case report patch test

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INTRODUCTION
Atopic Dermatitis (AD) is a chronically relapsing skin disease that occurs
most commonly during early infancy and childhood. It is frequently associated
with abnormalities in skin barrier function, allergen sensitization, and recurrent
skin infections.1 Atopy is defined as an inherited tendency to produce
immunoglobulin E (IgE) antibodies in response to minute amounts of common
environmental proteins such as pollen, house dust mites, and food allergens. 1,2
Dermatitis derives from the Greek “derma,” which means skin, and “itis,” which
means inflammation.2
Atopic Dermatitis (AD) affects about one-fifth of all individuals during their
lifetime, but the prevalence of the disease varies greatly throughout the world. In
several industrialised countries, the prevalence increased substantially between
1950 and 2000 so much that many refer to as the “allergic epidemic.”. However,
current indications point to eczema symptoms having levelled off or even having
decreased in some countries with a formerly very high prevalence, such as the
United Kingdom and New Zealand.2 This indicates that the allergic disease
epidemic is not increasing continually worldwide. Nevertheless, AD remains a
serious health concern, and in many countries, particularly in the developing
world, the disease is still very much on the rise.2
The appearance of the individual skin lesion in AD does not differ from
other eczemas such as contact eczema. In it’s acute form, eczema is characterised
by a lively red infiltrate with oedema, vesicles, oozing, and crusting;
lichenification, excoriations, papules, and nodules dominate the subacute and
chronic form. Accordingly, the diagnostic approach builds upon other
characteristics such as the distribution of the eczema as well as associated features
of the patient.1,2
The most widely used diagnostic criteria for AD were developed by Hanifin
and Rajka in 1980 and were later revised by the American Academy of
Dermatology.2 This set of criteria is primarily useful in clinical practice; another
set of diagnostic questions widely used in epidemiological research was

1

developed by the UK Working Party in 1994.2 The severity of eczema can be
graded according to several scoring systems such as Scoring Atopic Dermatitis
(SCORAD) and Eczema Area and Severity Index (EASI).3,4
Rapidly developing symptoms (type-1 reactions) caused by allergens in
allergic diseases can be easily diagnosed with detailed anamnesis, skin tests
and/or specific IgE level measurements. However, diagnostic approaches are
rather complex in late onset reactions, such as AD.1 Immediate-type
hypersensitivity is usually diagnosed by skin prick tests (SPTs) or by
measurement of serum-specific IgE. The disadvantage of SPT is the need for the
discontinuation of topical steroid and antihistamine treatment, which can lead to a
worsening of the preexisting AD. In addition, the requirement of intact skin
cannot always be fulfilled; this is especially true in childhood, when AD lesions
are commonly localized on the volar side of the forearms where SPT is usually
performed. In contrast, specific IgE measurement has no such limitations.3,5
Delayed, allergen-specific T-cell reactions also play an important role in the
pathogenesis of AD, but since it is not possible to detect these reactions using tests
of immediate-type hypersensitivity, a different kind of test needs to be used in
their diagnosis. The patch test is a standard method used for testing of delayedtype hypersensitivity reactions to contact allergens. 6 The atopy patch test (APT)
poses its modification, which is performed with allergens also known to elicit
immediate-type hypersensitivity reactions.7,8,9 In the diagnosis of food allergy,
APT can increase the diagnostic benefit of SPT and/or specific IgE measurement,
even if it is often necessary to verify results by a double-blind, placebo-controlled
food challenge. Sensitivity and specificity of APT varies depending on the type of
food allergen.7,8 In this paper, it has been reported a case of atopic dermatitis in
adult that has been treated with moisturizer, topical corticosteroid, sistemic
antihistamin and were done skin prick test and atopy patch test to identified
triggering factors.

