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Usefulness of Sweat Management for Patients with Adult Atopic Dermatitis, regardless of Sweat Allergy: A Pilot Study

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Background . Sweat is an aggravating factor in atopic dermatitis (AD), regardless of age. Sweat allergy may be involved in AD aggravated by sweating. Objective. We investigated whether sweat exacerbates adult AD symptoms and examined the extent of sweat allergy’s involvement. Method. We asked 34 AD patients (17 men, 17 women; mean age: 27.8 years) to record the extent to which sweat aggravated their symptoms on a 10-point numerical scale. Participant responses were compared with histamine release tests (HRT). Furthermore, 24 of the patients received instructions on methods of sweat management, and their outcomes were evaluated on a 10-point scale. Results. Sweat HRT results were class ≥ 2 in 13 patients, but HRT results were not correlated with the patients’ self-assessments of symptom aggravation by sweat. One month after receiving sweat management instructions, a low mean score of 4.6 was obtained regarding whether active sweating was good, but a high mean score of 7.0 was obtained in response to whether the sweat management instructions had been helpful. Conclusion . Our investigation showed that patients’ negative impressions of sweat might derive from crude personal experiences that are typically linked to sweating. Sweat management for patients with adult atopic dermatitis was extremely useful regardless of sweat allergy.
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Research Article
Usefulness of Sweat Management for Patients with Adult Atopic
Dermatitis, regardless of Sweat Allergy: A Pilot Study
Sakae Kaneko,1Hiroyuki Murota,2Susumu Murata,1Ichiro Katayama,2and Eishin Morita1
1Department of Dermatology, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo, Shimane 693-8501, Japan
2Department of Dermatology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
Correspondence should be addressed to Sakae Kaneko; kanekos@med.shimane-u.ac.jp
Received  June ; Revised  December ; Accepted  December ; Published  January 
Academic Editor: Adam Reich
Copyright ©  Sakae Kaneko et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background. Sweat is an aggravating factor in atopic dermatitis (AD), regardless of age. Sweat allergy may be involved in AD
aggravated by sweating. Objective. We investigated whether sweat exacerbates adult AD symptoms and examined the extent of sweat
allergy’s involvement. Method. We asked  AD patients ( men,  women; mean age: . years) to record the extent to which
sweat aggravated their symptoms on a -point numerical scale. Participant responses were compared with histamine release tests
(HRT). Furthermore,  of the patients received instructions on methods of sweat management, and their outcomes were evaluated
on a -point scale. Results. Sweat HRT results were class in  patients, but HRT results were not correlated with the patients’
self-assessments of symptom aggravation by sweat. One month aer receiving sweat management instructions, a low mean score
of . was obtained regarding whether active sweating was good, but a high mean score of . was obtained in response to whether
the sweat management instructions had been helpful. Conclusion. Our investigation showed that patients’ negative impressions of
sweat might derive from crude personal experiences that are typically linked to sweating. Sweat management for patients with adult
atopic dermatitis was extremely useful regardless of sweat allergy.
1. Introduction
Atopic dermatitis (AD) is a chronic relapsing eczematous
skin disease characterized by pruritus and inammation and
is accompanied by cutaneous physiological dysfunction [].
Numerous AD-triggering factors are known, such as irritants,
aeroallergens, food, microbial organisms, and sweat/sweating
[]. Skin testing with autologous sweat is positive in most
patients with AD [, ], and the clinical symptoms of children
with AD improve signicantly during the summer if they
take showers at school [, ]. Semipuried sweat antigen
from normal adults induced histamine release from the
basophils of % of patients with AD and % of patients
with cholinergic urticaria in Japan [, ]. e histamine
releaseinducedbysemipuriedsweatantigenismediated
by specic immunoglobulin E (IgE) [, ]. Sweat histamine
release tests (HRTs; Allerport, Kyowa Medex Co., Ltd.,
Tokyo, Japan) are covered by the Japanese health insurance
system.emainsweatantigenisMGL, produced as
a minor immunological antigen of Malassezia globosa with
posttranslational modication, cleaved, and secreted as a
 kDa major histamine-releasing sweat (Malassezia) antigen
[].
