A clinician's reference guide for the management of atopic dermatitis in Asians

Abstract

Background
Atopic dermatitis (AD) is a common skin condition among Asians. Recent studies have shown that Asian AD has a unique clinical and immunologic phenotype compared with European/American AD.

Objective
The Asian Academy of Dermatology and Venereology Expert Panel on Atopic Dermatitis developed this reference guide to provide a holistic and evidence-based approach in managing AD among Asians.

Methods
Electronic searches were performed to retrieve relevant systematic reviews and guidelines on AD. Recommendations were appraised for level of evidence and strength of recommendation based on the U.K. National Institute for Health and Care Excellence and Scottish Intercollegiate Guidelines Network guidelines. These practice points were based on the consensus recommendations discussed during the Asia Pacific Meeting of Experts in Dermatology held in Bali, Indonesia in October 2016 and April 2017.

Results
The Expert Panel recommends an approach to treatment based on disease severity. The use of moisturizers is recommended across all levels of AD severity, while topical steroids are recommended only for flares not controlled by conventional skin care and moisturizers. Causes of waning efficacy must be explored before using topical corticosteroids of higher potency. Topical calcineurin inhibitors are recommended for patients who have become recalcitrant to steroid, in chronic uninterrupted use, and when there is steroid atrophy, or when there is a need to treat sensitive areas and pediatric patients. Systemic steroids have a limited role in AD treatment and should be avoided if possible. Educational programs that allow a patient-centered approach in AD management are recommended as an adjunct to conventional therapies. Recommendations on the use of phototherapy, systemic drugs, and emerging treatments are also included.

Conclusion
The management of AD among Asians requires a holistic approach, integrating evidence-based treatments while considering accessibility and cultural acceptability.

Full text

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ABSTRACT
Background: Atopic dermatitis (AD) is a common skin condition among Asians. Recent
studies have shown that Asian AD has a unique clinical and immunologic phenotype
compared with European/American AD.
Objective: The Asian Academy of Dermatology and Venereology Expert Panel on Atopic
Dermatitis developed this reference guide to provide a holistic and evidence-based approach
in managing AD among Asians.
Methods: Electronic searches were performed to retrieve relevant systematic reviews and
guidelines on AD. Recommendations were appraised for level of evidence and strength of
recommendation based on the U.K. National Institute for Health and Care Excellence and
Scottish Intercollegiate Guidelines Network guidelines. These practice points were based
on the consensus recommendations discussed during the Asia Pacic Meeting of Experts in
Dermatology held in Bali, Indonesia in October 2016 and April 2017.
Results: The Expert Panel recommends an approach to treatment based on disease severity.
The use of moisturizers is recommended across all levels of AD severity, while topical steroids
are recommended only for ares not controlled by conventional skin care and moisturizers.
Causes of waning ecacy must be explored before using topical corticosteroids of higher
potency. Topical calcineurin inhibitors are recommended for patients who have become
recalcitrant to steroid, in chronic uninterrupted use, and when there is steroid atrophy, or
when there is a need to treat sensitive areas and pediatric patients. Systemic steroids have a
limited role in AD treatment and should be avoided if possible. Educational programs that
Asia Pac Allergy. 2018 Oct;8(4):e41
https://doi.org/10.5415/apallergy.2018.8.e41
pISSN 2233-8276·eISSN 2233-8268
Educational &
Teaching Material
Steven Chow 1,*, Chew Swee Seow2, Maria Victoria Dizon3, Kiran Godse4,
Henry Foong5, Vicheth Chan6, Tran Hau Khang7, Leihong Xiang8, Syarief Hidayat9,
M. Yulianto Listiawan10, Danang Triwahyudi11, Srie Prihianti Gondokaryono12,
Endang Sutedja12, Inne Arline Diana12, Oki Suwarsa12, Hartati Purbo Dharmadji12,
Agnes Sri Siswati13, Retno Danarti13, Retno Soebaryo14, and
Windy Keumala Budianti15; for the Asian Academy of Dermatology & Venereology
1Pantai Hospital, Kuala Lumpur, Malaysia
2National Skin Centre, Singapore, Singapore
3Makati Medical Center, Manila, the Philippines
4DY Patil School of Medicine, Nerul, Navi Mumbai, India
5Foong Skin Specialist Clinic, Ipoh, Malaysia
6Cadau Skin and Laser Clinic, Pnomh Penh, Cambodia
7Hanoi Medical University, Hanoi, Vietnam
8Fudan University, Shanghai, China
9League of ASEAN Dermatologic Societies, Kuala Lumpur, Malaysia
10Surabaya Skin Centre, Jawa Timur, Indonesia
11Rumah Sakit Metropolitan Medical Centre, Jakarta, Indonesia
12Univerity of Padjadjaran, Bandung, Indonesia
13Gadjah Mada University, Yogyakarta, Indonesia
14University of Indonesia, Jakarta, Indonesia
15Cipto Mangunkusumo Hospital, Jakarta, Indonesia
A clinician's reference guide for the
management of atopic dermatitis in
Asians
Received: Jul 24, 2018
Accepted: Oct 24, 2018
*Correspondence to
Steven Chow
Pantai Hospital Kuala Lumpur, No. A730, 7th
Floor, Block A, 8, Jalan Bukit Pantai, 59100
Kuala Lumpur, Malaysia.
Tel : +603-22826558
Fax: +603-92225273
E-mail: drstevenchow@gmail.com
Copyright © 2018. Asia Pacific Association of
Allergy, Asthma and Clinical Immunology.
This is an Open Access article distributed
under the terms of the Creative Commons
Attribution Non-Commercial License (https://
creativecommons.org/licenses/by-nc/4.0/)
which permits unrestricted non-commercial
use, distribution, and reproduction in any
medium, provided the original work is properly
cited.
ORCID iDs
Steven Chow
https://orcid.org/0000-0002-9094-2653
Author Contr ibutions
Conceptualization: Steven KW Chow, Chew
Swee Seow, Maria Victoria Dizon, Kiran Godse,
Henry Foong, Vicheth Chan, Tran Hau Khang,
Leihong Xiang, Syarief Hidayat, M. Yulianto
Listiawan, Danang Triwahyudi, Srie Prihianti
Gondokaryono, Endang Sutedja, Inne Arline
Diana, Oki Suwarsa, Hartati Purbo Dharmadji,
Agnes Sri Siswati, Retno Danarti, Retno
Soebaryo, Windy Keumala Budianti. Data
Review

