
Ariz) and the Pediatric Research Equity Act 1 (PREA-1) trial and
now serves as an investigator on PREA-2; and has served as a
consultant for Johnson & Johnson. N. Silverberg has received consultancy fees from Johnson & Johnson and Proctor & Gamble and
has received research support from the American Academy of
Dermatology. The rest of the authors declare that they have no
relevant conicts of interest.

Allergic contact dermatitis (ACD) is an immune-mediated

condition that is likely underrecognized in children. ACD is the
result of primary sensitization and secondary elicitation by
allergy-provoking haptens. A detailed clinical history and
physical examination may yield diagnosis. Patch testing is the
criterion standard diagnostic tool for conrming the diagnosis of
ACD in both children and adults. Herein, we present an
overview of pediatric ACD, an analysis of relevant current

literature on the topic, focused management recommendations,

and a discussion of existing knowledge gaps that must be
addressed by future research. 2015 American Academy of
Allergy, Asthma & Immunology (J Allergy Clin Immunol Pract
2015;3:661-7)

Equity Act 1 (PREA-1) trial and now serves as an investigator on PREA-2;

and has served as a consultant for Johnson & Johnson. N. Silverberg has
received consultancy fees from Johnson & Johnson and Proctor & Gamble
and has received research support from the American Academy of
Dermatology. The rest of the authors declare that they have no relevant
conicts of interest.
Received for publication January 20, 2015; revised manuscript received and
accepted for publication February 17, 2015.
Corresponding author: Sharon E. Jacob, MD, Department of Dermatology, Loma
Linda University, Faculty Medical Ofces, 11370 Anderson St, Ste 2600, Loma
Linda, CA 92354. E-mail: sjacob@contactderm.net.
2213-2198
2015 American Academy of Allergy, Asthma & Immunology
http://dx.doi.org/10.1016/j.jaip.2015.02.007

Medical Student, University of California San Diego, La Jolla

Chief, Pediatric Dermatology, M. Sinai Health Systems, Mt. Sinai St. LukesRoosevelt Hospital Center, New York
c
Departments of Dermatology, Preventive Medicine and Medical Social Sciences,
Feinberg School of Medicine at Northwestern University, Chicago
d
Fellowship Director, Pediatric Dermatology, The Childrens Hospital of Philadelphia, Philadelphia
e
Assistant Professor, Pediatrics and Dermatology, University of Pennsylvania School
of Medicine, Philadelphia
f
Associate Professor of Dermatology, Loma Linda University, Loma Linda
Conicts of interest: S. E. Jacob has received research support from the
Society for Pediatric Dermatology; has served as an independent investigator on the safety and efcacy of the Thin-Layer Rapid Use Epicutaneous
Patch Test (Smart Practice; Phoenix, Ariz) and the Pediatric Research
b

Key words: Allergic contact dermatitis; Atopic dermatitis;

Children; Pediatric; Nickel; Sensitization

661

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GOLDENBERG ET AL

Abbreviations used
ACD- Allergic contact dermatitis
ACDS- American Contact Dermatitis Society
AD- Atopic dermatitis
FDA- Food and Drug Administration
PPTR- Positive patch test reaction
PPD- Paraphenylynediamine
PREA-1- Pediatric Research Equity Act 1
RPPTR- Relevant positive patch test reaction

Allergic contact dermatitis (ACD) is a common immunemediated inammatory response to cutaneous allergens. Although
ACD may affect patients of all ages, its prevalence and signicance
within the pediatric population is likely underrecognized.1 ACD
presents with pruritic eczematous patches and plaques, making it
sometimes difcult to differentiate from atopic dermatitis (AD).
Untreated, persistent ACD may ultimately have substantial consequences on patients and their families quality of life due to
chronic pruritus, difculty sleeping, and recurrent infection. Thus,
a high index of suspicion and timely referrals for patch testing are
vital for suspected pediatric ACD.
Herein, we present an overview of pediatric ACD, analysis of
pertinent current literature, focused management recommendations, and a discussion of existing knowledge gaps to be
addressed by future research.

