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DECEMBER 2019
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Scratching the Surface: A Review of
Dermatitis
C M E
1 AMA PRA
ANCC
Category 1 CreditTM
1.5 Contact Hours
0.5 Pharmacology Contact Hour
Taylor E. Woo, MSc -  Medical Student -  Cumming School of Medicine -  University of Calgary -  Calgary, Alberta, Canada
Ranjani Somayaji, MD -  -  Department of Medicine -  Department of Dermatology -  University of Calgary - 
Calgary, Alberta, Canada
R.M. Haber, MD -  Professor -  Department of Medicine -  Department of Dermatology -  University of Calgary -  Calgary, Alberta,
Canada
Laurie Parsons, MD -  Clinical Associate Professor -  Department of Microbiology, Immunology and Infectious Diseases -  Univer
sity of Calgary -  Calgary, Alberta, Canada
Acknowledgments: The authors would like to thank the patients for agreeing to have their pictures taken for educational purposes. The author, faculty, staff, and planners,
including spouses/partners (if any), in any position to control the content of this CME/CNE activity have disclosed that they have no financial relationships with, or financial
interests in, any commercial companies relevant to this educational activity.
To earn CME credit, you must read the CME article and complete the quiz online, answering at least 13 of the 18 questions correctly.
This continuing educational activity will expire for physicians on December 31, 2021, and for nurses December 3, 2021.
All tests are now online only; take the test at http://cme.lww.com for physicians and www.nursingcenter.com for nurses. Complete CE/CME information is on the last page of this article.
GENERAL PURPOSE:
To present a case-based review illustrating atopic and contact dermatitis, including management of these conditions
using topical and systemic therapies.
TARGET AUDIENCE:
This continuing education activity is intended for physicians, physician assistants, nurse practitioners, and nurses with an
interest in skin and wound care.
LEARNING OBJECTIVES/OUTCOMES:
After participating in this educational activity, the participant should be better able to:
1. Review the prevalence, etiology, and consequences of the various types of dermatitis.
2. Describe the clinical manifestations and differential diagnosis of the various types of dermatitis.
3. Outline the treatment options for the various types of dermatitis.
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ABSTRACT
Eczematous reactions such as atopic dermatitis and contact
dermatitis are prevalent worldwide. Despite contrasting
pathophysiology, the diagnosis and management of these
dermatitides can be challenging for healthcare providers.
Differences in the distribution of the affected areas, duration of
onset, and associated symptoms may help to distinguish these
conditions. Diagnosis of the respective conditions is useful in
developing appropriate management plans. Herein, the authors
present a case-based review illustrating these different disease
entities. Management of these conditions, including the use of
topical and systemic therapies, is discussed.
KEYWORDS: atopic dermatitis, contact dermatitis, corticosteroids,
dermatitis, eczema, review, systemic therapy, topical therapy
ADV SKIN WOUND CARE 2019;32:542-9.
INTRODUCTION
Cutaneous disease is one of the leading contributors of disease
burden worldwide.1 According to a large cohort study of more
than 85 million patients, up to 25% of physician visits in the US
were attributable to skin-related conditions in 2013.2 The corre
sponding cost was estimated at $75 billion in direct healthcare
costs. Of the cutaneous manifestations of disease, atopic derma
titis (AD) and contact dermatitis (which encompasses irritant
contact dermatitis [ICD] and allergic contact dermatitis [ACD])
are of considerable interest because of their global prevalence. In
deed, AD is estimated to affect up to 20% of children worldwide.3
Contact dermatitis is the most common occupation-associated
skin condition, with ICD accounting for 80% of cases and ACD
constituting the remainder.4,5
Similarities in the clinical presentation of these conditions cre
ate a challenge for healthcare providers in accurately managing
these entities. This case-based review provides a diagnostic ap
proach to manage these common dermatitides.
Atopic Dermatitis
A 36-year old woman presents with an erythematous, pruritic, and
papulosquamous rash with secondary lichenification involving the
flexural areas of her elbows (Figure 1). Notably, the appearance of
the rash coincided with the onset of winter and has persisted since its
onset 3 months ago.