curation: Seow Chew Swee, Maria Victoria
Dizon, Kiran Godse, Henry Foong, Vicheth
Chan, Tran Hau Khang, Leihong Xiang, Syarief
Hidayat, M. Yulianto Listiawan, Danang
Triwahyudi, Srie Prihianti Gondokaryono,
Endang Sutedja, Inne Arline Diana, Oki
Suwarsa, Hartati Purbo Dharmadji, Agnes Sri
Siswati, Retno Danarti, Retno Soebaryo, Windy
Keumala Budianti. Funding acquisition: Syarief
Hidayat. Investigation: Steven KW Chow,
Chew Swee Seow, Kiran Godse, Henry Foong,
Tran Hau Khang, Inne Arline Diana, Retno
Danarti, Retno Soebaryo, Windy Keumala
Budianti. Project administration: Srie Prihianti
Gondokaryono. Resources: Srie Prihianti
Gondokaryono. Supervision: Chew Swee
Seow. Validation: Steven KW Chow. Writing -
original draft: Steven KW Chow, Chew Swee
Seow, Kiran Godse, Henry Foong, Tran Hau
Khang, Inne Arline Diana, Retno Danarti, Retno
Soebaryo, Windy Keumala Budianti. Writing
- review & editing: Chew Swee Seow, Maria
Victoria Dizon, Kiran Godse, Henry Foong,
Vicheth Chan, Tran Hau Khang, Leihong Xiang,
Syarief Hidayat, M. Yulianto Listiawan, Danang
Triwahyudi, Srie Prihianti Gondokaryono,
Endang Sutedja, Inne Arline Diana, Oki
Suwarsa, Hartati Purbo Dharmadji, Agnes Sri
Siswati, Retno Danarti, Retno Soebaryo, Windy
Keumala Budianti.
allow a patient-centered approach in AD management are recommended as an adjunct to
conventional therapies. Recommendations on the use of phototherapy, systemic drugs, and
emerging treatments are also included.
Conclusion: The management of AD among Asians requires a holistic approach, integrating
evidence-based treatments while considering accessibility and cultural acceptability.
Keywords: Asians; Atopic dermatitis; Eczema; Atopy; Dermatology
INTRODUCTION
Atopic dermatitis (AD), also referred to as atopic eczema, is a common skin condition among
Asians [1]. It is a chronic inammatory skin disease oen found in patients with personal
or family history of food allerg y, allergic rhinitis and/or asthma [2, 3]. Recent studies have
shown that AD may have several manifestations or phenotypes, such as extrinsic vs. intrinsic
AD [4], pediatric vs. adult AD [5], and European/American vs. Asian AD [6, 7].
Asian AD clinically presents with a more clearly demarcated lesion, more prominent scaling
and lichenication. Immunologic analyses have also shown that it has a unique cytokine
prole that closely resembles psoriasis [8, 9].
Challenges in AD management in Asia include variability in healthcare access in dierent
countries, generalists' level of condence in managing mild forms of AD, and misperceptions
by patients that only dermatologists can manage AD [8]. The Asian Academy of Dermatology
and Venereology Expert Panel on Atopic Dermatitis developed this reference guide to help
provide a holistic and evidence-based approach in managing AD among Asians.
MATERIALS AND METHODS
Electronic searches were performed on MEDLINE, Cochrane and Google Scholar to retrieve
systematic reviews and guidelines on AD published from 2000 to 2017. The following subject
headings or MeSH terms were used: ‘atopic dermatitis,’ ‘eczema,’ ‘Asian,’ ‘Chinese,’ ‘Japanese,’
‘Korean,’ ‘Thai,’ ‘Indonesian,’ ‘Filipino,’ ‘Singaporean,’ ‘Malaysian,’ ‘Indian,’ ‘guideline,’
‘management,’ ‘diagnosis,’ ‘treatment,’ ‘monitoring,’ ‘severity,’ ‘review,’ ‘meta-analysis,’
‘syst emat ic re view,’ ‘evi dence -base d,’ ‘laggrin,’ ‘pathophysiology,’ ‘intrinsic,’ ‘extrinsic,’
‘pediatric,’ ‘adult,’ ‘Caucasian’ and ‘prevalence.’ Only art icles in English were included.
This reference guide was based on the consensus recommendations discussed last October 2016
and April 2017 during the Asia Pacic Meeting of Experts in Dermatology held in Bali, Indonesia.
The recommendations were appraised based on the U.K. National Institute for Health and Care
Excellence and Scottish Intercollegiate Guidelines Network guidelines (Ta ble 1).
RESULTS AND DISCUSSION
Diagnosis of AD
The diagnosis of AD is clinical and is based on the morphology and distribution of the lesion,
as well as the associated signs and symptoms [10]. A widely used diagnostic criteria were
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published by Hanin and Rajka that consist of 4 Major and 23 Minor Criteria (Table 2). AD is
diagnosed when 3 major and 3 minor criteria are met [11].
There is currently no reliable biomarker to diagnose AD. A diagnostic work-up may be
performed in certain cases to help in prognostication, testing for allergic triggers or for
monitoring response to treatment. These tests include serum total immunoglobulin E (IgE)
levels, specic IgE levels and peripheral eosinophil count [4, 7, 12-14].
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Table 1. Level of evidence and strength of recommendation
Level of evidence Type of evidence
1++ High-quality meta analyses, high-quality systematic reviews of clinical trials with very little risk of bias
1+ Well-conducted meta-analyses, systematic review of clinical trials or well-conducted clinical trials with low risk of bias
1- Meta-analyses, systematic reviews of clinical trials or clinical trials with high risk of bias
2++ High-quality systematic reviews of cohort or case and control studies; cohort or case and control studies with very low risk of
bias and high probability of establishing a causal relationship
2+ Well-conducted cohort or case and control studies with low risk of bias and moderate probability of establishing a causal
relationship
2- Cohort or case control studies with high risk of bias and significant risk that the relationship is not causal
3Nonanalytical studies, such as case reports and case series
4Expert opinion
Strength of recommendation Evidence
A At least one meta-analysis, systematic review or clinical trial classified as 1++ and directly applicable to the target
population, or a volume of scientific evidence comprising studies classified as 1+ and which are highly consistent with each
other; evidence drawn from a NICE technology appraisal
B A body of scientific evidence comprising studies classified as 2++, directly applicable to the target population and highly
consistent with each other, or scientific evidence extrapolated from studies classified as 1++ or 1+
C A body of scientific evidence comprising studies classified as 2+, directly applicable to the target population and highly
consistent with each other, or scientific evidence extrapolated from studies classified as 2++
D Level 3 or 4 scientific evidence, or scientific evidence extrapolated from studies classified as 2+, or formal consensus
D (GPP) A good practice point (GPP) is a recommendation for best practice based on the experience of the Workgroup members
NICE, National Institute for Health and Care Excellence.
Table 2. The Hanifin and Rajka diagnostic criteria for atopic dermatitis
Major criteria
• Pruritus
• Dermatitis affecting flexural surfaces in adults and the face and extensors in infants
• Chronic or relapsing dermatitis
• Personal or family history of cutaneous or respiratory atopy
Minor criteria
• Features of the so-called “atopic facies”: facial pallor or erythema, hypopigmented patches, infraorbital darkening, infraorbital folds or wrinkles, cheilitis,
recurrent conjunctivitis, and anterior neck folds
• Triggers of atopic dermatitis: foods, emotional factors, environmental factors, and skin irritants such as wool, solvents, and sweat
• Complications of atopic dermatitis: susceptibility to cutaneous viral and bacterial infections, impaired cell-mediated immunity, immediate skin-test reactivity,
raised serum IgE, keratoconus, anterior subcapsular cataracts
• Others: early age of onset, dry skin, ichthyosis, hyperlinear palms, keratosis pilaris (plugged hair follicles of proximal extremities), hand and foot dermatitis,
nipple eczema, white dermatographism, and perifollicular accentuation
Exclusions
Scabies
Seborrheic dermatitis
Contact dermatitis (irritant or allergic)
Ichthyoses
Cutaneous T-cell lymphoma
Psoriasis
Photosensitivity dermatoses
Immune deficiency diseases
Erythroderma of other causes

Total IgE is elevated in approximately 80% of AD patients classied as extrinsic type. It is not
a diagnostic requirement, but it is helpful in determining prognosis or in choosing therapy.
In adults, a total serum IgE level of 200 IU/mL or greater may be considered high but this may
vary depending on the institution. The IgE cuto in infants varies according to age [14]. High
levels of IgE may reflect the long-term activity of AD but are oen non-specic and may be
seen in response to dierent allergens [1].
Specic IgE testing using blood serum specimens for food or inhalant allergens is
also nonspecic. However, it is preferable to skin prick testing for immediate or type I
hypersensitivity, especially in children. Preventing exposure to these allergens is expected to
improve/prevent exacerbation of rashes [15]. Peripheral eosinophil or mast cell counts are
oen nondiagnostic and are not recommended for routine use [15].
Practice point
: In some instances, a diagnostic work-up is done to help in prognostication,
testing for allergic triggers, or for monitoring response to treatment. [Level 4, good practice
point (GPP)]
Assessment of AD severity
Objective assessment of AD severity is important for appropriate management [10, 14, 16].
Generally, mild disease has a more remitted course, aects less body surface area (BSA), and
is associated with pruritus that is of lower intensity [17]. The SCOring Atopic Dermatitis or
SCORAD Index developed by the European Task Force on Atopic Dermatitis is a comprehensive
system used to assess AD severity [10, 13, 16, 18]. Although validated, this system combines
assessment of symptoms with observation of signs and is also more useful in pediatric patients
[19]. The Eczema Area and Severity Index (EASI) was hence developed incorporating disease
intensity and measurement of the total aected body area [19]. While the SCORAD looks at a
representative site for each of the 6 signs, the EASI assesses 4 signs in various areas (4 sites) of
the body and gives weight to the extent of the lesions [20]. Nonetheless, the EASI is limited by
its signicant emphasis on BSA measurements, which may be dicult to assess accurately and
uniformly [18]. Given the complexity of these assessment methods, the Three-Item Severity
(TIS) score is proposed as an alternative to the abovementioned systems for use in daily practice
(Tab le 3). It is based on the evaluation of erythema, edema or papulation and excoriation. The
TIS Score corresponds well with SCORAD and is suitable for use in routine clinical practice and
for screening purposes [13, 18, 21].
Practice point
: The TIS score correlates well with the more detailed SCORAD and can be used as
a screening tool or as a monitoring tool in practice and in epidemiological studies. [Level 2+, B]
Monitoring parameters for AD
AD poses a signicant burden on healthcare resources and to the quality of life (QoL) of
patients [22-24]. However, the measurement of QoL in infants, children and adolescents with
AD remains a challenge and lacks a universally reliable tool. Hence, routine QoL assessment
is not typically necessary [23].
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Table 3. The Three-Item Severity (TIS) score
Symptom Score (0, none → 3, severe)
Erythema 0, 1, 2, 3
Edema/papulation 0, 1, 2, 3
Excoriation 0, 1, 2, 3
TIS score: <3, mild; 3–5, moderate; ≥6, severe.