2

CASE REPORT

A 19 years old girl came to dermatovenereology outpatient clinic at dr.
Saiful Anwar General Hospital on September 16th 2015, with chief complaint red
patches on both of her arms and legs and also itchy mostly at night since 3 weeks
before admission and got worse in the last 3 days. Firstly, it appeared like small
red pimples and felt itch on her both arms and started to spread on her both legs.
She said that it happened after she ate meatballs and tongkol fish 3 weeks ago.
She keep scratching it all day long but the itch got worsen at night. She applied
inerson on the itch part of her body but not regularly and showed no
improvement.
From the history of the past illness, she had the same symptoms like this
since she was a child (the patient forgot when excactly). Sometimes got better by
it self but sometimes she has to go to general practitioners (GP) to get some
medication. The GP said that she had allergies. She usually use inerson® and
olive oil for her own medication but not regularly. The redness patch sometimes
dissapear but sometimes not. According to the patient, the itch began to appeared
everytime she eats meatball and tongkol fish, that is why she tried to avoid it. She
also felt itch and had runny nose or sneezing everytime she helps her mother to
clean the house or when the weather is cold. But if she has runny nose or sneezing
in the morning, it will become seldom or gone if she wears warm cloth or when
it’s already noon. She used to had wheals when she was a child and appeared
when the weather is cold. But she never experienced it again since she was in
junior high school. She had white and dry patches on her face when she was a
child, sometimes she had it now but not as often as when she was a child
(tratak’en). Sometimes she had itch on both of her eyes and only few times on her
nipples. She was the third and the last child.

3

From family history of atopy, her mother has the same eczema on both of
her arms and legs. She usually felt it when the weather is cold. Her first brother
has the same eczema. Her second sister has asthma. But all of her sibling already
married and live with their own family.
In patient daily environment, the patient use cotton mattres but not cleaned
every month, only change the sheeth every 2 weeks. She use dettol® soap for
everyday usage. Her skin is very dry but she uses hand and body lotion twice
daily. She sleeps on a bed bunk. Her father have pets like some chickens and
birds. There are a lot of wild cats wandering arround her house and sometimes
sleeps on her doormat or on her kitchen. She works as a administration on an
electricity housing supplier warehouse in Malang. She works from 8 am until 5
pm everyday except on Sunday.
From dermatological examination, on her face showed no periorbital
darkening (Figure 1A). On her trunk, upper right arm, upper and lower left arm,
upper and lower legs, showed multiple hyperpigmented patches with ill defined
border, irregular shape, varied in sizes (Figure 1B, D, F, G, H, I). On her right
lower arms showed multiple erythematous papules with ill defined border, round
shape, size ± ϕ 2-3mm (Figure 1E). On her dorsal feet showed multiple
hyperpigmented plaque with well defined border, well defined, varied in sizes,
some covered with white-yellowish rough scale (Figure 1J).

4

1A
Figure 1. A. There were no periorbital darkening, face palor, Dannie Morgan fold nor pityriasis
alba.

1B

1C

Figure 1. On her trunk and her back B. Showed multiple hyperpigmented patches with ill defined
border, irregular shape, varied in sizes (green arrow). C. No lession.

5

1D

1E

Figure 1. Form her left upper and lower arm D. Showed multiple hyperpigmented patches with ill
defined border, irregular shape, varied in sizes (green arrow). E. Showed erythematous papules,
multiple, round shape,with ill defined border, size ± ϕ 2-3mm (green arrow).

1
F

1G

Figure 1. On her left upper and lower arm. F. Showed multiple hyperpigmented patches with
irregular shape, varied in sizes, ill defined border (green arrow). G. Showed multiple
hyperpigmented patches with irregular shape, varied in sizes, ill defined border (green arrow).

6

1H
H

1I

Figure 1. On her both upper and lower legs. H. Showed multiple hyperpigmented papules with ill
difined border, round shape, varied in sizes. I. Showed multiple hyperpigmented macules with ill
defined border, irregular shape, and varied in sizes.

1J
Figure 1. On her dorsal feet J. Showed multiple hyperpigmented plaque with defined border,
varied in sizes, some covered with white-yellowish rough scale.

7

1
L

1
K

Figure 1. On her hands. K & L. Showed no lession.