Atopic dermatitis, commonly known as eczema, is an inflam
matory skin condition of significant morbidity worldwide.6 The
pathophysiology of AD is multifactorial and involves underlying
host factors, including epidermal barrier dysfunction, immune
dysregulation, and environmental conditions.7 Atopic dermatitis
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has a strong genetic component that accounts for approximately
90% of early-onset AD cases.8 Specifically, genetic mutations as
sociated with impaired skin barrier function, pH, and hydration
of the epidermis have been implicated in the pathogenesis of
AD.9 Individuals with AD are also at risk of developing asthma,
allergic rhinoconjunctivitis, and food allergies during their life
time.10,11 These conditions are referred to as the "atopic march"
and may present concurrently or following the development of
AD.12 Once established, AD may persist chronically or relapse
throughout an individual's lifetime. In addition, AD may predis
pose individuals to secondary infections such as Staphylococcus
aureus, which in turn can exacerbate AD disease severity.
Although seen in individuals of all ages, AD most frequently
occurs in childhood. Interestingly, new data suggest that there
is a U-shaped prevalence distribution with a high prevalence in
childhood that lessens in adulthood and increases again in older
age (>75 years). This is likely multifactorial and relates to skin
dysfunction in normal aging and/or pathology.13,14
Body areas affected by AD can vary by patient age (Figure 2).15
In infants, the extensor surfaces, forehead, and cheek areas are
commonly involved; the trunk is less frequently involved. During
childhood, involvement of the flexural folds (ie, front of elbow
crease) is most common. In the years of transition to adolescence
and adulthood, the flexural sites, wrists, ankles, and neck are
most often affected. During adulthood, involvement of the flex
ural surfaces, face, neck, and anterior chest is more common.16
Sparing of the groin and axillary regions is seen in all ages.
Although AD is a common entity, chronic dermatoses, infec
tious processes, and primary immunodeficiency may mimic the
presentation.17 Noninfectious dermatoses include contact derma
titis, seborrheic dermatitis, and psoriasis. Differentiating between
AD and contact dermatitis (ICD, ACD) can be challenging for
healthcare practitioners and is discussed in a later section. Early-
onset AD is often confused with seborrheic dermatitis, which
can be distinguished by its involvement of the scalp and absence
of pruritus. A diagnosis of psoriasis should be considered in the
case of well-demarcated patches with involvement of the groin.
Infectious processes such as scabies can be mistaken for AD but
may be differentiated by groin involvement and the accompanying
vesiculopustules found on the palms and soles.
Atopic dermatitis can have a spectrum of clinical presentations
over a lifetime. Acute presentations may accompany early-onset
AD and present as edematous, erythematous papules and plaques
with or without vesiculation. Subacute dermatitis presents with
scaling and/or crusting in addition to erythema. Chronic AD is as
sociated with dry, thickened plaques that may have features of
lichenification with a hardened or leathery appearance because of
consistent irritation and rubbing. Weeping or impetiginization may
be seen in association with S aureus  infection.18 Importantly, intense
pruritus is associated with all presentations of AD and is essential for
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Figure 1.
ATOPIC DERMATITIS
the diagnosis of the disease. Other associated cutaneous manifesta
tions include but are not limited to xerosis, ichthyosis vulgaris, and
keratosis pilaris. Postinflammatory hypopigmentation or hyperpig
mentation may be seen with AD, especially in patients of color.
Irritant Contact Dermatitis
A 42-year-old healthcare worker has developed a burning red eruption
over his dorsal hands bilaterally (Figure 3). The eruption improves over
the weekend but exacerbates during the work week. Just prior to the start
of this eruption, his facility instituted a new "safe hand" policy with
the use of a daily chlorhexidine scrub.
Irritant contact dermatitis results from direct exposure of the
skin to the cytotoxic effects of a chemical or physical agent. The
hands and face are the most commonly affected areas.19 It is as
sociated with occupations in the manufacturing industry, arts,
and food services, where exposure to irritating substances is
common. Healthcare providers are at considerable risk of ICD
because of frequent and repeated hand hygiene practices.20
Water, detergents, solvents, and oils are common causes, but
any substance that disrupts epithelial barrier function may re
sult in ICD.21 These exposures are influenced by the irritant's
concentration and pH levels, as well as duration of exposure.
