Download MINISTERUL SĂNĂTĂŢII REPUBLICII MOLDOVA

Moldavian Ministry of Health
STATE UNIVERSITY OF MEDICINE AND PHARMACY
“Nicolae Testemitsanu”
Faculty of Residency and Clinical Fellowship
Authors:
Florin Cenusha
Peter Martalog
Tatiana Gorelco
Tatiana Culeshin
Atopic dermatitis in children
Methodical indications
Kishinev 2010
CZU 616.5 – 053.2 (076.5)
Approved by Central Methodic Council of State University of Medicine and Pharmacy Nicolae
Testemitsanu, official report nr 1 from 18.02.2010
Authors:
Florin Cenusha – doctor of medical sciences, reader
Peter Martalog – doctor of medical sciences, reader
Tatiana Gorelco – doctor of medical sciences, pediatrician - allergologist
Tatiana Culeshin – doctor of medical sciences, pediatrician - allergologist
Methodological indications are edited for physicians - residents
Reviewers:
Susanna Shit, reader, doctor of medical sciences
Anna Guragata, reader, doctor of medical sciences.
Introduction
Main Principles:

Atopic dermatitis (AD) is a chronic allergic disease, upon which are IgE-dependent inflammation
and skin hyperreactivity.

AD develops in people with atopy (genetic predisposition to develop hypersensitivity reactions)
under
the action of external and internal factors and is one of the early manifestations of
systemic atopy.

Typical clinical manifestations of AD (widespread or localized) are: pruritus, persistent hyperemia
or transitory erythema, papulo-pustular vesicular eruptions, exudation, dry skin, desquamation,
excoriation, lichenification.

AD begins, as a rule, in the first months of life and is characterized by recurrent evolution.
Definition
Atopic dermatitis (AD) is a chronic allergic
disease, which develops in
predisposition to atopy, has a relapsed evolution
with a range
of age
people with hereditary
clinical particularities
and is
manifested by exudative and / or lichenoid eruptions, increased serum IgE levels and hypersensitivity to
specific and nonspecific irritation (allergic) .
Skin diseases phenotypically similar to AD, but which aren’t based on atopy in pathogenesis, are not
considered AD.
Terms used before - "atopic eczema", "endogenous eczema", "infantile eczema", "Brok atopic
neurodermitis”, " diffuse neurodermitis ", "prurigo-eczema" - according to contemporary classification
include the concept of AD. It should be pointed out that atopic eczema and atopic neurodermitis represent
the forms and stages of development of unique pathological process - the AD.
be used even
in the
presence
of minimal symptoms.
AD diagnosis should
This tactic allows
to
choose the
correct treatment and avoid more severe manifestations of atopy.
AD epidemiology
Main Principles:

Allergic diseases in children occupy the first place in the structure of all non-infectious diseases.

In the structure of allergic diseases in children, atopic dermatitis has the main place - 50-70% of
allergic diseases.

AD in children in developed countries is detected in 10-20% of the total child population.

Symptoms manifestation of AD in children is remarkable: in age up to 6 months - 60% of cases,
up to 1 year - 75%, up to 7 years - 80 - 90%.

In the last decades there has been a substantial morbidity increase of AD, is getting worse the
evolution of the disease, increases early invalidity.

AD is frequently associated with other allergic diseases: asthma - in 34%, allergic rhinitis - 25%,
relapsed laryngo-tracheitis - 10%, pollinosis - 8% of cases.

AD substantially affects quality of life, lead to a psychopathology personality formation, creates
difficulties in the choice of profession and family creation.

The real AD morbidity surpasses the actual official statistical data 5-10 times. This is related to
the use of different terminologies in diagnosis.
Allergic diseases can be easier to prevent, than treated. Treatment of early AD manifestations is far more
effective than treatment of advanced forms.
The risk factors in the development of atopic dermatitis in children
Main principles:

The main role in the development of AD in children belongs to the endogenous factors
(heredity, atopic skin hyperreactivity, impaired functional and biochemical processes of the skin),
which
in combination with various exogenous
factors (allergic
and
non-allergic)
leads to
development of the clinical picture of AD.