From general examination, the patient was compos mentis and looks well.
her blood pressure was 120/80 mmHG, pulse rate 80x/mnt, respiratory rate
20x/mnt, and her axilar temperature 37,3 ºC. Her IgE serum level was elevated
(1129 IU/mL).
The patient was diagnosed as AD, made clinicaly based on history taking
and physical examination. From Hanifin and Rajka criteria, on major sign were
found pruritus, typical morphology and distribution, tendency toward chronic or
chronically relapsing dermatitis, personal or family history of atopic disease :
asthma, allergic rhinitis, AD. On minor sign was found drynes on her skin,
elevated serum immunoglobulin E, early age onset, tendency toward non spesific
hand or foot dermatitis, history of nipple eczema, recurrent conjunctivitis,
pityriasis alba and food intolerance. Her SCORAD was 25,29 and include
moderate AD.
Table 1. SCORAD or score for AD.
Spread
Front

(%)
Face 0

(%)
Upper
torso 0

(%)
Arm right
and left 0

Back

Head 0

Intensity

---------Erythe
ma 1
----------

Upper
torso 0
-------Edema 0

Arm right
and left 9
--------Oozing 0

--------

---------

Subjective
sign

Pruritus
7

Insomnia

(%)
Gene
Talia
0

---------Excoria
tion 1
----------

(%)
Leg right n
left 18

(%)
Lower torso
2

Total

Leg right n
left 18
---------Lichenificat
ion 1
---------

Lower torso
2
------------Xerosis
2
-------------

49/5

7.5/2

7

8

Total score

25,29

The patient was given moisturizer cream, desoxymethasone ointment
twice daily, loratadine 10 mg once daily, also education about the disease, how to
maintain the moisture of the skin, and how to avoid the triggers so the patient can
make the exacerbation less happen. The patient came back after 14 days for the
follow up and showed with a good result. Her SCORAD score was 4 categorized
as mild AD.

2
B

2
A

Figure 2A & 2B. Follow up after 14 days. There were no lession.

2C

2D

9

Figure 2C & 2D. Follow up after 14 days. On the trunk and back showed multiple hyperpigmented
patches with irregular shape, varied in sizes, ill defined border.

2

2

Figure 2E and 2F. Follow up after 14 days. On the both legs showed multiple hyperpigmented
patches with irregular shape, varied in sizes, ill defined border.

2
Figure. 2G. Follow up after 14 days. The lession before was gone. Dryness (+).

The patient was educated to identify the triggering factor of her disease by
doing skin prick test and atopy patch test. Firstly, she was explained about the
procedure, the function of the test, and also the side effect that might could
happend during or after the test. Patient was told not to drink any drugs that can
decrease the prutitus such as loratadin, cold or flue medication that sold on over

10

the counter store, and the patient didn’t take any oral corticosteroid. Also there
wasn’t any flare during the test, or else the test can’t be done. Because the patient
was under 21 years old and didn’t accompanied by her mother, then she was told
to comeback later again with her mother for hospital policy on signing informed
concent. On December 14th 2015, she came to do the skin prick test. First we
make sure that the vollar area were free from any lession, the patient didn’t have
any flares and did all the instruction before. After that the mother’s patient signed
an informed concent for skin prick test.
Firstly we do the dermographism in the patient and if the result was
negative then we can do the skin prick test (Figure 3). Then we do the aseptic on
the upper right arm near the vollar area using alchohol and draw 1 for histamin
dihydrocloride (1mg/mL) as a positive control, 2 for coca as a negative control.
We put a drop of histamin using the cap of the steril lancet and use the steril lancet
to prick the droplet 1 mm into the skin without any bleeding. We do the same with
coca as a negative control. After 15 minutes there will be reaction on number 1
which as a positive control it will appeared as a wheal, in this case the wheal
diameters was ϕ 4,80 mm (+++) and the negative control didn’t appear at all
(Figure 4A and 4B).

3

4

4

Figure 3. Dermographism (green circle). 4A. Number 1 was histamin dihydrochloride (1mg/mL)
(green arrow) and number 2 was coca (red arrow). 4B. After 15 minutes appeared wheal on
number 1with ϕ 4,80mm (red arrow).