Additional contributors include both host factors (eg, age-
related epidermal barrier function) and environmental factors
(eg, humidity, temperature).
Acute exposure of the skin to the irritant results in the disrup
tion of the stratum corneum. Damage to the keratinocytes and a
corresponding inflammatory response give rise to erythema,
edema, vesiculation, and skin erosion. Continued and/or re
peated exposures to irritants may result in chronic ICD, which
presents with lichenification, excoriations, scaling, and fissures,
Figure 2.
THE DISTRIBUTION OF BODY SURFACES AFFECTED BY
ATOPIC DERMATITIS CHANGES WITH AGE
Involvement of extensor surfaces, forehead, and cheek areas is common in infants (<2 years).
In childhood, involvement of flexural folds is more commonly seen. In adults, involvement of the
flexural surface and the face, neck, and anterior chest is seen. In all ages, the groin and axillary
area is spared. (c) R. Somayaji, 2019.
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Figure 3.
IRRITANT CONTACT DERMATITIS
A, Dorsal view; B, palmar view.
which are the result of impaired transepidermal barrier recovery.
Inflammatory changes appear 8 to 24 hours following initial ex
posure to the irritant.
Multiple forms of ICD exist; cumulative ICD is the most prev
alent form, characterized by repeated, subthreshold exposure
to weak irritants impairing barrier function.21 Essentially,
although exposure to weak irritants would not normally re
sult in damage to the skin, the frequency at which the skin is
exposed exceeds the body's ability to repair its barrier func
tion. Ultimately, this pattern of irritant exposure results in
erythema, dryness, hyperkeratosis, and lichenification. Exposure
to a stronger irritant may result in erythematous, edematous
lesions and even necrosis of the affected area. This clinical
manifestation is often accompanied by a burning sensation,
pain, and blistering.
Figure 4.
ALLERGIC CONTACT DERMATITIS, HANDS
Allergic Contact Dermatitis
A 35-year-old hairdresser has begun to develop an intensely pruritic
rash involving her hands and distal forearms (Figures 4 and 5).
The eruption is on both the dorsal and palmar aspects of her hands
with more pronounced involvement on the palmar aspect. Small
vesicles  weeping clear  fluid are  often preceded by intense  pruritus
of the affected skin.
Compared with ICD, ACD accounts for a minority of occupa
tional contact dermatitis cases caused by exposure to external
agents.22 It has no age, race, or sex predilection and is seen most
commonly on the hands and face but may vary depending on the
allergen. For example, allergic reactions to nickel may be seen on
the umbilicus, ears, or neck from jewelry or belt buckles. After
nickel, the most common allergens that cause ACD in North America
include sulfate, fragrances, sanitary wipes (methylisothiazolinone),
neomycin, bacitracin, cobalt chloride, formaldehyde, balsam of
Peru, temporary tattoos (p-phenylenediamine), and sunscreen
products (benzophenone-3).23 When the associated allergens
are identified using patch testing, a reaction to topical corticoste
roids has been seen in up to 5.7% of cases.24 Establishing a clin
ical diagnosis in these cases may be difficult because of the
overlap between the underlying disease process and the reaction
to the corticosteroid. As such, topical steroid allergy should be
considered for cases in which topical corticosteroids fail to control
a presumed ACD case, or when a rash worsens despite adequate
steroid therapy.
Allergic contact dermatitis is a delayed-type hypersensitivity
immune response.25 The process starts with an initial exposure
and penetration of the allergen into the epidermis, followed by
a chain of physiologic processes that results in the sensitization
Figure 5.
ALLERGIC CONTACT DERMATITIS, FOREARMS
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of the body to the allergen. Upon re-exposure of the allergen, the
allergen-specific inflammatory cells activate and result in the
clinical manifestation of eczema. Importantly, the manifestation
is dependent on the characteristics and exposure pattern of the
allergen. Acute ACD commonly presents as a well-demarcated,
erythematous, pruritic patch or plaque with edema, blistering,
or weeping. If chronic, the eruption will often have signs of
lichenification or scale.