In the present study, we investigated whether sweat plays
a role in exacerbating adult AD symptoms and examined the
extent to which sweat allergy is involved.
2. Materials and Methods
2.1. Subjects. All patients were recruited from Shimane Uni-
versity Hospital between April  and March  before
they start sweating. We enrolled  patients with AD that was
diagnosedfollowingtheJapaneseDermatologicalAssocia-
tions criteria. e  enrolled patients included  men and 
women (mean age, . years; mean serum IgE,  IU/mL)
who received an HRT (Allerport, Kyowa Medex Co., Ltd.,
Tokyo, Japan). Histamine release percentage was (antigen
specic histamine release amount nonspecic histamine
release amount)/(total histamine release amount nonspe-
cic histamine release amount) ×. HRT class does not
Hindawi
BioMed Research International
Volume 2017, Article ID 8746745, 4 pages
https://doi.org/10.1155/2017/8746745
BioMed Research International
exceed histamine release cuto (histamine release percentage
%) stimulated by any antigen concentration sample. HRT
class exceed histamine release cuto stimulated by the
darkest antigen concentration sample. HRT class exceed
histamine release cuto stimulated by the darkest antigen
sampleandseconddarkantigenconcentration.HRTclass
exceed histamine release cuto stimulated by the darkest
antigen sample, second dark antigen, and third dark antigen
concentration. HRT class exceed histamine release cuto
stimulated by the thinnest antigen concentration sample.
Eczema Area and Severity Index (EASI) developed by the
EASI Evaluator Group (maximum  points) is used in this
study [].
2.2. Study Design. We asked the AD patients to record
the extent to which sweat aggravated their symptoms. e
participants recorded their responses using a -point numer-
ical scale, on which a score of  indicated that sweat was
the greatest aggravating factor. Participant responses were
compared with the classes of results obtained from the HRT
of blood samples.
In a second component to this study, we also instructed
 of the patients on methods of dealing with sweat (sweat
management). We subsequently evaluated the outcomes of
this instruction on a -point numerical scale. is study was
approved by the ethical committee of Shimane University and
thedeanoftheFacultyofMedicine(approvalnumber).
Inthecourseofoursweatmanagementinstructions,we
explained that it was ne to sweat profusely but additionally
requested that patients do at least one of the following: ()
shower at least once during the day (as soon as they sweat,
not since they came home), () wash the aected areas of
their skin with water, () apply wet wipes made of so
dough to irritated parts of their skin, and/or (4)change
their clothes when they became soaked with sweat. One
month aer this sweat management instruction, its outcomes
were determined via a questionnaire that used a -point
numerical scale.
2.3. Statistical Analysis. Spearman’s rank correlation test was
used to compare variables between groups. All analyses
were performed using STATA version (StataCorp, College
Station, TX, USA). A 𝑝value <. was considered statisti-
cally signicant. Continuous values are reported as means ±
standard deviations.
3. Results
In the HRT positive control test (anti-IgE antibody), of the
 participants tested negative and were excluded from the
analysis; both these participants were women. A mean sweat
HRT class of 1.44 ± 1.61 was recorded. During treatment,
patients were asked to respond to the following question
on a scale of – with a score of  indicating the greatest
degree of aggravation: “To what extent does sweat aggravate
your symptoms?” e mean of the patient scores was 5.85 ±
2.43. Blood was also collected, and correlations between the
original HRT results for sweat and patient responses were
Large
Small
0
2
4
6
8
10
01234
Contribution of sweat on
symptom aggravation
HRT class
F : e relationship between patients’ perceived symptom
aggravation due to sweat and histamine release test (HRT) results
(𝑁=32). Spearman’s rank correlation coecient revealed no
correlations (rs = −0.102,𝑝 = 0.286).
tested using Spearman’s rank correlation coecient. As can
be seen in Figure , no correlation was observed.