Patient monitoring forms with a written action plan have been used in many centers and are
suggested to positively aect compliance – as shown by a few small studies [25]. One such
tool is the Eczema Action Plan, a patient guide that provides instructions on the control and
rescue of AD. It is provided directly to patients and their caregivers [25]. More large scale
prospective studies are needed to support the routine use of these tools [26].
Practice point
: The use of patient monitoring forms with a written action plan may be used as
an optional tool for the patient to self-monitor ares. [Level 4, GPP]
The management of AD
The goals in AD management include reduction and prevention of symptoms to improve QoL
by safe and cost-eective means that are appropriate to the environment. The Expert Panel
recommends a stepwise approach to treatment based on the severity of disease (e.g., mild
disease warrants basic management and/or acute treatment, as needed, while moderate to
severe disease may require topical anti-inammatory and further assessment of recalcitrant
lesions). Basic therapeutic recommendations integrate Dr. Thiru Thirumoorthy's “ve pillars
of AD management” which include education, avoidance of triggers, rebuilding barrier
function, clearance of inammatory disorders, and control and elimination of the itch-
scratch cycle [16].
Education and avoidance of triggers
Education of the patient/caregiver must be communicated in lay person language and should
include regular discussions on short- and long-term goals of therapy [12, 15, 16, 27-29].
Therapeutic patient education is a patient-centered approach to AD management that entails
acquiring skills, such as self-management and treatment adaptation, which have been shown
to lead to better disease control [28, 30, 31].
The implementation of structured and multidisciplinary educational programs has led to
signicant improvements in subjective assessments of severity, itching and coping [29].
Educational programs dier in their type, content and organization [30]. Further studies
are needed to determine the cross-applicability and cost-eectiveness of these programs in
localities with dierent cultural norms [13].
Workshops carried out in a classroom setting or nurse-led educational sessions can improve
patient awareness of their disease and compliance [29, 32]. The use of standardized
instructional video may also be explored as a time-saving means of patient education [29].
Practice point
:
· Educational programs that allow a patient-centered approach in AD management are
recommended as an adjunct to conventional therapies. [Level 2+, C]
· Patient information leaets presented in a local language/dialect may be considered as
a cost-eective educational measure [30]. Instructional videos may also be explored.
[Level 4, GPP]
· Specialist dermatology nurses can hold brief educational sessions, which are known to
reduce AD severity. [Level 4, GPP]
· Specic topics may vary according to local practices; however, the following are common
themes that may be discussed during these sessions:
- Proactive treatment (in contrast to reactive treatment) to prevent outbreak, has been
strongly advocated recently.
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- Avoidance and modification of environmental triggers is just as important as therapy.
It encompasses lifestyle modification and avoidance of skin injury during ares.
- In the tropics, a hot and humid climate is a commonly reported cause of are and itch.
There is little information on the advice to be given regarding outdoor activities in
school and the choice of material for clothing.
- Basic measures of itch control include keeping the nails short and wearing loose, light
clothing and avoiding synthetic fabrics that dissipate heat and sweat poorly.
- Use of traditional medications may be a reason for ares of eczema.
· Food allergy in AD is debatable. The role of diet in the course and treatment of AD is
controversial and is not well understood. Some literature supports the idea that an
elimination diet may improve severe types of AD. However, practitioners should not
recommend otherwise healthy children to be deprived of nutrition due to unnecessary
food restrictions.
· Exposure to pets, provided that the pet is taken out of the home to get allergen exposure
to the child, is recommended in recent publications.
Topical therapy
Moisturizers
Moisturizers are the mainstay in AD management and should be used liberally and frequently,
especially during acute ares and in the prevention of relapse between breakouts, to moisten
and protect the skin [12, 16, 27]. Acceptability and availability of the moisturizer must be
considered [32].
Moisturizers that attract and bind water from the deeper epidermis to the subcutaneous
layer are known as humectants (Table 4). Those that form a hydrophobic lm to retard
transepidermal water loss (TEWL) are known as occlusives. Those that smoothen the skin
by lling the cracks between desquamating corneocytes are known as emollients [33, 34].
Some authors classify small molecular weight proteins into the class of ‘protein rejuvenators’
[35], while ceramide-dominant moisturizers are oen referred to as belonging to the class of
‘therapeutic moisturizers’ [36].
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Table 4. Classification of moisturizers according to their properties
Class Mode of action Some examples
Humectants Attract and bind water from
deeper epidermis to SC
Glycerin
Alpha hydroxy acids
Hyaluronic acid
Sorbitol
Urea
Occlusives Form a hydrophobic film to
retard TEWL of SC
Carnauba wax
Lanolin
Mineral oils
Olive oil
Petrolatum
Silicone
Emollients Smoothens skin by filling the
cracks between desquamating
corneocytes
Ceramide
Collagen
Colloidal oatmeal
Elastin
Glyceryl stearate
Isopropyl palmitate
Shea butter
Stearic acid
SC, subcutaneous layer; TEWL, transepidermal water loss.

