THE STUDY OF STAPHYLOCOCCUS AUREUS’S SUPERANTIGENS AND TREATMENT FOR PATIENT WITH ATOPIC DERMATITIS BY CEFUROXIM

MINISTRY OF EDUCATION AND TRAINING MINISTRY OF HEALTH
HANOI MEDICAL UNIVERSITY
CHAU VAN TRO
THE STUDY OF STAPHYLOCOCCUS AUREUS’S
SUPERANTIGENS AND TREATMENT FOR PATIENT WITH
ATOPIC DERMATITIS BY CEFUROXIM
Specialist: Dermatology
Code: 62 72 01 52

SUMMARY OF THESIS
HANOI - 2013
This thesis was completed at: HANOI MEDICAL UNIVERSITY
Academic Advisor:
Ass.Prof TRAN LAN ANH, PhD
Ass.Prof NGUYEN TAT THANG, PhD
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The thesis was presented to Dissertation Committee of HaNoi
medical university
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May find the thesis in library:
STUDIES RELATING TO THESIS WERE PUBLISHED
1. Chau Van Tro, Nguyen Tat Thang, Tran Lan Anh (2011)
"Study of Staphylococcus aureus’s superantigens in adult
patient with atopic dermatitis", Journal of practical
medicine, 4 (760), pp. 122-126.

2. Chau Van Tro, Nguyen Tat Thang, Tran Lan Anh (2012),
"Evaluation of treatment adult patient with subacute atopic
dermatitis by cefuroxim combined with topical
corticosteroids ", Journal of practical medicine, 5 (821), pp.
108 - 112.
INTRODUCTION
Atopic Dermatitis (AD) or atopic eczema (AE) is a common
chronic inflammatory skin disease. The prevalence is from 10 to
20% of the children population. So far the causes and mechanisms
of pathogenesis of AD still has not completely understood. The
treatment of AD has a lot of difficulties. The disease is recurrences,
so the prevalence diseases tend to be on the increase.
In the late 20th century, Michael J. Cork, Abeck. D et al,
Shuichi Higaki has found that Staphylococcus aureus played a very
important role in the mechanism of pathogenesis of the disease.
The studies of Adachi. Y et al, Strange. P et al, Yudate. T et
al have shown that Staphylococcus aureus secretes the enterotoxines
serves as an superantigen in the mechanism of pathogenesis of AD.
According to Gong. J. Q et al, Breuer. K et al, superantigens of
Staphylococcus aureus may penetrate the skin barrier and contribute
to the persistence and exacerbation of allergic skin inflamation in
AD through the stimulation of massive T cells.
Until now, the treatment of AD is primarily used anti-
histamine, topical corticosteroids, topical tacrolimus, pimecrolimus
and skincare with moistures. The use of antibiotics when there are
bacterial superinfections so that effect of treatment is not good.
Study of Gong. J. Q et al also shows a new strategy in the treatment
of AD is the use of antibiotics as important component of the overall
management of AD.
RESEARCH OBJECTIVES

1. Survey clinical characteristics and related factors to adult
AD in hospital of Dermato-Venereology of Ho Chi Minh
City from 08/2010 to 08/2012.
2. Determinate Staphylococcus aureus infection and
Staphylococcus aureus 's superantigens genes on the atopic
dermatitis adult patients.
3. Evaluate the effectiveness of treatment of subacute phase
adult atopic dermatitis by cefuroxim combine with topical
betamethasone dipropionate 0.05%.
NEW CONTRIBUTIONS OF DISSERTATION
The dissertation proved Staphylococcus aureus has very
important role in the mechanism of pathogenesis of atopic dermatitis,
making the onset or affect the degree of severity of the disease.
The dissertation also proved the effectiveness of the use of
oral antibiotics anti – Staphylococcus aureus as a measure of the
combined in the treatment of atopic dermatitis.
STRUCTURE OF DISSERTATION
Dissertation consists of 111 pages, excluding appendices and
reference , including 4 chapters , 32 tables, 2 charts, 5 pictures, 6
diagrams, 157 references (17 Vietnamese references, 140 English
references) and addendum. The layout of the thesis consists of
introduction (2 pages), overview (33 pages), subjects and methods
(17 pages), results (29 pages), discussion (27 pages), conclusion (2
pages) and recommendation (1 page), and there are 2 articles related
to the thesis has been published.
CHAPTER 1: OVERVIEW
1.1 Atopic dermatitis
Atopic dermatitis is a very common disease in dermatology.
The prevalence is increasing especially in the industrialized
countries. The prevalence is from 10 to 20% of the children

