ATOPIC DERMATITIS

1. INTRODUCTION
Eczema or atopic dermatitis is an inflammatory disorder of the skin of allergic,
chronic and intermittent (coursing outbreaks), initially characterized by inten
se itching, dry skin. It is a common pathology, since this is the most frequentl
y diagnosed dermatitis in primary care. It is also the most common skin disease
in childhood. Although it is a disease of chronic evolution, 60% go the first ye
ar of life, 25% do so later but in the first five years, and only 10% persist be
yond seven years, or reappear in adulthood or adolescence. There are plenty of t
erms that are synonymous with atopic dermatitis: prurigo, eczema flexurarum, Dia
tessaron pruritus, neurodermatitis, endogenous eczema, constitutional eczema, ex
udative eczema, atopic eczema. Itching is the most important symptom, and produc
es an inevitable scratching of erythematous lesions that can lead to eczematizat
ion of the skin, secondary infection, and eventually occur in the same lichenifi
cation (thickening of skin eczema, which takes on aspects of leather; occurs mai
nly around skin folds). For these symptoms will produce a significant change in
the quality of life. Is a major health concern, social and economic, due to the
increased incidence in a 100-200% in the last 30 years. The prevalence is differ
ent according to geographical areas, is more common in developed countries (wher
e the prevalence is 10 to 13%), and mainly in urban areas. In addition, no signi
ficant differences according to sex. Its clinical expression is variable and is
frequently associated to asthma, allergic rhinitis and food allergies.
2. PATHOGENESIS
2.1. Genetic factors
There are two basic genetic predisposing factors present in atopic dermatitis (A
D): 1. In these patients there is a special provision of the skin that facilitat
es the penetration of allergens, and therefore contact them with the individual'
s immune system. The causative factor of this disorder is unknown.
2. Misuse of Th2 immune responses: it seems that the mechanism of hypersensitivi
ty that causes this disease would be a mixed between type I and IV, and the dive
rsion of the immune response of LTH (partners) to Th2 (allergic-type response )
could have a role, but this has not been demonstrated, as yet unknown pathogenes
is.
2.2. Predisposing factors
Fina Skin characteristics (thin and friable) Low fat secretion alkaline pH Low L
ow sweat secretion secretory IgA Ac.Grasos altered composition (essential and ce
ramides) Dry skin (as it promotes the release of histamine) Water loss Liberatio
n mediators: prostaglandins and leukotrienes increased skin reactivity white Der
mographism: bleaching a few seconds of the red line produced after rubbing of th
e skin and skin whitening erythematous delayed after injection of cholinergic su
bstances. B-adrenergic blocking release of mediators: prostaglandins and leukotr
ienes All these factors facilitate skin inflammation (and thus exacerbate the it
ch), the penetration of allergens and bacterial colonization.
3. SYMPTOMS AND SIGNS
The initial morphology of the lesions is given by a follicular papule, and later
eczematous plaques that change in time as this, there are three forms of presen
tation of atopic dermatitis, which is most commonly associated with a particular
age: Acute Eczema: own infant, is characterized by vesicular and exudative lesi
ons on an erythematous base. Subacute Eczema: typical of childhood and is charac
terized by erythema and scaling.
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Chronic Eczema: own young adulthood, its clinical signs are basically the lichen
ification and hyperkeratosis.
Although this is the most frequent distribution, the three types of eczema can c
oexist on the same patient. A key factor for the geographical distribution of in
juries is the patient's age, according to this, there are three stages in atopic
dermatitis: Phase infant, child phase, and phase of the adolescent and the adul
t. Infant stage: occurs between the first and third month of life. It is charact
erized by an erythematous rash with papules elements and a large vesicular exuda
tive component, which primarily affects cheeks, forehead, ear folds, and scalp.
Occasionally spreads to the neck, trunk and extensor surface of limbs; also resp
ects the nasolabial triangle and the area of diaper rash. Its infancy: it appear
s between 2 and 12 years of age.€It is characterized by erythematous papular le
sions with a lower degree of exudation in the previous phase and there is a grea
ter tendency to lichenification by scratching. It typically affects the antecubi
tal and popliteal folds, but can also affect the facial region, eyelids, periora
l (cheilitis), atrial fold, wrists, hands, fingertip, ankles and feet. It is the
most common form of atopic dermatitis, and most of them disappear at 4-5 years
of age. Stage of adolescent and adult: papulación predominate clinically and li
chenification on the basis of intense xerosis (abnormally dry skin, which has a
flaky). The location is similar to that of the infant stage, with preferential a
lteration of the flexion creases and facial region.