EPIDEMIOLOGY
Pediatric cutaneous allergic sensitization was initially described
in 1931, when infantile delayed-type hypersensitivity to poison
ivy was rst reported.2 Nevertheless, it was believed that such
allergic reactions were uncommon due to widely held misconceptions that children were inherently limited in their
exposure to contact allergens and that the pediatric immune
system was immature.3-5 Studies have tried to quantify the
incidence of ACD and the prevalence of sensitization among
children with some success.
In 1986, Weston et al6 patch tested 314 healthy children to
assess sensitization rates. This landmark publication showed that
pediatric contact sensitization was not as rare as previously believed
(w20% had a reaction). Likewise, Bruckner et al7 assessed
sensitization rates in 95 asymptomatic children aged 6 months to
5 years with a new commercially available patch test kit (ThinLayer Rapid Use Epicutaneous Patch Test; Smart Practice;
Phoenix, Ariz). The overall incidence of sensitization in that study
was found to be 24.5%, with the youngest child demonstrating
reactivity at age 6 months.7 Although these studies showed substantial sensitization rates, they had small sample sizes and singlecenter recruitment biases and were not subsequently reproduced.
In Europe, a larger scale study by Burros et al8 tested 562 healthy
Portuguese schoolchildren and found a 13.3% sensitization rate.
Mortz et al9 studied healthy eighth-grade Danish schoolchildren
(Odense, Denmark) and found an overall 15.2% prevalence of
contact allergy in the 1501 subjects tested.
As expected, studies assessing children with suspected ACD
yielded signicantly higher sensitization rates. In Italy, Motolese
et al10 studied 53 affected children (ages 3 months to 2 years) and
found a 62% incidence of clinically relevant positive patch test reaction (RPPTR). In a retrospective review, Hogeling and Pratt11
noted in Ottawa that 55.8% of 100 children (aged 4-18 years) had

J ALLERGY CLIN IMMUNOL PRACT

SEPTEMBER/OCTOBER 2015

an RPPTR, with females predominating although other studies have

reported rates between 56.4% and 96.3%.12,13 Of note, Roul et al14
found a peak incidence of sensitization in children younger than 3
years within their 3-year retrospective study of 337 French children,
suggesting that signicant sensitization may be seen at earlier ages.
Jacob et al12 reported the rst pediatric US multicenter study of
65 symptomatic patients between 1 and 18 years old patch tested
between 2001 and 2006 in the University of Pennsylvania and the
University of Miami. The study reported an overall 83% positive
patch test reaction [PPTR] and 77% RPPTR.12 Belloni Fortina
et al15 evaluated 321 children younger than 3 years with suspected
ACD within a 6-year study period of 2002 to 2008 with the
nding of a 62.3% PPTR. Zug et al16 (the North American
Contact Dermatitis Research Group) reported a study of 391
North American children (0-18 years) referred for patch testing
(2001-2004) and compared their results with those for 9670 adult
patients also studied by the group. The pediatric group was not
different from the adult group in their overall RPPTR51.2%. In
a follow-up analysis of pediatric cases between 2005 and 2012 by
Zug et al, 883 children younger than 18 years were compared with
the cases reported between 2001 and 2004. The data were even
more striking than the previous study period, with 62.3% of the
subjects having a PPTR and 56.7% an RPPTR.17 The North
American Contact Dermatitis Research Group authors noted that
the specic differences in positive patch test and relevant positive
patch test frequencies between children and adults as well as test
periods conrm the importance of reporting periodic updates of
patch testing in children to enhance clinicians vigilance to clinically important allergens. Although the North American Contact
Dermatitis Research Group similarly reported the epidemiology of
ACD in adults with similar frequencies,18 it specically noted that
scattered generalized was the most common distribution in the
children (32.5%), whereas the hands were the most affected in the
adults (26.7%).17 This is important given the potential for nickel
to be associated with signicant idiopathic- and systemic-type
responses. Furthermore, it has been postulated that the systemic
nickel allergy syndrome may make patients more susceptible to
recurrent infections and dermatitis potentiation.19
To date, there has been one prospective pediatric study performed in the United States, notably the Pediatric Research
Equity Act 1 study (PREA-1), which found the 28 allergen and 1
negative control Thin-Layer Rapid Use Epicutaneous Patch Test
to be safe and efcacious in 102 children between 6 and 18 years
old at a single patch test institution,20 and the Pediatric Research
Equity Act 2 study is currently testing an expanded panel with an
additional 7 allergens in the same age group. Of note, Herro
et al21 assessed the frequency of sensitization in the PREA-1 trial
participants and found that 66% of nonatopic patients had at
least 1 positive reaction. Nevertheless, the true prevalence of
sensitization continues to be grossly underreported because of
deciencies in reporting and tracking.

