review article

TRIGGERS IN ATOPIC DERMATITIS/ECZEMA: SEPARATING FACT FROM

FICTION
Kannenberg SM, MBChB, MMed (Derm), Jordaan HF, MBChB, MMed (Derm), M Akad SA

Correspondence:
Division of Dermatology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University and
Tygerberg Academic Hospital

Email: surethak@sun.ac.za

ABSTRACT
Atopic dermatitis/eczema (ADE) is a common condition affecting up to 20% of children in some countries. Atopic
dermatitis/eczema impairs quality of life, not only of the patient, but also of family members. Due to the increasing
prevalence noticed in westernised populations since the 1940s, particular attention should be paid to triggers,
which may be contributing to this rise. Identifying a trigger is fraught with difficulty due to the fluctuating natural
course of ADE. Triggers of ADE include irritants (such as soap and detergents), allergens (including standard patch
test defined allergens, aeroallergens and food allergens), skin infections (such as Staphylococcus aureus, group A
streptococci, herpes simplex virus, malassezia and tinea infections) and others, including cigarette smoke exposure
and psychological stress. Many commonly believed triggers, such as extreme temperatures and exposure to sand,
have meagre supporting evidence. Nevertheless, they may aggravate the disease. The literature dealing with triggers
is sparse. In this article an overview will be given regarding the relevant literature dealing with this difficult topic.

TRIGGER - AN EVENT THAT PRECIPITATES OTHER EVENTS.
This is the definition of a trigger according to
thefreeonlinedictionary.com.
Atopic dermatitis/eczema (ADE) is a common condition
affecting up to 20% of children in some countries.
Atopic dermatitis/eczema impairs quality of life not only
physically, but also financially and emotionally, of the
patient and their families. Due to the increasing prevalence
noticed in westernised populations since the 1940s1-3,
particular attention should be paid to triggers, which may
be contributing to this rise.
Atopic dermatitis/eczema is a chronic inflammatory
disease caused by a complex interplay of genes, impaired
barrier function, immune dysfunction and environmental
factors, namely allergens and irritants. Skin lesions can be
classified as acute, sub-acute or chronic according to the
clinical morphology and microscopic findings. Incessant
pruritus is the only symptom of ADE and sufferers often
scratch themselves uncontrollably. Although pruritus may
be present in the first few weeks of life, parents become
more aware of the itch as the itch-scratch cycle matures,
when the patient is aged approximately 3 months. Pruritus
elicits rubbing and scratching leading to eczematisation
with eventual lichenification. Existing skin lesions of ADE
may also lichenify by a similar mechanism. The question is
often asked: is it the itch that rashes or the rash that itches?
More likely both statements are correct. Thus, any factor
that leads to pruritus in apparently normal skin or any factor
leading to worsening of existing eczema could be regarded
as a trigger. With this said one should keep in mind that
ADE intrinsically has an intermittent course with alternating
flares and remissions, often for unexplained reasons.
Various factors have been proposed as triggers for ADE,
mostly following epidemiological studies in which exposure
to these factors were associated with increased incidence
of ADE and/or exacerbation of established ADE. However,
studies related to this topic are of poor quality, and even
though clinical experience may dictate otherwise, good
scientific evidence for most triggers are lacking. The ideal
means by which the role of a flare factor in causing a flare
of disease is established, is to demonstrate a temporal
relationship between exposure and worsening of the
disease, a dose-response effect and, ideally, remission
of the flare following withdrawal of the relevant factor.

75
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
 review article
Table I: Triggers in Atopic Dermatitis/Eczema
TRIGGERS IN ATOPIC DERMATITIS/ECZEMA:
A. CHEMICAL IRRITANTS SUCH AS SOAPS, DETER-
GENTS AND CHLORINE
Soaps, bubble baths, detergents and surfactants (e.g.
sodium lauryl sulphate) emulsify surface and intercellular
lipids, which can then be washed off with water. They also
increase the pH of the skin, leading to increased protease
activity with premature desquamation of the stratum
corneum and therefore an impaired barrier function.