INFANT PHASE
CHILDREN'S STAGE
4. DIAGNOSIS
The diagnosis is mainly clinical and is based on the presence of at least three
major criteria + at least three minor criteria (Hanifin and Rajka criteria): Cri
teria Morphology and distribution more Itching Dermatitis typical chronic, persi
stent or recurrent personal and family history atopy; are atopic diseases (ie al
lergic diseases genetically determined) allergic asthma, allergic rhinitis and a
topic dermatitis. Minor criteria xerosis (dry skin) Ichthyosis (hereditary skin
disease that causes dry, scaly skin). Palmar Hyperlinearity. Keratosis pilaris (
form keratin plugs in hair follicles, giving the skin appearance of "goose bumps
") elevated serum IgE positive skin tests Start Early Age: 1-3 months Tendency T
endency to skin infections, nonspecific dermatitis Eczema hands and feet nipple
cheilitis (dry corners of the mouth) recurrent conjunctivitis Dennie-Morgan fold
: the existence of a double infraorbital fold (bottom)
Keratoconus, anterior subcapsular cataract
Periorbital darkening facial pallor or erythema Pityriasis alba: skin disorder i
n which patches appear on the same colorless, round or oval, with finely scaly t
exture, usually on the cheeks (bottom)
Pleats in front of the neck sweating itching wool intolerance and solvents perif
ollicular accentuation white Dermographism food intolerance Influence of environ
mental factors
5. DIFFERENTIAL DIAGNOSIS
Seborrheic Dermatitis: the differential diagnosis is more common in adults. The
suspicion if there is: Family history of early onset seborrheic dermatitis (befo
re month of life) no or mild itching erythemato-squamous lesions crusted with fa
t scale, without blistering, rounded, well
bounded without raised edge of variable size (right image) Location on the scalp
, mustache and intertriginous areas (where there are skin folds) Assignment to t
he diaper area and inguinal folds
Irritant contact dermatitis (diaper dermatitis) is the most important differenti
al diagnosis in children. Affect normal children (non-atopic) after exposure to
irritants such as saliva, urine, feces or detergents. Sometimes it may be associ
ated with Atopic Dermatitis and when it does, is less dry and less itchy than th
is. The differential diagnosis is straightforward, given the rash appears on the
irritated area (mainly the diaper area). Allergic Contact Dermatitis: lesions s
imilar to atopic dermatitis but limited to the area of contact with the allergen
ic material. Scabies or scabies: a contagious skin disease is rarely caused by t
he parasite Sarcoptes scabiei. Itching occurs mainly at night and is characteriz
ed by the presence of papules, vesicular exudative lesions similar to atopic der
matitis, but differs in the presence of acariana eminence in the form of beading
or furrow elevation (due to travel the parasite in the skin). It is located in
the folds between the toes, elbows, armpits, buttocks, breasts, glans penis, and
affects other family members residing with him.
Lichenoid dermatitis scabies or scabies: clinical manifestations flat papules, 2
-3 mm, sometimes hypopigmented, which are located on the back of the hands, elbo
ws or knees. Pruritus is absent or mild, and typically appear in the months of s
pring / summer, with spontaneous improvement. Other: Fungal dermatitis herpetifo
rmis Pityriasis Acrodermatitis enteropathica
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Histiocytosis X primary immunodeficiencies (Wiskott-Aldrich syndrome, Ataxia tel
angiectasia, Sind. HiperIgE).
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Netherton Syndrome Phenylketonuria
6. FOOD ALLERGY AND DA
We have seen that 50% of infants and young children with moderate or severe atop
ic dermatitis have food allergy proven by double-blind provocation tests, ie tha
t half of children with food allergy DA is involved in the exacerbation the tabl
e. The foods most frequently associated are the egg (mostly, 25%), milk, fish, w
heat, soybeans, peanuts and nuts, these foods are responsible for 90% of tests p
ositive double-blind provocation studies published. While allergies to eggs and
milk disappear with age, other food allergies are very persistent. Recent studie
s have found that the association of atopic dermatitis and egg allergy increases
the risk of respiratory allergic diseases at 4 years of age with a predictive v
alue of more than 80%.