Practice point
: The formulation of moisturizers must be suitable for the climate, humidity
and environmental conditions of the patient to ensure compliance. It is recommended to use
moisturizers across all levels of AD severity. [Level 1, A]
In Asia, traditional emollients such as virgin coconut oil are used [37, 38]. In patients with
mild to moderate AD, camellia oil has improved itch and helped reduce the use of medicated
topical ointments. Olive oil reduced the number of
Staphylococcus aureus
colonies but caused
erythema and reduced stratum corneum integrity. Virgin coconut oil improved SCORAD,
TEWL and skin capacitance scores, and reduced
S. aureus
colonization [37, 38].
There is insucient evidence on the use of oils in bath water or the use of acidic spring water [10].
However, consistent u se of moisturizers applied immediately aer bathing for at least 2 to 3 times
a day over aected and non-aected skin is recommended. “Double pajamas” (dry outer and moist
inner layer) as a form of wet dressing enhances the ecacy of the moisturizers and this form of wet-
wrap therapy with or without topical steroids can be used in moderate to severe AD [8].
New anti-inammatory agents are added into the formulation because of their steroid-
sparing eects (e.g., telmesteine, laggrin breakdown products,
Vitis vinifera
, ceramide-
dominant barrier repair lipids) [13, 37]. MAS063DP (Atopiclair) is a nonsteroidal barrier
repair cream that contains glycyrrhetinic acid,
V. vinifera
extract and telmesteine in
combination with shea butter (emollient) and hyaluronic acid (humectant) shown to be an
eective monotherapy for mild to moderate AD in pediatric and adult patients [13, 37]. In a
recent Cochrane review, MAS063DP was documented in at least four randomized trials to be
four times more eective in improving AD severity and led to more reduction of itch, fewer
ares, and improved patient satisfaction when compared to placebo (i.e., vehicle) [37].
Practice point
: Moisturizers should be applied directly on the skin aer bathing and for least 2
to 3 applications per day. [Level 1+, B]
Cleansers
There is no standard on the frequency or duration of bathing for patients with AD; however,
it is recommended to carefully remove crusted skin to eliminate bacterial contaminants.
The choice of cleansing products greatly inuence breakout in some patients. The use of
antiseptics (e.g., chlorhexidine, triclosan and potassium permanganate) while bathing has
not been shown to benet AD patients [10].
Alkaline and medicated soap removes the acid mantle of skin surface which has a normal pH of 5.5.
Use of nonsoap cleansers, such as glycerin, lauryl glucoside, tocopherol-based gels (e.g., Atopiclair
hydra), with low or neutral pH, hypoallergenic, and fragrance free is recommended [10].
Sodium hypochlorite bathing may be an option for some patients [39]. Strongly scrubbing
with a bath towel aer bathing is not recommended.
Practice point
: Limited usage of neutral to low pH, hypoallergenic, and fragrance-free nonsoap
cleansers is recommended. [Level 3, C]
Topical corticosteroids
Top ic a l co rt ic os te r oi ds a re r el ia bl e in co nt ro ll in g ares and are indicated for cases that
have failed to respond to adequate skin care and moisturizers. They are recommended for
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short-term use because of potential side eects. Steroids are grouped into seven classes
based on potency (Ta ble 5) [12-14, 27]. The availability of topical steroids may vary from
country to countr y.
Most cases of AD need only mild potency steroid. High potency topical steroid for ‘quick xes’
and in patients who have not responded to milder steroid is not recommended. Explore other
causes of waning ecacy, such as poor compliance and tachyphylaxis [10, 14]. Patients and
caregivers should be educated on misconceptions and possible ‘steroid phobia’ [10, 14, 16].
Practice point
:
· Application of topical steroids is useful for ares not typically controlled by conventional
skin care and moisturizers alone. [Level 1, A]
· It is recommended that doctors provide practical and workable instructions for patients
on the use of these topical medications. Explore causes of waning ecacy before using
topical corticosteroids of higher potency. [Level 1+, B]
Steroid dosage and fingertip units
The right choice of topical formulation ensures better treatment outcome. Lotion and gel
should be used in acute eczema with exudation and blisters, and to hairy regions. Ointment
is used for thick, dry areas, and to palms and soles. Cream can be used on all areas [37].
A close approximation of adequate dosage is determined by ‘ngertip units’ (FTU; Fig. 1).
FTU is the quantity of cream/ointment extruded from a tube with nozzle of 5-mm diameter
covering the length of the distal phalanx of the index nger. It is about 0.45 to 0.5 g of cream
and is sucient to cover an area of 300 cm2. The quantity of cream in a FTU varies with age:
adult male: 1 FTU provides 0.5 g; adult female: 1 FTU provides 0.4 g; child aged 4 years –
approximately 1/3 of adult amount. A rough guide of dosage is 1 g to face and neck, 8 g to trunk
(front and back), 4 g to arms, 6 g to legs, 1 g each to hands, feet and genitals [12, 16, 17, 27].
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Table 5. Topical steroids grouped according to potency
Class Drug Strength Dosage form
1Clobetasol propionate 0.05 Cream, foam, ointment
Diflorasone diacetate 0.05 Ointment
2Amcinonide 0.1Cream, lotion, ointment
Betamethasone dipropionate 0.05 Cream, foam, ointment, solution
Fluocinonide 0.05 Cream, gel, ointment, solution
Mometasone furoate 0.1Ointment
Triamcinolone acetonide 0.5Cream, ointment
3–4Betamethasone valerate 0.1Cream, foam, lotion, ointment
Fluocinolone acetonide 0.025 Cream, ointment
Fluticasone propionate 0.05 Cream
Fluticasone propionate 0.05 Ointment
Mometasone furoate 0.1Cream
Triamcinolone acetonide 0.1Cream, ointment
5Hydrocortisone butyrate 0.1Cream, ointment, solution
Hydrocortisone probutate 0.1Cream
Hydrocortisone valerate 0.2Cream, ointment
6Alclometasone dipropionate 0.05 Cream, ointment
Desonide 0.05 Cream, gel, foam, ointment
Fluocinolone acetonide 0.01 Cream, solution
7Dexamethasone 0.1Cream
Hydrocortisone 0.25, 0.5, 1Cream, lotion, ointment, solution
Hydrocortisone acetate 0.5–1Cream, ointment

Twice daily application for not more than 3 weeks is eective in most patients [13, 40].
Side eects, including possible hypothalamic-pituitary-adrenal axis suppression, should
be monitored, particularly in children who have chronically used topical corticosteroids.
Cutaneous side eects should be monitored in patients using potent steroids for longer
than the recommended period. However, no specic monitoring of systemic side eects is
recommended [10].
Practice point
: The FTU is easily understandable as a unit of measure for both patients
and clinicians. It is recommended to explain to the patient how to apply topical products
using this measure and to enable clinicians to condently advice patients without fear of
overdosing. [Level 4, GPP]
Topical calcineurin inhibitors
The topical calcineurin inhibitors (TCIs) tacrolimus and pimecrolimus have comparable
ecacy to topical steroid in patients with AD. TCIs are recommended for use in patients who
have become recalcitrant to steroid, in cases of prolonged uninterrupted use and when there
is steroid atrophy, or when there is a need to treat sensitive areas (e.g., face, anogenital area,
skin folds) and pediatric patients as a steroid-sparing agent [10, 41]. TCIs inhibit T-lymphocyte
function, which plays a central role in the development of inammatory reactions [12].
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Adolescent/adult
12 years
2.5 FTU (face & neck)
3 FTU (arm)
7 FTU (trunk including
buttock front and back)
1 FTU (hand, both sides)
6 FTU (leg)
2 FTU (foot)
Child
6–10 years
2.5 FTU (face & neck)
2.5 FTU (arm)
3.5 FTU (front)
5 FTU (back)
4.5 FTU (leg)
Child
3–5 years
1.5 FTU (face & neck)
3 FTU (arm)
3 FTU (front)
3.5 FTU (back)
4.5 FTU (leg)
Infant
1–2 years
1.5 FTU (face & neck)
1.5 FTU (arm)
2 FTU (front)
3 FTU (back)
2 FTU (leg)
Infant
3–6 months
1 FTU (face & neck)
1 FTU (arm)
1 FTU (front)
1.5 FTU (back)
1.5 FTU (leg)
FTU = amount of ointment expressed from a tube with a
5-mm diameter nozzle measured from the distal skin crease to the top
of the palmar surface of an adult’s index finger (~0.5 g)
1 FTU = adequate amount of ointment for “thin and even” application
to an area of skin equal to ~2 adult hands (fingers together)
Fig. 1. The Fingertip Unit (FTU) recommended for various age groups.

Because tacrolimus ointment and pimecrolimus cream may cause skin discomfort,
using topical corticosteroids should be considered rst to minimize TCI application site
reactions. The concomitant use of a topical corticosteroid with a TCI may be done for the
treatment of AD [41].
Tacrolimus ointment is usually applied externally aer bathing. A 0.1% tacrolimus ointment
for adults should be administered at a dose of 5 g or less. A 0.03% tacrolimus ointment for
children aged 2 to 5 years (<20 kg in body weight) should be given at a dose of not more than
1 g; for children aged 6 to 12 years (approximately 20 to 50 kg in body weight), at a dose of
2 to 4 g; and for children at least 13 years old (about 50 kg in body weight), a dose of up to 5
g. It should be administered at a maximum of twice per day. Pimecrolimus is available as a
1% cream and absorbed less than the tacrolimus ointment. When applied twice per day, an
interval of approximately 12 hours between applications is recommended.
Occlusive dressing therapy should not be used because it may cause absorption of the drug to
the bloodstream. Continuous external application of a tacrolimus ointment 2 to 3 times per
week aer remission induction can significantly inhibit the relapse of symptoms (proactive
therapy) [12, 16, 27, 41].
Proactive, intermittent use of TCI is recommended to help prevent relapses while reducing the
need for topical corticosteroids and is more eective than the use of emollients alone [12].
The disadvantage of using TCIs is that they are expensive and may cause burning and
stinging. Rare cases of skin malignancy have been reported but causal relationship has not
been established. Nonetheless, clinicians should be aware of the black-box warning on the
use of TCIs and discuss these as warranted [10]. TCIs do not increase the prevalence of
cutaneous viral infections with use of up to 5 years; however, physicians should inform their
patients of the theoretical risks. Routine blood monitoring of tacrolimus and pimecrolimus
levels is not recommended at this time [10].
Practice point
: TCIs are recommended for use in patients who have become recalcitrant to
steroid, in chronic uninterrupted use and when there is steroid atrophy, or when there is a
need to treat sensitive areas and pediatric patients. [Level 1+, B]
Phototherapy
Phototherapy may be used as second-line treatment in patients whose medical, physical,
and/or psychological states are greatly aected by their disease, which may include negative
impact on social or interpersonal interactions. Phototherapy can be used as maintenance
therapy in chronic disease and is oen used in severe AD [42]. While the mechanism
of action has not been fully elucidated, ultraviolet (UV) is thought to have local anti-
inflammatory and immunosuppressive action [41].
Phototherapy with narrowband ultraviolet B or UVB (UVBTL01) and UVA1 is most commonly
used. Medium-dose UVA1 may be used for control of acute flares while narrowband-UVB
may be used in the management of chronic AD [41, 43]. High dose UVA1 is useful for control
of acute exacerbations. PUVA is particularly useful in AD patients with thick lichenied and
keratotic palm and sole. PUVA (psoralen + UVA) lights are eective in patients with active
stable disease [13, 40, 41, 43].
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Phototherapy treatment of all forms should be under the active supervision of a physician
who is an expert in phototherapy techniques. The use of daylight phototherapy and home-
based phototherapy are options that are currently being explored [42].
Practice point
: Phototherapy is a second-line treatment, aer failure of rst-line treatment
(emollients, topical steroids, and TCIs). [Level 2+, C]
Systemic therapy
Systemic immunomodulatory agents may be used in cases that are refractor y to conventional
therapy, for severe disease with large body surface involvement making topical therapy
impractical, or in the event of complications of generalized exfoliative dermatitis [12, 16, 41,
42, 44]. The use of these agents is o-label in most cases. Generally, any patient who requires
systemic therapy should always be referred to a dermatologist [44].
Systemic steroids
Systemic steroids have limited role in AD treatment and should be avoided if possible. Judicious
use should be exclusively reserved for acute, severe exacerbations and as a short-term bridge
therapy to other systemic, steroid-sparing treatment [12, 13, 16, 42].
For adults, predn isolone 30 mg daily and tapering to 5 mg within 2–3 weeks may be used in AD
recalcitrant to topical therapy [13]. Other oral steroids used equivalent to prednisolone 5 mg are
dexamethasone 0.75 mg, methylprednisolone 4 mg, cortisone acetate 25 mg, hydrocortisone
20 mg, betamethasone 0.75 mg, triamcinolone 4 mg, and prednisone 5 mg [45].
In children, a dosage range of 0.5 to 1.0 mg/kg of prednisone or prednisolone as tablet or
oral solution for enteral administration, or triamcinolone acetonide as an intramuscular
injection, may be used [42]. Clinicians are advised to educate patients about the possibility of
adrenal suppression and of rebound ares upon treatment discontinuation [41, 42].
Practice point
: Oral steroids should not be used for all cases and should be given only at a
minimum dose and for the shortest duration possible in both adults and children. [Level 1++, A]
Cyclosporine
Cyclosporine is an immunosuppressant of T cells and decreases interleukin (IL)-2 production
[42]. It is fast-acting and largely well tolerated by children and inpatients in crisis. It
signicantly improves AD in the rst 1–2 months of therapy. It is especially fast in reducing
pruritus in adults and children with chronic severe AD [13, 16, 42].
Cyclosporine should be given at the lowest eective dose and the shortest treatment period,
as toxicity is related to both high dose and prolonged treatment. A standard dose of 150 to
300 mg/day of any oral preparation (e.g., microemulsion) divided into 2 doses, and taken at
the same time each day in adults may be sucient. The initial and maintenance doses will
depend on the disease severity and other comorbidities [42].
In children, the starting dose may range from 2.5 mg/kg/day and gradually increased until
clinical response is adequate (up to 4–5 mg/kg/day), and a course of up to 3 months is
satisfactory [12, 27, 41].
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Side eects are mostly predictable and dose-dependent; these include infection,
nephrotoxicity, hypertension, tremor, hypertrichosis, headache, gingival hyperplasia, and an
increased risk of skin cancer and lymphoma [42].
Practice point
: Monitoring of patients taking cyclosporine includes checking for baseline
blood pressure measurements x2, renal function testing, urinalysis with microscopy, fasting
lipid prole, complete blood count with dierentials (CBC), liver function, electrolytes,
uric acid, and testing for tuberculosis, human immunodeciency virus (HIV) and human
chorionic gonadotropin (HCG), if indicated [Level 1++, B].
Azathioprine
Azathioprine is a purine analog that inhibits DNA synthesis. It can be used as a rst-line
systemic agent in older children and teenagers with chronic long-term moderate to severe
AD with high total IgE when cyclosporine is neither eective nor indicated. The onset is slow,
typically up to 4 weeks, and it is not typically used as a rst-line medication in severe life-
impacting AD [13,. 40, 43].
Dosing in adults is 1 to 3 mg/kg but most guidelines limit use to 2.5 mg/kg/day given as a tablet or
compounded liquid, once a day. In children, 1 to 4 mg/kg/day is the allowed dose [12, 13, 42, 44].
Myelosuppression and hypersensitivity with skin rash, hepatitis, fever, oliguria, and
respiratory failure are rare but fatal adverse eects of azathioprine [27].
Practice point
: Monitoring of patients taking azathioprine includes checking for baseline
thiopurine methyltransferase or thiopurine S-methyltransferase (TPMT), CBC dierentials
and platelets, renal function, liver function, hepatitis B and C, and testing for tuberculosis,
HIV and HCG, if indicated. [Level 1++, B]
Methotrexate
Methotrexate is an antifolate metabolite that negatively aects T-cell function by blocking
DNA, RNA and purine synthesis. Its use in adults with AD has been demonstrated in trials
to be comparable to azathioprine. It is signicantly less immunosuppressive with preferable
long-term safety prole [12, 13, 16, 41, 44].
A standard dose is 7.5 to 10 mg of a solution given intramuscularly or subcutaneously once
a week. In children, the dose of 0.2 to 0.7 mg/kg per week has been demonstrated to be
eective and safe [42].
Short-term side eects include gastrointestinal upset and bone marrow suppression. Long-term
side eects include liver brosis, and a potential eect on spermatogenesis and ovulation [42].
Practice point
: Monitoring of patients taking methotrexate includes checking of CBC with
dierentials and platelets, renal function, liver function, hepatitis B and C, and screening for
tuberculosis, HIV and HCG, and pulmonary function tests, if indicated. [Level 1++, B]
Mycophenolate mofetil
Mycophenolate mofetil blocks the purine synthesis pathway by inhibition of the inosine
monophosphate dehydrogenase enzyme. It is useful for patients in whom other available
systemic therapies are contraindicated or not tolerated [12, 13, 16, 41, 44].
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There is currently limited data to make recommendations on the dosage of this drug but a short-
term oral dose of 1.0 to 1.5 g (up to 2 g) daily as monotherapy as an oral suspension, capsule or
tablet, may result in clearing of skin lesion in adults resistant to other treatments [42].
In children, a dose range of 12 to 40 mg/kg daily divided into two doses titrated up to 75 mg/kg
(3 g maximum) has been evaluated for pediatric AD patients. The suggested dosing in young
children is 40 to 50 mg/kg/day and in young adults is 30 mg/kg/day [42].
It is well tolerated but may cause nausea, vomiting and abdominal cramping in some
patients [42].
Practice point
: Monitoring in mycophenolate mofetil includes checking for CBC with
dierentials and platelets, renal function, liver function, and testing for tuberculosis, HIV
and HCG, if indicated. [Level 2+, C]
Antibiotics and antivirals
Antibiotics are needed where there is secondary bacterial infection and
S. aureus
is the
suspected pathogen. However, there is no role for long-term oral antibiotic prophylaxis in
clinically uninfected AD due to the risk of bacterial resistance and contact sensitization [12,
13, 16, 41, 44]. Acyclovir and valacyclovir should be instituted without delay to patients with
eczema herpeticum [12, 13, 16, 41, 44].
Topical antibiotics (e.g., fusidic acid, mupirocin) may be used for focal infections. However,
there is no evidence supporting their long-term use [13]. Creams are preferred for exudative
skin lesions while ointments are useful for dry lesions with desquamation [43].
The recommendation is that they should be applied twice a day with bandage or 3 times a day
without bandage for 7 to 10 days. Prolonged use of mupirocin may promote the emergence of
resistant strains and use beyond 10 days and is thus not recommended [28].
Practice point
:
· Systemic antibiotics may be used in the treatment of bacterial infections in conjunction
with other standard and appropriate treatments for AD. [Level 1+, B]
· Systemic antivirals are indicated for eczema herpeticum. [Level 2+, B]
· Topical antibiotics may be used for focal skin infections for 7 to 10 days. [Level 2+, B]
Antihistamines
AD patients who suer from dermographism, allergic rhinitis, severe itch, or other allergic
illnesses may require symptomatic relief with these agents. Antihistamines generally result in
partial relief [12, 16, 42].
Short-term, intermittent use of sedating antihistamines may be benecial owing to their
added eect of inducing sleep. However, nonsedating oral antihistamines do not have
sucient supporting evidence to be recommended in AD. Topical antihistamines are also not
recommended [41].
Practice point
: Patient reliance on systemic antihistamines may indicate that the treatment
plan is not sucient to manage the symptoms. [Level 2+, C]
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Complementary treatment for AD
The use of folk remedies or complementary/alternative therapies is deeply ingrained in the
culture of many countries in Asia [12, 13, 38, 40, 41, 44]. These are summarized in Table 6.
In general, there is limited evidence available that supports the routine use of these therapies.
Patients should be advised that these have not been suciently assessed for ecacy and
safety. Some traditional herbs may have unknown quantities of active contaminants (i.e.,
corticosteroids), potential interactions with other medications, and may contribute to ares
if the patient has hypersensitivity to any one of the ingredients [38].
Practice point
: Patients and their caregivers should be advised that complementary/alternative
therapies have not undergone sucient ecacy and safety evaluation. They should be
encouraged to share the use of such options during their visits. [Level 4, GPP]
Future research directions
There is emerging evidence on adjunctive therapies for AD. More information regarding the
safety and ecacy of these agents will be available in the future.
· Naltrexone is an opiate receptor antagonist that may be used in dicult-to-treat AD cases [13].
· Aprepitant , a new ne urokinin-rec eptor ant agonist, ha s been show n to be eective in resolving
chronic pruritus. More studies are needed to establish the role of these agents in AD [46].
· A new generation of moisturizers with antioxidants, such as vitamins, polyphenols, furfuryl
palmitate and grape seed oil with antipruritic agents, have been shown to signicantly
improve AD symptomatically at the same level as topical corticosteroids. More trials will be
available showing its eects on epidermal permeability barrier function in the future [46].
· Nutrient s upplement ation may be of benet in preventing AD development and in reducing
the severity of ares. The overall result of a meta-analysis suggests that probiotics could
be an option for the treatment of AD, especially for moderate to severe AD in children
and adults [47]. A recent systematic review identied
Lactobacillus rhamnosus
GG as the
most frequently studied probiotic strain for AD [48]. Further study is needed to better
understand the mechanism of these agents.
· Dupilumab, a biologic with IL-4 and IL-13-blocking activities, provided as 2 injections
a month has been shown to be highly eective. This option is useful for adults with
moderate-to-severe AD that has failed systemic treatment and may be available for
adolescents in the future. Consult your pharmacies and local formularies regarding
approval of this option [13, 49].
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Table 6. Complementary/alternative therapies used for atopic dermatitis
Treatment Description Overall implications
Acupressure Use of a small titanium bead to massage an acupoint
on the arm 3 times weekly to relieve pruritus and
lichenification
Studies limited by small number of subjects, absence of placebo and
unmonitored application
Acupuncture Use of acupuncture needles to relieve allergen-induced
itch intensity vs. placebo or antihistamine
Aromatherapy/massage Use of manual therapy for stress-relief is adjunctive in
treatment of atopic dermatitis symptoms; improves sleep
disruption
Counselling and the use of relaxation therapy could have confounded
any potential beneficial effects of the intervention; a much larger and
better designed trial of a more representative population is needed;
aromatherapy oils may be a contact allergen
Traditional herbs Use of various kinds of medicinal plants alone or in
combination with others as a decoction by boiling them in
water taken as a ‘tea’ or applied directly to the skin
Most extensively studied in this list; clearly reported and blinded
multinational trials which focus on outcomes such as quality of life and
adverse events (e.g., contaminant steroid toxicity, hepatotoxicity) are
necessary; quality control is a key issue