At the basis of AD development there is a genetically determined particularity (multifactorial
polygenic type of inheritance) of the immune response to allergen contact.

The immune response of atopic children is reflected by the prevalence of T-2 Helper, hyperproduction of total IgE and IgE-specific antibodies.

Skin hyperreactivity – is the basic factor in the risk for developing AD.

In families where parents are healthy, the risk of developing AD is 10-20%; in families where one
parent is suffering from diseases or allergic reactions, this risk is 40-50%; if both parents are allergic,
the risk is 80 - 90%.

Determination of the risk factors is required to give optimal prophylaxis and individual prognosis of
the disease.

Some exogenous factors (psycho-emotional efforts, weather changes, various pollutants, tobacco
smoke, food supplements) can cause AD exacerbation.

Among children in the early childhood the main cause of AD development is food allergy, in
children from 3 to 7 years increases the etiological importance of the habitual antigens and
fungal allergens, during puberty increases the influence of psycho-emotional factors.

Vaccination (especially against Diphtheria – Tetanus - Pertussis) in some children without clinical
and immunological status of evidence and without adequate prophylaxis is a trigger factor in the AD
development.
Food products, etiologically important for I year old children who suffer from AD:
Food product
Allergen (antigen)
Cow’s milk
Casein
Bovine serum albumin
Manifestation frequency
79 – 89%
β-lactalbumin
α-lactalbumin
Eggs
Ovalbumin
Ovo-mucoid
65 – 70%
Cereals
Gluten
30 – 40%
Soy
Protein S
20 – 25%
Fish
Paralbumin M
90 – 100%
Red or orange vegetables and Haptens (incomplete allergens)
40 – 45%
fruits
Food products - etiologic factors of food allergy (allergy according to the degree of activity)
High degree
Medium degree
The cow’s milk, fish, chicken
meat, eggs, strawberries,
raspberries, black currants,
blackberries, grapes, pineapple,
melon, nuts, honey, mushrooms,
mustard,tomatoes, carrots, beets,
celery, wheat, rye.
Pork, turkey, rabbit, potatoes,
Low degree
Horse meat, mutton (defatted),
zucchini, Turkish pumpkin,
peas, peaches, apricots, red
radishes, light color
currant, bananas, green peppers, pumpkins, green and
yellow apples, white cherries,
corn, buckwheat,
mossberry,
white currants,
gooseberry, plums, watermelon,
rice.
almonds, green cucumbers.
Atopic dermatitis classification
A universally accepted AD classification is not developed. At the same time most of clinics use
disease classification depending on the child's age, the affected area surface, the severity, the disease
period [9].
AD Classification according to age:
• Infant AD
• Child AD (up to 12 years)
• Adolescent AD (after 12 years)
AD Classification according to the affected area:
• Localized form when surface damage is less than 5% of skin tissue;
• Widespread form when surface damage extends from 5% to 50% of skin tissue.
• Diffuse form when surface damage exceeds 50% of skin tissue.
AD Classification by severity:
• Slight evolution;
• Moderate evolution;
• Severe evolution.
The severity of AD evolution is determined according to clinical symptoms of the disease:
For slight evolution are typical:
Hyperemia, exudation and insignificant skin excoriation (area <5%), papules, single vesicles, easy pruritus
that do not affect children's sleep, insignificant lymphadenopathy, no more than two acute exacerbation per
year.
For moderate evolution are typical:
Scratching, bleeding peels, damaged surface up to 50%, pruritus affecting the child's sleep, moderate
lymphadenopathy, up to four acute exacerbation per year.
For severe evolution are typical:
Massive outbreaks of exudation on the surface of more than 50%, erosions, fissures, bleeding scabs,
marked paroxysmal pruritus, sleep inversion, marked lymphadenopathy, more than four acute exacerbation
per year.
AD Classification according to the disease stage (period):
• acute stage (erythema, papule, vesicle, erosion, peels, excoriation).
• subacute stage (papules, excoriation, lichenification).
• chronic stage (lichenification, fibrinous papules).
Also there are a number of schemes (indices): SCORAD, EASI, SASSAD based on determination of AD
clinical manifestations severity. The most commonly used in our country is SCORAD scheme. The
final result is calculated by SCORAD index: Index SCORAD = A/ 5 + 7B / 2 + C where A, B and C are:
A. The spread - the spread area of the process (%). Calculate the area of skin desease is made according
to " number 9 law ": head and neck - 9%, anterior and posterior surface - each 18%, upper limbs - 9% ;
lower limbs - 18%, perineal region and genitals – each 1%.
B. The intensity of clinical manifestations is assessed based on six symptoms: erythema, edema / papule,
dry crusts/ moist exudation, excoriation, exudation, skin xerosis. Appreciation are made based on areas
with maximum clinical manifestation, xerosis - in not affected sectors. The degree of expression of the
each symptom is assessed by 4 - point scale: 0 - absent, 1 - poorly expressed, 2 – moderately expressed, 3 strongly expressed.
C. Subjective symptoms - pruritus and sleep disturbance. It is proposed the patient a 10 cm ruler to
show pruritus and sleep disorders intensity in the last three days. Every symptom is assessed from 0 to
10 points.
To appreciate the intensity of clinical manifestations to children less than 7 years can be used the
modification of the schedule SCORAD - TIS scheme, which is calculated as SCORAD index,
but only the parameters A and B by the following formula: A/5 + 7B/2.
The C parameter in children under 7 years is not appreciated, because children of this age are not able
to appreciate the subjective parameters such as pruritus and sleep disturbance level. SCORAD index total
score can range from 0 to 103 points.
Assessment based on the severity of AD SCORAD index values:
Index values
Severitaty of AD development
Up to 20 points
Slight evolution
From 20 to 40 points
Moderate evolution
Over 40 points
Severe evolution
Atopic dermatitis clinical manifestations
Anamnesis
In the AD suspects should be considered the following issues:

Did the patient had marked toxic erythema in the newborn period of life?

Is the patient bothered by pruritus?

Did the patient had allergic reactions to vaccines?

Did the patient had rash caused by any disturbances in food?

Did the level of expression of symptoms decrease after removing from nutrition the foods
with high allergic
potential,
those products
with histamine-liberating
action
and
high content of histamine?

Did the clinical manifestations decrease after antiallergic remedies administration?
In order to assess personal and hereditary antecedents is recommended to clarify the following moments:

The presence of pruritic eruption with characteristic localization and the evaluation conditions of
their improvement.

Family history of AD or other atopic diseases.

Eruption occurred as a result of a triggering factor (exposure to an allergen, stress, etc.).

Personal, family and environment factors.

Risk factors:

Tobacco smoke;

Contact with animal fur;

Contact with household chemicals, pollutants;

Contact with pollen and outdoor mold;

Early artificial nutrition;

Disorders in nutrition;

Antibiotics during pregnancy and lactation as well as antibiotic therapy in infancy;

Disorders in skin care;

Frequent respiratory diseases;

Functional disorders of the digestive tract.
Physical examination
Diagnostic criteria for AD [1,2,10]:
Common manifestations:

Pruritus

Typical morphology and localization

Early onset of disease

Chronic occurence with exacerbations

Familial or personal history of atopy
Frequent manifestations (seen in most of cases):

Skin infections

High IgE serum level

Non-specific dermatitis on hands and feet

Positive allergy skin tests

Skin xerosis

Periorbital hyperpigmentation
Occasional manifestations (nonspecific):

Focal erythema

Intolerance to certain food

Ichthyosis

Infraorbital fold Dennie – Morgan

Keratoconus

Nipple eczema

White pityriasis

Recurrent conjunctivitis

Wool intolerance

Pruritus from sweating
Diagnosis requires three common manifestation, and three frequent or casual symptoms.
Laboratory investigations in atopic dermatitis
Required laboratory investigation:

General blood analysis

IgE serum level

The level of IgE-antibodies to specific allergens

Allergy skin tests (allergologist)

Elimination diet
Recommended laboratory investigations:

Challenge tests (with certain allergens)

Urine summary

Serum biochemical indices (total protein, blood sugar, creatinine and urea, lactic dehydrogenase,
aspartate aminotransferase, alanine aminotransferase, bilirubin and its fractions).