In some cases, a diffuse or widespread rash may be seen in re
sponse to systemic exposure to an allergen to which the patient
was previously sensitized with a topical agent. This is referred
to as autoeczematization or an "id" reaction. This secondary der
matitis presents distally to the original dermatitis within 1 or
more weeks following the initial onset. There is a range of mor
phologic presentations, although it is usually symmetrical with
areas of erythematous papules and vesicles. Although the patho
genesis remains unclear, id reactions are seen in the context of
contact dermatitis and underlying infections.26-28
Differentiating AD, ICD, and ACD
Despite similar manifestations as an eczematous rash, there are
notable differences among these disease processes (Table 1).
Conceptualizing the physiologic processes of these entities
may be useful in understanding the differences. Briefly, the
mechanism driving the development of AD primarily involves
an endogenous problem of epithelial cell dysfunction.15 Conversely,
ICD and ACD are more consistent with exogenous exposure to an
irritant. Although allergens are highly diverse, fragrances and pre
29,30
servatives are most common.
Whereas the direct effects of the irritant primarily drive ICD,
ACD is a delayed-type hypersensitivity reaction caused by prior
sensitization and exposure to the allergen of interest. A thorough
history and physical examination can provide further insight into
these conditions. For instance, individuals with AD may describe
its onset during childhood with recurrent episodes following an
age-dependent pattern throughout their lifetime. In contrast, pa
tients with contact dermatitis may describe its onset following an
Table 1.
KEY FEATURES OF DERMATITIS BY TYPE
Endogenous
Exogenous
Atopic Dermatitis
Irritant Contact Dermatitis
Allergic Contact Dermatitis
Relevant
Erythematous, edematous rash which follows an Well-demarcated erythematous,
Typically a well-demarcated
features
age-dependent distribution
edematous rash with vesiculation
erythematous, edematous rash with
Chronically relapsing course
Improves with rest and worsens with vesiculation
Positive family history
repeated irritant exposure
Systemic exposure may produce a
diffuse rash on distal surfaces
Skin
Infants: facial and extensor involvement
Most commonly hands and feet
distribution
Children: flexural surfaces
Adult: flexural surfaces, neck, face, anterior chest
Diagnosis
Clinical
Clinical
Clinical and patch testing
Patch testing is the standard for
diagnosis; however, a negative result
does not rule out ACD
Symptoms
Intense pruritus
Burning/irritation, soreness
Pruritus
Duration of
May appear anytime in life
May appear acutely within 8-24 h
Lesions appear 24-72 h after
onset
Preferentially affects areas of dryness
of exposure
exposure
No sensitizing exposure is required
Requires sensitizing exposure
Treatment
Emollients
Irritant avoidance
Allergen avoidance
Topical corticosteroids
Emollients
Emollients
Topical calcineurin inhibitors
Topical corticosteroids
Topical corticosteroids
Crisaborole
Topical calcineurin inhibitors
Systemic
Systemic corticosteroids
Not typically used
Systemic corticosteroids
therapies
Phototherapy/psoralen and UV-A
Phototherapy/psoralen and UV-A
Dupilumab
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acute incident, such as exposure to strong irritants or after
employment at a new job where certain hygiene practices
are common.
Relying on the clinical morphology alone may not be enough
to distinguish ICD from ACD. As such, understanding the
area of distribution, duration of onset, and associated symp
toms may aid in diagnosis. Both ICD and ACD present as
sharply demarcated areas, but diffuse involvement of the dis
tal skin can be seen in ACD. The timeline from exposure to
the symptom onset is another distinguishing characteristic. In
cases of ICD, symptoms present in minutes to hours. In ACD,
onset is delayed and may occur up to 72 hours following re
peated exposure. Patients with ICD typically manifest with a
burning sensation, whereas pruritus is observed in ACD.
