Guidelines

Skin Appendage Disord 2015;1:187–196 Received: November 27, 2015

Accepted: February 12, 2016
DOI: 10.1159/000444682
Published online: March 23, 2016

Treatment of Seborrhoeic Dermatitis

in Asia: A Consensus Guide
Wai Kwong Cheong a Chi Keung Yeung b Raghunandan Govind Torsekar c
Dae Hun Suh d Rataporn Ungpakorn e Sandra Widaty f Noor Zalmy Azizan g
Maria Teresita Gabriel h Hau Khang Tran i Wei Sheng Chong j I-Hsin Shih k
Federica Dall'Oglio l Giuseppe Micali l
a
Specialist Skin Clinic, Singapore, Singapore; b Division of Dermatology, Department of Medicine, University of Hong
Kong, Hong Kong; c Department of Dermatology, Rajiv Gandhi Medical College and Chatrapathi Shivaji Maharaj
Hospital, Kalwa, Thane, India; d Department of Dermatology, Seoul National University College of Medicine, Seoul,
South Korea; e Skin and Aesthetic Lasers Clinic, Bumrungrad International Hospital, Bangkok, Thailand; f Department
of Dermato-Venereology and Medical Education Department, Universitas Indonesia, Kota Depok, Indonesia;
g
Department of Dermatology, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia; h Department of Dermatology,
Research Institute for Tropical Medicine, Manila, Philippines; i National Hospital of Dermatology and Venereology,
Hanoi, Vietnam; i Dermatology Unit, Department of General Medicine, Khoo Teck Puat Hospital, Singapore,
Singapore; k Department of Pediatric Dermatology, Chang Gung Children’s Hospital, Taipei, Republic of China;
l
Dermatology Clinic, University of Catania, Catania, Italyl

Key Words Asia at a meeting held in Singapore. The consensus group

Seborrhoeic dermatitis · Asia · Treatment · Diagnosis · developed a comprehensive algorithm to aid clinicians to
Consensus recommend appropriate treatment of SD in both adults and
children. In most cases, satisfactory therapeutic results can
be accomplished with topical antifungal agents or topical
Abstract corticosteroids. Non-steroidal anti-inflammatory agents
Seborrhoeic dermatitis (SD) is common in Asia. Its preva- with antifungal properties have been shown to be a viable
lence is estimated to be 1–5% in adults. However, larger pop- option for both acute and maintenance therapy.
ulation-based studies into the epidemiology of SD in Asia are © 2016 S. Karger AG, Basel
lacking, and the aetiology of SD may differ widely from West-
ern countries and in different parts of Asia. In addition, clini-
cally significant differences between Asian and Caucasian Introduction
skin have been reported. There is a need to define standard-
ized clinical diagnostic criteria and/or a grading system to Seborrhoeic dermatitis (SD) is a common chronic in-
help determine appropriate treatments for SD within Asia. flammatory disease of the skin, which manifests as scaly
With this in mind, experts from India, South Korea, Taiwan, reddish-brown itchy patches in sebaceous, gland-rich re-
Malaysia, Vietnam, Singapore, Thailand, the Philippines, In- gions of the scalp, face, and trunk [1]. It affects both chil-
donesia, and Italy convened to define the landscape of SD in dren and adults, with a higher incidence in infancy and