population. Causes and mechanisms of pathogenesis remains
unclear, related to multi factors such as: genes, allergens, nerve,
endocrine, immune changes, climate, infection Clinical symptoms
are plentiful such as: itching, insomnia, erythema, papules, oozing,
crusts, lichenfication… There are three phases of atopic dermatitis:
acute phase, subacute phase, and chronic phase. Currently there are
many measures for treatment the AD but the effectiveness of the
treatment is not high. The disease often relapse and influence on the
quality of life of the patient. AD becomes the burden on the family
and society.
1.2 The role of Staphylococcus aureus in AD
On the skin of healthy people, the ratio of Staphylococcus
aureus is about 5%. On the AD patients, the ratio of Staphylococcus
aureus from 55-75% on the non - lesion skin, 85-90% on the chronic
lesions, 80-100% of the acute lesions. It also found that the density
of the Staphylococcus aureus on acute inflammatory lesions 1,000
times higher than on the non – lesion skin in AD patients. So the
skin of the AD patients is a favorable environment for development
of Staphylococcus aureus.
The exact mechanism of the increase the ratio and the
number of Staphylococcus aureus on skin of AD patients still is
unknown. It may be a combination of the following mechanisms:
Skin barrier dysfunction, reducing the production of antibacterial
peptids in the skin (such as beta defensins and LL-37), reducing the
antimicrobial immune response of the skin, change the skin
pH That increase the adhesive of the Staphylococcus aureus on skin
of AD patients. When Staphylococcus aureus adhesive on the skin
they will produce enterotoxins that act as a superantigen enabled to
differentiate a large number of T cells into Th1 and Th2. The
differentiation that will produce cytokins such as IL4, IL5, IL10,

TNF-γ, Cytokins activate the inflammatory response to cause the
onset of AD.
1.3 Treatment of Staphylococcus aureus in patients with AD
So far, the scientists studied a lot of measures treatment of
Staphylococcus aureus in patients with AD.
Methods do not take antibiotics such as repair skin barrier
by moisturizing, use topical anti-inflammatory substances
(corticosteroids, calcineurin inhibitors ) to reduce adhesive of
Staphylococcus aureus on skin of AD patients.
The antiseptics: Bactericidal soap, KMnO4, povidone-iodine
10% … reduce the number of Staphylococcus aureus on the skin of
patients with AD, improve the clinical symptoms. However, these
substances may to irritate the skin.
Topical antibiotics: Topical antibiotics alone or in
combination with corticosteroids have effective in the treatment of
AD. However, using topical antibiotics have some disadvantages
such as have only effective at the location of the treatment, cause
allergic contact dermatitis, increase bacterial resistant. Therefore, the
new trend is the combination of oral antibiotics in the treatment of
AD. However, so far there is very little research on this issue.
CHAPTER 2: SUBJECTS AND METHODS
2.1 Subjects
128 AD patients, > 12 years old, visit to hospital of
Dermato-Venereology of Ho Chi Minh City from 08/2010 to
08/2012 and 40 healthy subjects, > 12 years old, does not have AD
or other skin diseases.
2.1.1 Diagnosis of AD: AD was diagnosed following the criteria of
Hanifin and Rajka.
2.1.2 Criteria of patient selection
Criteria of patient selection for clinical research, the ratio of

Staphylococcus aureus and genes encoding superantigens: AD
patients > 12 years old, no infected lesions, agreemen participant.
Criteria of patient selection for evaluating the effectiveness
of treatment AD by taking topical betamethasone dipropionate 5%
plus oral cefuroxim: sub – acute AD patients, ages from 12 to 60,
positive Staphylococcus aureus on lesions, agreemen participant.
2.1.3 Criteria of patient exclution: Patients used topical antibiotics
within 2 weeks and oral antibiotics within 1 month. Patients has
signs of heart, liver or lung severe diseases. Patients with
immunodeficiency (HIV/AIDS, diabetes, immune suppressant
medication ). Patients who are pregnant or are breastfeeding.
Patients suffering the side effects of corticosteroids such as skin
atrophy, vasodilation, hirsutisum Patients allergic to either
medication use (betamethasone dipropionate 0.05%) or cefuroxim.
2.2 Materials
Beprosone®: Betamethasone dipropionate 0.05% is average
topical corticosteroids, produced by HOE Pharmaceuticals Sdn Bhd,
Malaysia. Licensed in VietNam by decision No VN-0421-6, 17/QD-
QLD of Ministry of health.
Zinnat®: Cefuroxim is bactericidal antibiotic belong to two
generation Cefalosporin, tablets 500mg, produced by Glaxo
Operations UK Ltd, licensed in Viet Nam VN-8475-04 by decision
No. 85/QD-QLD of Ministry of health.
2.3 Methods
2.3.1 Study design: Cross-section, case - control and clinical trial.
2.3.2 Sample size
- Cross - sectional study (for object 1): Convenient sampling, select
all of the patients eligible for the study from August, 2010 to August,
2012.
- Case – control study (for object 2): sample size is estimated