11

After that, we continued with other allergen extracts such as dog’s hair
(number 4), chicken feather (number 5), house dust (number 6), raw cotton
(kapuk) (number 7), yeast (ragi) (number 8), mullet fish (ikan bandeng) (number
9), pindang fish (number 10), crab (number 11), wheat flour (number 12), cow’s
meat (number 13), chocolate (number 14), cob fish (ikan tongkol) (number 15),
pinapple (number 16), banana (number 17), peanuts (number 18), cow’s milk
(number 19), chicken’s meat (number 20), shrimp (number 21), orange (number
22), chicken egg whites (number 23), chicken egg yolk (number 24), duck egg
white (number 25), duck egg yolk (number 26), goat’s meat (number 27), tempe
(number 28), and papaya (number 29). With the same technique we use all
alergens on the patient’s right and left fore arm. After 15 minutes the reaction can
be seen and interperated. From all alergens only house dust mite (number 6) was
positive with diameter ϕ 4,65 mm (++). On crab allergen extract (number 11) also
appeared wheal with diameters ϕ 2,22 mm but not consider as a positive reaction.

12

13

4
C

4
E

4
D

4
F

4
G

Figure 4.C. drawn on vollar area for preperation of allergen extract prick test. D & E. A drop
different allergen was given and pricked on every number. F. Showed wheal on number 6 (ϕ 4,65
mm)(red arrow and red circle) and 11 (ϕ 2,22 mm) after 15 minutes. G. Showed no wheal.

After skin prick test was done, the patient came back on December

16th

2015

to do the atopy patch test. Firstly we make sure that the back area were free from
any lession, the patient didn’t have any flares and did all the instruction before.
The patient were explained once again about the function of the test, the
procedures, and the side effect that could happen during or after the test. After that
the patient agreed and signed an informed concent for atopy patch test. We do the
asepsis on the back of the patient using alchohol swab. By using the prick skin
allergens we applied it on the finn chamber with size 8 mm with a filter paper in
it, then aplied it on the patient back using white tape. We identified every alergens
and write it on the white tape with numbers label according to the numbers that
written on the skin prick test allergens (Figure 5A & 5B).
14

5A

5B

Figure 5A. Showed the back of the patient were clear from any lession. 5B. The finn chambers
were apllied on the back with the white tape after applying prick test allergens and then labelled by
the sequence number of prick allergens.

After labelled by the the sequnce number of prick allergens, we apllied
another white tape to ensure that the finn chambers were sttached firmly to the
patient back (Figure 5C). We educated the patient to did not do activities that are
too heavy that could make her sweats too much. We also told the patient not to
drink any medication, not to applied anything that can make the tape came off,
and if she felt itch it means that the allergens are giving reaction but if it she felt
burning sensation or pain sensation then she can take off the white tape. The
reading of the APT reactions are read after 48, and 72 hours.

5
C
Figure 5C. The atopy patch test were applied with another white tape to ensure the finn chamber
attached firmly.

15

After 48 hours we took off the white tape and all of the fin chambers to see
the reaction. The reading started 15 minutes after we took off the atopy patch. On
the left part were seen no reaction on the control which is coca (number 2) and
erythematous papules on histamin allergen (number 1) with interpretation ++.
Also seen erythematous papules on number 4 (dog’s hair), number 6 (house dust),
number 10 (pindang fish), and number 12 (wheat flour) (figure 5D and 5E).

5
D

5E

Figure 5D & E. Positive ++ on number 1, 4, 6, 10, 12. Showed few erithematous papules (red
arrow).

On the right side of the back seen few erithematous papules on number 18
(peanuts), 19 (cow’s milk), 21 (shrimp), 22 (orange), 27 (goat’s meat), and 28
(tempe) with interpretation were ++ (Figure 5F and 5G).

16

5
5
Figure 5F & G. Positive ++ on number 18, 19, 21, 22, 27,28. Showed few erithematous papules
(red arrow).

After 72 hours, the reading only seen on number 1, 4, 6, ,28 with some
erithematous papules and the interpretation was +++. Number 22 and 27 showed
less papules and erythema, the interpretation was + (Figure 5H and 5I).

5

5I

Figure 5H & 5I. Showed many spreading erythematous papules on number 1, 4, 6, and 28,
interpretation +++ and number 27 interpretation + (red arrow).

17

The patient was educated about the positive findings on prick test and
atopy patch test. She also told to avoid the trigering factors that already known
from the tests such as dog’s hair, house dust, and tempe.

18

Table 2. Result of SPT and APT
No.
1.
2.
4.
5.
6.
7.
8.
9.
10.
11.
12
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26
27.
28.
29.