Increased transepidermal water loss and dry skin are the
result, leading to pruritis and sensitivity to irritants.5-8
Whereas high concentrations of chlorine, as is found in
swimming pools, may have similar irritating effects on ADE
sufferers skin, the sterilising effect of dilute chlorine baths
is sometimes harnessed to decrease the bacterial load on
76
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
the skin of ADE patients. Soaps and detergents are the
most common causes of irritant contact dermatitis of the
hands and can trigger flares of ADE.9 Avoidance of irritants
are central in the management of ADE. When exposure is
unavoidable protective rubber gloves with a cotton lining
should be worn and application of appropriate emollients and
barrier creams should promptly follow the exposure. When
using shampoos, care should be taken to choose the correct
products, i.e. those approved for use in ADE, and extended
exposure, such as when washing the hair in the bath, should
be avoided. Patients with ADE may sometimes also develop
allergic contact dermatitis to surfactants. In a recent article
it was shown that atopic individuals were significantly
more likely to develop allergic contact dermatitis to the
surfactant cocamidopropyl betaine (CAPB).10 The authors
suggested that cleansers containing the surfactant sodium
review article
laureth sulfate (SLES) would be a safer alternative for the
atopic patient than products containing CAPB, as SLES is a
rare irritant and not a sensitiser.11
B. PHYSICAL IRRITANTS SUCH AS WOOL OR NYLON
Textile fibres have been reported to cause acute and
 make-up remover; bath, shaving and skin care products;
cumulative irritant and allergic contact dermatitis,
exacerbation of ADE and contact urticaria (e.g. nylon
causing allergic contact dermatitis and contact urticaria,
and wool causing acute and cumulative irritant dermatitis).12
The spiky texture of wool fibers is the main problematic
factor. Cotton is generally advised as an alternative, as it
is comfortable and can be layered in the winter to avoid
overheating and sweating. Unfortunately some studies
suggest that cotton may also present a roughness that
irritates the skin of children affected by ADE.13 Silk garments
have shown promising results as it has a very smooth non-
irritating texture, protects the covered areas against aero-
allergens and friction from clothing, and decreases the
possibility of scratching the skin with fingernails.14 Wool
products should therefore be avoided, cotton clothing be
used with caution and silk clothing be worn where possible.
Contrary to popular belief, laundry detergents are rare
causes of exacerbation of ADE.15 Clothes should be washed
in a mild detergent followed by the addition of a fabric
softener.16 To ensure no residual product in the clothing, an
extra rinse with clean water should be performed.
C. ALLERGIC CONTACT DERMATITIS TO TOILETRIES
AND PERFUMES
Patients with ADE are more likely than non-atopic
 to clinical relevance.22 A German cohort study demonstrated
individuals to develop hypersensitivity to allergens on
the standard patch test panel and, in particular, to metal
allergens including nickel, cobalt chloride and potassium
dichromate.17 They are also significantly more likely to
develop allergic contact dermatitis to formaldehyde
releasers, such as quaternium-15, imidazolidinyl urea,
1,3-Dimethylol-5,5-dimethylhydantoin (also known as
DMDM hydantoin), and 2-bromo-2-nitropropane-1,3-
diol. Formaldehyde releasers are used as preservatives in
toiletries, including perfumes and make-up. They are less
likely to develop reactions to parabens, formaldehyde, or
diazolidinyl urea.18 The preservative methylisothiazolinone
(MI) has the dubious honor of being selected the American
Contact Dermatitis Society Contact Allergen of the Year
for 2013 that after recent reports that this allergen has
shown an alarming increase in prevalence in different
European countries.19,20 A report from the USA documented
the same trend. The standard skin patch test used in South
Africa includes a methylchloroisothiazolinone (MCI)/MI
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
combination. Forty percent of MI contact allergy could be
missed however if this combination is used instead of the
less commonly available MI in isolation.20 MI is used as a
preservative in wet wipes and baby products (including
lotions and powders); cosmetics such as eyeliners and eye
hair care and hair-colouring products; nail care products,
deodorants, suntan products, and sunscreens, among
others. Occupational sources of MI include paints, inks,
glues, lacquers, varnishes, and cutting oils. Household
products containing MI include dishwashing liquid soaps
(even in some green household cleaning products),
laundry detergents, laundry stain removers, fabric softeners,
all-purpose cleansers, glass cleaners, and wood cleansers.20
 nderstandably avoiding all these products is very difficult
U
- even impossible. Sensitivities to these products often lead
to exacerbation of ADE and care should be taken when
choosing the correct products.