according to the following sample size calculator:
[ ]
2
21
2
22111222/1
)(
)1()1()1(2
PP
PPPPZPPZ
N
−
−+−+−
=
−−
βα
P1: Ratio of the positive Staphylococcus aureus in AD patients (80-
95%, depending on the study).
P2: Ratio of the positive Staphylococcus aureus in healthy subjects
(35-45%, depending on the study).
α: Probability of type 1 error (α = 0.05) → Z 1-α/2 = 1.96.
β: Probability of type 2 error → Z 1-β = 1.28.
We select P1 = 80%, P2 = 45% instead of the sample size calculator
 N = 40  The minimum sample size of each group is 40.
- Clinical trial (for object 3): Convenient sampling, select all of the
sub – acute AD patients during the period from 08/2010 to 08/2012,
eligible for the clinical trial stage and each group must be > 30
patients.
2.3.3 Steps to study
- Clinical examination to identify AD.

- Data collection
- Assess the severity of the disease by SCORAD:
Mild: SCORAD < 25
Moderate: SCORAD from 25 to 50
Severe: SCORAD > 50
- Assess the stage of the disease: acute, sub-acute and chronic
- Culture to identify Staphylococcus aureus: In AD patients, we
Culture and determine the Staphylococcus aureus on new lesions. In
healthy subjects, we culture and determines the Staphylococcus
aureus in the skin around the nostrils.
- Identify of the genes encoding superantigens: By multiplex PCR
(Polymerase Chain Reaction).
- Clinical trials: We Split AD patients randomly into two groups:
+ Group 1: Will be treated with a regimen including shower
by KMnO4 1/10,000, fexofenadin 60 mg (1 tablet /morning and 1
tablet / evening), cefuroxim 500 mg (1 tablet / morning and 1 tablet /
evening), beprosone ® apply twice /day.
+ Group 2: Will be treated with a regimen including shower
by KMnO4 1/10,000, fexofenadin 60 mg (1 tablet /morning and 1
tablet / evening), beprosone ® apply twice /day.
+ Duration of treatment: 2 weeks
+ Assess the result: Assess the clinical symptoms and
SCORAD score after a week of treatment, culture Staphylococcus
aureus at the end of week two.
2.4 Data processing: The data are processed and analysed by using
EpiInfo software in 2002.
- Descriptive statistics: Frequency, percentage is presented in the
form of table and diagram.
- Statistical analysis: Use χ ² and RR at 5% significance, confidence
intervals (CI) 95% to measure differences in the relationship of

results.
- Use One-Way-ANOVA to compare average scores of clinical
symptoms, SCORAD score of two groups before treatment, after 1
week of treatment, after 2 weeks of treatment.
2.5 Place and time of study: Place of study in hospital of Dermato-
Venereology of Ho Chi Minh City and NamKhoa Biotek company
(ISO 9001: 2000 and GMP/GLP of the WHO). Duration of study
from 08/2010 to 08/2012
2.6 Research ethics: Proposal of the research was through by the
Council of PhD proposal of Hanoi Medical University. The objects
of the study was announced, explained and agreed to voluntarily
participate in the study. All object information are kept secret
through the computerized. All Patients are paid for tests.
2.7 Limits of the study:
Superantigens are a relatively new concept. Their
mechanism are very complicated. Therefore, we accept the
mechanism of pathogenesis of superantigens in AD is explained on
the dermatologist journals of the World Health Organization website.
(
AD is a very complicated disease. The treatment is
depending on the stage of the disease. We conducted clinical trial
research on sub-acute phase. Because this stage occupy the majority
of AD.
CHAPTER 3: RESULTS
From 8/2010 to 08/2012, we studied 128 AD patients and 40 healthy
subjects.
3.1 Clinical characteristics and related factors of AD
3.1.1 Clinical characteristics
Ratio of clinical symptoms: Itching 100%, dry skin 78.91%,
insomnia 75% , non – pecific hand dermatitis 57.81%, cheilitis