Allergens
Histamin 1mg/mL
Coca (control)
dog’s hair 2,5 mg/ml
chicken feather 2,5 mg/ml
house dust 5 mg/ml
raw cotton 5 mg/ml
Yeast 1 mg/ml
mullet fish (bandeng) 2 mg/ml
pindang fish 2 mg/ml
Crab 2 mg/ml
wheat flour 1 mg/ml
cow’s meat 2 mg/ml
chocolate 1 mg/ml
cob fish (tongkol) 2 mg/ml
Pinapple 1 mg/ml
Banana 1 mg/ml
Peanuts 1 mg/ml
Cow’s milk 1 mg/ml
chicken’s meat 2 mg/ml
shrimp 2 mg/ml
Orange
chicken egg whites 1 mg/ml
chicken egg yolk 1 mg/ml
duck egg white 1 mg/ml
duck egg yolk 1 mg/ml
goat’s meat 2 mg/ml
tempe 1 mg/ml
Papaya 1 mg/ml

APT 48 hr
++
++
++
++
++
-

APT 72 hr
+++
+++
+++
+
+
+++
-

SPT
+++(4,80mm)
++(4,65mm)
-

DISCUSSION
The appearance of the individual skin lesion in AD does not differ from
other eczemas such as contact eczema. In its acute form, eczema is characterized
by a lively red infiltrate with oedema, vesicles, oozing, and crusting;
lichenification, excoriations, papules, and nodules dominate the subacute and
chronic form. Accordingly, the diagnostic approach builds upon other
characteristics such as the distribution of the eczema as well as associated features
of the patient.2 The typical patient with AD is a person with an early onset of itchy
eczema localised at typical sites such as the flexures of the elbows and knees in an
atopic patient or in a person with a familial predisposition to atopic disease. The
most widely used diagnostic criteria for atopic dermatitis were developed by
Hanifin and Rajka in 1980 and were later revised by the American Academy of
Dermatology (Figure 6).1,2

19

Figure 6. Hanifin Rajka criteria for AD.2

In this case the patient was diagnosed as AD, made clinicaly based on
history taking and physical examination. From Hanifin and Rajka criteria, on
major sign were found pruritus, typical morphology and distribution, tendency
toward chronic or chronically relapsing dermatitis, personal or family history of
atopic disease : asthma, allergic rhinitis, AD. On minor sign was found dryness on
her skin, elevated serum immunoglobulin E, early age onset, tendency toward non
specific hand or foot dermatitis, history of nipple eczema, recurrent conjunctivitis,
pityriasis alba and food intolerance.
Laboratory testing is not needed in the routine evaluation and treatment of
uncomplicated AD. Serum IgE levels are elevated in approximately 70–80% of
AD patients.1 This is associated with sensitization against inhalant and food
allergens and/or concomitant allergic rhinitis and asthma. In contrast, 20–30% of
AD patients have normal serum IgE levels. This subtype of AD has a lack of IgE
sensitization against inhalant or food allergens. However, some of these patients
may possess IgE sensitization against microbial antigens such as S. aureus toxins,
and Candida albicans or Malassezia sympodialis can be detected. As well, some
of these patients show positive reactions using the atopy patch test despite
negative immediate skin tests.1 We measure the patient IgE level by blood test and
showed high IgE level which is 1129 UI/ml.

20

Atopic Dermatitis (AD) is not curable, and many patients will experience a
chronic course of the disease. Accordingly, the treatment of AD aims to minimize
the number of exacerbations of the disease, so-called flares, second, reduce the
duration and degree of the flare, if flare occurs. The first aim relates primarily to
prevention; the second aim relates to treatment. Prevention is best attained by
trying to reduce the dryness of the skin, primarily via daily use of skin
moisturizing creams or emollients along with avoidance of specific and unspecific
irritants such as allergens and noncotton clothing. When dryness is reduced, the
desire to scratch will lessen and the risk of skin infection will decrease. Avoiding
long, hot baths further prevents skin dryness,but when a bath is taken, an
emollient should be applied directly after it to secure a moist epidermis and
augment the skin barrier function.1,2
Reducing the flare is warranted when actual eczema occurs or when mild
intermittent eczema worsens. Management of an eczema exacerbation requires
medical treatment often in the form of corticosteroid creams. 2 Topical
corticosteroids are the mainstay of the treatment for moderate to severe AD, both
in children and adults. Most patients benefit from treatment with mild to moderate
corticosteroid preparations, whereas only a small subset those with severe disease
needs potent preparations; very strong preparations are rarely needed. Mild and
moderate corticosteroid creams are reserved for children, while adults can be
treated with stronger preparations.2 In this case we gave emolient to the patient,
due to dryness of her skin and because the outcome of these patients SCORAD
are moderate level, then we give a moderate potency corticosteroid preparations.
Oral antihistamines are recommended for itching but have no effect on the
activity of the eczema. Non-sedating antihistamines should be used, but when
night-time