The ionogram (Na, K, Ca, Cl).
General blood analysis in some cases shows eosinophilia, which may serve as nonspecific sigh of the
disease; in case of secondary outbreaks infection neutrophilic leukocytosis is possible.
Appreciation the IgE serum level is not a specific test for atopic dermatitis. Low levels of total IgE in
serum does not indicate lack of atopia and does not exclude the diagnosis criteria for atopic dermatitis.
Allergy cutaneous testing (skin-prik test, scarification probes) is performed by the allergologist and aims to
detect IgE-induced allergic reactions. It is usually carried out by the method of scarification: skin
scarification of 4-5 mm with standard applying a drop of allergen in a concentration of 5000 U / ml
(1 unit =0.00001 mg protein nitrogen / 1 ml).
Appreciation the allergic reaction by skin scarification test
Test appreciation
Conventional sign
The visual image of allergic reaction
Negative
-
It is the same as the control test
Uncertain
+/-
Local redness, without swelling
Weakly positive
+
Swelling papule, 2-3 mm diameter and peri-papular
redness
Positive
++
Swelling papule with a diameter >3mm<5mm and peripapular redness
Intense positive
+++
Swelling papule with 5-10 mm diameter and peri-papular
redness
Excessively
positive
++++
Swelling papule with more than 10 mm diameter, peripapular redness and pseudopodies
The appreciation of the reaction is done after 20 min. It must be carried out in lack of acute
manifestations of the atopic dermatitis. Administration of the antihistaminic remedies, antidepressants,
neuroleptics decreases cutaneous receptor sensitivity and therefore may be a false negative results. For these
reasons named remedies need to be excluded for a period of 3-7 days before the examination.
Assessing the level of IgE-antibodies to specific allergens in blood serum is indicated to patients:

With diffuse forms of atopic dermatitis.

Who can’t be deprived of antihistaminic, antidepressants, neuroleptics therapy.

With skin allergy test
with dubious results, or absence
of
the
correlation between
clinical
manifestations and skin test results.

With high risk to develop anaphylactic reactions from any allergen in a skin test performance.

In infants.

In absence of allergens for allergy skin test and the existence of these to examine in vitro.
The elimination diet and challenge test with some allergens are indicated and performed by a
specialist doctor ( allergologist).
Hospitalization criteria for patients with atopic dermatitis
• Acute exacerbation of atopic dermatitis, accompanied by disorders of general condition.
• Widespread skin process, accompanied by secondary infection (bacterial, herpetic).
• Recurrent skin infections.
• AD in combination with other atopic diseases with severe evolution.
• Inefficiency of standard therapy carried out.
General principles of medical treatment in atopic dermatitis

Topical treatment (local) is a required and important section of the complex therapy of atopic
dermatitis.

Topical glucocorticosteroids (GCST) are first-line remedies in AD exacerbation treatment.

GCST presents the first step in the treatment of atopic dermatitis with moderate and severe
evolution.

In case of infectious complications are indicated a combination of topical remedies – containing
glucocorticosteroods, antibiotics and antifungals.

Calcium-neurin inhibitors are used in slight or moderate forms, or to improve the general state (after
treatment with GCST) in severe forms of AD.

Antiinflammatory remedies without glucocorticosteroids content which were previously used (tar,
naphthaline, ichthyol), at the moment because of low efficiency and high capacity of skin
photosensitivity are practically not used.

Emollient remedies are obligatorily used in AD therapy to improve dermal barrier function and to
recover the epidermal lipid layer.

Systemic antihistaminic therapy, both with sedative, and nonsedative remedies, is the main therapy
of AD in infants.

Systemic antibacterial therapy is indicated only to patients with severe skin infections, with fever,
intoxication, disturbances of general condition.

Immunosuppression therapy is used in very severe cases of AD, in inefficiency of other treatment
methods. There are recommended short courses of systemic glucocorticosteroids, cyclosporine,
azathioprine.