Subsequently,  of the patients received guidance about
the importance of sweating as a bodily function, having the
opportunity to sweat on a daily basis, and taking measures
to prevent excess sweat on the skin. Regarding the patients’
motivations to sweat on a daily basis, of the  participants
(one-third of the group) consciously worked up a sweat. With
regard to avoiding excess sweat on the skin,  patients took
showers, washed the aected areas with water, and used
wipesoneasilyaggravatedareas.
Onemonthaereducationonsweatmanagementwas
provided, patients were asked to rate the following two
statements. e rst statement was “It was good to sweat,”
for which a mean response score of 4.63 ± 2.20 was recorded.
e second statement was “e countermeasures for sweating
were helpful, for which the mean score was 7.04 ± 1.73.
Spearmans rank correlation test showed a positive correlation
between these values (Figure ). But there was no signicant
relation of EASI between before and aer education on sweat
management (𝑁=24:before10.8± 4.8,aer10.7±5.2). e
reasonmightbethatpatientsweremildcasesandobservation
period was short.
Furthermore, a negative correlation was found between
the patients’ impressions of sweating and the results of
the sweat HRT (Figure ). Patients with high HRT results
(positive reaction against semipuried protein derived from
healthy adults) did not have a favorable impression of sweat-
ing. However, many patients still thought that our sweating
education was helpful (Figure ), and no correlation was
found between HRT class and patients’ impressions of the
measures against excess sweat on the skin (Figure ).
4. Discussion
Patients may oen be directed to avoid sweating based on the
belief that sweat is an exacerbating factor for AD. Sweating
plays key roles in skin homeostasis, antimicrobial [], and
moisturizing eects [] and in skin surface pH regulation
BioMed Research International
0
2
4
6
8
10
0246810
Favorable
Bad
Favorable
Bad
Impact of sweat management
Impact of sweating on symptoms
F : e relationship between perception of sweat and the
degree of helpfulness provided by sweat management instructions at
month aer the instructions (𝑁=24). Spearman’s rank correlation
test showed a strong correlation between these values (rs = 0.348,
𝑝 = 0.0475).
Favorable
Bad
0
2
4
6
8
10
01234
HRT class
Impact of sweating on symptoms
F : e relationship between human sweat histamine release
test (HRT) class and the perception of sweat at month aer sweat
management (𝑁=23). Spearman’s rank correlation test indicated a
signicant correlation (rs = −0.411,𝑝 = 0.0271).
[]. Skin care with daily showering at an elementary school
was found to be eective for the treatment of atopic dermatitis
[]. However, few studies have evaluated the impact of sweat
education on the awareness of patients with AD. erefore,
we conducted a pilot study to investigate the impact of
educationonsweating.Wefoundnocorrelationbetween
the result of HRTs against sweat antigen and the degree
of a bad impression of sweat. Additionally, there was no
evident correlation between the degree of a bad impression
of sweat and the self-perceived extent of sweating aer
sweat management (Spearmans rank correlation test: rs =
0.0323,𝑝 = 0.438). erefore, this does not indicate that
excess sweating aggravates the symptom of AD. We also
analyzed HRTs against sweat in the group that received
sweat management education. e measurement results of
HRTs were not aected by receiving sweat management
instructions (Spearmans rank correlation test: rs = 0.0131,
𝑝 = 0.498). In fact, patients with a bad impression of sweat
showed high HRT results.
However, many patients still thought that taking mea-
sures against excess sweating was good. Furthermore, no
correlation was found between the results of the HRT and
patients’ favorable impression of countermeasures against
sweating.us,weconcludedthatitwasworthwhileto
oer proper guidance about sweat to patients with AD.
Unexpectedly, several subjects in our study are likely to think
that sweating is good for relieving their skin symptoms.
is might further be interpreted as suggesting that sweating
could be a mitigating factor in some cases, rather than an
aggravating factor.
In addition, we administered a separate questionnaire
survey to patients. In this questionnaire, patients were asked,
“Have you received guidance on what you should do aer
sweating?” No bad impressions were found in taking mea-
sures to avoid sweat on the skin. We found that three-fourths
of those surveyed have in fact been given such advice [].
is result also indicates that patient guidance for sweating
management is quite important.