itching

interferes

with

sleep,

sedating

antihistamines

are

recommended.2 In this case we use loratadin due to the the patient’s heavy
activity.
Scoring Atopic Dermatitis (SCORAD) is a clinical tool used to assess the
extent and severity of eczema. Dermatologists may use this tool before and after

21

treatment to determine whether the treatment has been effective. The scoring
include 3 measuring. First is area to determine extent, the sites affected by eczema
are shaded on a drawing of a body. The rule of 9 is used to calculate the affected
area (A) as a percentage of the whole body. Second is intensity, A representative
area of eczema is selected. In this area, the intensity of each of the following signs
is assessed as none (0), mild (1), moderate (2) or severe (3).


Redness



Swelling



Oozing / crusting



Scratch marks



Skin thickening (lichenification)



Dryness (this is assessed in an area where there is no inflammation)

The intensity scores are added together to give 'B' (maximum 18). And the third is
subjective symptoms i.e., itch and sleeplessness, are each scored by the patient or
relative using a visual analogue scale where 0 is no itch (or no sleeplessness) and
10 is the worst imaginable itch (or sleeplessness). These scores are added to give
'C' (maximum 20).3 In this case we measure the SCORAD with result 25,29 and
categorized as moderate atopic dermatitis.
The prick test is usually the most convenient test method for detecting
immunoglobulin E (IgE)-mediated allergy.5 Several requirements are advocated to
reach an ideal prick test. Some of them are controling the efect of medication.
Antihistamines of the so-called third generation, extensively used nowadays,
abolish the immediate reactivity of the skin usually for 1–3 days. This concerns
cetirizine, loratadine, fexofenadine, ebastine, mizolastine, and the newcomers
desloratadine and levocetirizine. Prick testing can be performed 3 days after
stopping treatment. Longer wash-out periods are needed with ketotifen (15 days)
and astemizole (4 weeks). Oral methylprednisolone more than 8 mg daily and

22

equivalent doses of other corticosteroids may also weaken the immediate
reactivity of the skin. Other drugs such as non-steroidal anti-inflammatory drugs
as well as topical application of corticosteroids do not affect prick test results
significantly.5 In this case we educated the patient to avoid ussage of antihistamin
drugs, cold or flue medication that sold on over the counter store, and the patient
didn’t take any oral corticosteroid
Large numbers of commercial prick test allergens are available; self-made
allergens can also be used. Drops of allergen solutions are applied to the volar
aspect of the forearm or to the upper part of the back. The flexures of the elbows
must be avoided, because this may give rise to not easily readable reactions, either
positive or negative. Other skin sites are not convenient as well. An important
point concerns the distance between the individual prick tests. These are applied
ideally 3–5 cm apart to avoid overlapping of reactions at reading. If such a
distance is not respected, difficulties in correct reading are obvious and no definite
conclusions can be drawn. This mistake in technology happens too often, even
among well-trained clinicians. When drops of allergen solutions are applied to the
skin, they are pierced with a special lancet. Allerbiopoint is a stainless steel lancet
(length: 1.1 mm; penetration angle 45°; presenting itself as a blister of ten sterile
disposable lancets). Puncture is made by gentle pressure; some authors, when
puncturing, exert a slight rotation movement to ensure better penetration of the
allergen. No bleeding may occur.5

23

Figure 7. Prick testing. (a) Prick test lancets; (b) Positive prick test to latex: positive and negative
controls.6