PATHOGENESIS
ACD results from a biphasic, delayed (type IV) hypersensitivity reaction comprising primary sensitization and secondary
elicitation. Sensitization occurs via direct cutaneous exposure to
allergens/haptens that are lipophilic molecules of less than 500
Daltons in molecular weight. Some allergens are potent sensitizers, and even a single exposure may be sufcient for sensitization to occur, for example, uroshiol in poison ivy. However,

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VOLUME 3, NUMBER 5

most allergens found in consumer products are weak sensitizers

that require repeated exposures for sensitization to occur, for
example, fragrances.22 The sensitization phase is clinically silent;
however, internal immune mechanisms may be ongoing for 10
to 15 days.23 The most common factor that predisposes toward
sensitization, especially to weaker allergens, is skin-barrier
disruption, for example, piercings, AD, or application of
topical antibiotics to wounds.
Elicitation of clinical manifestations of ACD usually occurs 72
to 96 hours after secondary, direct cutaneous, oral, or airborne
exposure to the same allergen. However, clinical ndings of ACD
may be present as early as 24 hours if multiple exposures occur.
Underlying immune system mechanisms of ACD are not fully
elucidated. Murine models have been developed to mimic human contact hypersensitivity reactions and to dissect the molecular changes. Unlike humans, however, mice have not been
found to be reactive to weak sensitizers such as nickel and
rubber and thus, the current models are not ideal.24 Studies have
found that human TL4 proteins are required for the development of nickel sensitization. Schmidt et al25 tested this theory
and found that TLR4-decient mice with transgenic expression
of human TLR4 were able to have efcient sensitization to nickel
with elicitation of contact hypersensitivity. Thus, these ndings
reect future directions both for new models for studying contact
dermatitis and for strategies for treatment.
Nevertheless, it is understood that haptens garner proinammatory properties, which induce migration and maturation
of dendritic cells, which ultimately travel to regional lymph
nodes and interact with T lymphocytes. This process has been
conrmed as a necessary step in the development of ACD.
Notably, T-celledepleted mice and patients with thymic aplasia
(Di George syndrome) cannot be sensitized.26
The elicitation phase involves diffusion of haptens into the
skin and activation of T lymphocytes. Although CD4 T lymphocytes appear to dominate within the immunologic response,
specically TH1,27 recent research is showing that other helper
cells, specically TH17, TH22, and TH29, are also important.24,28 Moreover, certain allergens have distinct immune poThus,
the
underlying
ACD
larization
patterns.24
immunopathophysiology involves complex interactions between
haptens, keratinocytes, dendritic cells, and T lymphocytic cells.

CLINICAL PRESENTATION
ACD classically presents as a localized, erythematous, eczematous eruption, often with geometric or linear patterns corresponding to sites of contact with the allergen (Figure 1). Acute
lesions may include vesicles on an edematous background,
whereas subacute and chronic lesions may present as papules and
plaques with secondary changes such as lichenication, from
accompanying severe pruritus and itch response. However, cases
of purpuric and pustular ACD have been reported.29,30
The location of the reaction can be a useful clue about the
inciting allergen, especially when the presentation is limited.17
Conversely, scattered generalized dermatitis could represent a
systemic ACD, in which ingestion of an allergen (in a sensitized
person) results in a cutaneous reaction of variable severity and
location. Notably, this may occur at the site of initial sensitization,
or have a more widespread distribution. A range of reference terms
exists to identify systemic ACD, including hematogenous contact
eczema, systemic allergic dermatitis, systemic contact

GOLDENBERG ET AL

663

FIGURE 1. Nickel dermatitis to ankle bracelet.

