Asia Pacific

pISSN 2233-8276 · eISSN 2233-8268

allergy Hypothesis & Experience
Review Article
http://dx.doi.org/10.5415/apallergy.2014.4.4.230
Asia Pac Allergy 2014;4:230-240

The role of antiseptic agents in atopic dermatitis
Melissa Lee*and Hugo Van Bever

Department of Paediatrics, University Children’s Medical Institute, Yong Loo Lin School of Medicine, Singapore 119077, Singapore

The skin of individuals with atopic dermatitis has a susceptibility to be colonized with Staphylococcus aureus. This has been
associated with increased frequency and severity of exacerbations of atopic dermatitis. Therefore, there is a growing interest in
the use of antiseptic agents to target primary bacterial colonization and infection. Antiseptic agents have been found to be better
tolerated and less likely to induce bacterial resistance as compared to antibiotics. There is also a wide variety of antiseptic agents
available. The efficacy of antiseptic agents has yet to be established as the studies reviewed previously have been small and of
suboptimal quality. This review discusses the rationale behind targeting S. aureus with antiseptic agents and presents findings
from a review of studies assessing the efficacy of antiseptics in atopic dermatitis in the last five years. Four studies were found,
including a bleach bath study which has already been reviewed elsewhere. The remaining 3 studies assessed the efficacy of
sodium hypochlorite containing cleansing body wash, sodium hypochlorite baths and 1% triclosan in leave on emollient. These
studies suggested some benefit for the inclusion of antiseptic use with the mainstay management of atopic dermatitis, including a
potential steroid sparring effect. However, there are many limitations to these studies which therefore warrant further investigation
on the impact of antiseptic use in atopic dermatitis.

Key words: Staphylococcus aureus; Atopic dermatitis; Anti-infective agents, local

INTRODUCTION rising eczema burden in most developing country settings
and in younger children [1-3]. Diagnosis depends on clinical
Atopic dermatitis (AD) is a chronic, relapsing and remitting assessment and the National Institute for Health and Care
inflammatory skin condition that usually develops in early Excellence (NICE) guideline recommends the use of the
childhood. Data derived from the International study of asthma validated criteria for AD (Table 1), which was derived from
and allergies in childhood (ISAAC) has shown a worldwide the Hanifin and Rajka diagnostic criteria [4, 5]. Most cases of
prevalence ranging from 2% to 20% with a tendency for higher childhood AD are mild with infrequent exacerbations and
prevalence in affluent European and Australasian settings, and minimal impact to quality of life. However, more severe AD

Correspondence: Melissa Lee This is an Open Access article distributed under the terms of the Creative
Commons Attribution. Non-Commercial License (http://creativecommons.
Department of Paediatrics, University Children’s Medical org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use,
Institute, Yong Loo Lin School of Medicine, National distribution, and reproduction in any medium, provided the original work is
University of Singapore, 21 Lower Kent Ridge Road, properly cited.
Singapore 119077, Singapore
Tel: +61 421 872 961
Fax: +61 8 93122348
E-mail: leeps.melissa@gmail.com