47.56%, anterior neck folds 42.18%, white dermographism 40.62%,
orbital darkening 26.56%, Dennie Morgan infraorbital folds 21.09%,
pityriasis alba 18.75%, keratosis pilaris 18.75%, ichthyosis vulgaris
7.81%, nipple eczema 3.9%.
The stage and the severity: Sub-acute phase 71.87%,
chronic phase 17.97%, and acute phase 10.16%. Average SCORAD
score is 12.35 ± 40.55. Moderate 44. 53%, severe 28.12%, and mild
27.34%.
3.1.2 Related factors of AD
Patient and family history has atopic diseases
Table 3.1: Ratio of patient and family history has atopic diseases
History AD
n (%)
Asthma
n (%)
Allergic rhinitis
n (%)
Patient (n = 128) 125 (97.65) 63 (49.22) 68 (53.13)
Father (n = 128) 75 (58.59) 23 (17.97) 32 (25)
Mother (n = 128) 27 (21.1%) 19 (14.84) 12 (9.37)
Brothers (n = 83) 42 (50.60) 33 (39.76) 51 (61.44)
Children (n = 67)) 29 (43.28) 17 (25.37) 15 (22.3)
Onset factors of AD

Chart 3.1: The majority of adult AD patients (55.47%) was
exacerbated by contact allergens.
The age of onset
Chart 3.2: The majority of AD patients (51.56%) has the age of
onset < 2 years old.
Relation between severity of AD with related factors

We used 2 x 2 table statistic analysis found that gender, age,
history of AD, asthma, allergic rhinitis does not affect the severity of
the disease. However, contact allergens and early age onset affects
severity of the disease.
3.2 Staphylococcus aureus and genes encoding superantigens of
Staphylococcus aureus on AD patients skin.
3.2.1 Ratio of Staphylococcus aureus positive in AD patients and
healthy subjects
Chart 3.3: Ratio of the Staphylococcus aureus positive on the lesions
of AD patients is higher than that on peri – notrils of healthy subjects
statistical significance p < 0.001; RR = 2.17; 95% CI (1.44 - 3.26).
We used 2 x 2 table statistic analysis found that the ratio of
Staphylococcus aureus positive in severe patient groups is higher
than that in the mild patient group statistical significance p = 0.001,
RR = 7.12; 95% CI (1.08-47.04).
The ratio of Staphylococcus aureus positive in acute and sub-acute
stage is higher than that in chronic stage statistical significance p =
0.015, RR = 1.38; 95% CI (1.006-1.90).
3.2.2 The genes encoding superantigens of Staphylococcus aureus
on AD patients skin and on healthy subjects
p < 0.001; RR = 2.17; 95% CI (1.44 – 3.26)
%
p < 0.001; RR = 8.65 ; 95% CI (1.29 – 57.9)
Chart 3.4: Ratio of the genes encoding superantigens of
Staphylococcus aureus on the lesions of AD patients is higher than
that on peri – notrils of healthy subjects statistical significance p =
0.0006; RR = 8.65; 95% CI (1.29-57.9).
We used 2 x 2 table statistic analysis found that the ratio of
the genes encoding superantigens of Staphylococcus aureus on the
lesions of severe AD patients is higher than that on the lesions of

mild AD patients no statistically significant with p = 0.04; RR =
1.58; 95%CI (0.95-2.67) and the ratio of the genes encoding
superantigens of Staphylococcus aureus on the lesions at the stage
acute, sub-acute and chronic difference not statistically significant
with p > 0.05.
3.3 Effective treatment adult AD patients by topical
betamethasone dipropionate 0.05% plus oral cefuroxim.
During the study period, 74 AD patients were eligible for the
clinical trial. We divided all the patients randomly into two groups.
Each group has 37 patients. However, during follow-up treatment (2
weeks), group 1 has 1 (2.7%) patient and group 2 has 5 (13.5%)
patients did not finish the study. Therefore, We analysis only 68
patients (group 1: 36 patients and group 2: 32 patients).
3.3.1 Comparison of therapeutic effect between two groups
Table 3.2 Comparison of therapeutic effect based on the mean of
SCORAD.
SCORAD
(Mean ± SD)
Group 1 Group 2 P value
Baseline 44.61 ± 8.34 43.03 ± 12.98 0.55
After 7 days treatment 26.69 ± 6.05 32.53 ± 9.31
After 14 days treatment 16.61 ± 3.85 23.41 ± 7.49
REDUCE SCORAD AFTER TREATMENT
After 7 days treatment -17.92 -10.5 0.003
After 14 days treatment -28 -19.62 < 0.001
Comments of the table 3.2
- Before treatment: Mean of SCORAD of group 1 was 44.61 ±
8.34, group 2 was 43.03 ± 12.98, the difference between the two
groups was not statistically significant with p = 0.55.
- After 7 days treatment: Mean of SCORAD of group 1 was 6.05