dermatitis, systemically induced allergic contact dermatitis, or

baboon syndrome.31-34 A more recently coined term for the
drug-related variant of baboon syndrome is symmetric drugrelated intertriginous and exural exanthema, which refers to the
development of erythema on exural areas after systemic (transcutaneous, transmucosal, oral, intravenous, intramuscular, or
inhalational) exposure to a drug in a previously sensitized individual.35 It seems that the most accurate and scientically plausible
term for all the above-discussed entities would be systemic reactivation of allergic contact dermatitis as proposed by Lachapelle.36
Pediatric ACD may also be misdiagnosed as AD because of the
commonality of eczematous dermatitis in the presentation of both
conditions. The barrier dysfunction of AD may predispose to easier
hapten penetration and ACD elicitation.21,37 In addition, topical
treatments for AD may themselves become allergens.38 Studies
show that children with AD have higher sensitization prevalence
than do children without AD, especially to certain allergens, such
as fragrances.21,39-41 Specically, Herro et al21 showed a 23%
difference in positive patch test results between atopic and nonatopic children aged 6 to 18 years. Furthermore, children with a
PPTR were found to be almost 3 times as likely to have a concurrent diagnosis of AD (34% vs 11.2%; P < .001).16 Recent
studies have found that laggrin gene mutations are associated with
an increased risk of nickel contact sensitization, possibly predisposing lgarrin-mutationecarrying children with AD to ACD.42
However, the relationship between ACD and AD is complex
and of much interest; thus, it justies further exploration.

DIAGNOSIS
Epicutaneous patch testing is the criterion standard for the
diagnosis of ACD.43 However, none of the currently available
patch testing devices is approved by the Food and Drug
Administration (FDA) for use in children younger than 18
years.44 As a result, providers customarily tailor patch testing to
the history of the pediatric patient, ultimately nding relevant
allergens and alleviating the suffering of their pediatric patients.
Well-gathered clinical history and a high index of suspicion for
pediatric ACD are necessary elements in garnering the correct
diagnosis. In tailoring pediatric patch tests, it is important to note
that children physiologically differ from adults. Infants have a
higher body surface area to volume ratio that predisposes them to

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GOLDENBERG ET AL

increased absorption of topical chemicals, decreased subcutaneous lipid deposition, which decreases the available volume for
toxin distribution, and an immature drug metabolism system.45
For this reason, some pediatric patch test practitioners modify
concentrations of allergens along the lines of Fishers proposition
in 197546 delineating that chemical concentrations of certain
patch tests be half dilution (S.E. Jacob, 2014; personal communication), while others halve the allergen contact-skin presentation
time for younger children, as outlined by the German Contact
Dermatitis Group.47
Skin biopsy is not routinely performed for the diagnosis of
contact dermatitis because history delineates between acute irritant and acute allergic reactions and the histopathology of
chronic dermatitis is frequently not specic.48 However, it may
be warranted in cases of recalcitrant dermatitis in which patch
testing was negative, or avoidance and topical treatments were
not sufcient at improving the symptoms. Moed et al49 performed biopsies on clinically normal skin after resolution of
initiated ACD or irritant contact dermatitis reactions in adults.
The authors reported that CD4 CCR10 inltrating cells and
CCL27 mRNA expression remained elevated 21 days after patch
testing in patients with induced ACD, but not irritant contact
dermatitis. Thus, although molecular testing may not be costeffective, experimental skin biopsies of patients with ACD may
yield helpful information for understanding the pathways of
human immunology.
Children are also unique in the cutaneous threshold for irritancy from certain allergens. In 2004, Johnke et al50 examined
562 infants (up to 18 months) for patch test reactivity to nickel
sulfate (200 mg/cm2); a reproducible positive reaction was seen in
only 8.6% of the cohort, and clinical relevance was found in only
1 infant. In a follow-up study in 2013, the same 26 infants who
tested positive to nickel at 12 and 18 months were offered repeat
patch testing at age 3 and 6 years.51 Mortz et al51 report that only
9.5% of the infants had reproducible nickel reactions at 3 or 6
years, and only 1 was clinically relevant. Thus, the authors
concluded that the initially positive reactions were most likely
irritation rather than true allergy owing to the patch test nickel
levels being excessively high for pediatric thresholds. However,
their results highlight the safety of repeated nickel patch tests in
their inability to cause patch-test sensitization, and that despite the
low reproducibility, patch testing in children with a high index of
suspicion for ACD yields accurate and necessary diagnoses.