When ICD and ACD cannot be distinguished clinically, patch
testing is necessary (the criterion standard for the diagnosis
of ACD).31
MANAGEMENT
The goals of treatment are to resolve the current skin eruption,
relieve symptoms, treat the underlying epithelial dysfunction,
and engage in maintenance therapy to reduce the risk of future
symptoms. In all cases, education is the cornerstone of manage
ment to identify and avoid known exacerbating factors. In the
case of ICD and ACD, protective equipment such as gloves
should be used when working with known irritants.32 General
care includes a regular skin care routine and the use of moistur
izers to protect against dry skin.33-35 Using moisturizers reduces
xerosis, pruritus, erythema, fissuring, and lichenification, thereby
lessening the severity of disease.36 In AD, moisturizers are associ
ated with extension to the time of flare, a reduction in the number
of flares, and less corticosteroid required to achieve control.37,38
Although various formulations exist, including ointments and
creams, no particular preparation has been shown to be signifi
cantly more effective.
Topical corticosteroids and calcineurin inhibitors are used
in the first-line medical management of AD, ICD, and ACD.
Although topical corticosteroids are observed to be effica
cious in ACD, however, the evidence surrounding their use
in ICD remains unclear.39,40 Topical corticosteroids are used
in localized dermatitis involving less than 10% of the body
surface area.41 Steroids typically come in cream, lotion, or
ointment formulations. The choice of steroid vehicle is influ
enced by the severity and location of the lesion, as well as the
extent of xerosis (Table 2). High-potency corticosteroids should
be avoided in intertriginous areas and areas of thin skin, includ
ing the face, flexural surfaces, eyelids, and the anogenital re
gion because of the risk of cutaneous atrophy.36 In addition,
striae (stretch marks) and telangiectasia may result from pro
longed use. Options for mild to moderate cases of dermatitis
on the body include a triamcinolone acetonide 0.1% or a
clobetasol propionate 0.05% cream or ointment.36,42,43 Pro
viders should expect resolution of the rash within several
days following a once- or twice-daily application of topical
corticosteroid.44
Steroid-sparing therapies include topical calcineurin inhibitors
such as pimecrolimus 1% cream for mild or moderate disease
and tacrolimus 0.03% to 0.1% ointment for moderate to severe
disease.43,45,46 Common adverse reactions associated with topi
cal calcineurin inhibitors include local stinging and/or burning.
In addition, topical calcineurin inhibitors contain a black box
warning for increased lymphoma risk,47 but postmarketing sur
veillance since the early 2000s has not substantiated this risk. Re
cent developments in topical therapies for the treatment of mild
to moderate AD include crisaborole 2% ointment.36,48 Intermit
tent use of these topical agents can be continued after the initial
rash has been resolved, once or twice per week. Proactive use of
mild-potency topical corticosteroids or topical calcineurin inhibi
tors once or twice per week is recommended to reduce the recur
rence of flares.36
Systemic therapies (such as systemic steroids) are occasionally
used in AD and ACD but not typically in ICD. Systemic cortico
steroids are reserved for cases that involve greater than 10% of
the body surface area.41 In ACD, systemic corticosteroids are
used in cases of severe poison ivy, disseminated ACD, or failure
of topical therapies.49 In AD, systemic steroids are reserved for
acute, severe exacerbations as bridge therapy to topical cortico
steroids. However, systemic corticosteroids are not recom
mended as a long-term treatment for dermatitis.
Narrowband UV-B phototherapy or psoralen and UV-A may
be used in cases of AD and ACD. In particular, the use of narrow-
band UV-B phototherapy in patients with moderate to severe AD
has resulted in significant clinical improvement.50 However, its
utility is limited by patient adherence, owing to the frequency
of treatments and sparse location of treatment facilities.
Table 2.
EXAMPLES OF TOPICAL CORTICOSTEROIDS44
Mild Potency
(Class 6/7)
Moderate Potency
(Class 4/5)
High Potency (Class 1)
Desonide 0.05%
Mometasone
Betamethasone
Hydrocortisone
2.5%
furoate 0.1%
Betamethasone
valerate 0.1%
dipropionate 0.05%
Clobetasol propionate
0.05%
Triamcinolone
acetonide
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Recently, a new systemic therapy for the treatment of AD has
emerged. Dupilumab is an injectable systemic therapy used for
patients recalcitrant to topical treatments.51,52 However, there is
currently no evidence for the use of these novel therapies in
ACD or ICD.