± 26.69, group 2 was 9.31 ± 32.53, mean SCORAD of group 1
reduces 17.92 and mean SCORAD of group 2 reduced 10.05.
Mean SCORAD of group 1 reduced more than group 2
statistically significant with p = 0.003.
- After 14 days treatment: Mean of SCORAD of group 1 was
3.85 ± 16.61, group 2 was 7.49 ± 23.41, mean SCORAD of
group 1 reduced 28 and mean SCORAD of group 2 reduced
19.62. Mean SCORAD of group 1 reduced more than group 2
statistically significant with p < 0.001.
Table 3.3 Comparison of therapeutic effect based on clinical
symptoms
Clinical signs Group 1
(Mean±SD)
Group 2
(Mean±SD)
P value
C = Itching + Insomnia
- Baseline
- After 7 days treatment
- After 14 days treatment
8.11±3.23
3.44±1.98
1.55±0.87
8.81±3.35
4.75±2.37
2.62±1.36
0.38
0.016
0.0002
B = Erythema + edema/papules + oozing/crusts + excoriations +

lichenification + dryness
- Baseline
- After 7 days treatment
- After 14 days treatment
9.80±2.02
6.36±2.93
3.6 ±1.10
9.09±2.99
7.15±2.31
5.22±1.91
0.25
0.22
0.0001
A = Area of lesions
- Baseline
- After 7 days treatment
- After 14 days treatment
13.50±5.22
13.19±5.05
12.64±4.90
11.72±3.72
11.25±3.29
11.20±3.64
0.11
0.075
0.25
Comments of the table 3.3
C = Itching + insomnia
- Before treatment: Mean of C of group 1 was 8.11 ± 3.23, group
2 was 3.35 ± 8.81, the difference between the two groups was

not statistically significant with p = 0.38.
- After 7 days treatment: Mean of C of group 1 was 3.44 ± 1.98,
group 2 was 4.75 ± 2.37. Mean C of group 1 reduced much more
than mean C of group 2 statistically significant with p = 0.016.
- After 14 days treatment: Mean of C of group 1 was 1.55 ± 0.87,
group 2 was 1.36 ± 2.62. Mean C of group 1 reduced much more
than mean C of group 2 statistically significant with p < 0.0002.
B = Erythema + edema/papules + oozing/crusts + excoriations +
lichenification + dryness
- Before treatment: Mean of B of group 1 was 9.80 ± 2.02, group
2 was 9.09 ± 2.99, the difference between the two groups was
not statistically significant with p = 0.25.
- After 7 days treatment: Mean of B of group 1 was 6.36 ± 2.93,
group 2 was 7.15 ± 2.31. Mean B of group 1 reduced much more
than mean B of group 2 but the difference was not statistically
significant with p = 0.22.
- After 14 days treatment: Mean of B of group 1 was 3.61 ± 1.10,
group 2 was 5.22 ± 1.91. Mean B of group 1 reduced much more
than mean B of group 2 statistically significant with p = 0.0002.
A = Area of the lesions
- Before treatment: Mean of A of group 1 was 13.50 ± 5.22,
group 2 was 11.72 ± 3.72, the difference between the two groups
was not statistically significant with p = 0.11.
- After 7 days treatment: Mean of A of group 1 was 13.19 ±
5.05, group 2 was 11.25 ± 3.29. Mean B of group 1 reduced
much more than mean B of group 2 but the difference was not
statistically significant with p = 0.075.
- After 14 days treatment: Mean of A of group 1 was 12.64 ±
4.90, group 2 was 11.20 ± 3.64. Mean A of group 1 reduced
much more than mean A of group 2 but the difference was not