Hyposensibilization specific therapy is not recommended for patients with AD. At the same time it
may be highly effective in cases of asthma, associated rhinoconjunctivitis.
Topical glucocorticoids are indicated for children with moderate, severe or continually recurrent form of
atopic dermatitis, in case of resistance in other forms of treatment. [1, 2, 3, 4]. Depending on the therapeutic
potency, GCST is divided into several classes (or groups), in Europe there are 4 classes.
European GCST classification [1, 2, 9, 11]:
CLASS
I – low potency
DRUG NAME
Hydrocortisone acetate 0,5%,1%,2,5%
Prednisolone 0,5%
II- medium potency
Mazipredon hydrochloride 0,25%
Hydrocortisone 17 – butyrate 0,1%
Fluocinolone acetonide 0,025%
Flumethasone pivalate 0,02%
Fluocortolon 0,25%
III-high potency
Betamethasone valerate 0,1%
Triamcinolone acetonide 0,1%
Methylprednisolone aceponate 0,1%
Budesonide 0,025%
Halometasone monohydrate 0,05%
Mometasone furoate 0,1%
IV-extreme potency
Clobetasol propionate 0,05%
Halcinonid 0,1%
The GCST administration rules:
1.
Not to be used with the purpose of AD prophylaxis.
2. The contemporary GCST can be used in any skin area (excluding periorbital area).
3. Are prefered remedies with high efficiency and long term action.
4. Start the treatment with high potency glucocorticosteroids (3 – 5 days), then continue with medium
and low potency remedies.
5. GCST are used till the liquidation of the disease symptoms (including the pruritus).
6. Treatment duration varies from 3 to 5 days, till 1 month of daily administration (if is necessary a
longer cure is possible, in an intermittent manner).
7. Children under 2 years old are indicated non-fluorinated remedies.
8. Infectious complications need to be treated before the GCST indication.
9. Not recommended to use the IV class remedies (very active) in children under 14 years old.
Contraindications for topical glucocorticosteroids administration:
1. Tuberculosis and cutaneous syphilis
2. Viral infections (chickenpox, herpes simplex)
3. High patient’s sensibility towards the remedy components.
Frecvently used topical glucocorticosteroids in the AD treatment in children:
Drug name
Administration is allows from :
Drug administration frecvency
Hydrocortisone acetate
Birth
2 times in 24 hours
Prednisolone
More than 1 month
2 times in 24 hours
Methylprednisolone aceponate
6 months
1 time in 24 hours
Hydrocortisone 17-butyrate
6 months
1 – 2 times in 24 hours
Mometasone furoate
6 months
1 time in 24 hours
Adverse effects of long term GCST administration:
Local

Skin atrophy

Skin eruptions, acne, striae

Hypertrichosis

Secondary skin infection (bacterial,fungal)

Disorders of skin pigmentation

Tachyphilaxis.
Systemic:

Hypothalamic-pituitary-adrenal axis suppression

Growth retention

Cushing syndrome development.
The causes of GCST adverse effects:

Uncontrolled GCST administration, especially the fluorinated ones

Using the method of GCST dissolving

The use of GCST during the disease remission

Using GCST on large skin areas (>20%)
Topical immunomodulators (calcium-neurin inhibitors) presents a nonsteroidal antiinflammatory
medication. In medical practice are used two remedies: Pimecrolimus cream and Tacrolimus ointment [2,8].
In RM 1% Pimecrolimus cream is registered.

Is given to children under 3 months.

Apply on any sections of the skin.

Is indicated for children with slight and moderate AD forms or with an improved general condition
(after complete the GCST cure) in severe dermatitis.

The risk of developing secondary skin infection is lower in patients treated with pimecrolimus,
compared with patients treated with GCST.

Patients who used pimecrolimus are recommended to minimize exposure to sunlight.
Topical remedies with antibacterial and antifungal effects are efficient in the treatment of patients with AD
complicated with bacterial or fungal skin infection [9, 11]. To avoid fungal infection expansion on
antibacterial therapy background it is indicated the administration of combinated remedies, with
bacteriostatic and antifungal content (eg, Natamycin + Neomycin + Hydrocortisone or Betamethasone +
Gentamycin + Clotrimazole).
Emollient remedies, because they reduce inflammation and relaxe the skin are included in the recent
therapeutic standards of atopic dermatitis [2, 3, 7, 9]. This group includes traditionally used remedies
(Lanolin, Dexapantenol) and contemporary curative cosmetic remedies.
Rules for emollient administration:

Use daily, no more than twice a day.