© 2016 S. Karger AG, Basel Giuseppe Micali, MD

2296–9195/16/0014–0187$39.50/0 Dermatology Clinic, University of Catania
AOU Policlinico-Vittorio Emanuele
E-Mail karger@karger.com
Via Santa Sofia, 78, IT–95123 Catania (Italy)
www.karger.com/sad
E-Mail cldermct @ gmail.com
mid-adulthood (age 30–60 years) [2–4]. In infants, SD drome) [16]. The prevalence of SD in HIV patients was
frequently follows an uneventful course, and generally reported as 47.0% in Thailand, 19.2% in Malaysia, and
clears by 6–12 months of age (3 months in most Asian 17.0% in Korea [17–19].
infants) [5]. It may appear again in individuals in their
teens and twenties and may then generally follow a wax-
ing and waning course throughout adulthood. Differences between Asian and Non-Asian Skin
The distribution of SD is typically symmetrical and le-
sions range from being mild, patchy, and scaling to being Clinically significant differences between Asian and
widespread, thick, and with adherent crusts [1, 2]. The Caucasian skin have been reported, and these differenc-
lesions may have a red, smooth, glazed appearance in skin es may impact the management of SD in Asians. The
folds. SD of the trunk may appear in the presternal area most obvious difference between ethnic groups relates
and in body folds, including the axillae, navel, groin, and to skin colour, secondary to the presence of melanin
inframammary and anogenital areas. Common sites of [20]. The photo-protective properties of melanin may
involvement are hairy areas of the head, including the influence the rate at which skin ages, with Caucasians
scalp, the scalp margin, eyebrows, eyelashes, the mous- showing an earlier onset of photo-aging than Asians [20,
tache, the beard, along with the forehead, nasolabial folds, 21]. Asian skin is more prone to postinflammatory hy-
external ear canals, and postauricular creases [2, 5]. perpigmentation than Caucasian skin [20, 22]. Differ-
ences have also been observed in the stratum corneum
of Asians compared with that of non-Asians [20]. Al-
Epidemiology of SD in Asia though evidence regarding transepidermal water loss in
Asian skin is contradictory, there are reports of Asians
SD has been reported to affect approximately 1–5% of having a lower transepidermal water loss than other rac-
the population worldwide, depending on the country es [20]. However, a study in similarly aged Japanese and
studied [1, 6–8]. A limited number of studies have inves- German women detected no significant differences in
tigated the epidemiology of SD in Asia [9–14]. In a Ko- transepidermal water loss between the two races [23].
rean cross-sectional study of military personnel, SD was Similarly, there was no difference in transdermal water
ranked as the third most troublesome skin disease after loss between Japanese and French volunteers whose
atopic dermatitis and tinea cruris; the prevalence of SD physiological parameters were investigated at three dif-
was 2.1% [9]. A study in India reported that 13.4% of ferent skin sites [24]. The interpretation of such data
children aged <5 years had SD, with the prevalence peak- must take into account the ambient humidity, which can
ing during infancy and decreasing steadily with age [10]. dramatically alter observations. Studies generally indi-
In Indian adults with scalp dermatoses, 18.7% of cases cate that Asians have higher stratum corneum water
were attributed to SD [11]. Furthermore, data from Sin- content [25] and higher stratum corneum lipid levels
gapore revealed an SD prevalence of 3.2% in children but than other races [20, 26, 27]. Investigations involving
of 7.0% in adults [12]. In Asian individuals aged 12–20 the removal of the stratum corneum by tape stripping
years, the prevalence of SD varied widely between tropi- indicated that Asian skin may have a poor barrier func-
cal cities and countries (i.e., Macao 2.7%, Guangzhou tion [28–30]. Asians compared with non-Asians have a
2.9%, Malaysia 17.2%, and Indonesia 26.5%) [13]. A heightened dermatological response to irritants com-
cross-sectional study conducted in Japan found that the monly found in topical, over-the-counter, or cosmetic
prevalence of SD among 67,448 patients attending hos- preparations [23, 31–35]. In a study in Japanese patients
pital dermatology clinics was 3.28% [14]. The wide vari- with photo-damaged skin, tretinoin caused a higher
ation in prevalence rates obtained in these studies is like- than anticipated level of irritation than that previously
ly to be a reflection of the high variability of the SD ex- reported in Caucasians [34]. In another study in which
pression [15]. participants underwent a skin patch test on the forearm
Similar to Western countries, in Asia there is an in- with sodium lauryl sulphate, significant subjective sen-
creased trend for SD in patients with immunosuppres- sory differences were found between Japanese and Ger-
sion (e.g., organ transplant recipients, AIDS patients), man women [23]. Increased skin reactivity was observed
neurological or psychiatric conditions (e.g., Parkinson’s in Asian subjects compared with Caucasian subjects in
disease, tardive dyskinesia, depression), or genetic disor- an analysis of results compiled from 9 acute irritation
ders (e.g., Down’s syndrome, cardiofaciocutaneous syn- patch test studies [31]. Similarly, in a study involving

188 Skin Appendage Disord 2015;1:187–196 Cheong  et al.

 