D. FOOD ALLERGENS
The role of food in ADE has always been and remains
controversial. Cases where an early onset and increased
severity of AD, and where gastrointestinal tract symptoms
are prominent, a food allergen should be considered.21
This topic will be discussed in more detail elsewhere in this
journal.
E. AEROALLERGENS
Sensitisation to aeroallergens does not necessarily translate
that sensitisation pattern changes throughout childhood,
with the prevalence of sensitisation increased steadily
throughout childhood. Sensitisation prevalence hierarchy
(grass > birch pollens > HDM > cat > dog) was maintained
from age 5 years onwards.23 Performing and interpreting
allergy tests (such as skin prick tests and atopy patch
tests) require special training, may be expensive and time-
consuming. Aeroallergen testing may identify those children
with AD at risk for the development of airway disease, so
testing should be considered in children with severe ADE
and specific IgE to aeroallergens. Additional indications
for testing would be in children with AD and typical airway
disease symptoms and seasonal variation.24 Unfortunately,
desensitisation does not seem to improve the ADE in
patients with proven sensitivity to aeroallergens.25
(i) House dust mite (HDM)
The House Dust Mite (HDM) [Dermatophagoides

pteronyssinus] is a tiny insect, 0.25-0.3 mm in length, too
77
 review article
small to see with the naked eye and is a cosmopolitan guest
in human habitation. The mites mainly live in mattresses
and bedrooms as part of the dust. Dust mites feed on
organic detritus such as flakes of shed human skin and
flourish in the stable environment of dwellings. Some
people with eczema are allergic to HDM. HDM affect ADE
via two different mechanisms, including a direct proteolytic
activity and an immunological action inducing an IgE-
mediated response. Two proteins, namely Der p 1 and Der
p 2, show direct proteolytic activity causing increased
barrier disruption.26 Of note is that these proteases may
also cleave lung epithelium and may thereby lead to
respiratory symptoms.27 In the literature as many studies
show improvement with HDM avoidance as those showing
no improvement. HDM is ubiquitous in the environment
and many of the currently suggested techniques are time-
consuming and expensive. Given the conflicting results
of the studies, allergen avoidance measures cannot be
recommended to relieve symptoms at this time.28 However,
some people with severe recalcitrant eczema may consider
trying to clear house dust mite from their home, as much as
possible. The management of HDM is beyond the scope of
this article.
(ii) Animal dander
Some ADE patients report allergic reactions after contact
with animals such as cats, dogs and horses. Dander refers
to loose scales formed on the skin and shed from the coat
or feathers of various animals. The literature is inconsistent
regarding the relationship between ADE and animal dander
exposure. A recent meta-analysis reported a favourable
effect of exposure to dogs and other pets on the risk of
AD in children, whereas no association could be shown
with exposure to cats.29 Tolerance of their own pet is often
reported but this tolerance may be lost when the individuals
are removed from the home. Some practitioners recommend
the removal of the pet in cases of severe allergy, while others
suggest limited managed exposure, e.g. not sharing a bed
with the pet. One has to keep the psychological distress
of pet removal in mind, though, as a report was published
where children chose their pets as one of their three most
favourite items. Removal of the pet may not be justified.30
(iii) Pollen
A seasonal variation in the ADE may be a good indication
of a pollen-sensitive ADE. In a study published in 2005,
it was found that children with a summer-type pattern
experienced more symptoms on days with high grass-
pollen count.31 The likelihood of pollen as aeroallergen in
patients with symptoms on air-exposed surfaces (such
78
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
as the face, dcolletage, lower arm and hands) is also
much higher and especially if the patient shows less or
no involvement on skin surfaces covered with clothes.32
Airborne pollens are the most difficult of aeroallergens to
avoid. During windy periods the pollens may be carried long
distances from the plant. Some cases may have symptoms
limited to a particular time of year and then it is advisable
to avoid open-air activities. If possible, spending summers
in pollen-free areas such as the seacoast or high-mountains
should be considered. As patients carry the pollens on
their skin and hair, daily cleansing including hair washing is
recommended in the problematic time of year. Hanging the
washing in open air to dry should be avoided and regular
vacuum cleaning should be performed.33
(iv) Mold
A review article published in 2013 could not find any strong
evidence implicating molds as a triggering factor for ADE.34
(v) Cockroach
Cockroach allergens can induce positive patch test
reactions in patients with ADE,35 however the role of
cockroach antigen has not been proven with well-controlled
clinical studies.36
F. INFECTIONS
Patients with ADE display a significant decrease in the
expressions of antimicrobial peptides (AMP) and exhibit
innate and adaptive immune defects, which explain their
increased susceptibility to skin infections due to bacteria,
fungi or viruses.