90 80 70 60 50 40 30 20 10 0 0-1 years = /> 2 TCAlm. (+) TCInh. (+)
In the left graph shows the percentage of children sensitized to food allergens
(ie, presenting IgE
specifically, it corresponds with the bar on the left) and inhalant allergens (r
ight bar) depending on their age. As can be seen, over 90%
of children under one year are sensitized to food, and that awareness declines w
ith age, whereas sensitization to inhalant allergens increases with age. It is i
mportant to understand that in children with atopic dermatitis the presence of s
pecific IgE to a food does not mean that the food involved in the exacerbation o
f DA box, therefore, before removing the food we verify their participation by:
1. Identify and relate with clinical / allergen by clinical history and examinat
ion. 2. To identify IgE-mediated sensitization to / or allergen / s by skin test
s or specific serum IgE. It has been more profitable than making a
patch test (which is used for diagnosis of type IV hypersensitivity) that a Pric
k-test (hypersensitivity type I), especially if still positive on the second tes
t is performed. 3. Evidence that sensitization to the allergen / s is responsibl
e for the clinic by controlled challenge test, this test is that: The exclusion
diet for 2 weeks is followed by improved oral provocation is followed by deterio
ration, in which provocation case involves no risk, since the most that can happ
en is that exacerbate atopic dermatitis box. In studies this test is done with d
ouble blind
7. TREATMENT OF THE DA
The two pillars of the treatment of AD are antihistamines (necessary to eliminat
e the itching and so break the vicious circle itch-scratch-eczema-pruritus that
superinfection), and measures of a toilet, taking care not to damage the fragile
skin of these patients. 1. Standards for skin care: Good doctor-patient relatio
nship (TALK). Curative Treatment There is no single cause. The removal of the fo
od that exacerbates the DA box (positive oral challenge), although we have seen
that does not solve the background skin hyperreactivity. Favorable prognosis "?
General skin care: adequate hydration (fundamental): Reduce frequency of use of
soap, mild soap and avoid using deodorants and scented soaps. Be reduced as much
as possible (1-2 times / week) the bath, using warm water and avoiding long bat
hs. The 50% glycerin rosewater is better than soap. It extends to apply a massag
e to the skin is dried with cotton. Use moisturizers frequently (at least 2 time
s a day, ideally 2-4 times a day or more), especially after bathing, exercise, s
wimming, washing, etc. For broadcast applications are preferred lotions. The bat
hrooms with the addition of colloids are useful to hydrate the skin. Add half a
cup of corn flour (cornstarch ®) or oats (Aveenoderm
bañoidal ®,
Aveenoderm
emo-colloidal ®).
Also
there
pills
dermatological (Aveenobar ®). Avoid irritating and aggravating factors to reduc
e itching and scratching: Avoid too tight or irritating clothing (wool, fur or a
nimal hair). We recommend cotton clothing for its porosity and softness, especia
lly underwear and pajamas. Wash clothes with a mild detergent without perfumes a
nd rinse thoroughly. Avoid starch clothes. Keep soft ambient temperature of the
room. Caring for the nails are well trimmed. You can use cotton gloves at night
if necessary. Avoid contact with animals, dust, sprays and perfumes. If there is
eczema on the feet, avoid sneakers and rubber soles. Change socks frequently.€
Skin Care question: Wash daily with warm water without detergent + bath oil. The
bathrooms should be short and warm water with oatmeal gel does not harm the ski
n, and then perform a proper hydration products recommended by your doctor. Ster
oid creams are only used in severe cases. 2. Elimination of allergens: If the pa
tient has a history of exacerbation of skin lesions after taking a meal, and spe
cific skin tests are positive (oral challenge), these foods should be eliminated
from the diet. If it is an essential nutrient, such as milk for babies, your do
ctor may recommend non-allergenic substitute. However, the elimination of the fo
od fails to fully control the disease. If environmental factors are suspected, s
uch as allergy to pollen, dust mites, animal dander, are also taken appropriate
measures to avoid contact with these allergens: mattress covers and pillows (if
skin test (PC) +) Elimination of pets, etc. . (If PC +) No smoking in house Wear
soft cotton or linen Avoid overheating the room 3. Pharmacological treatment of
atopic dermatitis: Antihistamines are very useful to relieve itching, and there
fore needed to break the vicious circle.