DOI: 10.1159/000444682
Caucasian and Japanese women, the acute irritant re- contention, more specific studies are needed to assess
sponse tended to be greater in the Japanese volunteers, species-specific molecular typing in large patient groups
reaching statistical significance with the stronger irri- of diverse ethnicity.
tants [35]. Interestingly, 1 study reported no differences
in skin pain perception between Chinese, Malay, and In-
dian participants [36]. Further well-designed studies Treatment of SD
comparing the structure and physiology of Asian skin
with Caucasian skin are warranted. The goal of SD treatment is not only to alleviate signs
and symptoms of the condition but also to promote nor-
malization of skin structure and function [44]. SD has
Pathogenesis of SD been found to significantly impact a patient’s quality of
life [16], and treatment should be addressed to improve
Although the general causes of SD, including interac- skin symptoms as well as quality of life.
tion of Malassezia spp. with sebaceous lipids, seborrhoea, In Western countries, topical treatments with anti-
immune dysfunction, neurogenic factors, and emotional fungals and anti-inflammatory drugs have been exten-
stress [1, 5, 37], are considered similar in Asian and West- sively studied in patients with SD [8, 45, 46]. Although
ern countries, ethnicity and geography are significant as- guidelines for the treatment of SD are generally lacking
pects determining the degree of pathogenic association [8], recent evidence-based Danish guidelines have rec-
between Malassezia spp. and SD. Both M. globosa and M. ommended antifungal azoles as first-line treatment
restricta are considered the predominant species in West- [47]. The same paper indicates that a short course of
ern countries, whereas a relative predominance of M. re- topical corticosteroid or topical calcineurin inhibitors,
stricta in lesional skin from SD patients is evident in East both having an anti-inflammatory effect, may be con-
Asian countries [38–40]. In Korea, for example, analysis sidered beneficial [47]; systemic treatment of SD with
of scalp scales from SD patients revealed the presence of oral antifungals may be advised in selected patients [47,
Malassezia spp. in 85% of cases, M. restricta in 47.5%, but 48].
M. globosa in only 27.5% [39]. Conversely, in Thailand, a
study in infants with SD showed a predominance of M. Treatment of SD in Asia: Critical Issues
furfur [41]. When treating Asian SD patients, the physician needs
The extent to which Malassezia spp. are associated to consider not only the possible differences in aetiology
with the presence of dandruff in SD patients also ap- between Asian and Western skin, but also a number of
pears to vary markedly throughout Asia. For instance, other sociological, economic, and cultural differences
Iranian researchers reported that only 24.5% of SD pa- [49]. For example, the ratio of dermatologists to the
tients with dandruff had positive cultures for Malasse- overall population is very low in many Asian countries
zia spp. [42]. The corresponding percentage in an In- [49], meaning that most patients with SD are generally
dian study was 84%, and Malassezia spp. density was not treated by dermatologists. In addition, there is a
significantly associated (p < 0.001) with dandruff sever- wide availability of over-the-counter medications, cos-
ity [43]. In addition, the rate of Malassezia spp. isolation meceuticals, and generics as well as a variety of unprov-
from SD patients was significantly greater (p < 0.01) in en and unorthodox treatments within Asia [49]. This
Southern rather than other regions of India [43]. Re- may result in more Asian SD patients self-treating or
gional climatic conditions need to be taken into account seeking treatment from beauticians and other non-
when the pathogenesis of SD is being considered [10, health-care personnel, therefore increasing the risk of
20]. Heat, humidity, and sweat are known to aggravate irritating or inappropriate treatments [49]. In addition,
SD symptoms, especially scalp itch. Sunlight and the significant differences in the acceptance, availability,
high ultraviolet index typical of tropical climates may and insurance support for treatment modalities for der-
also exacerbate SD symptoms. Overall, these findings matological conditions vary from country to country
suggest that regional differences in hereditary aspects of within Asia [49].
host susceptibility (e.g., skin constitution, inflamma- In the light of the impact of these various factors, there
tion) and in climatic conditions facilitating Malassezia is a need to have common treatment strategies for SD pa-
spp. growth may affect local distribution and pathoge- tients within Asian. Therefore, an expert consensus panel
nicity of this opportunistic pathogen. To clarify this of twelve dermatologists from India, South Korea, Tai-

Management of Seborrhoeic Dermatitis in Skin Appendage Disord 2015;1:187–196 189

Asia DOI: 10.1159/000444682
Table 1. Treatment products for SD of the scalp and hairy areas

Class of product Formulation Instructions for use

Mild SD
Topical antifungals Ciclopirox 1 – 1.5% shampoo 2 – 3 times weekly
Ketoconazole 1 – 2% shampoo, 2% foaming gel,
20 mg/g hydrogel
AIAFp e.g. Piroctone olamine/bisabolol/ 2 – 3 times weekly
glycyrrhetic acid/lactoferrin shampoo
Keratolytics Salicylic acid 3% shampoo Salicylic acid: 2 – 3 times weekly
Tar 1 – 2% shampoo Tar: 1 – 2 times weekly
Other agents Selenium sulphide 2.5% shampoo 2 – 3 times weekly
Zinc pyrithione 1 – 2% shampoo
Topical corticosteroids Class I
(class I–II) Hydrocortisone 1% liniment and solution, 0.1% lotion Once daily for up to 4 weeks
Class II
Alclometasone 0.05% ointment
Desonide 0.05% cream
Moderate-to-severe SD
Topical corticosteroids Class I
(class I–II) Hydrocortisone 1% liniment and solution, 0.1% lotion Once daily for up to 4 weeks
Class II
Alclometasone 0.05% ointment
Desonide 0.05% cream
Topical corticosteroids Class III Twice weekly, applied for 5 min, for 2 weeks
(class III–IV) Fluocinolone acetonide 0.01% shampoo
Class IV Twice weekly, applied for 5 min, for 2 weeks
Clobetasol propionate 0.05% shampoo
Systemic antifungals Itraconazole 100-mg caps First month: 200 mg/day for 1 week, then 200
mg/day for 2 days/month up to 11 months
Terbinafine 250-mg caps Continuous regimen: 250 mg/day for 4 – 6
weeks
Intermittent regimen: 250 mg/day for 12 days
per month for 3 months
Fluconazole 50-mg caps 50 mg/day for 2 weeks or 200 – 300 mg weekly
for 2 – 4 weeks

wan, Malaysia, Vietnam, Singapore, Thailand, the Philip- this approach was based on grade levels in the Strength-
pines, Indonesia, and Italy was convened in Singapore on of-Recommendation Taxonomy (SORT) scheme [50].
the 26–27 September 2014. Each recommendation was also graded by the level of ev-
idence according to the March 2009 Oxford Centre for
Evidence-Based Medicine levels of evidence [51].
Consensus Recommendations for SD in Asia
Treatment
The specific practice recommendations identified by SD of the Scalp and Hairy Areas
this consensus group for the treatment of SD in Asian In adults, SD is a chronic condition that is likely to re-
adults and infants are outlined in the subsequent subsec- cur after treatment (category A, level 2b). Hence, patients
tions. The panel used a consensus approach to determine should be counselled about the need for proper skin care
recommendations about each clinical aspect addressed; [5]. Treatment selection should consider drug efficacy,

190 Skin Appendage Disord 2015;1:187–196 Cheong  et al.

 

DOI: 10.1159/000444682
Table 2. Treatment products for non-scalp SD

Class of product Formulation Instructions for use

Mild SD
Topical antifungals Ciclopirox 1% cream Twice daily for 4 weeks
Ketoconazole 2% cream
AIAFp e.g. Piroctone olamine/alglycera/
bisabolol cream
Topical corticosteroids (class I) Hydrocortisone 1% cream and ointment
Topical calcineurin inhibitors* Pimecrolimus 1% cream
Tacrolimus 0.1% ointment
Moderate-to-severe SD
Topical corticosteroids Alclometasone 0 – 05% ointment Twice daily for 4 weeks
(class II) Desonide 0.05% cream
Systemic antifungals Itraconazole 100-mg caps First month: 200 mg/day for 1 week, then 200 mg/day
for 2 days/month up to 11 months
Terbinafine 250-mg caps Continuous regimen: 250 mg/day for 4 – 6 weeks
Intermittent regimen: 250 mg/day for 12 days per
month for 3 months
Fluconazole 50-mg caps 50 mg/day for 2 weeks or 200 – 300 mg weekly for 2 – 4
weeks

* Off-label use.