(i) Bacterial: e.g. Staphylococcus aureus (S. aureus) and
group A streptococcus
Patients with ADE are more susceptible to colonisation
by S. aureus because of dysfunction of the innate and
adaptive immune systems.37 A study published in 2013
found that the S. aureus colonisation rate was higher in ADE
patients as compared with non-ADE patients, and that the
rate was higher in acute lesions of ADE patients versus
chronic lesions.38 The colonisation rate increased with age
and the more severe cases demonstrated higher rates of
colonisation rates. The severity of ADE decreased when
treated for S. aureus.39 S. aureus produces superantigens,
which affects the immune system by stimulating T cells
to produce pro-inflammatory cytokines by a non-MHC,
restricted mechanism and suppresses T regulatory cells.
By this mechanism S. aureus superantigens increase
Th2- mediated responses, which in turn suppresses
antimicrobial responses in atopic skin. Superantigens also
review article
induce corticosteroid resistance as well as the production of
IL-31, a very pruritogenic cytokine that regulates filaggrin
expression.40 In a study by Leung et al, 60% of patients with
moderate to severe AD were found to have IgE antibodies
to S. aureus exotoxins. In this way, S. aureus may also trigger
an allergic response via allergen-specific activation of
Fc3RI-bearing effector cells (e.g. mast cells).41
The fact that nasal S. aureus carriage of caregivers may
be a potential source of re-colonisation in children with
AD should be kept in mind when treating this problem.
Treatment should thereby be extended to include the whole
family.42 Care should be taken when using emollient tubs a
clean spoon should be used to decant the desired amount
into another container to avoid introduction of S. aureus or
other skin organisms into the primary container. A study by
Carr et al published in 2008, found that more than half of
the containers tested revealed some sort of bacterial
growth. S. aureus contributed to a quarter of bacterial
growth in their study.43
A retrospective review from 2011 showed that children with
ADE and group A streptococcal infections were more prone
to invasive disease, including bacteremia and septicaemia,
than those infected with S. aureus alone.44
(ii) Fungal
Malassezia yeasts are commensal fungi forming part of
the biofilm of the skin. It has always been considered to
be unable to cause significant problems, but in recent
literature this theory is being questioned. Increased levels
of IgE to Malessezia have been found to be associated with
refractory cases of head and neck dermatitis.45,46 Some
of these cases have been found to show improvement on
systemic antifungal treatments.47
Patients with ADE are more prone to develop acute
and chronic dermatophyte and candida infections.
These infections lead to pruritus and the activation of
the itch-scratch-cycle and should therefore be treated
appropriately.48
(iii) Viral
Viral infections, including herpes simplex and varicella
zoster viruses, in patients with ADE may be very serious. Due
to the impaired barrier function and local immunological
disturbance, sometimes aggravated by the use of topical
corticosteroids, viral infections can spread rapidly over
the body. Molluscum contagiosum, in particular, may be a
persistent problem disseminating due to autoinoculation
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
(via scratching).49
G. CIGARETTE SMOKE
The literature on whether gestational and perinatal
exposure to cigarette smoke may be associated with the
onset of childhood ADE is inconclusive. A study published
in 2011, however, managed to show that adult onset ADE
may be influenced by cumulative and current exposure to
cigarette smoke, whether via environmental or personal
cigarette smoke exposure.50 An increased risk of hand
eczema was found to be associated with smoking more
than 10 cigarettes per day.51
H. Psychological stress
Psychological stress impairs the barrier function, favours
a shift in immunity toward a Th2 response, is associated
with an abnormal hypothalamic-pituitary-adrenal axis and
produces neuropeptides in the skin leading to neurogenic
inflammation.52 ADE also causes psychological stress in
the patient as well as the family. A clear association of
psychological stress triggering ADE could not be confirmed
by a meta-analysis of the available literature by Williams
et al conducted in 2007.30 However, some people react
to stress by habit scratching. This may activate the itch-
scratch cycle and can make eczema worse. Avoid scratching
as much as possible, keep fingernails short, consider
wearing cotton gloves at night, and opt rather for rubbing if
possible. Psychological and stress-reduction interventions
may decrease pruritus, scratching and thereby patient well-
being.