FREQUENT ALLERGENS
Childrens exposure and susceptibility to allergens differs from
that in adults simply because of inherent differences in their
immediate environments. Based on the most recent North
American Contact Dermatitis Group data, the top 10 allergens
via PPTRs in children (0-18 years old) include nickel (28.1%),
cobalt (12.3%), neomycin (7.1%), Myroxylon perierae (balsam of
Peru) (5.7%), lanolin alcohol (5.5%), fragrance mix (5.2%),
bacitracin (5.2%), carmine (3.8%), paraphenylenediamine
(3.3%), and quaternium 15 (3.2%).17
Nickel is the most frequent allergen in adult and pediatric
populations found to be positive in patch-tested populations.
Nickel contact dermatitis can produce localized or systemic
dermatitis with extensive morbidity.52 It is ubiquitous in our
environment and can be found in a wide range of daily-use items
such as jewelry, keys, zippers, computers, school chairs, personal

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SEPTEMBER/OCTOBER 2015

electronics, toys, and even food.52 Nickel sensitization is the

second highest prevalent allergy in patients with AD (13.1%).42
And patients with AD are more likely to have long-standing issues with nickel ACD, with few losing patch test positivity over
time.19 An association between nickel sensitization has been
found with loss-of-function laggrin mutation and AD.42
Thyssen et al53 speculate that such ndings may be explained
by the nickel-chelating abilities of laggrin that ultimately lead to
an accumulation of nickel in the upper part of the skin. Thus,
when laggrin is lost, nickel may enter the lower layers of the
epidermis more easily and thus lead to sensitization.
In Denmark and the European Union, legislation limiting
nickel content in products has been in effect for over 20 years.53 A
study on Danish schoolgirls comparing those with pierced ears
before the legislation to those with pierced ears postlegislation
found a 13% reduction in nickel sensitization.54 However, nickel
from electronic products such as mobile phones55 and iPads,56
foods, such as chocolate,57 and toys58 continues to affect children worldwide. Prompted by the signicant increase in the
detection of nickel in children noted between 2004 and 2008, and
nickel being designated by the journal of the American Contact
Dermatitis Society (ACDS) Dermatitis as the Allergy of the Year,
the American Academy of Dermatology developed a nickel
workgroup that through partnership with the American Medical
Association outreached the Consumer Product Safety Commission
who stated that the ASTM International (formerly known as the
American Society for Testing and Materials) had developed and
adopted a voluntary safety standard on childrens metal jewelry
(F2923-11). Subsequently, the Nickel Allergy Alliance formed to
track the growing number of conrmed nickel dermatitis cases and
serve as a voice for those concerned with the increasing prevalence
of nickel allergy in the United States. In 2015, the ACDS and the
Nickel Allergy Alliance coendorsed a resolution to the Advisory
Board of the American Academy of Dermatology Patient Safety
and Quality Committee recommending the issuance of a health
advisory regarding the high sensitization rates to nickel in the
United States and a recommendation for mandatory national
nickel directive, akin to the European Nickel Directive, to regulate
the allowable release of nickel.
Paraphenylynediamine (PPD) is 1 of 5 chemicals labeled by
the US Consumer Product Safety Commission as a strong
sensitizer. It has high utility in the mainstream consumer world
as a permanent hair dye, with an allowable concentration regulated at less than 6%. Unfortunately, despite being banned from
products used on the skin since 1938,59 it is commonly found
unregulated in children-oriented products such as temporary
tattoos and black henna skin designs and inks, with PPD concentrations upwards of 30%.60,61 In 2001, the FDA centralized
the monitoring of PPD-related ACD with the establishment of a
MedWatch hotline (1-800-332-1088).62 A recent report from
FDA data showed 12 cases of urticarial (17%) reactions due to
temporary tattoos,63 echoing published reports on the dangerous
anaphylactic-type reactions from PPD.64-66 However, overall
there has been a decrease in reported PPD cases since the initiation of the FDA informational Web site and hotline63 and a
joint safety alert by the American Academy of Dermatology and
the ACDS, suggesting that such governmental measures and
societal education play an important role in reducing the incidence of ACD.
Interestingly, children with AD (barrier dysfunction) present
with heightened sensitizations to Myroxylon pereirae (balsam of