CONCLUSION
Given the importance and prevalence of atopic and contact der
matitis within the modern context, establishing an accurate diag
nosis is critical in guiding management. Managing these
conditions involves education, avoidance of the provoking agent,
and treatment of flares using topical agents. However, the effi
cacy of newly developed immunologic therapies in contact der
matitis is not well understood. Future research investigating the
potential use of these treatments could provide new avenues
for managing dermatitis.
PRACTICE PEARLS
-  Atopic dermatitis, ACD, and ICD are common dermatologic
conditions encountered in clinical practice.
-  Atopic dermatitis most commonly presents in childhood and
patients will often have a family history of the condition.
-  Identifying and avoiding triggers are the cornerstone of treat
ment for ACD and ICD.
-  Education, maintenance therapies, and a regular skin care
routine with moisturizers are key to managing and decreasing
episodes for all forms of dermatitis.
-  Patients should avoid the use of high-potency corticosteroids
in intertriginous areas and areas of thin skin because of the risk
of cutaneous atrophy.- 
REFERENCES
1. Hay RJ, Johns NE, Williams HC, et al. The global burden of skin disease in 2010: an analysis
of the prevalence and impact of skin conditions. J Invest Dermatol 2014;134:1527-34.
2. Lim HW, Collins SAB, Resneck JS, et al. The burden of skin disease in the United States.
J Am Acad Dermatol 2017;76:958-972.
3. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab 2015;66:8-16.
4. Tovar R, Leikin JB. Irritants and corrosives. Emerg Med Clin North Am 2015;33:117-31.
5. Peiser M, Tralau T, Heidler J, et al. Allergic contact dermatitis: epidemiology, molecular
mechanisms, in vitro methods and regulatory aspects. Current knowledge assembled at
an international workshop at BfR, Germany. Cell Mol Life Sci 2012;69:763-81.
6. Carroll CL, Balkrishnan R, Feldman SR, et al. The burden of atopic dermatitis: impact on the
patient, family, and society. Pediatr Dermatol 2005;22:192-9.
7. David Boothe W, Tarbox JA, Tarbox MB. Atopic dermatitis: pathophysiology. In: Advances in
Experimental Medicine and Biology. New York, NY: Springer International Publishing; 2017;
21-37.
8. Bataille V, Lens M, Spector TD. The use of the twin model to investigate the genetics and
epigenetics of skin diseases with genomic, transcriptomic and methylation data. J Eur
Acad Dermatology Venereol 2012;26:1067-73.
9. Sandilands A, Sutherland C, Irvine AD, et al. Filaggrin in the frontline: role in skin barrier
function and disease. J Cell Sci 2009;122:1285-94.
10. Elias PM, Steinhoff M. 'Outside-to-inside' (and now back 'outside' pathogenic mechanisims
in atopic dermatitis. J Invest Dermatol 2009;128:1067-70.
11. Ellis CN, Drake LA, Prendergast MM, et al. Cost of atopic dermatitis and eczema in the United
States. J Am Acad Dermatol 2002;46:361-70.
12. Spergel JM, Paller AS. Atopic dermatitis and the atopic march. J Allergy Clin Immunol 2003;
112:118-27.
13. Abuabara K, Magyari AM, Hoffstad O, et al. Development and validation of an algorithm to
accurately identify atopic eczema patients in primary care electronic health records from
the UK. J Invest Dermatol Aug 2017;137(8):1655-1662.
14. Voelker R. Older adults may fuel an upturn in eczema cases. JAMA 2019;321(11):
1038-1039.
15. Weidinger S, Novak N. Atopic dermatitis. Lancet 2016;387:1109-22.
16. Garmhausen D, Hagemann T, Bieber T, et al. Characterization of different courses of atopic
dermatitis in adolescent and adult patients. Allergy 2013;68:498-506.
17. Barrett M, Luu M. Differential diagnosis of atopic dermatitis. Immunol Allergy Clin North Am
2017;37:11-34.
18. Kong HH, Oh J, Deming C, et al. Temporal shifts in the skin microbiome associated with
disease flares and treatment in children with atopic dermatitis. Genome Res 2012;22:850-9.
19. McDonald JC, Beck MH, Chen Y, et al. Incidence by occupation and industry of work-related
skin diseases in the United Kingdom, 1996-2001. Occup Med (Chic Ill) 2006;56:398-405.