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Symptomatic treatment (the outbreak): Topical corticosteroids (best creams ointm
ents): steroid creams should be reserved for major injuries and will be used for
short periods of time (3 days). Topical antibiotics in case of an injury from b
ecoming infected: â ¢ â ¢ fusidic acid (S. Aaureus) Mupirocin
Pimecrolimus (1% for> 2 years): is a corticosteroid drug of nature that acts sel
ectively on the skin by inhibiting the synthesis and release of inflammatory cyt
okines in T lymphocytes (which are key cells in the pathogenesis of atopic derma
titis ), and inhibiting mast cells. In this way, reduces itching and erythema as
sociated with atopic dermatitis. This drug has been specifically developed to tr
eat inflammatory skin diseases. Tacrolimus (0.03% for> 2 years) (0.1% only in ad
ults): a drug with action similar to above, since both are topical calcineurin i
nhibitors. The potency of 0.1% Tacrolimus is similar to that of glucocorticoster
oids (GCE) potent topical, being greater than that of Tacrolimus 0.03% and 1% Pi
mecrolimus, which have the same power as potent topical GCE media. Both drugs ca
n only be used in over 2 years. Tacrolimus and Pimecrolimus To use is necessary
to take the precautions indicated by the FDA and the EMEA, as has been the use o
f these drugs may increase the incidence of certain cancers. Therefore only be u
sed in outbreaks and for the shortest time possible.
Therapeutic step in atopic dermatitis
In early stages (in which there is only dry skin) is treated the patient with ba
sic measures: skin hydration, emollients, avoiding irritants and identifying and
avoiding potential triggers. When the DA is now moderate, these measures will b
e added to potent topical corticosteroids, low-medium and / or topical calcineur
in inhibitors (tacrolimus 0.03% or pimecrolimus 1%). Faced with a moderate or se
vere AD, the patient was treated with topical corticosteroids and / or topical c
alcineurin inhibitors (tacrolimus 1%). Finally, faced with a recalcitrant and se
vere AD (which usually occurs in adults), systemic treatment is administered wit
h cyclosporine A therapy or UV (ultraviolet).
Cutaneous mastocytosis
The cutaneous mastocytosis encompass a set of rare diseases characterized by an
accumulation of mast cells in the skin, with or without involvement of other org
ans or systems.
1. Classification of mastocytosis
Cutaneous Mastocytosis Urticaria pigmentosa Mastocytoma solitary eruptive macula
r telangiectasia perstans Mastocytosis Mastocytosis, diffuse cutaneous malignant
systemic mastocytosis (mast cell leukemia)
2. Cutaneous mastocytosis
The etiology is unknown. Both sexes are affected equally. It is more common in C
aucasians. There are two peaks of incidence: under 6 years and between 20 and 40
years. Most cases are sporadic and only rarely there are other family members a
ffected.
2.1. Urticaria pigmentosa
It is the clinical form of mastocytosis more frequent, and mainly affects infant
s and children. The lesions may be present at birth, but more often is the appea
rance in different outbreaks during the first months to about 2 years old.
Local Events: The rash consists of multiple nodules or papules maculo-pigmented
(reddish-brown) sometimes become vesicular, with undefined borders and centripet
al distribution, symmetrical and widespread. The size of lesions ranging from se
veral millimeters to several centimeters. The lesions have a pathognomonic diagn
ostic sign and known as the Darier sign. Is that a gentle friction on the skin t
riggers a white urticarial reaction with itching, erythema and local swelling, a
nd even hives, this effect is produced by the degranulation of mast cells accumu
lated in the skin with subsequent release of inflammatory mediators.
Urticaria Pigmentosa (LEFT) AND SIGN OF DARIEN (DCHA)
General Manifestations: The general symptoms are more common in larger cases of
the disease. They are caused by the degranulation of mast cells that occurs spon
taneously as a result of friction of injuries or exposure to different predispos
ing factors such granulation: physical stimuli: Exercise of the skin friction ho
t or cold baths (extreme changes temperature) Drugs (produce nonspecific release
of mediators): Analgesics: salicylates, diclofenac, morphine Antibiotics: amino
glycosides, amphotericin B Muscle relaxants (nondepolarizing) Parasympathomimeti
c Sympathomimetics
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Food: Fish: tuna, sardines, shellfish ... Cheese: Emmental, Gorgonzola, Parmesan
... Vegetables: spinach, tomato, eggplant ... Fruits: strawberries, citrus, ban
anas ... Nuts Meats: sausages, smoked meat ... Alcoholic Beverages Miscellaneous
: eggs, chocolate ...