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VOLUME 3, NUMBER 5

Peru), with studies reporting that up to 20% of the patients with

AD have a PPTR and specically 19% have reactions to
fragrance mix-1.21 M perierae and its cross-reactive chemicals
boast wide use in various aromatic products, lotions, ketchups,
make-up, and toothpaste and as a avoring additive in soft
drinks.67
Notably, other allergens have been emerging as top sensitizers
owing to their prevalent use in child care products. Cocamidopropyl betaine has been reportedly used as a surfactant in
cleaning products for children.12 Because soaps and detergents
are known to exacerbate skin barrier disruption, AD has been
found to be associated with cocamidopropyl betaineeinduced
contact hypersensitivity.68 Methylchloroisothiazolinone/methylisothiazolinone, the ACDS 2013 allergen of the year,69 may be
found in wet wipes, frequently used for infants and young
children, and shampoos.43 Methylisothiazolinone should be
tested individually because testing only for the mix misses 40%
of the reactions. In addition, testing may be necessary for propylene glycol, which may be found in personal care products and
topical prescriptions.70 Moreover, with the rising prevalence of
AD in children, the use of topical corticosteroids (and the vehicle
ingredients in the preparation) in this population as mainstay
treatment has risen exponentially. The incidence of ACD due to
topical corticosteroids ranges from 0.2% to 6%, with the overthe-counter class A steroids leading the group with an estimated sensitization rate of 5.72%.71

MANAGEMENT
The focus of ACD treatment is correct diagnosis, avoidance,
and prevention. A detailed history and, if necessary, patch testing
may reveal the underlying responsible allergenic culprits. An indepth discussion with the patient may be warranted to explain
the steps to prevention, specically, avoidance. National organizations such as the ACDS and the Mayo clinic offer services to
help providers and patients identify common sources of allergens.72,73 When avoidance is not sufcient, topical and at times
systemic therapies may be initiated.74 Because this is beyond the
scope of this article, other resources may provide more detailed
information on the various therapeutic options for such
cases.71,74,75 Topical corticosteroids should be used with caution
because they may become sources of sensitization. Corticosteroidsparing agents such as topical calcineurin inhibitors may be
considered instead.
For systemic ACD associated with nickel or balsam of Peru,
for example, dietary modications may be warranted. Several
studies have proposed diets to reduce cutaneous ares.76,77
Because these diets tend to be cumbersome, point-based systems have been designed to allow for selection of foods by lower
point assignments.78,79
GAPS IN KNOWLEDGE
Despite the presence of more than 3380 peer-reviewed publications on the topic of pediatric ACD (PubMed search results
(Dermatitis, Allergic Contact OR contact dermatitis OR patch
testing) AND (child* OR pediatric), December 30, 2014), there
still remain many gaps in our knowledge base regarding the
condition, its relationships to other ailments, its overall public
health impact, and future preventative measures.
Studies report an overall incidence of ACD ranging between
1% and 6% of the total US population.80 However, the true

GOLDENBERG ET AL

665

prevalence of sensitization in children is unknown because many

cases are either undiagnosed or misdiagnosed, unreported, or
both. To enact change in manufacturing goods or protective
legislation, a factual foundation of the severity of the problem is
needed. Thus, large, multicenter, multicollaborative population
studies are necessary to gather information, provide generalizable
results, and initiate research advances in the eld of pediatric
ACD. In November 2014, the Loma Linda University launched
a pediatric contact dermatitis provider and case registry.81 This
multicenter (national) project has the potential to yield
comprehensive information on the prevalence of pediatric patch
testing, and may serve as the basis for future legislative changes.82

CONCLUSIONS
The relationship between ACD and AD is complex and
renders further study. Patients with recalcitrant AD warrant an
in-depth diagnostic workup for underlying sensitizations and
ACD because both conditions have similar presentations. ACD
is a common pediatric problem that warrants national attention,
research, and action. Last, nickel-limiting directives are active in
many developed countries including Denmark, the European
Union, Korea, and China83; however, the United States is still
lagging behind these innovative initiatives. Collaborations between researchers, manufacturers, policymakers, and patients are
necessary to enact change that will help protect the children of
our future from unnecessary suffering from nickel dermatitis and
other identied allergens.
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