Received: April 30, 2014
Accepted: September 12, 2014

http://apallergy.org

26]. such as the bends of the elbows or behind the knees (or visible dermatitis on the cheeks and/or extensor areas in children aged 18 months or under) • Visible flexural dermatitis involving the skin creases. There is also an understanding be isolated from the skin of 5–30% of unaffected individuals that individuals with skin disease may be genetically predisposed [17. It has been important role in the disease process [8]. SA can or calcineurin inhibitors [28-31]. 12].org/10. 17] in patients with AD. 21-23]. including been linked to AD prevalence in the first and second years increased synthesis of extracellular matrix adhesins. visual problems and STAPHYLOCOCCAL COLONIZATION IN impaired dental hygiene [6. It also allows the entry of pathogenic strains being reisolated after months of adequate SA superantigens (SSAgs).Antiseptic agents in atopic dermatitis Table 1. thus treatment [17. Colonization with SA within the first year of life has to microscopic structural changes in the skin barrier. with dysfunction enhances SA colonization. 7]. as well as allergens and irritants. Collectively. rapid recolonization [27]. association between severe AD and multiple comorbid chronic health disorders. ATOPIC ECZEMA Much remains to be understood about the complex pathophysiology of AD. 12. † Asian. Clinical Guideline No.29-fold risk of moderate to severe AD in and fibrinogen for SA [32. with the permission of the Royal College of Obstetricians and Gynaecologists on behalf of the National Collaborating Centre for Women’s and Children’s Health. The skin of patients with suggested that the underlying allergic skin inflammation of atopic eczema has a tendency to be colonized by SA [8-12]. alkaline skin surface pH [34-36] and reduced production of Staphylococcal colonization also persists despite eradication endogenous antimicrobial peptides due to defective innate strategies with studies showing recurrence in almost 100% of immune responses [10. this skin barrier patients with eczema after antistaphylococcal treatment. 22]. 2007. such as asthma. black Caribbean. an early childhood. hay fever. it is widely accepted that the Extensive research has shown that the propensity for SA skin commensal microorganism Staphylococcus aureus (SA) has an colonization is complex and multifactorial [12]. although this link has been disputed [24. The role in several reservoirs such as the anterior nares. fibronectin of life and poses a 4. The clinical significance of colonization SSAgs are exotoxins produced by SA which play a key role in apallergy. such as the bends of the elbows or behind the knees (or visible dermatitis on the cheeks and/or extensor areas in children aged 18 months or under) • Personal history of flexural dermatitis (or visible dermatitis on the cheeks and/or extensor areas in children aged 18 months or under) • Personal history of dry skin in the last 12 months • Personal history of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative of children aged under 4 years) • Onset of signs and symptoms under the age of 2 years (this criterion should not be used in children aged under 4 years * Reproduced from National Institute for Health and Care Excellence. reduced skin lipid content. both atopic and nonatopic. 33]. food allergies. such as corticosteroids skin lesions can be as high as 73% [18-20]. and black African children may have atopic eczema affecting the extensor surfaces rather than the flexures. however. In comparison. It has been reported showing significantly reduced colonization on the skin following that self-contamination from these reservoir sites or colonized topical anti-inflammatory drugs alone.230 231 . Family members also often serve as a source of contributing to exacerbation of skin disease [10].4.doi. 25]. Atopic Eczema in Children. Diagnostic criteria of atopic dermatitis* [4] Atopic eczema should be diagnosed when a child† has an itchy skin condition plus ≥3 of the following: • Visible flexural dermatitis involving the skin creases. as well as matrix adhesins which facilitate SA adherence [12]. recurrent ear infections. the axillae and the of inflammation and bacterial adherence is based on studies perianal region [16.org http://dx.57 London: National Institute for Health and Clinical Excellence. is correlated with poorer overall health. impaired sleep and is that there may be a correlation between SA colonization with increased healthcare utilization [6.2014. and discoid or follicular patterns may be more common. There also appears to be an severity and exacerbation of disease [11. 7]. This AD may contribute to increased colonization of SA as skin bacteria has been isolated from up to 90% of lesional skin [13-15] inflammation injures the skin barrier and exposes extracellular and has also been found in clinically uninfected areas.5415/apallergy.