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Other: X-ray high molecular weight polymers intravenous (dextran) Emotional stre
ss jellyfish Bacterial toxins and insect bites (mosquitoes, wasps, bees) Ascaris
General symptoms are seizures flushing (redness brilliant general, the more impo
rtant in the face and upper third of the chest, lasting less than 30 minutes), p
ruritus, headache, palpitations, abdominal cramps and sometimes vomiting and dia
rrhea, we do the differential diagnosis of this table with the "Chinese restaura
nt syndrome" caused by the consumption of MSG, which is characterized by flushin
g, hypotension and
bronchospasm. The most severe episodes of syncope and hypotension accompany impo
rtant thing you can progress to shock and death. Bronchospasm is rare but has be
en reported after administration of salicylates. The release of heparin can indu
ce hemorrhagic diathesis. The prognosis is good, presenting spontaneous regressi
on of lesions on puberty in 50% of cases, and another 25% in adulthood. In the a
dult form may have a chronic course and there may be complications with infiltra
tion of the bone marrow and other organs (systemic mastocytosis).
2.2. Solitary mastocytoma
The solitary mastocytoma represents 10% of cases of mastocytosis in childhood. L
esion usually consists of a single (exceptionally there may be 3 or 4 lesions as
nodules or plaques), which initially presented as recurrent vesicles and evanes
cent appearing subsequently infiltrated plate, elastic consistency and color
pink, yellow or brownish above the area of vesicles. The surface has a cobblesto
ne or "orange peel" and hyperpigmentation (due to chronic release of mediators)
may be important. The lesion is round or oval, with a diameter ranging between 1
and 5 cm. As in the urticaria pigmentosa, the lesions are present at birth or a
ppear during the first months of life. Areas of choice are the wrists, elbows an
d trunk. Another similarity with urticaria pigmentosa is that any trauma or fric
tion over the injury can cause it to take a look urticarial (Darier sign). The p
rognosis of solitary mastocytoma is good. Children with a solitary lesion rarely
acquire new lesions after two months of the appearance of it, and it tends to r
egress spontaneously during early childhood. General symptoms associated with so
litary mastocytoma are rare, but may occur rarely and be serious.
Solitary mastocytoma
2.3. Diffuse cutaneous mastocytosis
This rare clinical form of mastocytosis is characterized by diffuse involvement
of the skin rather than the individual lesions, as there is a diffuse infiltrati
on of mast cells in the dermis. It mainly affects the trunk and proximal extremi
ties root. Patients are usually asymptomatic at birth,€developed in early thick
ening of the skin, which becomes pink or yellow color and texture similar to ora
nge peel, the alterations described are accentuated in flexural areas.
In some cases the disease causes intense itching widespread, even in the absence
of visible skin changes. Blisters are common, recurrent, intractable pruritus a
nd systemic involvement and flushing crisis. The course is usually progressive a
nd the prognosis is not good, because it often develops a systemic disease.
Diffuse Cutaneous Mastocytosis
2.4. Telangiectasia macular eruptive perstans
This name is given to the form of mastocytosis in which the telangiectasia is th
e predominant clinical fact of the eruption. It usually occurs mainly in adolesc
ents and adults. It consists of red telangiectatic macules hyperpigmented, unlik
e other forms of mastocytosis, urticarial show relatively little response. It is
a disease that tends to be persistent and very resistant to treatment.
MACULAR ERUPT Telangiectasia perstans
3. DIAGNOSIS
The diagnosis of different forms of cutaneous mastocytosis is mainly clinical, w
ith emphasis on Darier's sign, which is pathognomonic, and positive in more than
90% of cases. We perform various complementary investigations to ascertain the
stage of the disease, and in all cases is indicated skin biopsy confirming the d
iagnosis. Mastocytosis in children usually limited to affect the skin, so there
will be no further investigation unless it relates to extracutaneous symptoms. I
n contrast, patients who start the disease in adulthood is often systemic mastoc
ytosis with involvement of bone marrow and other organs. Therefore, in adult pat
ients with cutaneous mastocytosis addition to the above there will be a complete
blood and urine together with bone marrow biopsy, quantification of histamine o
r some of its metabolites in urine for 24 hours, and quantification of serum try
ptase.
4. TREATMENT
Avoidance of agents that trigger mast cell degranulation, and symptomatic treatm
ent with antihistamines H1 mainly but can also be used cromolyn sodium or topica
l steroids. In advanced cases PUVA photochemotherapy is used (which reduces itch
ing and improves the injuries), and interferon alpha in aggressive forms.
Sorry for a commission so long ... Is all of the slides and adding little in cla
ss. I tried to post pictures because I think it helps, but if you think that say
it is too.
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