Transcript Allergic dermatoses

ALLERGIC DERMATOSES
Lector: Shkilna M.
Content
1. Allergic diseases
2. Contact dermatitis
3. Atopic dermatitis
 Clinical Phases
 Treatment of atopic dermatitis
4. Urticaria
 Causes of urticaria
 Classification of urticaria
 Treatment of urticaria
WHY DO WE GET ALLERGIES?
Immune system designed to protect from lifethreatening infection.
Co-evolution of components of the immune system
with common pathogens
–
–
–
–
Viruses
Protozoae & Helminths
Bacteria
Fungi
Evolutionary pressure has generated an immune system
able to respond to these diseases.
Important questions in allergy
The main topics of concern
Food safety
(allergenicity of food:
composite and genetically
modified foods)
Biological factors
(safety of vaccination)
Chemical factors
(products highly
aggressive for the skin
medication )
TERMINOLOGY
Dermatitis =
Dermat
+
refers to skin
itis
means
“inflamed”
(thus, inflamed skin)
Other examples: arthritis, colitis, encephalitis, etc.
Allergic dermatoses
A. Nonimmunologic
Toxic / Pharmacologic
Non-Toxic / Intolerance
Bacterial food
poisoning
Heavy metal
poisoning
Scromboid fish
poisoning
Caffeine
Alcohol
Histamine
Lactase deficiency
Galactosemia
Pancreatic
insufficiency
Gallbladder / liver
disease
Hiatal hernia
Gustatory rhinitis
Anorexia nervosa
Allergic dermatoses
B. Immunologic Spectrum
Non-IgE Mediated
IgE-Mediated
Oral Allergy
Syndrome
Anaphylaxis
Urticaria
Allergic Rhinitis
Acute
Bronchospasm
Eosinophilic esophagitis
Eosinophilic gastritis
Eosinophilic gastroenteritis
Atopic dermatitis
Asthma
Protein-Induced Enterocolitis
Protein-Induced Enteropathy
Eosinophilic proctitis
Dermatitis herpetiformis
Food-induced Pulmonary Hemosiderosis
TYPES OF DERMATITIS
Allergic contact dermatitis
Irritant contact dermatitis
Atopic dermatitis
Other types
IT IS PRECIPITATED BY
EXTERNAL SOURCES
OR INTERNAL ONES
(ENDOGENOUS or
EXOGENOUS)
Exogenous: contact
DERMATITIS (acute)
Irritant, allergic and infective.
Endogenous: chronic atopic
dermatitis, neurodermatis,
and other types
Contact Dermatitis
Cell mediated reaction involving sensitized
T lymphocytes.
Etiology
– Irritant form: Chemical insult to skin. No
previous sensitizing event.
– Allergic form is delayed-hypersensitivity
reaction. Skin sensitized from initial exposure.
During next exposure patient has reaction.
Allergic contact dermatitis
The term “contact dermatitis” describes an inflammation of
the skin caused by contact with external agents.
Allergic contact dermatitis is a delayed-type hypersensitivity
reaction due to the contact with a chemical to which the
individual has previously been sensitized.
Possible allergens are found in jewellery, personal care
products, topical medications, plants and work-related
materials.
Usually, the eczematous reaction develops within 24 to 72
hours after contact with the causative chemical in a sensitized
individual.
Allergic Contact Dermatitis
Figure 19.7
COMMON ALLERGENS
Nickel
Benzocaine
Fragrance
Mercaptomix
Black rubber mix
PPD
Potassium dichromate
Cinammic aldehyde
Quaternium 15
Jewelry, foods
anesthetics
perfumes, personal care products
rubber gloves
rubber gloves
black hair dye
leather, spackling, detergents
fragrance, toothpaste
preservative personal care products
Nickel
Most common allergen tested by the
NACDG, with 14% of patients reacting to it
Relevance has been estimated to be 50%
Commonly used in jewelry, buckles, snaps,
and other metal-containing objects
High rate of sensitivity attributed to ear
piercing
Dimethylglyoxime test to determine if a
particular item contains nickel
Individuals with nickel allergy should avoid
custom jewelry, and can usually wear
stainless steel or gold
Nickel Dermatitis
Common presentations are
dermatitis on the ears, under a
necklace or a watch back, or
on the mid-abdomen caused
by a belt buckle, zipper, or
snap
Eyelid dermatitis from metal
eyelash curlers can be seen
Photos from dermatlas.org
Neomycin Sulfate
Most commonly used topical antibiotic
Most common sensitizer among
topical antibiotics
Found in many OTC preparations:
bacterial ointments, hemorrhoid
creams, and otic and opthalmic
preparations
Frequently used with other
antibacterial agents, such as bacitracin
and polymyxin, as well as
corticosteroids
Co-reactivity is commonly seen with
neomycin and bacitracin
13 year old boy developed an itchy allergic contact dermatitis
from a topical antibiotic. www.dermatlas.org
Quaternium-15
Preservative that is an effective
biocide against Pseudomonas, as
well as other bacteria and fungi
Most common preservative to
cause ACD
Found in shampoos, moisturizers,
conditioners, and soaps
80% of those reacting to
quarternium-15 are also
formaldehyde sensitive
Hand dermatititis due to
quaternium-15 in a moisturiser
dermnetnz.org/dermatitis/quaternium
IRRITANT CONTACT DEMATITIS
Non-immunologic
inflammatory reaction of
the skin due to an
external agent
Varied morphology
Clinical types
– Chemical burns
– Irritant reactions
– Acute irritant contact
dermatitis
– Chronic irritant contact
dermatitis
COMMON IRRITANTS
Water
Skin cleansers
Industrial cleaning agents
Acids and alkalis
Oils and organic solvents
Oxidizing and reducing
agents
Plants
Animal products
CONTACT DEMATITIS
Allergic contact dermatitis
(Nickel)
IRRITANT CONTACT DEMATITIS
Atopic dermatitis
Atopic dermatitis is a chronic
inflammatory disease of the
skin primarily seen in the
pediatric age group
Characterized by dry skin,
pruritus, erythema, edema,
scaling, excoriations, oozing,
lichenification
Increasing prevalence, rising
costs
Together with asthma and
allergic rhinitis forms part of
the ‘atopic triad’
ATOPIC DERMATITIS:
EXACERBATING FACTORS
(TRIGGERS)
Anxiety/stress
Climatic factors
– Temperature
– Humidity
Irritants
– Detergents/solvents
– Wool or other rough material
– Perspiration
Allergens (contact, inhalant & food)
Infections (staph and strep)
Atopic Dermatitis
High level of IgE
antibodies to House dust
mites
IgE bound to
Langerhans cells in
atopic skin
Food exacerbates
symptoms in some
patients: eggs, peanuts,
cow’s milk represent up
to 75% of positive test.
Clinical Phases
Infantile Phase ( 0-2 years )
Childhood Phase ( 2-12 years )
Adult Phase (puberty onwards)
Infantile ( 0-2 years )
Atopic Dermatitis
60% of case AD present
in the first year of life,
after 2 months of age
Begin as itchy erythema
of the cheeks
Distribution include
scalp, neck, forehead,
wrist, and extensors
May become desquamate
leading to erythroderma.
Egg, peanut, milk, wheat, fish, soy, and chicken may exacerbate infantile AD
Childhood ( 2-12 years )
Atopic Dermatitis
Characterized by less acute
lesions
Distribution: antecubital and
popliteal fossae, flexor wrist,
eyelids, and face.
Persistent rubbing and
scratching leads to lichenified
plaques and excoriations
Severe atopic dermatitis
involving more than 50% of
body surface area is
associated with growth
retardation.
Adult (puberty onwards) Atopic
Dermatitis
Distribution: antecubital
and popliteal fossae, the
front side of the neck,
the forehead, and area
around the eyes.
Atopic individuals are at
greater risk of
developing hand
dermatitis than are the
rest of the population
70% develop hand
dermatitis some times in
their lives
FLARE FACTORS IN
ATOPIC DERMATITIS
TREATMENT OF ATOPIC DERMATITIS
Identify and control “flare factors”
Topical treatments
– Glucocorticosteroids
– Newer “non-steroidal” TIMs
Emollients
– Moisturizers
– Baths with added lubricants
Systemic treatments
– Oral antihistamine (a cornerstone of treatment)
– Oral antibiotics
– Systemic steroids
– Immunosuppression (phototherapy, cytotoxic drugs)
Urticaria affects up to 2% of the population at some time in a
lifetime
Transitory (individual episodes < 24h duration) red skin
swellings with itching
No desquamation, rarely affects mucous membranes
Associated with angioedema in about 40% of cases
SYMPTOMS of Urticaria:• Intense itching.
• Burning.
• Sense of heat.
LESION
• Starts as red erythematous macules.
• Soon paleoedematous wheals develop.
• Irregular, asymmetrical.
• Velvetty to touch.
• Erythema well defined, fades on pressure.
• Subside within few hours without leaving any trace.
• Dermographism positive.
• Wheals develop along line of scratching or pressure.
Pathogenesis
In urticaria, a chemical called
histamine is released from the
cells in our skin. This causes
fluid from blood vessels
underneath the surface of our
skin to leak out. This results in
the raised patches (weals) that
you see on the surface of our
skin.
The histamine also causes the
weals to itch.
If urticaria affects the deeper
layers of skin, it can cause
even larger swellings, called
angioedema.
Urticaria and angioedema can
occur together or separately.
What are the causes of urticaria?
Allergy (foods such as nuts & shellfish, pollen, exposure to
animals, bee stings etc.)
Medications (such as aspirin, penicillin etc.)
Insect bites (papular urticaria)
Infections (viral, bacterial, fungal)
Chemical
Stress
Autoimmune
Heat or cold
Sun (solar urticaria)
Exercise (Cholinergic urticaria)
Pressure (from tight fitting clothing)
Water (aquagenic urticaria)
Vibrations
Idiopathic (unknown)
Differentiating Acute from Chronic Urticaria (Hives)
Acute Urticaria (Hives)
Duration of few days to few weeks
Incidence of 15-20% of population
Etiology usually detected
Most cases are mild and never seen by physician
Chronic Urticaria (Hives)
Duration greater than six weeks
Ranges from continuous (almost daily) to recurrent (symptom
free intervals of days to many weeks)
Course variable from months to years
Incidence of up to 3% of population
Etiology not found in 90-95% of cases = IDIOPATHIC (cause
unknown or not determined)
Chronic urticaria is further subclassified into several distinct entities
Classification of chronic urticaria
Chronic urticaria
Urticarial
vasculitis
Physical
urticaria
Autoimmune
urticaria
Ordinary
chronic
urticaria
Contact
urticaria
Idiopathic
chronic
urticaria
Schnitzler’s
syndrome
Physical urticaria
Dermatographic: Reaction
when skin is scratched (very
common)
Cholinergic: Reaction to body heat,
such as when exercising or after
a hot shower
Physical urticaria
Delayed Pressure Urticaria : reaction to standing for long
periods, bra-straps, elastic bands on undergarments, belts
Physical urticaria
Solar urticaria : Reaction to
direct sunlight (rare, though more
common in those with fair skin)
Cold urticaria : Reaction to cold,
such as ice, cold air or water - worse with
sudden change in temperature
Physical urticaria
Aquagenic urticaria: reaction
to water
Heat urticaria: reaction to
hot food or objects
URTICARIAL Vasculitis
Papular urticaria
Urticaria Pigmentosa
(mastocytosis)
Contact urticaria
Skin Prick Test (SPT)
Specific
Sensitive
Simple to perform
Rapid (result in 15-20
min)
Educational for patient
Intradermal Skin Test (IDT)
More sensitive than skin prick test
May induce false positive
reactions
May induce systemic reactions
Should be done only if skin prick
test is negative and allergen is
highly suspect.
Treatment of urticaria
Avoid provoking factor
Oral antihistamine :
H1 BLOCKER: Sedative antihistamine
DIPHENHYDRAMINE,
HYDROXYZIN,
PROMITHAZINE,
TRIPROLIDIN
Low sedative antihistamine: ASTEMIZOLE, TERFINADIN,
LORATIDIN, CETRIZIN,
DESLORATIDIN
Doxepin
H2 BLOCKER
In acute sever urticaria we can
start Treatment by IM
antihistamine , I.V. steroid
{hydrocortisone} and S.C.
adrenaline
Systemic steroids
Topical Treatment usually
CALAMIN lotion
Resistant chronic urticaria as
CYCLOSPORIN,
METHOTREXATE
Leukotrein receptor antagonist:
Zafilukast, Montelukast
Thank you for your attention!