and proteases in the pathogenesis of AD. there is a theoretical basis for interleukin (IL) 4 and interferon-γ. cutaneous lymphocyte-associated antigen. clinically infected skin disease and the prophylactic treatment There is also an emerging role on the impact of environmental of individuals who are at risk of colonization or infection. in addition to cytokines such as eczema (Table 2). enhancing entry of other SA-derived molecules. of inducing bacterial resistance. 47]. SSAg. cysteine- to trigger an enhanced inflammatory response through the and metalloproteases [46. Induction of corticosteroid resistance Exposes the ECM adhesins which lead to enhanced adherence of SA to the skin Protease secretion Induction of skin barrier breakdown. such as serine-.2014. term topical corticosteroid use may lead to adverse effects such Treatment strategies can be divided into the management of as local irritation. AD. which is an incentive to management as long agents as ancillary therapy for the management of AD. Antiseptics represent an alternative and fungi. [26. T helper cell. dust mites. or act as allergens of antiseptics over antibiotics are that they have low potential themselves. APC. induce SSAg-specific IgE antibodies which trigger inflammatory mediator release from sensitized mast cells and basophils • Direct stimulation of APC and keratinocytes causing release of proinflammatory cytokines e. Staphylococcus aureus. also produce proteases which may enhance the to topical antibiotics in patients with AD. 42]. SSAgs can also induce corticosteroid resistance. antigen presenting cell. SA. 45] Superantigen Penetrate the skin barrier contributing to chronic inflammation which directly leads to further injury to the skin barrier • Stimulation of massive T cells causing cytokine release e. SA. extracellular matrix. 44]. rarely cause delayed-type Table 2. 47]. They have the ability Extracellular proteases produced by SA. Staphylococcal superantigen.Asia Pacific allergy Lee M and Bever HV.doi. pollen as antiseptic agents [49. Interleukin. 50]. TNF-α. have also been quantified in the eradication of SA in patients with eczema in order to prevent the sera of most patients with AD compared to normal controls aggravation of skin disease. 40]. allergens and irritants which perpetuates the chronic inflammatory nature of AD Cleavage of endogenous protease inhibitors Induction of proinflammatory and proallergic responses Promotion of Th2 skewed adaptive immune responses IgE production IL. [12]. skin atrophy and skin depigmentation [5]. ECM. CLA+. and contribute to the inflammatory response [45]. This has led to the hypothesis that eradication of SA may lead to a steroid There has been wide interest in the use of antistaphylococcal sparring effect [11]. IL-1. tumour necrosis factor. 37-39].4. atopic dermatitis. the chronic inflammatory nature of AD. Th. have been found in in vivo mice stimulation of a variety of T-cell clones and cytokine secretions studies to compromise the epidermal permeability barrier [48].g.. IL-12 which enhance infiltration of T cells to skin lesions • Expansion of skin-homing CLA+ T cells amplifying the initial cutaneous inflammation in AD • Augmentation of allergen-induced skin inflammation. toxic shock syndrome ability to inactivate some human plasma proteases inhibitors and toxin-1 and staphylococcal enterotoxins and their role has been interact with host defense mechanisms and tissue components established in several immunohistological studies based on in a complex manner that further augments the infection process SA strains isolated from the lesional skin of patients with AD and enhances SA survival [46.4.230 apallergy.Summary of potential mechanisms by which Staphylococcus aureus induces and exacerbates atopic dermatitis [12.IL-4 • Act as an allergen. and have been shown to decrease with treatment [11.5415/apallergy. Over 70% of SA strains isolated from the skin of AD patients These bacterial proteases are also insensitive to and have the produce superantigens such as alpha-toxin.org . in addition to ranges from the use of systemic and topical antibiotics as well environmental allergens such as cockroaches. TNF. There is also a positive correlation between colonization with superantigen producing strains of SA and clinical severity of AD THE RATIONALE FOR ANTISEPTIC USE IN [41. Consequently. The main advantages passage of allergens across the skin barrier. 232 http://dx.org/10. which ATOPIC ECZEMA may increase the severity of skin disease [43. Increased levels of antistaphylococcal superantigen SA infection is therefore related to the pathogenesis of specific IgE and IgM antibodies.g.