I. Dust and sand
HDM resides in dust and in that way exposure to dust may
trigger ADE, as HDM is a well-known trigger of ADE. Sand is
a commonly believed trigger of ADE, but no clear evidence
could be found in the literature to prove this.
J. Extreme temperature and humidity
The role of humidity and extreme temperature in ADE is
unclear. These factors should be avoided where possible.30
K. Other possible triggers
Sweat may act as an irritant and thereby lead to
exacerbation of ADE. Decreased sweating may also trigger
ADE as it causes xerosis.53 Hormonal changes during
pregnancy and during the menstrual cycle may affect
ADE.54 Air-conditioning decreases the moisture in the air
and may further contribute to the deterioration of ADE, if
the filters are not cleaned regularly. Hard water does not
have scientific evidence of triggering ADE.55
79
 review article
CONCLUSION
ADE has a significant impact on the quality of life of the
individual suffering with this condition, but also on the rest
of the family. Many triggers of ADE have been identified.
Some have solid scientific evidence and should be avoided or
amended as such. Others have no- or inconclusive evidence
and this should be conveyed to ADE patients. Studies on
triggers of ADE are ongoing and we should endeavor to
continue to separate fact from fiction.
DECLARATION OF CONFLICT OF INTEREST
The authors declare no conflict of interest.
REFERENCES
1. Taylor B, Wadsworth J, Wadsworth M, et al. Changes in the reported prevalence
of childhood eczema since the 1039-1945 war. Lancet 1984;2:1255-57.
2. Williams HC. Is the prevalence of atopic dermatitis increasing? Clin Exp Dermatol
1992;17:385-91.
3. Yura A, Shimizu T. Trends in the prevalence of atopic dermatitis in school children:
longitudinal study in Osaka Prefecture, Japan, from 1985-1997. Br J Dermatol
2001;115:966-73.
4. Langan SM, Williams HC. What causes worsening of eczema? A systematic
review. Br J Dermatol 2006;155:504-14.
5. Abe T, Ohkido M, Yamamoto K. Studies on skin surface barrier function: skin
surface lipids and transepidermal water loss in atopic skin during childhood. J
Dermatol 1978;5:223-39.
6.  White MI, McEwan Jenkinson D, Lloyd DH. The effect of washing on the
thickness of the stratum corneum in normal and atopic individuals. Br J Dermatol
1987;116:525-30.
7. Froebe CL, Simion FA, Rhein LD, Cagan RH, Kligman A. Stratum corneum lipid
removal by surfactants: relation to in vivo irritation. Dermatologica 1990;181:277-
83.
8. Ananthapadmanabhan KP, Moore DJ, Subramanyan L, et al. Cleansing without
compromise; the impact of cleansers on the skin barrier and the technology of
mild cleansing. Dermatol Ther 2004;17(suppl 1):16-25.
9. Meding B, Swanbeck G. Prevalence of hand eczema in an industrial city. Br J
Dermatol 1987;116:627-34.
10. Shaughnessy C, Malajian D, Belsito D. Cutaneous delayed-type hypersensitivity
in patients with atopic dermatitis: Reactivity to surfactants. J Am Acad Dermatol
http://dx.doi.org/10.1016/j.jaad.2013.12.009. (article in press)
11. Robinson V, Bergfeld W, Belsito D, et al. Final report of the amended safety
assessment of sodium laureth sulfate and related salts of sulfated ethoxylated
alcohols. Int J Toxicol 2010;29:151-61.
12. Hatch KL, Maibach HI. Textile fiber dermatitis. Contact Dermatitis 1985;12:111.
13. Bendsoe N, Bjornberg A, Asnes H. Itching from wool fibers in atopic dermatitis.
Contact Dermatitis 1987;17:2122.
