16

Occlusive Therapy in Atopic Dermatitis

Misha M. Heller1, Eric S. Lee2, Faranak Kamangar3,
Wilson Liao4 and John Y. M. Koo4
1University of Southern California, Keck School of Medicine, Los Angeles, California
2University of Nebraska Medical Center, College of Medicine, Omaha, Nebraska
3University of California Davis, School of Medicine, Sacramento, California
4University of California San Francisco, Department of Dermatology

San Francisco, California

USA

1. Introduction
The treatment of atopic dermatitis (AD) can be challenging for dermatologists and other
healthcare professionals. Conventional treatments consisting of emollients and topical
corticosteroids are often insufficient for severe and/or refractory AD. Other therapies
include systemic corticosteroids, photochemotherapy using psoralen and ultraviolet-A light,
and cyclosporine. However, all of these approaches have potentially serious side effects and
relative contraindications, especially in children. Over the past two decades, occlusive
therapy has been advocated as a safe and effective treatment modality for individuals with
acute erythrodermic AD and those with severe and/or refractory AD. (Nicol 1987;
Goodyear et al. 1991; Bridgman 1995; Devillers and Oranje 2005)
Occlusive therapy usually involves the application of emollients, antiseptics, or topical
corticosteroids under either wet wrap dressings (WWD) or dry wrap dressings (DWD). This
consists of moistened open-weave cotton tubular bandages (eg. Tubifast, Tubigauz) in
WWD occlusion, versus dry gauze, plastic wraps, or hydrocolloid dressings (eg.
Duoderm) in DWD occlusion. (Nicol 1987; Goodyear et al. 1991; Bridgman 1995)
More recently, however, occlusion alone using a hydrogel patch has been utilized. The
theory is that a major component in the pathophysiology of AD is barrier dysfunction. In
fact, many current therapies target this barrier defect (i.e., pseudoceramide moisturizers and
skin barrier emulsions). As such, an ideal repair mechanism would completely eliminate
microbe and allergen penetration and transepidermal water loss in AD, both of which lead
to xerosis, hypersensitivity, pruritus, and inflammation. The hydrogel patch, therefore,
offers an innovative approach to complete barrier repair. (Park et al. 2011)
Regardless of the treatment approach, occlusive therapy offers many advantageous such as
a cooling effect on inflamed skin, increased penetration of topical agents, enhanced skin
hydration, and a barrier to external antigens and trauma (i.e. scratching). Reported
disadvantages include the cumbersome and time-consuming nature of the application
process, risk of allergic reaction to the occlusive material itself, and possible increased risk of
infectious complications such as folliculitis, furunculosis, or cellulitis. An additional concern
is that occlusion may cause skin maceration if used incorrectly, or can paradoxically

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promote skin dryness if too little topicals are applied. (Nicol 1987; Goodyear et al. 1991;
Bridgman 1995; Krakowski et al. 2008)
Occlusion alone of both normal and lesional eczematous skin can result in increased density
of cutaneous microbial flora. (Aly et al. 1978; Rajka et al. 1981) Moreover, there is a positive
association between Staphylococcus aureus (S. aureus) colonization and disease severity.
(Williams 2000) These findings suggest that occlusion, by increasing the density of S. aureus,
might push already colonized eczematous skin into the realm of clinical infection. In

-defensin, is depressed in patients with AD such that eczematous skin possesses decreased
addition, innate production of cutaneous anti-microbial peptides, such as sphingosine and

natural resistance to bacterial invasion (Arikawa et al. 2002; Ong et al. 2002) Thus, evidence
of clinically apparent skin infection may be a contraindication to occlusive therapy, as it may
exacerbate the infection. (Aly et al. 1978) However, the possibility that S. aureus colonization
may complicate occlusive therapy has not been adequately addressed to date.
Another concern is that the use of topical corticosteroids under occlusion may relate to an
increased potential for absorption and greater incidences of possible adverse effects. Most
attention has been focused on the risk of skin atrophy and striae, hypothalamic-pituitary-
adrenal (HPA) axis suppression, as well as growth impairment in children.
Ultimately, this chapter aims to examine current evidence on the safety and efficacy of
occlusive therapy in the treatment of AD.

2. Methods
Studies on the use of occlusive therapy for the treatment of atopic dermatitis were identified
in PubMed and Embase Medline databases from January 1966 to April 2011, using the key
terms “occlusion,” “occlusive dressings”, “occlusive therapy,” “wet wrap,” “wet dressings,”
“dry wrap,” “dry dressings,” “atopic dermatitis,” “dermatitis,” and “eczema.” Key terms
were also searched in combination. Reference lists of relevant publications were manually
searched for additional relevant studies. The search was limited to original studies and
review articles published in English or with English abstracts, in humans. Studies of small
size and those that did not use a controlled or randomized study design were included due
to the dearth of published literature on this topic. Publications meeting these criteria were
then reviewed for study design, population, disease severity or type, study size, efficacy,
and safety. The topical agent used, dilution, and type and period of occlusive therapy were
also noted, when such information was made available in the publication. In addition,
response to therapy was seen as improvement in disease severity or symptoms from
baseline, improvement in SCORing Atopic Dermatitis (SCORAD), and/or improvement in
Eczema Area and Severity Index (EASI) score, depending on what information was
provided. Of note, SCORAD is composite score of eczema severity based on the surface area
involved, intensity of symptoms, and subjective symptoms such as sleep disturbance and
pruritus. EASI is a 12-point scoring system of disease severity assessing erythema,
induration, lichenification, pruritus, and excoriation. Finally, conclusions were drawn from
the results of these studies bearing in mind standard clinical practice.

3. Studies on occlusive therapy

There are a total of 19 studies evaluating the use of occlusive therapy in AD (Table 1).
Fourteen studies used WWD, 5 of which were randomized controlled trials. All WWD

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*Dilution and concentration noted when provided in the article

Table 1. Studies on Occlusive Therapy (HCT = Hydrocortisone, RCT = randomized
control trial)

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occlusion studies demonstrated efficacy in severe or acute, moderate and chronic AD.
Among the 4 studies examining DWD, only one used a randomized controlled design. All,
except one, DWD studies demonstrated improvements in AD. There is also one study that
used an impermeable hydrogel patch consisting of about 50% water content. The hydrogel
patch alone demonstrated improvements in AD, comparable to that of corticosteroid use
alone. Increased cutaneous bacterial counts or clinical infections were reported in 4 out of
the 15 studies using WWD and all 4 studies using DWD.

3.1 Wet wrap dressings

The following is a detailed description of the 14 studies evaluating the efficacy of WWD in
the treatment of AD (Table 2). Occlusive therapy was first introduced by Goodyear et al. in
1991. Goodyear et al. (1991) evaluated the inpatient use of WWD occlusion for acute
erythrodermic eczema. This WWD technique involved the application of open-weave cotton
tubular dressings (Tubegauz) impregnanted with hydrocortisone 1% cream (if child <2
years of age) or 10% dilution of bemethasone valerate (if child > 2 years of age) twice daily.
All 30 children responded well to WWD occlusion, with no relapses noted at 2 weeks
follow-up. Interestingly, an attempt at long-term home therapy using WWD, following the
inpatient therapy, in 5 patients was unsuccessful due to reports of inconvenience, increased
bacterial infections, and prolonged HPA axis suppression. (Goodyear 1991)
Mallon et al. (1994) studied the use of WWD in chronic severe eczema in 21 children.
Eczema was managed using topical steroid creams (i.e. hydrocortisone 0.5% or 10% dilution
betamethosone 0.1% cream) and emollients under WWD daily for less than 5 days. All
patients responded well to WWD therapy. The treatment was also well-tolerated. Majority
of parents (20/21) reported decreased use topical steroid per week following the
introduction of WWD therapy. (Mallon et al. 1994)
Abeck et al. (1999) treated 6 patients (3 children and 3 adults) with acute exacerbated atopic
eczema with basic emollients in combination with chlorhexidine-soaked dressings for 3 days.
The study observed improvements in disease severity based on SCORAD score. Patients also
reported decreased itch and sleep loss following WWD therapy. In addition, there was a
reduction of S. aureus counts that paralleled skin improvement. (Abeck et al. 1999)
In a study of 31 children with severe refractory AD, Wolkerstorfer et al. (2000) investigated
the efficacy of various cortiocosteroid dilutions under WWD occlusion. Participants were
divided into 3 treatment groups. The first group consisted of 18 children, who were treated
with 50% dilution of fluticasone propionate 0.05% (FP) cream under WWD for 2 weeks. In
the second group, 5 children with symmetrically localized AD were treated with different
dilutions (10%, 25% and 50%) of FP cream on the left and the right side of the body under
WWD for one week and then 10% dilution of FP cream under WWD the following week. In
the third group, 8 children were treated with 0% (i.e. only emollient), 5%, 10%, or 25%
dilutions of FP cream applied to the entire body under WWD. After just one week of
therapy, significant improvement in disease severity was observed, without noticeable
differences between 5%, 10%, or 25% dilutions of FP cream under WWD. Less improvement
was observed in the second week of therapy. In terms of skin infections, mild-to-moderate
folliculitis was reported in a large proportion of the children, with 33% (6/18) children in
the first group, 40% (2/5) children in the second group, and 63% (5/8) children in the third
group. There was also one case of furunculosis in the third group. Interestingly, generalized
folliculitis was noted in both of the children treated with only emollient during the first
week. These findings suggests that although WWD occlusion may foster bacterial growth,

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Table 2. Outcomes of Studies on Wet Wrap Dressing Occlusion (DPD = deoxypyridinoline,

HPA = hypothalamic-pituitary-adrenal, HRQoL = Health Related Quality of Life)