twice weekly antiseptic to induce resistance [49]. antiseptics used in this added to emollient may be applied on a daily basis on the whole setting may be a suitable alternative as they have less potential body or on affected areas. One percent to 2% triclosan or 0. Whilst the RCT concluded that there was crusting and consequently. [51] involved agents [11. 12.9 in the treatment group and 17. However. Antiseptics in clinically infected eczema didecyldimethylammoniumchloride. However. p = 0. involving 1.Antiseptic agents in atopic dermatitis hypersensitivities or allergic reactions and come in a variety randomized controlled trials (RCTs). Bath-Hextall et al. particularly with the fears of the emergence of antibiotic- [5]. Therefore. 51.2014. povidone iodine.5415/apallergy.9 although a number of studies showed that topical or systemic points. potassium permanganate. Clinically infected or ‘impetiginised’ skin disease can were pretreated with oral cephalexin then treated with either be characterized by increased erythema. Topical antibiotics. unable to perform a group analysis [50]. With regards to the use of topical antiseptic no significant difference in global outcome for clinically infected agents. silk coated textiles and special silk fabric. 60]. in uninfected eczema [50]. can be used not achieved despite pretreatment with daily cephalexin for 2 for no longer than two weeks in patients with clinical infection weeks followed by 3 months of twice daily intranasal mupirocin in localized areas. sodium hypochlorite or they were superior than standard therapy in clinically infected bleach and chlorhexidine gluconate [49]. antibiotics were able to reduce colonization density. mainly because of an increasing resistance problem worldwide Topical antiseptics in clinically uninfected eczema [55-58].4. inclusion criteria and treatment protocol in the apallergy.5% to 1% chlorhexidine resistant strains of SA [56. Alternatively. bacterial load [49]. the the setting of uninfected skin in AD against exacerbation is less short term use of antiseptics. clear and remains a controversial area in the management of can also be used as adjunct therapy to reduce bacterial load AD.doi. [50. Antiseptic baths can be particularly useful in reducing arm) for 3 months. children with atopic eczema [5]. good scientific data on the subject 31 children with clinically infected moderate to severe AD who are rare. A review by Schnopp et al.7 in the placebo group) [50. However.org http://dx. the Cochrane review found one poorly reported study eczema when oral antibiotics were compared with placebo or assessing the benefit of povidone-iodine in 15 children and when topical steroid antibiotic combinations were compared adults with clinically infected mild to moderate AD but was with steroid alone [50].017 at 1 month. such as triclosan or chlorhexidine. chlorhexidine. Given the contradictory results available. of preparations to suit individual needs.org/10. This study by Huang et al. Antibiotic reduced clinical severity of clinically infected AD in the treatment treatment alone has no impact on allergic skin inflammation arm based on eczema area and severity index (EASI) scores (7. it would be prudent to be restrictive in prescribing antibiotics. 52]. including 51].004 at 3 months). it appears that of good quality large RCTs and found that there is no good the recommendations for the topical use of antibiotics and evidence to support the use of antistaphylococcal agents antiseptics are not substantiated by good quality clinical data [49. The review found one that disease flares caused by secondary infection with SA requires RCT assessing the effect of an antibacterial bath additive on and responds to treatment with antibiotics and antiseptic clinically infected AD. the benefit of antibiotic use in AD is treatment for 5 consecutive days each month and twice weekly still disputed with a Cochrane review presenting studies showing bleach baths [51]. [49] 50]. 54].1 points. 59] performed a systemic review of 26 endpoints.229 participants. resulting the study was criticized as it was unclear if any adjustment was in partial improvement of skin lesions [17. Of further clinical relevance is that eradication of SA was preparations combined with topical corticosteroids. differing [50] and Birnie et al. The Cochrane review reported a lack bathes have been recommended [49]. 53. Antiseptics include of interventions to reduce SA in eczema to determine whether triclosan. In a Cochrane review released in 2010. superficial pustular intranasal mupirocin ointment and bleach baths (treatment arm) eruption or purulent exudation with crusting and can spread or intranasal petrolatum ointment and plain water baths (placebo easily [5]. bleach. The role of antistaphylococcal agents used preventively in For children with AD and are prone to recurrent infections.230 233 . It is widely accepted or clinically uninfected atopic eczema. presented 15 studies which assessed the efficacy of a range of antiseptic treatments including triclosan. p = 0. The NICE made for the differing baseline EASI scores between the two guideline recommends a one to two weeks course of flucloxicillin group of patients who were treated for more than one month as first-line treatment to treat widespread infection with SA in (26. However.