Prick testing of allergens needs the concomitant use of controls, positive and
negative. Histamine chlorhydrate solution (1-10 mg/ml) to measure direct
reactivity to histamine. Saline and/or the vehicle of the allergens is used as a
negative control.5 In this case we use histamin 1 mg/ml as a positive control and
coca as a negative control.
After 15 min, the allergen and control droplets are wiped off with soft
paper tissue. Conventional time reading is 15–20 min, as we are evaluating an
immunological immediatetype 1 reaction. Reading prick test reactions needs
careful evaluation and interpretation, taking into account several parameters of
prime importance. The negative control ought to be negative; if positive, it raises
questions about the reading of allergen prick tests. Its main interest is therefore to
detect false-positive reactions.5 In this case the coca’s reading was negative and
the histamin’s reading was positive (+++).
Reading and interprating prick test should be measure carefully. These are
some parameters that should be notice on reading prick test:

24

● Wheal and flare reactions to positive controls, which appear around the piercing
usually in minutes, are measured in terms of diameters and surface areas
● Allergen prick test results are usually expressed as the mean of the longest
diameter of the wheal and the largest diameter perpendicular to it.
● Reactions greater than 3 mm and at least half of that produced by histamine are
regarded as positive. Reactions smaller than those produced by histamine may not
be clinically significant.
● If the patient has dermographism (factitious urticaria), skin piercing produces
usually small (1–2 mm) wheals, which may make the interpretation of the results
very difficult.5
There is a clear-cut difference in terms of readings between patch testing
and prick testing. Patch testing is a codified procedure that does not imply any
control, whereas prick testing is invariably submitted to controls either positive or
negative in order to achieve correct interpretation of the results. The final goal in
prick testing is to assess (either past or current) the relevance. The practical means
to conclude “likely,” “possible,” “doubtful,” or “not traced” relevance. 5 In this
case the result was positive ++ on house dust becouse the diameter was more than
3 mm or at least more than half of the positive control (4,80mm) which is
4,65mm.
Atopic patch test (APT) can be used as a diagnostic tool in characterizing
patients with allergen triggered AD.7,8,9 Shankar K, Chakravarthi M studied about
APT using prick test allergens in aluminium patch test chambers. 8 The antigens
are loaded in aluminium patch test chambers with filter paper using the dropper
provided by the manufacturer. A drop from the dropper was approximately 1/16
ml. The test site was upper back. The antigens used were dust mites: D. farinae,
D. pteronyssinus, pollens of Cynodon dactylon and Parthenium hysterophorus,
foods like rice, wheat, milk, egg and dog and cat epithelia. 8 The reading was taken
after 48 and 72 hours and interpretation and Grading of APT reaction was done
according to the guidelines by European task force on AD consensus (Figure

25

8).7,8,9 After 48 hours, were seen erythematous papules on number 4 (dog’s hair),
number 6 (house dust), number 10 (pindang fish), and number 12 (wheat flour).
And also after 72 hours, the reading only seen on number 1, 4, 6, ,28 with some
erithematous papules and the interpretation was +++. Number 22 and 27 the
interpretation was +.

Figure 8. Grading APT reactions.7
Finn Chamber is a round aluminum patch test device which provides good
occlusion because of the chamber design. The 8 mm inner diameter provides a 50
mm2 area and about 20 μL volume. The outer diameter is 11 mm and the distance
between the chambers is 20 mm. Apart from standard 8 mm (inner diameter) Finn
Chambers®, large 12 mm (inner diameter) Finn Chambers can be purchased (200
strips of one chamber). These are of special interest when using the APT. For
liquid allergens, place a filter paper disk in the chamber, and apply one drop of
liquid, just sufficient to soak the disk. Petrolatum patches can be made up a few
hours in advance; liquid patches should be made up at the last minute.6 In this case
we use finn chamber 8 mm size due to lack of the size 12 mm. We also use filter
paper disk to apply the allergens and immediately applied to the back area.
Dust mites are considered to be the most important triggering agent for AD.
In a study conducted in Croaotia by Kuljanac et al, on Dermatophagoides
pteronyssinus with APT and concluded that APT may detect the trigger factor in
AD patients.7 According to Turjamaa et al., and werfel et all, among the allergens
26