potential for side effects as well as cosmetic acceptability treatment with antifungal or AIAFp shampoo, 2 days of
(category B, level 4). Wherever possible, patient self- potent-to-very potent topical corticosteroid shampoo
treatment should be avoided, to minimize the likelihood (class III and IV), containing fluocinolone acetonide
of inappropriate treatment, SD symptom exacerbation, 0.01% (class III) or clobetasol propionate 0.05% (class IV)
and variability in treatment response. for up to 2 weeks [45, 58–60] (category A, level 1b). In
For SD of the scalp and hairy areas, the panel recom- case of more resistant disease, systemic antifungals may
mends the treatments summarized in table 1 (category A, be added [47, 48]. For long-term maintenance, antifun-
level 1b). For mild forms, a topical approach is recom- gal, AIAFp, or other shampoos active on SD may be used
mended starting with ketoconazole or ciclopirox, or alter- once or twice weekly (category B, level 5).
natively selenium sulphide/zinc pyrithione, or keratolytic
shampoos [8, 52]. Similarly to non-scalp SD [53–56], SD of Non-Scalp Areas
non-steroidal and anti-inflammatory with antifungal For SD of the non-scalp areas, the panel recommends
properties (AIAFp) shampoo may represent a viable op- the treatments summarized in table 2 (category A, level
tion, as reported in a recent randomized, single-blind 1b). For the treatment of mild, non-scalp SD in adults,
clinical trial [57]. In case of failure, add a 4-week course especially on the face, the use of antifungal creams (e.g.,
with a weak-to-moderately potent corticosteroid [class I ketoconazole 2% cream, ciclopirox 1% cream) or AIAFp
and II according to the Anatomical Therapeutic Chemi- cream is preferred [52]. Topical antifungals represent the
cal (ATC) classification by the World Health Organiza- most common approach, and in the past years AIAFp
tion (WHO)] followed by its gradual discontinuation cream has clearly demonstrated efficacy and tolerability
[52]. in the treatment of mild-to-moderate SD of the face [53–
For moderate-to-severe forms, especially if itchy, a 56, 61] (category A, level 1b). In case of failure, a combi-
combination of antifungal or AIAFp shampoo with weak- nation of both antifungals and AIAFp agents may be con-
to-moderately potent (class I–II) topical corticosteroids sidered. If no improvement is seen or in case a more rap-
for up to 4 weeks is recommended [52]; in case of no im- id control of SD signs and symptoms is desired, a weakly
provement, consider to include in the weekly routine potent topical corticosteroid (class I according to the

Management of Seborrhoeic Dermatitis in Skin Appendage Disord 2015;1:187–196 191

Asia DOI: 10.1159/000444682
 Color version available online
Assessment of severity of SD of
the scalp and hairy areas

Mild Moderate to severe

Antifungal shampoo Combine antifungal or AIAFp shampoo

or with
AIAFp shampoo weak to moderately potent (class I–II) topical
or corticosteroids for up to 4 weeks
Selenium sulphide/zinc pyrithione/tar shampoo

Improvement No improvement Improvement No improvement

Gradually Add weak to moderately Gradually Continue AIAFp or

discontinue potent (class I–II) topical discontinue antifungal shampoo, and
treatment until corticosteroids for up to treatment until add potent to very potent
remission 4 weeks remission (class III–IV) corticosteroid
shampoo twice a week for
2 weeks

No improvement

Add
systemic
antifungals

Fig. 1. Proposed therapeutic algorithm for adult SD of the scalp and hairy areas. AIAFp = Nonsteroidal anti-in-
flammatory agent with antifungal properties.

ATC by WHO) once or twice daily for up to 2 weeks may tive for mild-to-severe SD refractory cases (category A,
be added [4]. If successful, the use of a topical corticoste- level 1b).
roid may be extended for an additional 2 weeks. The use The above recommendations are summarized in fig-
of AIAFp cream may be considered for maintenance ures 1 and 2.
treatment.
For moderate-to-severe non-scalp SD, topical moder- Treatment in Infants
ately potent corticosteroids (class II according to the ATC SD of the Scalp and Hairy Areas
by WHO) may be used up to a maximum of 2 weeks in SD management in infants involves advising simple
combination with AIAFp or topical antifungals. This ap- measures, such as regular washing of the scalp with baby
proach will achieve the most rapid control of SD signs and shampoo and gentle brushing to loosen scales [62]. The
symptoms. In case of clinical improvement, the use of a daily use of white petrolatum may help to soften scales. If
topical corticosteroid may be considered for an addition- these measures are not effective, ketoconazole 2% sham-
al 2 weeks. If the response is not satisfactory, the use of poo could be used until the condition resolves [62, 63]
systemic antifungals should be considered. Finally, topi- (category A, level 1b). The clinical efficacy of AIAFp
cal calcineurin inhibitor agents may represent an alterna- cream in infants has been demonstrated in a multicentre,