The overall mean reduction in IGA score from AN UPDATED REVIEW OF STUDIES ASSESS. 10. week 4. and 0. n = 12). we 14. equivalent to 0. Clinical response was measured topical anti-inflammatory and emollient therapy.230 apallergy.22.005% sodium hypochlorite baths in 36 patients aged other antiseptic agents [49]. n = 6). n = 11).01. n =18). Furthermore.Asia Pacific allergy Lee M and Bever HV.2014. placebo-controlled study assessing the efficacy better tolerated. Patients were given either 100mL of 5% sodium hypochlorite of a 0. including the bleach bath study by Huang et al. Acceptability and Follow-up was performed at baseline. studies made it challenging to determine the benefit of a questionnaire completed by parents [66].org . The It appears that there is growing interest in the role of sodium authors acknowledged that the limitations of the study were that hypochlorite in the management of AD. baseline to final measurement was 0. Given the growing potential of antiseptic use in AE. They were instructed AD who also had lesional cultures positive for SA at baseline. There were no reports of patients developing infective antimicrobial activity was not assessed in this review.01. [51] was also highly accepted and tolerated by patients and their which has already been reviewed [49. is easily accessible and cheaper compared to of 0.8 at 1 month (p = 0.4.01.9% at 1 month (p < 0. n = 13). n =13). Traditional dilute this pilot study and should include the impact on the usage of bleach baths have concentrations that range from 50 parts per the patient’s topical and systemic regimen and whether it has million (ppm. 0.002. [67] performed a 2-month prospective randomized.8 at 2 months (p = 0. Its assessing the clinical efficacy of sodium hypochlorite containing antimicrobial effect is probably due its ability to cause irreversible body wash is thus needed to confirm the encouraging results of aggregation of essential bacterial proteins [65]. n = 10).7% at 2 weeks (p = 0. PubMed was searched for studies final measurement in all patients was 14. week 2.001. sodium hypochlorite is double-blinded. 50]. of water) to 90 ppm (0. 0. The overall mean reduction from baseline to last five years (to March 2014).5415/apallergy. Its antistaphylococcal it was a small non blinded study that lacked a placebo arm and activity.005% being shown to be safe and effective [61-64]. and week tolerability of the product was also assessed retrospectively using 8 (end) of treatment [67]. to soak neck down in these baths for 10 minutes. equivalent to half a cup of bleach Wong et al. points—1. sodium statistically significant reduction in bacterial count was found at hypochlorite.4. triclosan. and 16.8% (p = 0. parents with high scores recorded on the patient satisfaction questionnaire. The use of sodium hypochlorite gel cleanser Table 3. n = 12). 0.0061% sodium hypochlorite containing cleansing body (bleach treatment arm) or distilled water (placebo arm) and wash in 18 children with clinically uninfected moderate to severe instructed to add this into 100 L of water. chlorhexidine. between 2 and 30 years old with uninfected moderate to severe In a pilot feasibility study. n = 18).6% at 2 months (p = 0. Response to treatment was assessed 234 http://dx. The use of sodium antibacterial therapy in AE. [66] assessed the efficacy AD. with concentrations as study lost to follow up [66]. n = 6).005.8% at3 months reviewed studies assessing the efficacy of antiseptics in AD in the (p = 0. twice a week Patients used the wash three days a week for 12 weeks and for two months. n = 11). The efficacy of fabrics treated to provide trend. Patients also unanimously preferred this product Sodium hypochlorite in AD management over traditional dilute sodium hypochlorite bleach baths [66]. percentage of body surface area (BSA) affected.9 (p = 0.001.005%. Aqueous cream using an investigator global assessment (IGA) score and the as soap was provided to standardize their bathing regimen.005.001. The ING ANTISEPTIC USE IN ATOPIC ECZEMA mean reduction from baseline of BSA affected was 10. Patients then rinsed off with normal tap water were allowed to continue with their individualized topical and and were allowed to maintain their individualized regimen of systemic treatment regimen. A key finding was the importance hypochlorite gel cleanser was reported to result in statistically of anti-inflammatory therapy and its role in reducing bacterial significant mean reductions in IGA scores at all follow-up time colonization. in half a tub of water) [66]. with 4 studies found.org/10. despite following a decreasing and eczema or AD. has been had many of the retrospective patients in the initial phase of the established in in vitro and in vivo studies. A in English containing bleach.0 at 2 weeks (p = 0.25 cup bleach in half a tub any benefit in clinically infected AD. course of the study.doi. including against methicillin-resistant SA. A larger randomized controlled study low as 0.01. Ryan et al. povidone iodine or potassium permanganate 1 month only (p = 0. The results exacerbations requiring oral antibiotic treatment during the were hand searched for relevant studies.9 at 3 months (p = 0.009%.