In general, sweat has been thought to aggravate AD
by allergic reaction against the Malassezia antigen or by
impaired skin homeostasis due to decreased sweating. Our
study found that patients’ impression of “sweat is bad”
might have come from crude personal experiences which are
ordinarily linked with sweating (e.g., associations between
sweating and hot environments, exercise, and nervousness).
5. Conclusions
Sweat management for patients with adult atopic dermatitis
was extremely useful, regardless of sweat (Malassezia) aller-
giesorbadimpressionforsweating.
Competing Interests
e authors declare no conict of interests.
Acknowledgments
is work was supported in part by Health and Labor
Sciences Research Grants (Research on Intractable Diseases)
fromtheJapaneseMinistryofHealth,LaborandWelfare.An
earlier version of this work was presented as an abstract at the
rd Eastern Asia Dermatology Congress, Jeju, .
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... exercise, walking, or bathing), but they should also rinse sweat off to not leave excessive sweat on the skin surface. Kaneko et al. investigated the impact of these instructions ("incorporating activities with sweating" and "rinsing sweat off") on patients' global assessment (n=23) (37). Results showed that approximately 25% of patients felt that following these instructions had a favorable impact on their symptoms. ...
... worsening of itching and dermatitis (37). Elucidation of the mechanism leading to disease aggravation by sweat is an urgent task to achieve long-term control of AD. ...
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... 26 Furthermore, patients with a high HRT classification displayed discomfort to sweating. 27 By contrast, no association between the ASwST and AD disease severity was reported. 4 In daily clinical practice, many AD patients complain of the worsening of their disease by sweating. ...
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... Sweat management in these children includes changing out of sweat-soaked clothes, gently wiping off excessive sweat using a soft damp towel, or quick showering soon after sweating, followed by emollient use. 52,53 Commercial wet wipes or "baby wipes" should be avoided due to increased risk for allergic contact dermatitis from fragrance and preservatives. ...
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... In fact, Kaneko et al. reported the usefulness of sweat management for patients with adult AD regardless of the reactivity in a sweat allergy test by using semi-purified sweat antigen. 40 The identification of such antigens in sweat should be the scope of future studies. ...
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Antimicrobial peptides are an integral part of the epithelial innate defense system. Dermcidin (DCD) is a recently discovered antimicrobial peptide with a broad spectrum of activity. It is constitutively expressed in human eccrine sweat glands and secreted into sweat. Patients with atopic dermatitis (AD) have recurrent bacterial or viral skin infections and pronounced colonization with Staphylococcus aureus. We hypothesized that patients with AD have a reduced amount of DCD peptides in sweat contributing to the compromised constitutive innate skin defense. Therefore, we performed semiquantitative and quantitative analyses of DCD peptides in sweat of AD patients and healthy subjects using surface-enhanced laser desorption ionization time-of-flight mass spectrometry and ELISA. The data indicate that the amount of several DCD-derived peptides in sweat of patients with AD is significantly reduced. Furthermore, compared with atopic patients without previous infectious complications, AD patients with a history of bacterial and viral skin infections were found to have significantly less DCD-1 and DCD-1L in their sweat. To analyze whether the reduced amount of DCD in sweat of AD patients correlates with a decreased innate defense, we determined the antimicrobial activity of sweat in vivo. We showed that in healthy subjects, sweating leads to a reduction of viable bacteria on the skin surface, but this does not occur in patients with AD. These data indicate that reduced expression of DCD in sweat of patients with AD may contribute to the high susceptibility of these patients to skin infections and altered skin colonization.