statistically significant with p = 0.25.
Table 3.4: Results of Staphylococcus aureus cultured of 2 groups
after the 14 days treatment
Staphylococcus
aureus
Group 1 Group 2 P value
Positive 3 (8.33%) 25 (78.12%) P < 0.001
Negative
Total
33 (91.67%)
36 (100%)
7 (21.88%)
32 (100%)
Comments of the table 3.4: After the 14 days treatment, 91.7% of
the patients in Group 1 had resulted Staphylococcus aureus negative;
21.88% of the patients in Group 2 had resulted Staphylococcus
aureus negative. Ratio of Staphylococcus aureus negative in Group 1
was more than that of group 2 statistically significant with p < 0.001;
RR = 5.1; 95% CI (2.57-10.12).
3.3.2 Adverse effects of 2 medications: During 2 weeks treatment
we not recorded any adverse effects of the medicine in both groups
Chapter 4: DISCUSSION
4.1 Clinical features and related factors of Atopic Dermatitis
4.1.1 Clinical features
Pruritus: Pruritus is the main symptom and one of the main criteria
for diagnosing Atopic Dermatitis (AD). According to medical books,
80-100% of patients with AD experience symptoms of pruritus. In
our research, 100% of our patients had pruritus. Pruritus causes
scratching and rubbing leading to secondary lesions such as
infection, hardened skin, scratches, etc. Pruritus also causes

insomnia, which impinges on patients’ quality of life.
Insomnia: In our research, 75% of our patients developed insomnia.
Like other chronic diseases, AD greatly affects patients’ mental
health. It progresses chronically, recurs repeatedly, which has bad
effects on patients’ quality of life, brings on worry, depression, and
insomnia.
Dry skin: According to our research results, 78.91% of the patients
experienced dry skin. According to medical books, patients with this
symptom make up around 50-70% of all AD patients. The causes of
dry skin lie in the decreased filaggrin and ceramide production as
well as the increased trans-epidermal water loss. Dry skin makes
patients feel pruritusy, be prone to stimuli, and worsens the disease
process. Therefore, applying moisturizing creams or lotions plays a
crutial role in AD treatment.
Other symptoms such as: Palmar and plantar dermatitis, cheilitis,
skin folds on the anterior aspect of the throat, white dermographism,
periocular darkening of the skin, infraorbitary (Dennie-Morgan) skin
fold, pityriasis alba, keratosis pilaris, ichthyosis, nipple eczema are
also common symptoms in patients with AD.
4.1.2 Related factors
In our research on 128 adults with AD, males made up
58.6%, higher than females with 41.4%. The youngest age was 13,
the eldest was 78, and the average age was 37.65 ± 14.09 with a high
proportion of the group of 21-40 (56.25%). An occupation requiring
frequent exposure to allergens plays an important role in the
triggering or aggravation of the disease. Proportions of occupations
in our research were as follow: of all subjects, 35.16% were office
workers, 21.87% were students, 21.09% were farmers, 14.06% were
freelancers, and 7.81% were workers. Georaphy is also one of the
significant epidemiological characteristics of AD. AD is more

common in urban areas than in the rural ones, particularly common
in industrialized zones. In our research, 64.8% of the patients lived in
Ho Chi Minh City while only 35.2% lived in other provinces. The
atopic factor in AD was evident in the patients having concurrent
allergic diseases such as asthma and allergic rhinitis. Figures in our
research have shown that of all AD patients, 97.65% had a family
history of AD, 49.22% had history of asthma, and 53.13% had
history of allergic rhinitis. AD is proved to be have a hereditary
component. Recently, scientists have indentified a lot of genes
related to AD, which lie on chromosomes: 11q13, 5q31-33, and
16p11.2-11.1. As can be seen from our research figures, our AD
patients had family history as follow: 58.59% of them had an AD-
affected father, 17.97% had an asthma-affected father, and 25% had
a allergic-rhinitis-affected father; the percentages of those who had a
mother affected by AD, asthma, and allergic rhinitis were 21.1%,
14.84%, and 9.37% respectively; the percentages for having an
affected sibling were 50.60%, 39.76%, and 61.44% respectively; and
for having an affected child were 43.28%, 25.37%, and 22.39%
respectively.
Triggering factors play a crucial role in the pathogenesis of
AD. They are diverse and plentiful, usually divided into 3 groups:
aeroallergens, contact allergens and food allergens. Our research
results have shown that of all AD patients, 55.47% had contact
allergens as triggering factor, 28.12% had food allergens as
triggering factor, 12.5% had aeroallergens as triggering factor, and
3.91% did not show a clear triggering factor.
4.2 S.aureus and the superantigen-encoding genes of S.aureus in
AD patients
4.2.1 Compare S.aureus detection results between AD and
healthy group