product.Antiseptic agents in atopic dermatitis Table 3.org/10.230 235 . atopic dermatitis. * Diagnosis based on Hanifin and Rajka Criteria. The study reported a papulation. (2010) [69] 27-Day double blinded placebo controlled randomized Severity assessed according to SCORAD Index 1% Triclosan in leave on emollient trial involving 60 patients 12 to 40 years old with mild to Presence of adverse events moderate AD* according to SCORAD Index Amounts of topical corticosteroids and study cream 0. followed by either study cream or vehicle control applied twice daily on the whole body Huang et al. trunk and lower limbs) diluted bleach baths resulted in clinically improved AD from and a physician’s assessment of erythema.org http://dx. stable on a 4-point scale.2014. (2013) [66] 12 week open-label nonrandomized feasibility study of Clinical response based on IGA score and percentage of Sodium hypochlorite 18 children over 6 months with uninfected moderate BSA affected containing cleansing body wash to severe AD according to IGA score and positive Secondary endpoints included change in quantitative lesional cultures for Staphylococcus aureus at baseline bacterial load from baseline. placebo-controlled Efficacy assessed using EASI score. Efficacy assessed using EASI scores Intranasal mupirocin ointment controlled study involving 31 patients. Overall. investigator global assessment.025% betamethasone valerate cream was provided used for concurrent use over eczematous areas for the first 27 days. with moderate to severe AD determined with IGA and clinical signs of secondary bacterial infections† All patients received oral cephalexin for 14 days prior to administration of treatment or placebo (intranasal petrolatum ointment and plain water baths) Each patient maintained a stable regimen of topical anti-inflammatory medication and emollient therapy throughout the study period AD. patient adherence and satisfaction individualized topical and systemic treatment regimens were continued Wong et al.doi.001) suggesting clinical was assessed using visual analog scale and bacteriological improvement was achieved and sustained after 1 month of assessment was performed by calculating SA density from a treatment. body surface area. regimen of topical anti-inflammatory and emollient Patients’ assessment of overall response and intensity therapy maintained of itch assessed using visual analog scale was also Aqueous cream as soap was issued to standardize assessed bathing regime S. a validated composite score of BSA from also assessed [67]. eczema area and severity index. a validated Sodium hypochlorite baths study involving 36 patients between 2 and 30 years old composite score of BSA from four regions (head with uninfected moderate to severe AD* according to and neck. EASI.4. significant reduction in EASI scores between the treatment and Patients’ assessment of overall response and intensity of itch placebo groups at 1 and 2 months (p < 0. edema/ Patients soaked in diluted bleach or distilled water induration/population. There was also significant improvement in EASI scores swab of the worst affected sites. twice a week for 2 months. SCORing Atopic Dermatitis. Safety based on clinical adverse and various clinical parameters corresponding to the upper limbs. SCORAD. BSA. trunk and lower limbs) and Rajka and Langeland Criteria 1989 a physician’s assessment of erythema. Antiseptic treatment Author/antiseptic assessed Details Outcomes measured Ryan et al. events reported by patients or observed by the physician was trunk and lower limbs (areas of the body submerged in the baths) apallergy. (2009) [51] 3-Month randomized. edema/induration/ 1 month and was tolerated by patients. aureus density was determined using quantitative bacterial cultures Tan et al. placebo. upper limbs. crusting and/or pustule. investigator-blinded. (2013) [67] 2-Month prospective. IGA.5415/apallergy. the study reported that the use of four regions (head and neck. using the EASI score. †Weeping. excoriation and lichenification on a 4-point scale. 6 months to 17 and sodium hypochlorite baths years of age. upper limbs. randomized. excoriation and lichenification baths for 10 minutes. tolerability of the Treatment given three times a week for 12 weeks.