found to be relevant in atopic eczema, food allergens (mostly in children) and
aeroallergens are the most important.10,11 Environmental substances like
aeroallergens produce flares in some patients with atopic eczema. Moreover
aeroallergen avoidance, especially with regard to house dust mites, can result in
marked improvement of skin lesions. An epicutaneous patch test, APT, with type 1
allergens known to elicit IgE-mediated reactions, and the evaluation of
eczematous skin lesions after 24–72 h can be used as a diagnostic tool in
characterizing patients with aeroallergen and food-triggered AE. Atopy patch
testing (APT) has been investigated as a potential tool to identify foods which
may cause late-type symptoms such as exacerbation of AD.12
Another study done by Miroslav Necas, about APT using aeroallergen
prick testing, using histamin 10mg/ml as a positive control and salone solution as
a negative control. The allergens were applied to the patients’ backs during the
remission of atopic dermatitis. The first reading was made after 48 hours and the
second after 72 hours. The evaluation of the reactions was made according to the
ETFAD group recommendations, showed the most common allergen were house
dust mite allergens (12.8%), followed by grass and plant pollen (10.4%) and dog
allergens (8%).13 From this case, positive result on hause dust found on both test,
SPT and APT. Beside that, it has positive result on dog’s hair allergen and tempe
(+++) and weak reasult on orange (+).

27

SUMMARY
We reported a case of a 19 years old girl with atopic dermatitis who
presented by chief complaint red patches on both of her arms and legs since 3
weeks ago and got worse in the last 3 days. From history taking and clinical
appearence fit to hanifin and rajka criteria for atopic dermatitis. SCORAD was
used as severity score with the value of 25,29. The therapy was given, emolient,
desoxymethasone ointment twice daily, loratadine 10 mg once daily, also
education about the disease. The patient is also done skin prick test and atopy
patch test to identify the triggering factors of her disease. The result of the SPT
was house dust mite (++) and also for the APT are positive on dog’s hair, house
dust, and tempe. Patient then aducated about the result and to avoid the triggerring
factors.

28

REFFERENCES
1. Leung YM, Eichenfield FL,& Boguniewicz M. AD (Atopic Eczema) In :
Fitzpatrick’s Dermatology In General Medicine, 8 th edition, edited by
Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffel DJ, and Wolff K,
2012; p 165-182.
2. Thomsen FS. AD: Natural History, Diagnosis, and Treatment. ISRN Allergy,
2014, article ID 354250 p: 1-7
3.

Liska M, Gutova V, Panzner P, Brodska P. The Clinical Relevance of
Various Hypersensitivity Tests in Patients with AD as Assessed by Their
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4. Hanifin MJ, Thurston M, Omoto M, Cherill R,et all, The eczema area and
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Dermatology, 2001. vol. 10, no. 1, pp. 11–18.
5. Lachapelle MJ, Maibach IH. The Metodology Of Open (Non-Prick) Testing,
Prick Testing, And It’s Variants In : Patch Testing And Prick Testing, A
Practical Guide, 2nd edition, edited by Lachapelle MJ, Maibach IH, 2009;
p:141-51.
6. Lachapelle MJ, Maibach IH. Patch Testing Metodology In : Patch Testing
And Prick Testing, A Practical Guide, 2nd edition, edited by Lachapelle MJ,
Maibach IH, 2009; p:33-67.
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Testing, A Practical Guide, 2nd edition, edited by Lachapelle MJ, Maibach
IH, 2009; p: 121-6
8. Shankar K, Chakravarthi M. Atopic Patch testing. Indian J Dermatol
Venereol Leprol, 2008; p:467-70.
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Allergy In Children With Atopic Eczema Dermatitis Syndrome. Roczniki
Akademii Medycznej w Bialymstoku.2005;p: 261- 67.
10. Turjanmaa K, Darsow2 U, Niggemann3 B, Ranc K, Vanto5 T, Werfel6 T.
Present status of the atopy patch test. Allergy 2006: 61: 1377–1384.
11. Werfel T, Ballmer-Weber B, Eigenmann PA, Niggemann B, Ranc F,
Turjanmaa F, Worm M. Eczematous reactions to food in atopic eczema.
Allergy 2007: 62: 723–728
12. Tončić R.J, Lipozenčić J. Role and Significance of Atopy Patch Test. Acta
Dermataovenerol Croat 2010;18(1):38-55
13. Necas

M. Atopy Patch Testing
Dermatovenerologica. 2013;22:39-42.

with

airborne

allergens.

Acta

29

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