14. Ricci G, Patrizi A, Bendandi B, et al. Clinical effectiveness of a silk fabric in the
treatment of atopic dermatitis. Br J Dermatol 2004;150:127-31.
15. Belsito D, Fransway A, Fowler J Jr, et al. Allergic contact dermatitis to detergents:
a multicenter study to assess prevalence. J Am Acad Dermatol 2002;46:200-
206.
16. Hermanns JF, Goffin V, Arrese JE. Beneficial effects of softened fabrics on atopic
skin. Dermatology 2001;202(2):167-70.
17. Malajian D, Belsito D. Cutaneous delayed-type hypersensitivity in patients with
atopic dermatitis. J Am Acad Dermatol 2013;69:232-37.
18. Shaughnessy C, Malajian D, Belsito D. Cutaneous delayed-type hypersensitivity
in patients with atopic dermatitis: Reactivity to topical preservatives. J Am Acad
Dermatol 2014;70:102-107.
19. Urwin R, Wilkinson M. Methylchloroisothiazolinone and methylisothiazolinone
contact allergy: a new epidemic. Contact Dermatitis 2013;68:253255. 50. Lee C, Chuang H, Hong C, et al. Lifetime exposure to cigarette smoking and the
20. Castanedo-Tardana M, Zug K. Methylisothiazolinone. Dermatitis 2013;24(1):2-6.
21. Werfel T, Ballmer-Weber B, Eigenmann PA, et al. Eczematous reactions to food in
atopic eczema: position paper of the EAACI and GA2LEN. Allergy 2007;62:723-
28.
22. De Benedictis F, Franceschini F, Hill D, et al. The allergic sensitization in infants
with atopic eczema from different countries. Allergy 2009;64:295-303.
23. Matricardi P, Bockelbrink A, Keil T, et al. Dynamic evolution of serum
immunoglobulin E to airborne allergens throughout childhood: results from the
multicenter allergy study birth cohort. Clin Exp Allergy 2009;39:1551-57.
24. Spergel JM. Epidemiology of atopic dermatitis and atopic march in children.
Immunol Allergy Clin North Am 2010;30:269-80.
25. Darsow U. Allergen-specific immunotherapy for atopic eczema: updated. Curr
Opin Allergy Clin Immunol 2012;12:665-69.
26. Deleuran M, Ellingsen A, Paludan K, et al. Purified Der p 1 and p 2 patch tests in
80
Current Allergy & Clinical Immunology 2014 June Vol 27 No.2
patients with atopic dermatitis: evidence for both allergenicity and proteolytic
irritancy. Acta Derm Venereol 1998;78:241-43.
27. Winton H, Wan H, Cannell M, et al. Class specific inhibition of house dust mite
proteinases which cleave cell adhesion, induce cell death and which increase the
permeability of lung epithelium. Br J Pharmacol 1998;124:1048-59.
28. De Bruin Weller M, Knulst A, Meijer Y, et al. Evaluation of the child with atopic
dermatitis. Clinical & Experimental Allergy 2012;42:35262.
29. Pelucchi C, Galeone C, Bach JF, et al. Pet exposure and risk of atopic dermatitis at
the pediatric age: a meta-analysis of birth cohort studies. J Allergy Clin Immunol
2013;132(3):616-62.
30. Atopic Eczema in Children Management of Atopic Eczema in Children from Birth
up to the Age of 12 Years. NICE Clinical Guidelines, No. 57 National Collaborating
Centre for Womens and Childrens Health (UK).London: RCOG Press; December
2007. 69-71
31. Kramer U, Weidinger S, Darsow U, et al. Seasonality in symptom severity
influenced by temperature or grass pollen: results of a panel study in children
with eczema. J Invest Dermatol 2005;124:514-23.
32. Wheatley L, Platts-Mills T. Role of inhalant allergens in atopic dermatitis. In:
Leung DYM, Greaves MW, eds. Allergic Skin Disease: a Multidisciplinary Approach.
Marcel Dekker, New York, 2000.
33. G Pnyai G, Hidvgi B, Nmeth I, et al. Contact and aeroallergens in adulthood
atopic dermatitis. J Eur Acad Dermatol Venereol 2008;22:1346-55.