or from the reduction in SA colonization with antimicrobials. It was all age groups [67]. at 2 months in the treatment group. [51] suggesting that clinically reported in 15 patients however only 4 were considered related to improvement in AD does not require complete eradication of SA treatment and included transient stinging pain after application [67]. There group.2014. p > 0. –9. treatment and follow-up and since patients were responsible for the authors reported significantly lower amount of topical steroid administering their own treatment. 15.06–5. good quality studies assessing the relationship between sites not exposed to the antiseptic. 95% CI. whether it has any implications in disease may also reflect a shift in skin flora. however this was not significant (–11.99 for control group.05) [69]. A low potency corticosteroid was allowed to be Limitations of this study were that it was a small study with short used concurrently during the treatment period and interestingly. Future studies also need to further assess the relationship steroid sparring effect by reducing local SA enterotoxin induced between degree of SA colonization and clinical severity of AD corticosteroid resistance [43.86 vs. The improvement Triclosan in AD management in EASI scores in the treatment group also corresponded to a One study presented in this review was a double blinded significant reduction in percentage BSA affected at 2 months (p RCT assessing the efficacy of emollient containing 1% triclosan = 0. such as the nares. as not statistically significant. The use of bleach baths was also associated reported that emollient containing 1% triclosan significantly with a reduction in density of SA over time. Whilst the head and neck severity and that AD treatments diversify skin bacteria preceding of patients in the treatment group showed improvement in the improvements in disease activity [68]. respectively. thus implying a true double blinded study as patients would have been able to steroid sparring and synergistic effect of 1% triclosan containing differentiate between bleach and placebo on the basis of odour. this was not statistically significant and may have been due to partial submersion of these areas. Of patients in the treatment who withdrew from the study due to adverse events [69]. this study was not a control (22 g and 44. it was found SA was greater As the skin of patients with AD has intrinsic properties that during disease flares and correlated with worsened disease increase susceptibility to SA colonization. although this was reduced AD severity at day 14 compared to vehicle control.05). Furthermore. in a separate study assessing the temporal shifts in the skin microbiome associated with disease flares and treatment in children with AD [68]. Adverse events were bleach bath study by Huang et al. No patients for treatment group vs. There was also no statistical difference determined by mean SCORAD change from baseline (–8.71.4. Based on ribosomal RNA bacterial gene CONCLUSIONS sequencing performed on DNA obtained directly from serial skin sampling of children with AD. persistent colonization requires further investigation as there is also a paucity of long despite treatment in patients may reflect recolonization from term. This resolved spontaneously overall assessment of response between treatment and placebo even with continued use of the cream.2 g. the study was not performed application by patients in the treatment group compared to the in a controlled environment. p < 0.– in colony counts between the treatment and placebo groups at 4.05). 44]. and was found to be safe and highly acceptable either 1 or 2 months.Asia Pacific allergy Lee M and Bever HV.230 apallergy. as opposed to to corticosteroid potency required and how it affects clinical being solely related to reduction in SA colonization.5415/apallergy.002). Improvement on amount of corticosteroid used.8% experienced side effects which included burning/ was also improvement of severity at day 27 in the treatment stinging and mild dry skin. [51] in their own bleach bath SA colonization associated with antiseptic use produces this study. There were no statistically significant differences in patient’s of 1% triclosan containing emollient. A similar proportion of patients in the group. this putative effect hypochlorite is bactericidal in vitro [62].1 placebo group also experienced similar side effects. Whilst dilute sodium analysis was performed [69]. no bacteriological not be necessary for disease improvement.46. emollient [69]. 95% CI. These findings were similarly found in the to patients after a study period of 27 days. p < 0. These improvements appeared to be evident across in 60 patients with mild to moderate uninfected AD [69]. above outcomes.2–8. it is unlikely that the use 236 http://dx. Therefore. 13.doi.org . It has been suggested that the reduction of This was recognized by Huang et al. withdrew from the study because of intolerance to the baths [67]. its impact members of the household who may be carriers. 27.org/10.4. Since this study was performed since it appears complete eradication of SA colonization may in patients with clinically uninfected eczema.75. as suggested outcome. There were no subjects groups at either 1 or 2 months.

Asher MI. Optimal management requires The studies available on the role of antiseptic agents in the addressing the key factors known to cause exacerbation of management of AD suggest some benefit for the inclusion of disease. Williams HC.230 237 . topical calcineurin inhibitors. with the aim of eradicating It may also be difficult to achieve patient compliance thus primary infection. these studies should reduce microbial colonization thus reducing the risk of secondary assess whether any flares or infected exacerbations occur with infection and the need for specific antimicrobial therapy [8. this can be utilized for long-term control and should be applied on to previously eczematous skin in a ‘proactive’ approach: -Monotherapy with either a TCI or a lowest potency topical corticosteroid used intermittently or an alternation of the two agents SA colonization -Daily use of emollients and topical corticosteroids to reduce colonization -Use of antiseptic agents may be considered -Judicious use of antibiotics in secondary infection TCI. The RCTs and should assess long-term efficacy. The approach of adding antiseptic avoidance. appearing skin is not immunologically normal and is often ISAAC Phase Three Study Group. together with daily application of emollient [73]. 72].124:1251-8. will be of long-term benefit. Clayton TO. Practical conclusions for the clinician [5. the high rates of recolonization. emollients to enable the repair and protection of the agents to emollients and body washes is a convenient measure skin barrier with proper hydration and topical anti-inflammatory of introducing an additional agent into the AD management agents such as corticosteroids or calcineurin inhibitors. of antistaphylococcal therapy alone. there are many limitations to these and reducing skin inflammation. However.org http://dx. The reported steroid sparring effect There is also an emerging rationale for a ‘proactive’ approach to associated with antiseptic use should also be further investigated. tailored to the individual: Allergens -Allergen identification and avoidance. the mainstay studies which therefore warrant further investigation on the of AD management. In particular. Recent perspectives on the global epidemiology of apallergy. the management of AD to achieve long-term remission between flares.5415/apallergy.2014. primarily targeting improvement in skin barrier function antiseptic use. Chronic inflammation Topical anti-inflammatory agents such as corticosteroids or calcineurin inhibitors: -Induction therapy: during periods of exacerbation whereby a variety of protocols may be utilized as initial therapy until an acceptable level of clearance is achieved: -High potency topical corticosteroids -Lowest effective potency topical corticosteroids -TCI -Topical corticosteroid/ TCI combinations -Maintenance therapy: once exacerbations have been controlled. Flohr C. Global variations in prevalence of colonized by SA [8. the adverse effects of their long-term use cannot be ignored. 73. continued antiseptic use. SA.org/10. Robertson CF. tolerability use of emollients and topical corticosteroids alone are able to and cost effectiveness.4. Future studies need to be large scale double blinded remain important therapeutic options (Table 4) [70. which constitutes irritant and allergen impact of antiseptic use in AD. Skin barrier dysfunction -Daily use of emollients. This involves continued intermittent application of low dose topical anti-inflammatory agent over previously eczematous REFERENCES but now normal looking skin.doi. Consequently. Odhiambo JA. Again. 71]. 74]. particularly with hindering the reported benefits of this ‘proactive’ approach.e23. this is based on the recognition that normal 1. will regimen. Staphylococcus aureus. 2. safety. However.Antiseptic agents in atopic dermatitis Table 4. the proactive approach of eczema symptoms in children from ISAAC Phase Three. 10. J Allergy Clin topical anti-inflammatory agents is considered ‘offlabel’ use and Immunol 2009. 71] Key factors to address.

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