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Background: Sweat is a major aggravating factor of atopic dermatitis (AD) and approximately 80% of patients with AD show type I hypersensitivity against sweat. Objective: To identify and characterize an antigen in sweat that induces histamine release from basophils of patients with AD. Methods: Basophil histamine-releasing activity in sweat was purified by a combination of chromatographies, and proteins were analyzed with mass spectrometry. Recombinant proteins of the sweat antigen were generated, and their biological characteristics were studied by immunoblots, histamine release tests, and neutralization assays. Results: We identified a fungal protein, MGL_1304, derived from Malassezia globosa (M globosa) in the purified sweat antigen. Recombinant MGL_1304 induced histamine release from basophils of most of the patients with AD, in accordance with the semi-purified sweat antigen. Moreover, recombinant MGL_1304 abolished the binding of serum IgE of patients with AD to the semi-purified sweat antigen, or vice versa in immunoblot analysis, and attenuated the sensitization of RBL-48 mast cells expressing human FcɛRI by serum IgE. Studies of truncated mutants of MGL_1304 indicated that IgE of patients with AD recognized the conformational structure of MGL_1304 rather than short peptide sequences. Western blot analysis of the whole lysate, the culture supernatant of M globosa, and the semi-purified sweat antigen showed that MGL_1304 was produced as a minor immunological antigen of M globosa with posttranslational modification, cleaved, and secreted as a 17-kDa major histamine-releasing sweat antigen. Conclusion: MGL_1304 is a major allergen in human sweat and could cause type I allergy in patients with AD.
Article
Auteur(s) : Hiroyuki Murota, Aya Takahashi, Megumi Nishioka, Saki Matsui, Mika Terao, Shun Kitaba, Ichiro Katayama Department of Dermatology, Osaka University, 2-2, Yamadaoka, 565-0871 Suita, Japan Sweat is thought to exacerbate the symptoms of atopic dermatitis (AD) [1, 2]. It is known that the pH of sweat and skin surfaces increases with time [3]; thus, old sweat might cause skin barrier dysfunction and promote infection. Such susceptibility to environmental factors and infection are considered [...]
Article
Atopic dermatitis (AD) is a chronic relapsing eczematous skin disease characterized by pruritus and inflammation and accompanied by cutaneous physiological dysfunction (dry and barrier-disrupted skin). Most of the patients have atopic diathesis. A standard guideline for the management (diagnosis, severity classification and therapy) of AD has been established. In our guideline, the necessity of dermatological training is emphasized in order to assure diagnostic skill and to enable evaluation of the severity of AD. The definitive diagnosis of AD requires the presence of all three features: (i) pruritus; (ii) typical morphology and distribution; and (iii) chronic and chronically relapsing course. For the severity classification of AD, three elements of eruption (erythema/acute papules, exudation/crusts and chronic papules/nodules/lichenification) are evaluated in the most severely affected part of each of the five body regions (head/neck, anterior trunk, posterior trunk, upper limbs and lower limbs). The areas of eruption on the five body regions are also evaluated, and both scores are totaled (maximum 60 points). The present standard therapies for AD consist of the use of topical corticosteroids and tacrolimus ointment as the main treatment for the inflammation, topical application of emollients to treat the cutaneous physiological dysfunction, systemic antihistamines and anti-allergic drugs as adjunctive treatments for pruritus, avoidance of apparent exacerbating factors, psychological counseling and advice about daily life. Tacrolimus ointment (0.1%) and its low-density ointment (0.03%) are available for adult patients and 2-15-year-old patients, respectively. The importance of the correct selection of topical corticosteroids according to the severity of the eruption is also emphasized. Furthermore, deliberate use of oral cyclosporine for severe recalcitrant adult AD is referred.
Article
For elementary school children with atopic dermatitis, a skin care program using shower therapy was performed during the school lunch break for 6 weeks from June to July in 2004 and 2005. All 53 participants showed an improvement in their atopic dermatitis during the 6-week periods studied. Skin care with daily showering at an elementary school was thus found to be effective for the treatment of atopic dermatitis.