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the addition of topical corticosteroids to the treatment regimen appeared to provide some
protective benefits. (Wolkerstorfer et al. 2000)
Tang (2000) treated 10 children experiencing a flare of facial eczema with WWD occlusion.
Children were initiated on an intermittent treatment regimen involving 10% dilution of
mometasone furoate 0.1% cream or ointment under WWD applied for 2-3 hours once daily
for a few consecutive days. All parents reported good treatment response. No cutaneous
side effects were observed from topical corticosteroid use. (Tang 2000)
Pei et al. (2001) performed a randomized control trial of 40 children with moderate-to-severe
AD. Prior to starting the study, all patient were instructed to apply 0.005% flucinolone
acetonide cream twice daily for 2 weeks to standardize treatment medications. Patient were
then randomized to receive 10% dilution of 0.1% mometasone furoate ointment or 10%
dilution of 0.005% fluticasone propionate ointment. These topical agents were applied once
a day for 2 weeks without WWD. After this 2-week period of open application, patients
were further randomized to receive the same topical agent for 2 more weeks without WWD,
or for 2 more weeks under WWD. Only 30 patients (75%) entered into this second phase of
the study since their disease severity had failed to improve by more than 50% after the
initial 2 weeks of open topical application. In other words, only patients whose disease was
refractory to a 2-week period of conventional open therapy continued in the study.
Ultimately, there were a total of 27 patients who completed the study. One child receiving
fluticasone propionate ointment dropped out of the study because the patient was unable to
tolerate WWD. The study found that significantly greater improvements in disease severity
and extent in patients using WWD, as compared to controls. These results suggest that
WWD may be an effective second-line therapy in children whose disease is refractory to
conventional open topical corticosteroids. (Pei et al. 2001)
Schnopp et al. (2002) examined the effect of WWD in a randomized control study of 20
inpatients with exacerbated AD. Children received either a topical corticosteroid
preparation (mometasone furoate 0.1%) or a steroid-free preparation (its vehicle) under
WWD, applied twice daily for 5 days to the tested area in a left-right study. Disease severity
at day 3 and day 5 continuously improved in both groups; however, the mometasone
furoate-treated group showed significantly greater irmprovements. Staphylococcus aureus
bacterial counts initially decreased during the first 3 days of treatment in both groups. At
day 5, bacterial counts continued to decrease in the steroid-treated group, but bacterial
counts increased in the vehicle-treated group. There were no reported clinical signs of
bacterial superinfection in either the steroid or vehicle groups. The study concluded that
WWD were useful in treatment of exacerbated AD, with applications of topical
corticosteroids showing better efficacy than steroid-free emollients. (Schnopp et al. 2002)
Devillers et al. (2002) evaluated the use of WWD in refractory AD in 12 adults and 14
children. WWD were applied daily and re-wettted every 2-3 hours for 1 week in an
inpatient setting. Patients used 5% dilution of FP cream under WWD on affected areas of the
face. As for the body, a side-to-side comparison study was performed, in which adults
applied 10% and 25% dilutions of FP cream and children applied 5% and 10% dilutions of
FP cream. Disease severity improved dramatically during the one week of inpatient therapy.
There was no difference in improvement between dilutions applied to each side of the body.
Following inpatient therapy, 8 adults and 13 children continued treatment at home with less
potent dilutions of FP cream. Exacerbation of AD occurred in 3 adults and 2 children.
Infectious complications included localized folliculitis (4 reported cases), secondary
impetigo (2 reported cases), localized Pseudomonas aeruginosa infection, cellulitis of the left

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cheek in a patient without a facial mask, and purulent conjunctivitis in a patient with a facial
mask. These complications may be attributed to variations in standard protocal for WWD
application, such as prolonged (>8 hours) occlusion and the frequent rewetting procedure.
(Devillers et al. 2002)
McGowan et al. (2003) examined the effects of WWD therapy using topical corticosteroids
on short-term growth and bone turnover in 8 prepubertal children, ranging from 3-8 years
of age. Tubular bandages were applied over 10% or 25% dilutions of beclomethasone
dipropionate for 24 hours each day for 2 weeks. After 2 weeks, frequency of tubular
bandages was reduced to overnight use for one week and then as required for the remainder
of the treatment period. Occlusive dressings were applied for a median duration of 12 weeks
(range 2 – 18 weeks). Short-term growth was assessed by measuring lower leg length
velocity by knemometry, while bone turnover was assessed by urinary deoxypyridinoline
excretion. (McGowan et al. 2003) (See Section 3.4 Cutaneous and Systemic Side Effects for
further discussion of this study)
In randomized control trial, Beattie and Lewis-Jones (2004) compared the use of 1%
hydrocortisone under WWD to conventional open therapy in 19 children with moderate,
widespread AD. The control group applied 1% hydrocortisone twice daily for 2 weeks,
without WWD. In the study group, patients applied 1% hydrocortisone once in the morning
for 2 weeks, with WWD twice daily for the first week and then only at night for the second
week. Both groups were allowed to apply non-steroidal emollients as often as necessary.
Beattie and Lewis Jones (2004) found no difference in clinical improvement between the
control group and the study group. The authors, therefore, concluded that conventional
open therapy using 1% hydrocortisone and emollients alone appeared to be as effective as
using 1% hydrocortisone under WWD for moderate AD. Despite these findings, it is
important to note that the use of 1% hydrocortisone is a less potent choice than what is
generally used in clinical practice when treating moderate AD. If the authors had evaluated
the use of a mid-potency topical corticosteroid under WWD, the degree of improvement
between the study and control groups might have been markedly different. In terms of
health related quality of life, Beattie and Lewis-Jones (2004) found greater improvements in
the non-WWD control group than the WWD group for both the child and the family.
Children in the non-WWD control group also reported more sleep than the WWD group,
but there was no significant difference for itch between treatment groups. In regards to
infections, 2 of the 10 (20%) children in the WWD group experienced folliculitis, one of
which had to be withdrawal from the study. There were no reported clinical infections in the
non-WWD control group. (Beattie and Lewis-Jones 2004)
Foelster-Holst et al. (2006) conducted a randomized, controlled study of 24 adults and
children with acute episodes of AD. This was left-right comparison study, in which patients
had skin lesions symmetrically affecting both arms or legs. One arm or leg was randomly
treated with the topical prednicarbat (a medium potency corticosteroid), with WWD using a
tubular bandage. The other extremity received topical prednicarbat alone. After 48-72 hours
of therapy, both groups showed improvement of the local SCORAD, but the improvement
in the WWD group was significantly better. No adverse effects were observed in either
treatment group. (Foelster-Holst et al. 2006)
Hindley et al. (2006) carried a randomized, control trial to investigate the efficacy of WWD
as compared to conventional topically applied corticosteroids. This 4-week study consisted
of a total of 50 children with moderate-to-severe eczema. In the conventional treatment
group, patients had emollients applied as needed and 1% hydrocortisone ointment (or more

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potent topical steroids, if necessary) applied twice daily. In the WWD treatment group,
patients had wet wraps applied daily for a 24-hour period over 1% hydrocortisone ointment
(or more potent topical steroids, if necessary) during the first week, followed by wet wraps
applied for a 12- or 24-hour period depending on disease progress for the remaining three
weeks. When wet wraps were applied for only a 12-hour period, 1% hydrocortisone and
emollients were used during the non-wet wrap period. Both treatment groups demonstrated
improvement in overall SCORAD scores; however, there was no significant difference
between the conventional and WWD treatment groups. Five out of 23 (22%) children in the
WWD treatment group required antibiotics for skin infections, as compared to none of the
children in the conventional treatment group. The authors conclude that 4-weeks of
maintenance WWD treatment may be associated with more skin infections than
conventional treatment. (Hindley et al. 2006) However, it is important to realize that in
clinical practice, physicians usually do not use WWD for maintenance therapy of AD over a
4-week duration. Instead, physicians are more likely to use WWD in settings of acute
generalized eczematous flares for 3-7 days to induce disease remission. (Williams 2006) Lee
et al. (2007) examined the therapeutic efficacy of WWD and the mechanism behind its
therapeutic efficacy in treatment of AD. Ten patients with severe AD received WWD
(without steroid treatment) for 7–14 days. SCORAD was used to assess AD severity,
immediately following the end of treatment and 7 days after termination of treatment.
Transepidermal water loss, water content in the corneum, and lipid amount of skin surface
were also measured. The SCORAD was significantly reduced after WWD therapy.
Additionally, epidermal water content was increased and transepidermal water loss was
decreased following WWD therapy; these results were maintained 1 week after terminating
therapy. In atopic lesions, increased release of lamellar bodies and restoration of
intercellular lipid lamellar structure was observed. The authors speculated that increased
secretion of lamellar bodies induced with WWD occlusion may lead to recovery of the
abnormal epidermal barrier and clinical improvement in AD. (Lee et al. 2007)
In a clinical study of six children with moderate to severe AD, Hon et al. (2007) tested the
efficiacy of WWD occlusion using Tubifast® garments with mometasone furoate 0.1%
cream. Short-term use of WWD occlusion over 3 days demonstrated improvement in disease
severity based on SCORAD. In addition, a wrist motion monitor was used to measure
nocturnal itch, which showed that average scratching activity was significantly reduced by
20–60% on day 3 of treatment. Furthermore, WWD was effective in improving quality of life
in these children. (Hon et al. 2007)
Since its introduction by Goodyear et al. (1991) nearly two decades ago, WWD occlusion has
been extensively used as a relatively safe and effective treatment modality for children with
acute erythrodermic AD and those with severe and/or refractory AD. The most effective
topical corticosteroid to be used is still uncertain, but 10% dilutions of potent topical
corcorticosteroid are most commonly used. Protocols on adminstration and duration of
WWD occlusion can vary between studies. (Oranje et al. 2006) (See Table 3)
Advantages of WWD occlusion include a rapid therapeutic response, reduction in itch and
sleep disturbances, and a possible decreased topical corticosteroid use. Disadvantages
include high cost, the need for specialized training, increased potential for topical
corticosteroid absorption, and increased incidences of folliculitis and other cutaneous
infections. (Oranje et al. 2006)
However, the application of WWD has become less time-consuming and more feasible for
home use with development of Tubifast® garments manufactured by Medlock Medical®

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(available since 2003). With the introduction of these garments, wet wrapping can be done in
20–25 minutes. Tubifast garments® are available as tights for babies aged 6–24 months, vests
for children 6 months through 14 years, and socks and leggings in all sizes. These washable
garments are absorbent, holding enough water to remain moist for hours, and are elastic
and able to conform to the contours of the body. (Page 2005)

1. Choose the appropriate width of the tubular bandages and cut these to size to fit
the affected body areas (i.e. arms, legs, trunk). Alternatively, Tubifast® garments
can be used.
2. Apply the appropriate dilution of topical corticosteroids (e.g. fluticasone propionate
0.05% cream, mometasone furoate 0.1% cream) on the involved skin. In general, diluted
steroids in emollients of 1:9 are applied to the face of all patients and body of infants,
while diluted steroids in emollients of 1:9 or 1:3 are applied on the body of adults.
3. Wet the pieces of tubular bandage in lukewarm water. Alternatively, if Tubifast®
garments are used, then the inner garment is moistened using a plant sprayer.
4. Apply the first layer of wet tubular bandages. Connect the arm and leg pieces to the
trunk. Apply the facial mask, if necessary. Alternatively, if Tubifast® garments are
used, the inner garment is moistened using a plant spray.
5. Apply the second layer of dry tubular bandage. Again, connect the arm and leg
pieces to the trunk. Apply the facial mask, if necessary. Alternatively, if Tubifast®
garments are used, a second dry Tubifast® garment is placed over the wet one.
6. Re-wet the tubular bandages every 2-3 hours. Alternatively, if Tubifast® garments
are used, re-wet the inner Tubifast® garment every 2-3 hours.
7. Repeat procedures #1-6 (described above) daily.
8. After 7 days of occlusive therapy, the dilution of topical corticosteroids (e.g.
fluticasone propionate 0.05% cream, mometasone furoate 0.1% cream) is applied on
the involved skin for 4-7 consecutive days.
Table 3. Protocol for Wet Wrap Dressing occlusion
Finally, in a review article, Devillers and Oranje (2006) made the following conclusions
regarding WWD occlusion with a grade C of recommendation. 1) WWD using cream or
ointment and a double layer of cotton bandages, with a moist first layer and a dry second
layer, is an efficacious short-term treatment for children with severe and/or refractory
AD.2) The use of WWD with diluted topical corticosteroids is a more efficacious treatment
than wet-wrap dressings with emollients only for children with severe and/or refractory
AD. 3) The use of WWD with diluted topical corticosteroids is a safe intervention treatment
for children with severe and/or refractory AD for up to 14 days, with temporary systemic
bioactivity of the corticosteroids as the only reported serious adverse effect. 4) Lowering the
absolute amount of applied topical corticosteroid to once daily application and further
dilution can reduce potential risks. (Devillers and Oranje 2006)

3.2 Dry wrap dressings

DWD occlusion in AD has been less well studied (Table 4). Specifically, Rajka et al. (1981)
examined the effect of dry occlusion on skin microbial flora. Occlusion using plastic film was
applied to 10 patients with AD. A significant increase in the density of S. aureus was observed
after 24 hours of dry occlusion. Notably, 2 of the 10 patients had tiny pustules or crusts
following dry occlusion. But, there were no reports of AD exacerbation. (Rajka et al. 1981)

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Table 4. Outcomes of Studies on Dry Wrap Dressing Occlusion

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Geraldez et al. (1989), in a randomized controlled study of 60 patients with lichen simplex
chronicus, observed more infections and other adverse events in patients treated with
diflucortolone valerate 0.3% ointment under occlusion as compared those treated without
occlusion. Among the patients using dry occlusion, 2 patients (7%) developed pustular
lesions surrounding the affected sites, one (3%) had erythema, and one (3%) had
hyperpigmentation. None in the control group experienced any side effects. The control
group also reported greater improvements in both pruritus and lichenication. The authors
noted that the difference in the observed efficacy may be due to poorer absorption of the
ointment that tended to adhere to the plastic occlusive material. Furthermore, the adverse
events seen in the treatment group may have resulted from the combination of both the
ointment vehicle and the nature of the plastic occlusive material that created an over-
occlusive environment, thereby favoring microbial proliferation and/or contact
sensitization. (Geraldez et al. 1989)
Volden et al. (1992) treated 48 patients with chronic, therapy-resistant AD, with once-weekly
application of clobetasol propionate lotion under hydrocolloid (Duoderm) occlusive
dressings. Of the 48 patients, 44 (92%) had complete resolution of lesions, and 4 (8%) had
partial response (defined as >50% clearance). There were also 2 (4%) patients with mild
folliculitis. The authors conclude that adverse events were both mild and infrequent.
(Volden 1992)
Gauger et al. (2003) further addressed the concern of skin colonization with S. aureus using
occlusion therapy for AD. A side-to-side comparative study of 15 patients with generalized
or localized AD was performed, in which the flexures of the elbows were covered with
silver-coated textiles on one arm and cotton on the other arm for one week. The study found
a significant decrease in S. aureus colonization on the lesions covered with silver-coated
textile just 2 days after initiation of therapy and lasting until the end of the treatment.
Additional, a significantly less amount of S. aureus was observed on the silver-coated textile
sites than the cotton sites at the end of the treatment. Clinical improvement further
correlated with the reduction of bacterial colonization. Thus, the silver-coated textile
appeared to not only improve active lesions of AD, but also mitigate the potential pro-
microbial effects of dry occlusion alone. (Gauger et al. 2003)
Ultimately, DWD occlusion appears to improve disease severity and is perhaps most
beneficial in chronic treatment-resistant eczematous lesions. However, there is too little data
to determine whether occlusion, in particular DWD occlusion, predisposes skin bacterial
growth. But, it seems reasonable to conclude that the addition of antimicrobial topical
agents (e.g. antiseptic or silver preparations) to occlusive therapy might be helpful in
countering the potential risk of infection. (Abeck et al. 1999; Gauger 2006)

3.3 Hydrogel patch

In a pilot study of 15 patients, Park et al. (2011) evaluated the efficacy and safety of a
hydrogel patch for AD treatment. The hydrogel patch used in this study was composed of
an adhesive, thin, flexible, hydrogel layer on an impermeable urethane surface. Unlike
hydrocolloid dressings (e.g. Duoderm) with low water content, the hydrogel patch
consisted of approximately 50% water. In this 6-week study, patients applied the hydrogel
patch over one lesion for 6-8 hours daily and triamcinolone (TAC) 0.1% cream twice daily
to another lesion. Erythema, induration, lichenification, excoriation, and total EASI scores
significantly improved compared to baseline in both the hydrogel patch and TAC groups.

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Improvement in pruritis was observed in both treatment groups, but was only statistically
significant in the TAC group. At week 4, there was no significant difference in all sub-
scores between the patch and TAC groups (except pruritus, as stated above).
Improvement was maintained after discontinuing treatment for 2 weeks. No adverse
events from steroid use occurred. This study appears to demonstrate that instant
correction of the dysfunctional skin barrier with the hydrogel patch can improve signs
and symptoms of AD comparable to TAC 0.1% cream. Thus, the hydrogel patch may
provide a new approach to occlusive therapy without the potential risks of topical
corticosteroid use (Park et al. 2011)

3.4 Cutaneous and systemic side effects

Topical corticosteroid use can cause both cutaneous and systemic side effects, most
significantly laboratory adrenal insufficiency. Risk factors include the use of high potency
corticosteroids, occlusive or prolonged therapy, and application to thin- or barrier-
compromised skin lesions. (Levin and Maibach 2002) Occlusive therapy with topical
corticosteroids does not appear to be associated with an increased incidence of local non-
infectious side effects, such as skin atrophy and striae. This is most likely because nearly all
studies have examined limited treatment durations and diluted topical corticosteroids.
However, several studies demonstrated either lowering of morning cortisol levels
(Hartmann and Lahmann 1977; Goodyear et al. 1991), loss of diurnal cortisol rhythm
(Hartmann and Lahmann 1977), or overt laboratory HPA suppression with WWD
(Wolkerstorfer et al. 2000; Devillers et al. 2002). Importantly, nearly all cases of decreased
cortisol levels proved to be transient, returning to normal ranges within weeks of
discontinuing therapy.
Specifically, Goodyear et al. (1991) found that 0900 hour cortisol levels were suppressed
immediately after treatment with WWD, but returned to normal 2 weeks following therapy.
Following this observation by Goodyear et al. (1991) of a transient lowering of morning
cortisol levels (Goodyear et al. 1991), Wolkerstorfer et al. (2000) decided to examine the
effects of different corticosteroid dilutions under WWD occlusion on HPA axis supression
in children with severe refractory AD. Only 3 out of the 18 children in the first treatment
group (i.e. 50% dilution of FP cream) and none of the 5 children in the second treatment
group (i.e. 10%, 25% and 50% dilutions of FP cream) demonstrated HPA axis suppression
based on 0900 hour serum cortisol measurements following 2 weeks of WWD occlusion.
In the third treatment group (i.e. 0%, 5%, 10%, or 25% dilutions of FP cream applied to the
whole body), children demonstrated HPA axis suppression based on 0600 hour serum
cortisol measurements, which was associated with the absolute amount of applied
corticosteroid. To be more specific, a dose–response relationship was observed with an
absolute amount of topical corticosteroid applied. Patients using 800 µg m-2 daily
(equivalent to 1.6 g FP 0.05% cream) had an approximately 80% improvement, while
patients using absolute amounts >957 µg m-2 daily had no greater improvement. Patients
using absolute amounts ≤800 µg m-2 daily had no suppression of the HPA axis. This
suggests that weaker dilutions of topical corticosteroid may have a lower risk of HPA axis
suppression, while still maintaining comparable efficacy to more potent dilutions of
topical corticosteroid. (Wolkerstorfer et al. 2000)
Similarly, Devillers et al. (2002) found a significant decrease in early-morning serum cortisol
levels following 1-week of inpatient WWD therapy. Transient cortisol levels below the
normal range were observed after 4 days in 3 children and after one week in 2 adults. One

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Occlusive Therapy in Atopic Dermatitis 283

adult, who also taking inhaled steroids, developed prolonged suppression of the HPA axis,
in combination with several abdominal striae. (Devillers et al. 2002)
As for the effect of occlusive therapy using topical corticosteroids on bone development,
McGowan et al. (2003) examined short-term growth and bone turnover in prepubertal
children undergoing WWD occlusion for AD. Knemometry, a technique estimating the
distance between the heel and knee of the sitting child, was used as a non-invasive
measurement of lower leg length, in combination with 24-hour urinary deoxypyridinoline
excretion to evaluate bone turnover. Lower leg length and urinary deoxypyridinoline
levels for all children remained similar in pre-treatment measurements and during
therapy. This suggests that WWD occlusion for a limited duration does not impact growth
parameters. (McGowan et al. 2003)

4. Occlusion in clinical practice

Occlusive therapy, in particular WWD occlusion, can be useful as a ‘stepped-up’ therapy in
controlling acute erythrodermic AD or as a second-line therapy for severe and/or refractory
disease. There is limited convincing data that WWD occlusion is superior to conventional
open application of topical corticosteroids. However, occlusive therapy represents an
important alternative to currently available, but often undesirable standard treatment
modalities for AD. A few drawbacks of standard therapies include dependency on super-
potent topical corticosteroids, frequent and inconvenient sessions of phototherapy, and serious
systemic side effects with oral medications (e.g. nephrotoxicity with cyclosporine use).
Based on the studies on occlusive therapy, it appears that the greatest benefits of topical
corticosteroids under occlusion is achieved during the first week of therapy. This suggests
that if used as ‘rescue’ therapy for acute flares or intermittently for maintenance, durations
of up to 1 week might be adequate (Wolkerstorfer et al. 2000; Pei et al. 2001). Anecdotally,
long-term effects are thought to be sustained when WWD occlusion are continued with
emollients for 2–4 more weeks to improve skin hydration (Nicol 1987). Variations in
protocol regarding duration of WWD occlusion and rewetting procedures possibly
contributed to differences observed in efficacy and incidence of infection. It may, therefore,
be advisable to limit occlusion to less than 8 hours duration, apply WWD no more than
twice daily, and avoid rewetting procedures.
It is difficult to ascertain the extent to which occlusion may promote bacterial colonization.
However, the use of anti-bacterial agents, when applied alone or under occlusion, appears
to not only inhibit bacterial colonization, but also reduce disease severity. (Abeck et al. 1999;
Brockow et al. 1999; Gauger 2006) Thus, it seems logical that antibacterials, whether topical
or systemic, might be a beneficial adjunct to occlusive therapy helping to decrease the
potential risk of clinical infection. As such, topical antibacterials in combination with topical
corticosteroids under occlusion may be useful when treating small areas of skin for a limited
period of time, while systemic antibacterials in combination with topical corticosteroid
under occlusion may more be appropriate when treating larger areas of involvement. Yet,
the use of antibacterials must be weighed against the potential risk of antimicrobial
resistance and contact sensitization. (Williams 2000; Zhai and Maibach 2001)
More specifically, according to Williams (2000), there are three categories of patients with AD:
1) those with obvious clinical infection, in whom anti-staphylococcal therapy is essential, 2)
those with mild disease and a lower density of S. aureus colonization, in whom no evidence
supports additional benefit of anti-staphylococcal therapy, and 3) those with fissured or

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284 Atopic Dermatitis – Disease Etiology and Clinical Management

cracked eczema without overt signs of infection such as crusting or folliculitis. (Williams 2000)
While the latter group of patients carry an intermediate to high levels of S. aureus, studies are
contradictory regarding the clinical benefits of anti-staphylococcal therapy in these patients.
Clinicians may choose to institute antimicrobial therapy, in combination with topical
corticosteroids under occlusion. If poorly responsive to WWD occlusion, addition of
corticosteroid with topical or oral antibiotics has been helpful anecdotally, suggesting that
subclinical infection or heavy colonization may impede response to topical corticosteroids.
(Nicol 1987) Despite half a century of topical corticosteroid use in eczematous skin, the clinical
criteria for the addition of a topical antimicrobial agents remains to be determined.
In terms of the concern for adrenal suppression with topical corticosteroids under occlusion,
the minimal available data suggests that a decrease in cortisol levels can occur, but these
effects are generally transient. The use of mid- or high-potency corticosteroid, an ointment
vehicle, occlusion, and a disrupted skin barrier are all contributing factors that can increase
the risk of systemic side effects including this possibilty of adrenal suppression. Of note,
there has been only one suggested fatal case of adrenal insuffiency from topical
corticosteroid use. However, the details of this case are limited. It is known that the patient
was an 11-year old girl with generalized psoriasis being treated with betamethasone cream
under occlusion for a prolonged durations. However, the concentration and the exact
quantity of betamethasone cream applied, as well as the duration of therapy are unknown.
(Levin and Maibach 2002)
Several strategies may be used to limit the potential for such complications. Possible options
include using occlusive therapy only intermittently, reducing topical corticosteroid potency
gradually as inflamed skin improves, and applying occlusion only once-daily. Studies have
demonstrated that twice-daily application of topical corticosteroids to be no more effective
than once-daily regimens and more prone to systemic side effects. (Lagos and Maibach 1998;
Green et al. 2005) In addition, diluting topical corticosteroids may be helpful in reducing the
risk of serious side effects. However, such preparations may alter the physiochemical
properties of the agent and may not serve to reduce disease activity. (Haigh and Smith 1991;
Gao and Li Wan Po 1994; Ohtani et al. 2002; Kizu et al. 2004) Furthermore, the application of
a hydrogel patch, which appeared to have similar efficacy as topical corticosteroid use, may
potentially serve as an ideal method of treating AD while avoiding topical corticosteroids.
(Park et al. 2011) But, additional studies on the efficacy of the hydrogel patch in the
treatment of AD are needed. Ultimately, if prolonged topical corticosteroid use is required
in certain patients with refractory disease, adrenal function may be monitored using
morning plasma cortisol and urinary steroid levels, in combination with rapid ACTH
stimulation testing, while evaluating the patient for cutaneous atrophy or Cushingoid
features (Levin and Maibach 2002). But, the rare occurence of topical corticosteroid-induced
Addison’s disease makes this suggestion impractical for most patients.
Topical immunosuppressive agents such as pimecrolimus or tacrolimus under occlusion
have not yet been studied extensively. These agents might represent a valuable non-
steroidal alternative, though systemic absorption should be measured to confirm that
immunosuppressive levels have not been reached. An open-label study evaluating topical
pimecrolimus cream 1% in the treatment of chronic hand dermatitis showed that twice-daily
application under occlusion was safe and effective, resulting in low pimecrolimus blood
levels. (Thaci et al. 2003) Beyeler et al. (2006) reported a case of a female patient treated with
tacrolimus 0.1% ointment under occlusion with Unna’s paste boots (zinc bandages), whose

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Occlusive Therapy in Atopic Dermatitis 285

serum levels had reached 12.9 μg/l after 5 days of treatment, corresponding to high-dose
immunosuppression. Beyeler et al. (2006) attributed the increased systemic absorption to the
combination of severely damaged skin barrier function, application of tacrolimus to a large
surface area, and occlusion under zinc bandages. (Beyerler et al. 2006)
The wide variation in occlusive techniques and predominance of uncontrolled trials with
small sample sizes make direct comparison of studies evaluating the safety and efficacy of
occlusive therapy difficult. Limited numbers of studies using control groups restricts the
conclusions that can be drawn regarding the benefit of occlusive therapy versus
conventional therapies. However, it can be concluded that occlusive therapy has been
shown, both formally and anecdotally, to be very effective in severe or exacerbated AD. It,
therefore, offers an important alternative or adjunct therapy to more commonly used
approaches. The randomized controlled trials described in this chapter resulted in divergent
outcomes regarding infectious complications and efficacy. Differences could be related to
the study populations (i.e. exacerbated versus moderate AD) or different topical
corticosteroid application regimens.
While the exact mechanism of action of occlusive therapy is still unknown, a recent pilot
study demonstrated significant down-regulation of 7 serum chemokines following WWD
occlusion for 1 week in 6 children with severe AD. Of these, 4 chemokines are considered to
be potential serum markers for the disease activity of AD. (Ong et al. 2008) In another study
evaluating WWD occlusion using diluted tacrolimus and fluticasone propionate cream in
APOC1 mice with AD, WWD occlusion improved transepidermal water loss, reinforcing
that this may be one of the therapeutic aspects of occlusive therapy. (Oranje et al. 2009)
Future studies should evaluate the efficacy of occlusive therapy versus open topical
corticosteroid application with measurements on the differences in systemic absorption.
Studies should also investigate the impact of varying the durations of occlusive therapy.
Given the number of protocols utilizing inpatient or specialized nurse-assisted visits, it
would be useful to understand the contribution of professional supervised application. To
our knowledge, no studies to date have evaluated occlusion as preventive therapy (i.e., to
prevent disease flares and maintain cutaneous hydration).

5. Conclusion
WWD occlusion may be a reasonable first-line therapy for acute exacerbations of AD and
second-line therapy for refractory disease. DWD occlusion appears to be efficacious having
relatively low risk of infectious complications and may be particularly useful in treatment of
chronic AD lesions. However, it remains unclear if occlusive therapy offers significant
advantageous over conventional open therapy. The risk of infection associated with
occlusive therapy, while greater than open therapies, seems to be manageable and may be
mitigated by limiting the duration of occlusion, avoiding rewetting and perhaps adding
antibacterial agents. Transient changes in morning cortisol levels and rare clinical HPA
suppression seen with the use of topical corticosteroids under occlusion are concerning side
effects, but are likely related to corticosteroid potency and the absolute amount applied. The
hydrogel patch offers an innovative approach to the treatment of AD instantly correcting the
barrier defect, and it may have similar efficacy as topical corticosteroids without the
systemic risks. Further controlled studies are needed to better evaluate the risks and benefits
of these occlusive modalities in the treatment of AD.

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286 Atopic Dermatitis – Disease Etiology and Clinical Management

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Hartmann, F. and J. J. Lahmann (1977). Effect of the external use of triamcinolone acetonide
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 Atopic Dermatitis - Disease Etiology and Clinical Management
Edited by Dr. Jorge Esparza-Gordillo

ISBN 978-953-51-0110-9
Hard cover, 414 pages
Publisher InTech
Published online 22, February, 2012
Published in print edition February, 2012

Atopic Dermatitis is a common disease characterized by inflamed, itching and dry skin. This relapsing allergic
disorder has complex etiology and shows a remarkably high clinical heterogeneity which complicates the
diagnosis and clinical management. This book is divided into 4 sections. The first section (Disease Etiology)
describes some of the physiological mechanisms underlying Atopic Dermatitis, including alterations in the
immune system and the skin-barrier function. The important role of host-microorganism interactions on the
pathophysiology of Atopic Dermatitis is discussed in the second section (Microorganisms in Atopic Dermatitis).
An overview of the clinical diagnostic criteria and the disease management protocols commonly used is given
in the third section (Diagnosis and Clinical Management). The last section (New Treatments) describes new
therapeutic approaches that are not widely used but are currently being studied due to preliminary evidence
showing a clinical benefit for Atopic Dermatitis.

How to reference
In order to correctly reference this scholarly work, feel free to copy and paste the following:

Misha M. Heller, Eric S. Lee, Faranak Kamangar, Wilson Liao and John Y. M. Koo (2012). Occlusive Therapy
in Atopic Dermatitis, Atopic Dermatitis - Disease Etiology and Clinical Management, Dr. Jorge Esparza-Gordillo
(Ed.), ISBN: 978-953-51-0110-9, InTech, Available from: http://www.intechopen.com/books/atopic-dermatitis-
disease-etiology-and-clinical-management/occlusive-therapy-in-atopic-dermatitis

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