192 Skin Appendage Disord 2015;1:187–196 Cheong  et al.

 

DOI: 10.1159/000444682
 Color version available online
Assessment of severity of SD
of non-scalp areas

Mild Moderate to severe

Topical antifungals Combine mid-potency topical

or corticosteroid for 1–2 weeks
AIAFp with AIAFp
or
topical antifungals

Improvement No improvement

Improvement No improvement
Combine any of the two above

Extend treatment Add systemic

for an additional antifungals
Extend treatment 2 weeks
until remission Improvement No improvement
No improvement

Add low-potency topical

corticosteroids for 2 weeks
Switch to TCI*
to either one of the above
topicals

Improvement No improvement

Extend Switch to TCI*

treatment with
topical
corticosteroid
for 2 additional
weeks

Fig. 2. Proposed therapeutic algorithm for adult non-scalp SD. AIAFp = Nonsteroidal anti-inflammatory agent
with antifungal properties; TCI = topical calcineurin inhibitors. * Off-label use.

double-blind, placebo-controlled, parallel-group study in Conclusions

infants with cradle cap, in whom there was a significant
difference in the reduction of scaling between the treat- Because the skin of Asians compared with non-Asians
ment and placebo groups [64]. is more reactive to irritants, topical agents with irritant
potential, and therefore with the likelihood to complicate
SD of Non-Scalp Areas SD lesions [31], should be avoided. In particular, cosmet-
The use of ketoconazole 2% cream is advised alone or ic products containing alcohol, soap and shaving cream,
together with a weakly potent topical corticosteroid (class I greasy emollients, and any known trigger factors, if they
according to the ATC by WHO) [65] (category A, level 5). cause irritation, should be changed for more gentle prod-
All therapeutic options are listed in table 3. ucts. Finally, the presence of dry or damp conditions in

Management of Seborrhoeic Dermatitis in Skin Appendage Disord 2015;1:187–196 193

Asia DOI: 10.1159/000444682
Table 3. Treatment products for infantile SD

Class of product Formulation Instructions for use Notes

Scalp and hairy areas

Topical antifungals Ketoconazole 2% shampoo Shampoo: twice a week for 4 One small trial on 13 patients (age: <1
weeks year) showed no systemic absorption or
change in liver function after 1 month
of use
Emollients White petrolatum ointment Daily use Softens scales to help ease manual
removal (e.g. with a soft brush)
AIAFp e.g. Piroctone olamine/alglycera/ Every 12 h Effective for cradle cap
bisabolol cream
Non-scalp areas
Topical Ketoconazole 2% cream Once daily for up to 7 days May be used alone or in combination
antifungals with topical corticosteroids
Topical corti- Hydrocortisone 1% cream Once daily for up to 7 days Limit surface area application
costeroids (class I)

the workplace/living place, a facilitating factor for SD Statement of Ethics

common in many Asia countries, should also be consid-
Published research complies with the guidelines for human
ered [66] (category B, level 5). studies and animal welfare regulations.

Acknowledgments
Disclosure Statement
Editorial support for the preparation of this manuscript was
The authors have received honoraria for their participation in
given by Dr. Dennis Malvin H. Malgapo of MIMS Pte. Ltd. through
the Asia Pacific Seborrheic Dermatitis Leaders’ Summit 2014. Dr.
an unrestricted educational grant by A. Menarini Asia-Pacific Pte.
Wai Kwong Cheong is a speaker for Galderma and for L’Oréal and
Ltd.
a member of the Advisory Board for P & G Olay Pro-X Global Der-
matologist Alliance.

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DOI: 10.1159/000444682