20. Behroozy A, Keegel TG. Wet-work exposure: a main risk factor for occupational hand
dermatitis. Saf Health Work 2014;5:175-80.
21. Slodownik D, Lee A, Nixon R. Irritant contact dermatitis: a review. Australas J Dermatol 2008;
49:1-11.
22. Fartasch M. Ultrastructure of the epidermal barrier after irritation. Microsc Res Tech 1997;37:
193-9.
23. DeKoven JG, Warshaw EM, Belsito DV, et al. North American Contact Dermatitis Group patch
test results 2013-2014. Dermatitis 2017;28:33-46.
24. Davis MDP, 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;56:921-7.
25. Kaplan DH, Igyarto BZ, Gaspari AA. Early immune events in the induction of allergic contact
dermatitis. Nat Rev Immunol 2012;12:114-24.
26. Sharma V, Beyer DJ, Paruthi S, et al. Prominent pruritic periumbilical papules: allergic
contact dermatitis to nickel. Pediatr Dermatol;19:106-9.
27. Takci Z, Tekin O, Karadag AS. A Pediculid case: autosensitization dermatitis caused by
pediculosis capitis. Turkish J Parasitol 2012;36:185-7.
28. Lee SY, Lee DR, You CE, et al. Autosensitization dermatitis associated with propolis-induced
allergic contact dermatitis. J Drugs Dermatol 2006;5:458-60.
29. DeKoven JG, Warshaw EM, Zug KA, et al. North American Contact Dermatitis Group patch
test results: 2015-2016. Dermatitis 2018;29(6):297-309.
30. Findings from Mayo Clinic yields new findings on allergies (prevalence of allergen
sensitization detected by patch tests). Immunotherapy Weekly 2018;2192.
31. Nelson JL, Mowad CM. Allergic contact dermatitis: patch testing beyond the TRUE Test.
J Clin Aesthet Dermatol 2010;3:36-41.
32. Wigger-Alberti W, Elsner P. Preventive measures in contact dermatitis. Clin Dermatol 1997;
15:661-5.
33. Berndt U, Wigger-Alberti W, Gabard B, et al. Efficacy of a barrier cream and its vehicle as
protective measures against occupational irritant contact dermatitis. Contact Dermatitis
2000;42:77-80.
34. Martin SF, Rustemeyer T, Thyssen JP. Recent advances in understanding and managing
contact dermatitis. F1000Research 2018;7:810.
35. Bauer A, Ronsch H, Elsner P, et al. Interventions for preventing occupational irritant hand
dermatitis. Cochrane Database Syst Rev 2018;4:CD004414.
36. Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic
dermatitis: section 2. Management and treatment of atopic dermatitis with topical
therapies. J Am Acad Dermatol 2014;71:116-32.
37. van Zuuren Esther J, Zbys F, Robin C, et al. Emollients and moisturisers for eczema.
Cochrane Database Syst Rev 2017;2:CD012119.
38. Miller DW, Koch SB, Yentzer BA, et al. An over-the-counter moisturizer is as clinically
effective as, and more cost-effective than, prescription barrier creams in the treatment of
children with mild-to-moderate atopic dermatitis: a randomized, controlled trial. J Drugs
Dermatol 2011;10:531-7.
39. Levin C, Maibach HI. An overview of the efficacy of topical corticosteroids in experimental
human nickel contact dermatitis. Contact Dermatitis 2000;43:317-21.
40. van der Valk PGM, Maibach HI. Do topical corticosteroids modulate skin irritation in human
beings? Assessment by transepidermal water loss and visual scoring. J Am Acad
Dermatol 1989;21:519-22.
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41. Gooderham M. Management of adult moderate-to-severe atopic dermatitis: a practical guide
for primary care. Skin Therapy Lett 2017;12.
42. Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment and
prevention. J Am Acad Dermatol 2005;53:845.e1-845.e13.
43. Carr WW. Topical calcineurin inhibitors for atopic dermatitis: review and treatment
recommendations. Pediatr Drugs 2013;15:303-10.