According to our research, the proportion of having S.aureus
in lesion areas of AD patients was 81.25%, which was higher than
that in healthy people’s outside nostril area (37.5%). The difference
had a statistical significance with p<0.001, RR = 2.17, 95% CI (1.44
– 3.26). Our findings are in accordance with other researches in the
world. In 1997, Goh, C.L. et al conducted a study on 33 AD patients
in Singapore showing that the S.aureus detection proportion in lesion
areas of AD patients was 89%, in their healthy skin area was 42%, in
their outside nostril area was 55%, which was higher than that in
healthy skin area of the healthy group being 5%, in outside nostril
area being 35%. This result is also in accordance with findings of
other authors like Abeck D. et al, Higaki S. et al, Breuer K. et al.
From these above findings, it can be seen that the proportion of
S.aureus detection in lesion area of AD patients are higher than that
in healthy people’s skin.
4.2.2 Compare detection results of superantigen-encoding genes
of S.aureus between AD and healthy group
Our research figures have shown that 119 samples were
positive, including 104 samples taken from lesion areas of AD
patients, 15 samples taken from outside nostril area of the healthy
group. All of the samples were tested with PCR experiment to find
superantigen-encoding gene segments. Of 104 samples taken from
lesion area, there were 60 samples having superantigen-encoding
genes, which is equivalent to 57.69%, whereas there was only 1
sample from the healthy group having superantigen-encoding genes,
equivalent to 6.67%. This difference had a statistical significance
with p = 0.0006, RR = 8.65; 95%CI (1.29 – 57.9). According to
Breuer K. et al, the proportion of superantigen detection
implemented by Latex methodology was 31%. According to Tomi
N.S. et al, who carried out a research on 25 patients with AD, the

proportion of superantigen detection implemented by Latex
methodology is 44%. According to McFadden, J.P. et al research,
65% of S.aureuses isolated from lesion area of AD patients secrete
superantigen. There were differences in those figures, but they were
insignificant. These differences were resulted from the fact that those
authors indentified superantigen by Latex methodology while we did
it by PCR methodology.
4.3 Compare the effectiveness of treatment for AD adults in
subacute phase between the two groups
4.3.1 Compare the effective treatment based on average
SCORAD
Before the treatment, the average SCORAD of group 1 was
44.61 ± 8.34, the average SCORAD of group 2 was 43.03 ± 12.98 -
the difference between the two groups had no statistical significance
with p = 0.55. At 7 days after the treatment, the average SCORAD
of group 1 fell from 43.03 ± 12.98 to 26.69 ± 6.05 (fell by 17.92
points); the average SCORAD of group 2 went down from 43.03 ±
12.98 to 32.53 ± 9.31 (fell by 10.05 points). It can be seen clearly
that the average SCORAD scores of both groups experienced a
meaningful decline after 7 days since the commencement of the
treatment. After 14 days of treatment, the average SCORAD of
group 1 continued to decrease to 16.61 ± 3.85 (decreased 28 points
compared to the initial score), and that of group 2 decreased to 23.41
± 7.49 (decreased 19.62 points compared to the initial score). That
decrease of group 2 was a result of merely applying topical
corticosteroid. This is in accordance with medical books and
instruction of treatment, which says that applying topical
corticosteroid is highly effective and still the first option in treating
AD. However, comparison between the decrease levels of the 2
groups has shown that after 7 days of treatment, the everage

SCORAD of group 1 saw a higher decrease than that of group 2,
which had a statistical significance with p = 0.003; and after 14 days
of treatment, the score of group 1 continued to see a higher decrease
than that of group 2, which had a statistical significance with p <
0.001. These figures of comparison indicate that using oral
antibiotics in combination with applying topical corticosteroides
leads to a higher decrease in SCORAD compared to merely applying
corticosteroid. This finding is in accordance with findings of 2
researches of Ewing C.I et al and Boguniewicz M et al.
4.3.2 Compare the effectiveness of treatment based on clinical
symptoms
Assessment of the severity degree of AD according to
SCORAD scale is based on scores of clinical symptoms: C = pruritus
+ insomnia; B=erythema + papules/edema +
exudation/desquamation + scabbing + lichenified lesions + dry skin;
A = extent of the lesion. Therefore, we made a comparison between
the 2 regimens in terms of effectiveness of treatment, based on the
everage score of the above clinical symptoms.
C = pruritus + insomnia: Before the treatment, this score of group
1 was 8.11 ± 3.23, while that of group 2 was 8.81 ± 3.35, and the
difference between the two figures had no statistical significance
with p = 0.38. After 7 days of treatment, the scores of group 1 and
group 2 fell to 3.44 ± 1.98 and 4.75 ± 2.37 respectively. After 14
days of treatment, the figures continued to go down to 1.55 ± 0.87
and 2.62 ± 1.36 respectively. It can be seen clearly that the average
scores of the same group at the time of the 7
th
day and the 14
th
day of