· Omalizumab, an anti-IgE antibody, is eective in patients with AD and asthma with blood
IgE of 30–700 IU. It is currently available for use for asthma and chronic spontaneous
urticaria [13].
· Intravenous immunoglobulin has not been shown to be eective in recent studies and is
not recommended for use in AD [40].
· To date, the role of vitamin D supplementation in AD remains to be unclear. It is known
that cathelicidins in the skin are relatively decient in individuals with AD, and that vitamin
D may mediate the expression of innate cathelicidins in the skin. Interventional studies
have yielded mixed results [13, 29, 40].
· A phosphodiesterase 4 inhibitor, roumilast, is one of the latest nonsteroidal topical
therapy options in the armamentarium of AD management [50].
· Novel targeting agents used to treat recalcitrant pruritus have been evaluated in a small
number of studies. Specic mediators and pathways, such as the protease-activated receptor 2,
the H4 histamine pathway and the transient receptor potential vanilloid (TRPV) ion channels,
are continually being studied in the development of topical antipruritic options [51]. Apart
from their antipruritic properties, TRPV1 antagonists appear to play a role in maintaining
epidermal barrier function and may be available as an option in the near future [52].
ACKNOWLEDGEMENTS
The Asian Academy of Dermatology & Venereology has received publication support and
funding from A. Menarini Pte Ltd but has maintained editorial independence. Dr Dennis
Malvin H. Malgapo of MIMS Pte Ltd provided editorial and technical writing support. The
authors have no competing interests to disclose.
REFERENCES
1. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab 2015;66 Suppl 1:8-16.
PUBMED | CROSSREF
2. Leung DY, Boguniewicz M, Howell MD, Nomura I, Hamid QA. New insights into atopic dermatitis. J Clin
Invest 2004;113:651-7.
PUBMED | CROSSREF
3. Leung DY. New insights into atopic dermatitis: role of skin barrier and immune dysregulation. Allergol
Int 2013;62:151-61.
PUBMED | CROSSREF
4. Suárez-Fariñas M, Dhingra N, Gittler J, Shemer A, Cardinale I, de Guzman Strong C, Krueger JG,
Guttman-Yassky E. Intrinsic atopic dermatitis shows similar TH2 and higher TH17 immune activation
compared with extrinsic atopic dermatitis. J Allergy Clin Immunol 2013;132:361-70.
PUBMED | CROSSREF
5. Kim KH. Overview of atopic dermatitis. Asia Pac Allerg y 2013;3:79-87.
PUBMED | CROSSREF
6. Chen H, Common JE, Haines RL, Balakrishnan A, Brown SJ, Goh CS, Cordell HJ, Sandilands A, Campbell
LE, Kroboth K, Irvine AD, Goh DL, Tang MB, van Bever HP, Giam YC, McLean WH, Lane EB. Wide
spectrum of laggrin-null mutations in atopic dermatitis highlights dierences between Singaporean
Chinese and European populations. Br J Dermatol 2011;165:106-14.
PUBMED | CROSSREF
7. Noda S, Suárez-Fariñas M, Ungar B, Kim SJ, de Guzman Strong C, Xu H, Peng X, Estrada YD, Nakajima
S, Honda T, Shin JU, Lee H, Krueger JG, Lee KH, Kabashima K, Guttman-Yassky E. The Asian atopic
dermatitis phenotype combines features of atopic dermatitis and psoriasis with increased TH17
polarization. J Allergy Clin Immunol 2015;136:1254-64.
PUBMED | CROSSREF
15/18https://apallergy.org https://doi.org/10.5415/apallergy.2018.8.e41
Atopic dermat itis in Asians

8. Chan YC, Tay YK, Sugito TL, Boediardja SA, Chau DD, Nguyen KV, Yee KC, Alias M, Hussein S, Dizon MV,
Roa F, Chan YH, Wananukul S, Kullavanijaya P, Singalavanija S, Cheong WK. A study on the knowledge,
attitudes and practices of Southeast Asian dermatologists in the management of atopic dermatitis. Ann
Acad Med Singapore 2006;35:794-803.
PUBMED
9. Ho SG, Chan HH. The Asian dermatologic patient: review of common pigmentary disorders and
cutaneous diseases. Am J Clin Dermatol 2009;10:153-68.
PUBMED | CROSSREF
10. Eicheneld LF, Tom WL, Berger TG, Krol A, Paller AS, Schwarzenberger K, Bergman JN, Chamlin SL,
Cohen DE, Cooper KD, Cordoro KM, Davis DM, Feldman SR, Hanin JM, Margolis DJ, Silverman RA,
Simpson EL, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Sidbury R. 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.
PUBMED | CROSSREF
11. Hanin JM, Rajka G. Diagnostic features of atopic eczema. Acta Derm Venereol (Stockh) 1980;92:44-7.
12. Katayama I, Aihara M, Ohya Y, Saeki H, Shimojo N, Shoji S, Taniguchi M, Yamada H; Japanese Society of
Allergology. Japanese guidelines for atopic dermatitis 2017. Allergol Int 2017;66:230-47.
PUBMED | CROSSREF
13. Nankervis H, Thomas KS, Delamere FM, Barbarot S, Rogers NK, Williams HC. Scoping systematic review
of treatments for eczema. Southampton (UK): NIHR Journals Librar y; 2016.
14. Saeki H, Nakahara T, Tanaka A, Kabashima K, Sugaya M, Murota H, Ebihara T, Kataoka Y, Aihara M,
Etoh T, Katoh N; Committee for Clinical Practice Guidelines for the Management of Atopic Dermatitis
of Japanese Dermatological Association. Clinical Practice Guidelines for the Management of Atopic
Dermatitis 2016. J Dermatol 2016;43:1117-45.
PUBMED | CROSSREF
15. Eicheneld LF, Tom WL, Chamlin SL, Feldman SR, Hanin JM, Simpson EL, Berger TG, Bergman JN,
Cohen DE, Cooper KD, Cordoro KM, Davis DM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K,
Silverman RA, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Sidbury R. Guidelines of
care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J
Am Acad Dermatol 2014;70:338-51.
PUBMED | CROSSREF
16. Rubel D, Thirumoorthy T, Soebaryo RW, Weng SC, Gabriel TM, Villafuerte LL, Chu CY, Dhar S, Parikh
D, Wong LC, Lo KK; Asia-Pacic Consensus Group for Atopic Dermatitis. Consensus guidelines for the
management of atopic dermatitis: an Asia-Pacic perspective. J Dermatol 2013;40:160-71.
PUBMED | CROSSREF
17. Eicheneld LF, Boguniewicz M, Simpson EL, Russell JJ, Block JK, Feldman SR, Clark AR, Toe S, Dunn
JD, Paller AS. Translating atopic dermatitis management guidelines into practice for primary care
providers. Pediatrics 2015;136:554-65.
PUBMED | CROSSREF
18. Oranje AP. Practical issues on interpretation of scoring atopic dermatitis: SCORAD Index, objective
SCORAD, patient-oriented SCORAD and Three-Item Severity score. Curr Probl Dermatol 2011;41:149-55.
PUBMED | CROSSREF
19. Hanin JM, Thurston M, Omoto M, Cherill R, Toe SJ, Graeber M. The eczema area and severity index
(EASI): assessment of reliability in atopic dermatitis. EASI Evaluator Group. Exp Dermatol 2001;10:11-8.
PUBMED | CROSSREF
20. Grinich EE, Schmitt J, Küster D, Spuls PI, Williams HC, Chalmers JR, Thomas KS, Apfelbacher C, Prinsen
CAC, Furue M, Stuart B, Carter B, Simpson EL. Standardized reporting of the Eczema Area and Severity
Index (EASI) and the Patient-Oriented Eczema Measure (P OEM): a recommendation by the Harmonising
Outcome Measures for Eczema (HOME) Initiative. Br J Dermatol 2018;179:540-1.
PUBMED
21. Wolkerstorfer A, de Waard van der Spek FB, Glazenburg EJ, Mulder PG, Oranje AP. Scoring the severity of
atopic dermatitis: three item severity score as a rough system for daily practice and as a pre-screening tool
for studies. Acta Derm Venereol 1999;79:356-9.
PUBMED | CROSSREF
22. Chu CY. Measuring quality of l ife in infa nts, children a nd adolescents with eczema. B r J Dermatol 2017;176:848-9.
PUBMED | CROSSREF
23. Heinl D, Prinsen CA, Deckert S, Chalmers JR, Drucker AM, Ofenloch R, Humphreys R, Sach T, Chamlin
SL, Schmitt J, Apfelbacher C. Measurement properties of adult quality-of-life measurement instruments
for eczema: a systematic review. Allergy 2016;71:358-70.
PUBMED | CROSSREF
16/18
https://apallergy.org https://doi.org/10.5415/apallergy.2018.8.e41
Atopic dermat itis in Asians

24. Leung DY, Guttman-Yassky E. Assessing the current treatment of atopic dermatitis: Unmet needs. J
Allergy Clin Immunol 2017;139 (4S):S47-8.
PUBMED | CROSSREF
25. My Eczema Action Plan [Internet]. [cited 2018 Oct 25]. Available from: https://www.kairos2.com/my_
eczema_action_plan.pdf/.
26. Ridd MJ, King AJL, Le Roux E, Waldecker A, Huntley AL. Systematic review of self-management
interventions for people with eczema. Br J Dermatol 2017;177:719-34.
PUBMED | CROSSREF
27. Kim JE, Kim HJ, Lew BL, Lee KH, Hong SP, Jang YH, Park KY, Seo SJ, Bae JM, Choi EH, Suhr KB, Lee
SC, Ko HC, Park YL, Son SW, Seo YJ, Lee YW, Cho SH, Park CW, Roh JY. Consensus Guidelines for the
Treatment of Atopic Dermatitis in Korea (Part I): General Management and Topical Treatment. Ann
Dermatol 2015;27:563-77.
PUBMED | CROSSREF
28. Stalder JF, Bernier C, Ball A, De Raeve L, Gieler U, Deleuran M, Marcoux D, Eicheneld LF, Lio P, Lewis-
Jones S, Gelmetti C, Takaoka R, Chiaverini C, Misery L, Barbarot S; Oriented Patient-Education Net work
in Dermatology (OPENED). Therapeutic patient education in atopic dermatitis: worldwide experiences.
Pediatr Dermatol 2013;30:329-34.
PUBMED | CROSSREF
29. Sidbury R, Tom WL, Bergman JN, Cooper KD, Silverman RA, Berger TG, Chamlin SL, Cohen DE, Cordoro
KM, Davis DM, Feldman SR, Hanin JM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K, Simpson EL,
Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Eicheneld LF. Guidelines of care for the
management of atopic dermatitis: Section 4. Prevention of disease ares and use of adjunctive therapies
and approaches. J Am Acad Dermatol 2014;71:1218-33.
PUBMED | CROSSREF
30. Barbarot S, Bernier C, Deleuran M, De Raeve L, Eicheneld L, El Hachem M, Gelmetti C, Gieler U, Lio
P, Marcoux D, Morren MA, Torrelo A, Stalder JF; Oriented Patient-Education Network in Dermatology.
Therapeutic patient education in children with atopic dermatitis: position paper on objectives and
recommendations. Pediatr Dermatol 2013;30:199-206.
PUBMED | CROSSREF
31. Gonzales F, Ramdane N, Delebarre-Sauvage C, Modiano P, Duhamel A, Lasek A. Monitoring of topical
corticosteroid phobia in a population of parents with children with atopic dermatitis using the TOPICOP®
scale: prevalence, risk factors and the impact of therapeutic patient education. J Eur Acad Dermatol
Venereol 2017;31:e172-4.
PUBMED | CROSSREF
32. Giam YC, Hebert AA, Dizon MV, Van Bever H, Tiongco-Recto M, Kim KH, Soebono H, Munasir Z, Diana
IA, Luk DC. A review on the role of moisturizers for atopic dermatitis. Asia Pac Allergy 2016;6:120-8.
PUBMED | CROSSREF
33. Arkwright PD, Motala C, Subramanian H, Spergel J, Schneider LC, Wollenberg A; Atopic Dermatitis
Working Group of the Allergic Skin Diseases Committee of the AAAAI. Man agement of dicult-to-treat
atopic dermatitis. J Allergy Clin Immunol Pract 2013;1:142-51.
PUBMED | CROSSREF
34. Varothai S, Nitayavardhana S, Kulthanan K. Moisturizers for patients with atopic dermatitis. Asian Pac J
Allergy Immunol 2013;31:91-8.
PUBMED
35. Sethi A, Kaur T, Malhotra SK, Gambhir ML. Moisturizers: the slippery road. Indian J Dermatol
2016;61:279-87.
PUBMED | CROSSREF
36. Koh MJ, Giam YC, Liew HM, Foong AY, Chong JH, Wong SM, Tang MB, Ho MS, Tan LS, Mason JM, Cork
MJ. Comparison of the Simple Patient-Centric Atopic Dermatitis Scoring System PEST with SCORAD
in young children using a ceramide dominant therapeutic moisturizer. Dermatol Ther (Heidelb)
2017;7:383-93.
PUBMED | CROSSREF
37. van Zuuren EJ, Fedorowicz Z, Christensen R, Lavrijsen A, Arents BW. Emollients and moisturisers for
eczema. Cochrane Database Syst Rev 2017;2:CD012119.
PUBMED
38. Vieira BL, Lim NR, Lohman ME, Lio PA. Complementary and alternative medicine for atopic dermatitis:
an evidence-based review. Am J Clin Dermatol 2016;17:557-81.
PUBMED | CROSSREF
39. Wollenberg A, Oranje A, Deleuran M, Simon D, Szalai Z, Kunz B, Svensson A, Barbarot S, von Kobyletzki
L, Taieb A, de Bruin-Weller M, Werfel T, Trzeciak M, Vestergard C, Ring J, Darsow U; European Task Force
17/18https://apallergy.org https://doi.org/10.5415/apallergy.2018.8.e41
Atopic dermat itis in Asians

on Atopic Dermatitis/EADV Eczema Task Force. ETFAD/EADV Eczema task force 2015 position paper
on diagnosis and treatment of atopic dermatitis in adult and paediatric patients. J Eur Acad Dermatol
Venereol 2016;30:729-47.
PUBMED | CROSSREF
40. Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic eczema. Health Technol
Assess 2000;4:1-191.
PUBMED
41. Chu CY, Lee CH, Shih IH, Chen HC, Huang PH, Yang CY, Wang WJ, Chen YJ, Sheu HM, Wang WM, Lee
WR, Lo YH, Dai YS, Wang LF, Tsai TF, Yang CH. Taiwanese Dermatological Association consensus for the
management of atopic dermatitis. Dermatol Sin 2015;33:220-30.
CROSSREF
42. Sidbury R, D avis DM, Cohen DE, Cordoro KM, Berger TG, Bergman JN, Chamlin SL, Cooper KD,
Feldman SR, Hanin JM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K, Silverman RA, Simpson EL,
Tom WL, Williams HC, Elmets CA, Block J, Harrod CG, Begolka WS, Eicheneld LF; American Academy
of Dermatology. Guidelines of care for the management of atopic dermatitis: section 3. Management and
treatment with phototherapy and systemic agents. J Am Acad Dermatol 2014;71:327-49.
PUBMED | CROSSREF
43. Galli E, Neri I, Ricci G, Baldo E, Barone M, Belloni Fortina A , Bernardini R, Berti I, Caarelli C, Calamelli
E, Capra L, Carello R, Cipriani F, Comberiati P, Diociaiuti A, El Hachem M, Fontana E, Gruber M,
Haddock E, Maiello N, Meglio P, Patrizi A, Peroni D, Scarponi D, Wielander I, Eicheneld LF. Consensus
conference on clinical management of pediatric atopic dermatitis. Ital J Pediatr 2016;42:26.
PUBMED | CROSSREF
44. Kim JE, Kim HJ, Lew BL, Lee KH, Hong SP, Jang YH, Park KY, Seo SJ, Bae JM, Choi EH, Suhr KB, Lee
SC, Ko HC, Park YL, Son SW, Seo YJ, Lee YW, Cho SH, Park CW, Roh JY. Consensus Guidelines for the
Treatment of Atopic Dermatitis in Korea (Part II): Systemic Treatment. Ann Dermatol 2015;27:578-92.
PUBMED | CROSSREF
45. Liu D, Ahmet A, Ward L, Krishnamoorthy P, Mandelcorn ED, Leigh R, Brown JP, Cohen A, Kim H. A
practical guide to the monitoring and management of the complications of systemic corticosteroid
therapy. Allergy Asthma Clin Immunol 2013;9:30.
PUBMED | CROSSREF
46. Man G, Elias PM, Man MQ. Therapeutic benets of enhancing permeability barrier for atopic eczema.
Dermatologica Sin 2015;33:84-9.
CROSSREF
47. Foolad N, Brezinski EA, Chase EP, Armstrong AW. Eect of nutrient supplementation on atopic dermatitis
in children: a systematic review of probiotics, prebiotics, formula, and fatty acids. JAMA Dermatol
2013;149:350-5.
PUBMED | CROSSREF
48. Kim SO, Ah YM, Yu YM, Choi KH, Shin WG, Lee JY. Eects of probiotics for the treatment of atopic
dermatitis: a meta-analysis of randomized controlled trials. Ann Allerg y Asthma Immunol 2014;113:217-26.
PUBMED | CROSSREF
49. Ariëns LFM, Bakker DS, van der Scha J, Garritsen FM, Thijs JL, de Bruin-Weller MS. Dupilumab in atopic
dermatitis: rationale, latest evidence and place in therapy. Ther Adv Chronic Dis 2018;9:159-70.
PUBMED | CROSSREF
50. Sakkas LI, Mavropoulos A, Bogdanos DP. Phosphodiesterase 4 inhibitors in immune-mediated diseases:
mode of action, clinical applications, current and future perspectives. Curr Med Chem 2017;24:3054-67.
PUBMED | CROSSREF
51. Tey HL, Yosipovitch G. Targeted treatment of pruritus: a look into the future. Br J Dermatol 2011;165:5-17.
PUBMED | CROSSREF
52. Bonchak JG, Swerlick RA. Emerging therapies for atopic dermatitis: TRPV1 antagonists. J Am Acad
Dermatol 2018;78 (3S1):S63-6.
PUBMED | CROSSREF
18/18
https://apallergy.org https://doi.org/10.5415/apallergy.2018.8.e41
Atopic dermat itis in Asians