34. Torley D, Futamura M, Williams H, et al. Whats new in atopic eczema? An
analysis of systematic reviews published in 2010-2011. Clin Exp Dermatol
2013;38:449-56.
35. Michel S, Yawalkar N, Schnyder B, et al. Eczematous skin reaction to atopy patch
testing with cockroach in patients with atopic dermatitis. J Investig Allergol Clin
Immunol 2009;19(3):173-79.
36. Caubet J, Eigenmann P. Allergic Triggers in Atopic Dermatitis. Immunol Allergy
Clin N Am 2010;30:289307.
37. De Benedetto A, Agnihothri R, McGirt LY, et al. Atopic dermatitis: a disease
caused by innate immune defects? J Invest Dermatol 2009;129:14-30.
38. Park H, Kim C, Huh I, et al. Staphylococcus aureus Colonization in Acute
and Chronic Skin Lesions of Patients with Atopic Dermatitis. Ann Dermatol
2013;25(4):410-16.
39. Huang J, Abrams M, Tlougan B, et al. Treatment of Staphylococcus aureus
colonization in atopic dermatitis decreases disease severity. Pediatrics
2009;123:e808-e814.
40. Spaulding A, Salgado-Pabn W, Kohler P, et al. Staphylococcal and Streptococcal
Superantigen Exotoxins. Clin Microbiol Rev 2013;26(3):422.
41. Leung D, Harbeck R, Bina P, et al. Presence of IgE antibodies to staphylococcal
exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group
of allergens. J Clin Invest 1993;92(3):1374-80.
42. Patel G, Wyatt H, Kubiak E, et al. Staphylococcus aureus colonization of children
with atopic eczema and their parents. Acta Derm Venereol 2001;81:366-67.
43. Carr J, Akram M, Sultan A, L. Hunter, et al. Contamination of emollient creams
and ointments with Staphylococcus aureus in children with atopic eczema. Br J
Dermatol 2008;159 (Suppl. 1):114.
44. Sugarman J, Hersh A, Okamura T, et al. A Retrospective Review of Streptococcal
Infections in Pediatric Atopic Dermatitis. Ped Dermatol 2011;28(3):230-34.
45. Zhang E, Tanaka T, Tajima M, et al. Anti-Malassezia-specific IgE antibodies
production in Japanese patients with head and neck atopic dermatitis:
relationship between the level of specific IgE antibody and the colonization
frequency of cutaneous Malassezia species and clinical severity. J Allergy (Cairo)
2011;2011:645-70.
46. Darabi K, Hostetler S, Bechtel M, et al. The role of Malassezia in atopic dermatitis
affecting the head and neck of adults. J Am Acad Dermatol 2009;60:125-36.
47. Back O, Bartosik J. Systemic ketoconazole for yeast allergic patients with atopic
dermatitis. J Eur Acad Dermatol Venereol 2001;15:34-38.
48. Faergemann J. Atopic dermatitis and fungi. Clin Microbiol Rev 2002;15(4):545-
63.
49. Shiohara T, Sato Y, Takahashi R, et al. Increased susceptibility to cutaneous viral
infections in atopic dermatitis: the roles of regulatory T cells and innate immune
defects. Curr Probl Dermatol 2011;41:125-35.
development of adult-onset atopic dermatitis. Br J Dermatol 2011;164:483-89.
51. Meding B, Alderling M, Albin M et al. Does tobacco smoking influence the
occurrence of hand eczema? Br J Dermatol 2009;160:514-18.
52. Arndt J, Smith N, Tausk F. Stress and Atopic Dermatitis Current Allergy and
Asthma Reports 2008;8:312-17.
53. Paul C, Maumus-Robert S, Mazereeuw-Hautier J, et al. Prevalence and risk factors
for xerosis in the elderly: a cross-sectional epidemiological study in primary care.
Dermatology 2011;223(3):260-65.
54. Rimoin L, Kwatra S, Yosipovitch G. Female-specific pruritus from childhood
to postmenopause: clinical features, hormonal factors, and treatment
considerations. Dermatol Ther 2013;26(2):157-67.
55. McNally N, Phillips D. Geographical studies of atopic dermatitis. In: Atopic
dermatitis. The epidemiology, causes and prevention of atopic dermatitis. Ed HC
Williams. Cambridge University Press 2000;71-84.