It is given together with GCST and calcium-neurin inhibitors and during remission, in absence of
symptoms.

In order to avoid tachyphylaxis the remedy substitution is required every 3-4 weeks.
With the purpose of skin cleansing is recommended:
 Daily baths.

The use of hygienic products (soap, shampoo, gel) with a neutral pH.

Aviod the sponge.
Systemic treatment includes the use of antihistaminic, antibacterial, immunosuppressant remedies.
Antihistaminic remedies are the most commonly used remedies in atopid dermatitis therapy [1, 2]. They are
indicated in case of impossibility to eliminate allergens from the patient’s usual environment, in constant
contact with the removed allergens, to reduce and suppress the skin allergic inflammation, the cutaneous
pruritus. Sedative and nonsedative antihistaminic therapy (1st and 2nd generations) is quilified as the main
therapy in atopic dermatitis in children.
1st generation drugs (sedative)
2nd generation drugs (nonsedative)
Dimetinden
Loratadine
Quifenadine
Desloratadine
Clemastine
Cetirisine
Chloropyramine
Levocetirisine
Cyproheptadine
Fexofenadine
Sedative antihistaminic remedies

Must not be used for a long time or continuously.

Use only in acute exacerbation, in short courses before bedtime.

Not recommended for patients with AD, in combination with asthma or allergic rhinitis.
Adverse effects: tachyphylaxis, sleepiness, cognitive function depression, M-colinolitical effects.
Nonsedative antihistaminic remedies

Are used for a long time control in nocturnal and diurnal pruritus.

Almost do not manifest sedative effects, possess antiinflamatory effect.

They are used in the treatment of patients with AD, in association with asthma or allergic rhinitis.
Systemic antibiotics (Spiromycin, Azithromycin, Cefuroxime, Ceftriaxone) is recommended for patients
with severe, confirmed bacterial skin infections. Aren’t used in case of absence of dermal infection
symptoms. Do not influence the AD evolution. Long – term administration for other purposes (eg. Standard
therapy in resistant to treatment forms) is not recommended [ 10].
Systemic glucocorticosteroids (Prednisolone, Dexamethasone) are indicated in short cures [1, 3, 6].

Used in severe atopic dermatitis resistant to topical glucocorticosteroid and antihistaminic treatment.

Are given in aggressive pruritic syndrome on a diffuse skin disease background.

When used for a long time period, there are significant adverse effects.
Immunosuppressant remedies
Cyclosporine A, Azathioprine are efficient in severe atopic dermatitis which do not respond in other
treatment modalities [5]. For the reason of multiple toxicity and secondary effects, their use is very limited.
Cyclosporine is used more frequently in short courses, on average 8 weeks.
Adequate management in atopic dermatitis has the following objectives:

Minimal or no symptoms.

Minimum acute episodes.

No emergency visits to the doctor or hospital.

Lack of complications.

Minimum or no secondary effects caused by medication.
Continuous monitoring is essential in achieving the therapeutic goals. During these visits is analysed and
modified the treatment program, the medications and the control of the treatment level.
Monitoring of patients with atopic dermatitis.

Patients return to the medical visit 2-4 weeks after the first visit, and then – every 3 months.

When established the AD control, regular maintenance visits remain essential.

Number of visits to doctor and appreciation of the control level depends on the initial pathology
severity to a certain patient and the patient’s educational level regarding to measures necessary to
maintain AD control.

\
Level of control should be established in certain intervals of time by the doctor and the patient.
Annex 1
Diagnostic algorhythm in atopic dermatitis
Symptoms and manifestations
Differential
diagnosis.
Diagnosis of
concomitant diseases
Hanifin &
Rajca
[1, 2]
Severity appreciation
SCORAD
EASI
SASSAD
Symptoms stability
Factors that promote
exacerbation
Food allergy
Household, pollen
allergy. Allergy to
medicines
Infection.
Environmental
conditions
DIAGNOSIS
Annex 2
Stepped therapy of atopic dermatitis in children
AD forms that don’t
respond to treatment
The intensity
Moderate or expressed
AD manifestations
Slight or moderate AD
manifestations
Dermal xerosis
Skin cleansing
IV Step
III Step
II Step
I Step
Systemic immunosuppresive,
GCST, 2nd generation
antihistaminics, phototherapy.
2nd
generation
systemic
antihistamines, medium and
high potency GCST (1st line), to
stabilization
(reduced
symptoms) – calcium-neurin
inhibitors (2nd line)
2nd generation systemic
antihistamines, low and
medium potency GCST (1st
line), calcium-neurin
inhibitors (2nd line)
The main therapy: emollient,
hydratanting remedies,
remove trigger
Annex 3
Medication used in atopic dermatitis treatment
Medications ( in
Dose
Daily dose/24 hours
brackets – trading
Number of daily
administration
name)
SYSTEMIC ANTIHISTAMINIC MEDICATION
Sedative antihistamines ( Ist generation)
Dimetinden
Drops 1 ml (20 drops)
Up to 1 year 3 – 10
(Fenistil)
1 mg – 10 ml
drops; from 1 to 3 years
– 10-15 drops; over 3
3
years – 15-20 drops
Quifenadine
Tablet 0,01g, 0,025g;
From 1 to 3 years 0,005
(Fencarol)
powder 0,01g
g; 3-7 years – 0,01 g;
2-3
over 12 years – 0,025g
Clemastine
Tablet 0,001 g;
From 1 to 6 years – 0,25
(Clemastine, Tavegyl)
ampoules 2,0 ml (1
mg; from 6 to 12 years
mg/ml)
– 0,5 mg; over 12 years
2
– 0,001g
Chloropyramine
Tablet 0,025 g;
Up to 1 year – 0,002 –
(Suprastine)
ampoules 2%, each 1,0-
0,005 g; from 1 to 6
2,0 ml
years – 0,005 – 0,015 g;
2-3
from 6 to 12 years –
0,015 – 0,025 g.
Intramuscularly –0,5 –
1,0 mg/kg. Intravenous
– 1/3 from
intramuscular dose.
Cyproheptadine
Tablet 0,004 g;
From 6 months to 2
(Cyproheptadine,
syrup 0,4 mg/ml (2
years 0,4 mg/kg; 2-6
Peritol)
mg/5 ml) – 100 ml
years 6 mg/day; 6-14
years 12 mg/day
3
Nonsedative antihistamines (2nd generation)
Loratadine
Tablet 10 mg;
From 2 to 12 years,
(Agistam, Clarisens,
Drinkable suspension 5
with body weight less
Claritin, Erolin,
mg/5ml – 120 ml
than 30 kg – 5 mg; over
1
30 kg – 10 mg.
Flonidan,
Klarifer,Lomilan, Lora10, Loraderm-KMP,
Loratadine 10-SL)
Cetirizine (Cetirizine
Drops 1 ml (20 drops)
From 6 months to 1
SL, Letizen, Parlazin,
10 mg – 10 ml; drops 1
year – 5 drops once;
Zyrtec)
ml (20 drops) 10 mg –
from 1 to 2 years – 5
20 ml; tablet 10 mg
drops twice ; from 2 to
1-2
6 years – 5 drops twice
or 10 drops once; over 6
years – 20 drops or 1
tablet once
Dezloratadine
Syrup 0,5 mg/ml 100
From 6 months to 1
(Aerius)
ml; tablet 5 mg.
year – 2 ml; from 1 to 6
years – 2,5 ml; from 6
1
to 12 years – 5 ml; over
12 years – 10 ml or 1
tablet
Levocetirizine
Drops 1 ml (20 drops)
From 2 to 6 years – 5
(Xyzal)
5 mg – 20 ml;
drops twice; over 6
tablet 5 mg
years – 1 tablet or 20
1-2
drops once
Fexofenadine
Tablet 30 mg, 120 mg,
From 6 to 12 years – 30
(Telfast)
180 mg.
mg twice; over 12 years
– 120 mg or 180 mg
once
1-2
CORTICOSTEROID REMEDIES
Systemic glucocorticosteroids
Methylprednisolone
Tablet 4 mg; ampoules
0,25-0,2 mg/kg/day
40 mg/ml
Prednisolone
1-3
Tablet 5 mg; ampoules
1 – 2 mg/kg/day for 3 –
25 mg/1ml or 30 mg/ml
10 days (maximum 60
1-3
mg/day)
Dexamethasone
Tablet 4 mg; ampoules
0,15 – 0,45 mg/kg/day
4 mg/ml
for 3-10 days
1-2
Topical glucocorticoids
Hydrocortisone acetate
Ointment 1% - 35 g şi
Localy, from birth
50 g; cream 2,5% 10 g.
2
Ointment 0,5% - 10 g şi
Localy, from the age of
20 g
1 month
Methylprednisolone
Ointment 0,1% - 15g;
Localy, from 6 months
aceponate (Advantan)
cream 0,1% - 15g.
Hydrocortisone 17 –
Ointment 0,1% - 20 g.
Prednisolone acetate
2
1
Localy, from 6 months
butyrate (Locoid)
1-2
Mometasone furoate
Ointment 0,1% - 15g;
(Elocom)
cream 0,1% - 15g.
Localy, from 6 months
1
Preparate combinate
Natamycin + Neomycin
Cream 15 g; ointment
+ Hydrocortisone
15 g.
Localy, from 1 year
2
(Pimafucort)
Betamethasone +
Gentamycin +
Clotrimazole (Triderm,
Acriderm GC)
Cream 30 g
Localy, from 2 years
2
CALCIUM-NEURIN INHIBITORS
Pimecrolimus (Elidel)
Cream1% - 15g and 30g Localy, from 3 months
2
IMMUNOSUPPRESSIVE REMEDIES
Cyclosporine (Sandim-
Capsules 25 mg; 50 mg;
2,5 – 5,0 mg/kg body
mun, Sandimmun
100mg.
weight
Neoral)
2
REFERENCES:
1. Consensus Conference on Pediatric Atopic Dermatitis J. Am. Acad. Dermatol.2003; 49: 1088 –
1095.
2. Consensus Report EAACI/AAAAI/PRACTALL Diagnosis and treatment of atopic dermatitis in
children and adults. J. Of Allergy and Clin. Immunol. And Allergy, 2006: (61): 969-987.
3. Ellis C., Luger T., Abeck D. Et al. International consensus Conference on Atopic Dermatitis II
(ICCAD II): clinical update and current treatment strategies. Br. J. Dermatol., 2003 May; 148 Suppl.
63:3-10.
4. Hanifin J. M., Gupta A. K., Rajagopalan R. Intermittent dosing of fluticasone propionate cream for
reducing the risk relapse in atopic dermatitis patients. Br. J. Dermatol., 2002; 147(3): 528-537.
5. Harper J.I., Ahmed I., Barclay G. Et al. Cyclosporin for severe childhood dermatitis: short course
versus continuous therapy. Br. J. Dermatol., 2000: 142(1): 52-58.
6. Hoare C., Li Wan Po A., Williams H. Systematic review of treatments for atopic dermatitis.//Health.
Technol. Assess. 2000;Vol.4, P. 1-191.
7. Shav J. C. Atopic dermatitis. Up To Date December 29, 2003.
8. Wahn U., Bos J. D., Goodfield M. et al. Efficacy and Safety of Pimecrolimus Cream in the LongTerm Management of Atopic Dermatitis in Children.// Pediatrics.-2002.-Vol 110(el).
9. Аллергология и иммунология. Под ред. Баранова А.А. и Хаитова Р.М. – Москва, 2008, с.1074.
10. Минаева Н.В., Корюкина И.П. Атопический дерматит у детей: диагностика, лечение,
профилактика. Пермь, 2007, 32 с.
11. Педиатрия. Клинические рекомендации. Под ред. Баранова А.А. – М.: «ГОЭТАР-Медиа». –
2007.- с.17 – 35.
12. Dermatita atopică la copil. Protocolul clinic naţional (PCN – 79). Chişinău 2008.