44. Ference JD, Last AR. Choosing topical corticosteroids. Am Fam Physician 2009;79:135-40.
45. Belsito D, Wilson DC, Warshaw E, et al. A prospective randomized clinical trial of 0.1% tacrolimus
ointment in a model of chronic allergic contact dermatitis. J Am Acad Dermatol 2006;55:40-6.
46. Pacor ML, Di Lorenzo G, Martinelli N, et al. Tacrolimus ointment in nickel sulphate-induced
steroid-resistant allergic contact dermatitis. Allergy Asthma Proc 2006;27:527-31.
47. Castellsague J, Kuiper JG, Pottegard A, et al. A cohort study on the risk of lymphoma and skin
cancer in users of topical tacrolimus, pimecrolimus, and corticosteroids (Joint European longitudinal
lymphoma and skin cancer evaluation-JOELLE study). Clin Epidemiol 2018;10:299-310.
48. Akama T, Baker SJ, Zhang YK, et al. Discovery and structure-activity study of a novel
benzoxaborole anti-inflammatory agent (AN2728) for the potential topical treatment of
psoriasis and atopic dermatitis. Bioorganic Med Chem Lett 2009;19:2129-32.
49. Usatine RP, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician
2010;82:249-55.
50. Tintle et al. 2011. Reversal of atopic dermatitis with narrow band UVB phototherapy and
biomarkers for therapeutic response. J Allergy Clin Immunol 128(3):583-584.
51. Sidbury R, Davis, Dawn M, et al. Guidelines of care for the management of atopic dermatitis:
part 3: management and treatment with phototherapy and systemic agents. J Am Acad
Dermatology 2014;71:327-49.
52. Blauvelt A, de Bruin-Weller M, Gooderham M, et al. Long-term management of moderate-to
severe atopic dermatitis with dupilumab and concomitant topical corticosteroids (LIBERTY AD
CHRONOS): a 1-year, randomised, double-blinded, placebo-controlled, phase 3 trial. Lancet
2017;389:2287-303.
For more than 153 additional continuing education articles related to Skin and Wound Care topics,
go to NursingCenter.com/CE.
CONTINUING MEDICAL EDUCATION INFORMATION FOR PHYSICIANS
and DOs only. All other healthcare professionals participating in this activity will receive a certificate
Lippincott Continuing Medical Education Institute, Inc., is accredited by the Accreditation
of participation that may be useful to your individual profession's CE requirements.
Council for Continuing Medical Education to provide continuing medical education
for physicians.
CONTINUING EDUCATION INSTRUCTIONS
Lippincott Continuing Medical Education Institute, Inc., designates this journal-based CME activity for

 Read the article beginning on page 542. For nurses who wish to take the test for CNE contact
a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should claim only the credit
hours, visit http://nursing.ceconnection.com. For physicians who wish to take the test for CME
commensurate with the extent of their participation in the activity.
credit, visit http://cme.lww.com. Under the Journal option, select Advances in Skin and Wound Care
and click on the title of the CE activity.
PROVIDER ACCREDITATION INFORMATION FOR NURSES

 You will need to register your personal CE Planner account before taking online tests. Your planner
Lippincott Professional Development will award 1.5 contact hours including 0.5 pharmacology credits
will keep track of all your Lippincott Professional Development online CE activities for you.
for this continuing nursing education activity.

 There is only one correct answer for each question. A passing score for this test is 13 correct
LPD is accredited as a provider of continuing nursing education by the American Nurses Credentialing
answers. If you pass, you can print your certificate of earned contact hours or credit and access
Center's Commission on Accreditation.
the answer key. Nurses who fail have the option of taking the test again at no additional cost. Only the
This activity is also provider approved by the California Board of Registered Nursing, Provider
first entry sent by physicians will be accepted for credit.
Number CEP 11749 for 1.5 contact hours. LWW is also an approved provider by the District of
Columbia, Georgia, and Florida CE Broker #50-1223.
Registration Deadline: December 31, 2021 (physicians); December 3, 2021 (nurses).
PAYMENT
OTHER HEALTH PROFESSIONALS
This activity provides ANCC credit for nurses and AMA PRA Category 1 CreditTM for MDs

The registration fee for this CE activity is $17.95 for nurses; $22.00 for physicians.
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