treatment declined considerably compared to the initial score. This is
in accordance with Kawashima, M. et al, in whose research,
fexofenadine used 60 mg twice/day was proved to be more effective
than placebo in reducing pruritus for AD patients, which has a
statistical significance with p = 0.005. On the other hand, applying
topical corticosterods also had effect of reducing pruritus for 77 AD
patients through the mechanism of mechanism of anti-inflammatory
and immunomodulatory. But when we compared the average scores
of 2 symptoms of pruritus and insomnia of the 2 groups on the 7
th
and the 14
th
day of treatment, we saw that the score of group 1 fell by
a greater degree, which has a statistical significance with p = 0.016
(at the time of the 7
th
day) and p = 0.002 (at the time of the 14
th
day).
This indicates that applying topical corticosteroid in combination
with oral antibiotics can reduce the symptoms of pruritus and
insomnia faster than the methodology of merely applying topical
corticosterods. The reason is that antibiotics reduce S.aureus on skin,
reduce superantigen secretion, indirectly reduce inflammatory
response, reduce cytokines release, and reduce symptoms of pruritus
and insomnia.
B = erythema + papules/oedema + exudation/desquamation +
scabbing + lichenification + dry skin: Before the treatment, group
1’s score was 9.80 ± 2.02, group 2’s score was 9.09 ± 2.99, and the
difference between the 2 figures had no statistical significance with p

= 0.25. After 7 days of treatment, the figure of group 1 fell to 6.36 ±
2.93 while that of group 2 fell to 7.15 ± 2.31, which meant the
average B score of group 1 fell by a greater degree than that of group
2 but the difference had no statistical significance with p = 0.22.
After 14 days of treatment, the average B of group 1 continued to
decrease to 3.61 ± 1.10 while that of group 2 decreased to 5.22 ±
1.91, which meant the average B of group 1 fell by a greater degree
than that of group 2 with a statistical significance of p = 0.002. So
the combination with oral antibiotics started to take effect of
reducing the clinical symptoms of AD from the 7
th
day of treatment
to the 14
th
day. We have not been able to consult any documents
assessing the effectiveness of using oral antibiotics based on the
clinical symptoms of AD, therefore we cannot compare our findings
with other authors.
A = extent of the lesion: Before the treatment, the average A of
group 1 and group 2 were 13.50 ± 5.22 and 11.72 ± 3.72
respectively, and the difference had no statistical significance with p
= 0.11. After 7 days of treatment, the figures were 13.19 ± 5.05 and
11.25 ± 3.29 respectively, and the difference had no statistical
meaning with p = 0.075. After 14 days of treatment, the figures were
12.64 ± 4.90 and 11.20 ± 3.64 respectively, and the difference had no
statistical significance with p = 0.25. These findings are in
accordance with that of Ewing, C.I. et al. This is also in accordance
with the clinical reality that during AD treatment, the symptoms of
pruritus, insomnia, erythema, papules/oedema,
exudation/desquamation, scabbing, lichenified lesions, dry skin

lessen first and the extent of lesion lessens more slowly.
4.3.3 S.aureus detection results on the 14
th
day of treatment of
the two groups
Before the treatment, the patients of the 2 groups tested
positive for S.aureus. After 14 days of treatment, 91.7% of group 1
and 21.88% of group 2 tested negative for it, and the difference
between the two figures had a statistical significance with p < 0.001,
RR = 5.1; 95%CI (2.57 – 10.12). Our findings are in accordance with
Weinberg, E. et al. The result that 21.88% of group 2 (who did not
use antibiotics) were negative for S.aureus is thanks to the fact that
applying topical corticosteroid is effective in reducing aureus on AD
patients’ skin.
CONCLUSION
Through our research on 128 adult patients with AD and 40
healthy subjects at the Ho-Chi-Minh City Hospital of Dermatology-
Venereology from August, 2010 to August, 2012, we have drawn to
conclusions as follow:
1. Clinical features and factors related to adult patients with AD
Clinical features: Common clinical symptoms: pruritus
100%, dry skin 78.91%, insomnia 75%, the other symptoms made up
for lower proportions. Subacute phase 71.87%, chronic phase
17.97%, and acute phase 10.16%. Severity of AD: Moderate
44.53%, severe 28.12%, and mild 27.34%.