Article
We previously demonstrated that the semipurified human sweat antigen causes skin reactions and histamine release from basophils via specific IgE in patients with atopic dermatitis (AD). Patients with cholinergic urticaria (ChU) also develop skin reactions and histamine release of basophils in response to autologous sweat. To study whether or not patients with ChU share sensitivity for the sweat antigen with patients with AD and to study the clinical characteristics among patients with ChU and the relationship with histamine-release activity of basophils. The sweat antigen that induces histamine release from basophils of patients with AD was prepared by Con-A, anion-exchange and reverse-phase chromatography. Relationships between histamine-release activity against the sweat antigen and clinical features of patients with ChU were analysed. Twenty-three of 35 patients with ChU showed > 5% net histamine release in response to the semipurified sweat antigen, whereas none of healthy controls did so. In patients with ChU, histamine release in response to semipurified sweat antigen significantly correlated with the level of serum IgE and eosinophil numbers in peripheral blood. Incidence of each atopic disease in patients with ChU tended to be higher than in the general Japanese population. When the patients were categorized according to their responses in the histamine release test, the positive group tended to show a higher incidence of AD and bronchial asthma compared with the negative group. ChU and AD may share hypersensitivity to common antigens in sweat. The sweat allergy and atopic diathesis are associated with each other.
Of 45 patients with atopic dermatitis skin-tested with their own sweat, 43 showed positive immediate-type skin reactions to titres between 1 and 256. Of 22 non-atopic patients 18 showed negative reactions. Skin reactivity of the atopic patients to the sweat and house dust did not run parallel. Radioallergosorbent test (RAST) using the sweat collected from a healthy subject detected IgE antibody in 24 atopic patients with a score from 0.5 to 3.5, whereas all the control subjects showed the score 0. This IgE antibody to sweat did not cross-react with the mite extract (Dermatophagoides farinae) or Staphylococcus aureus. These results indicate that atopic patients have specific IgE antibody to sweat.
Article
Atopic dermatitis is a hereditary disorder, frequently associated with allergic rhinitis and bronchial asthma. The disease may be influenced by many triggering factors such as irritants, aeroallergens, food, microbial organisms, sex hormones, stress factors, sweating, and climatologic factors. Moreover, it is important to be aware of contact allergy as a complicating factor. This review deals with recent clinical, experimental, and some therapeutic data on these triggering factors.
Article
Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD). To examine the sweating function in AD in a quantitative manner. We investigated the sweating response of lesional and non-lesional skin of adult patients with AD by a quantitative sudomotor axon reflex test in which the axon reflex is stimulated by acetylcholine iontophoresis. Sweat volume on the volar aspect of the forearm was measured in 18 adult patients with AD and in 40 non-atopic controls; five patients with Sjögren's syndrome were also studied as disease comparators. We also evaluated the sweating function in four AD patients after topical corticosteroid therapy. Latency time, direct (DIR) sweat volume and axon reflex-mediated indirect (AXR) sweat volume were the variables studied. The latency time in AD patients was significantly prolonged and AXR sweat volume significantly reduced compared with those in non-atopic control subjects. The latency time and AXR sweat volume of lesional AD skin were significantly more prolonged and reduced, respectively, than those of non-lesional skin. In contrast, the DIR sweat volume of lesional or non-lesional AD skin induced by direct stimulation with acetylcholine was only slightly reduced when compared with that in non-atopic controls. Latency time and sweat volumes of lesional and non-lesional AD skin improved after topical corticosteroid therapy. These results suggest that the impaired sweat response in AD is attributable to an abnormal sudomotor axon reflex, which is reversed by topical corticosteroid administration.
Article
Sweating aggravates itch in atopic dermatitis, but the mechanism is unclear. In this study, we examined the involvement of type I hypersensitivity in the aggravation of atopic dermatitis by sweating. Skin tests with autologous sweat were positive in 56 of 66 patients (84.4%) with atopic dermatitis, but only in 3 of 27 healthy volunteers (11.1%). Sweat samples from both patients and healthy volunteers induced varying degrees of histamine release from basophils of patients with atopic dermatitis. However, the histamine release was impaired by removal of IgE on the basophils. Incubation of basophils with myeloma IgE before sensitization with serum of patients blocked the ability to release histamine-induced sweat. IgE antibody against antigen(s) in sweat may be present in serum of patients with atopic dermatitis. Key words: