ALLERGIC DERMATOSES Lector: Shkilna M.. Content 1. Allergic diseases 2. Contact dermatitis 3. Atopic dermatitis  Clinical Phases  Treatment of atopic.

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Presentation transcript:

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 life- threatening 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 Food safety (allergenicity of food: composite and genetically modified foods) Biological factors (safety of vaccination ) Chemical factors (products highly aggressive for the skin medication ) The main topics of concern

TERMINOLOGY Dermatitis = Dermat+itis Dermatitis = Dermat+itis refers to skin means refers to skin means“inflamed” (thus, inflamed skin) Other examples: arthritis, colitis, encephalitis, etc. Other examples: arthritis, colitis, encephalitis, etc.

Allergic dermatoses Toxic / Pharmacologic Non-Toxic / Intolerance Bacterial food poisoning Heavy metal poisoning Scromboid fish poisoning CaffeineAlcoholHistamine A. Nonimmunologic Lactase deficiency Galactosemia Pancreatic insufficiency Gallbladder / liver disease Hiatal hernia Gustatory rhinitis Anorexia nervosa

Eosinophilic esophagitis Eosinophilic gastritis Eosinophilic gastroenteritis Atopic dermatitis Asthma Allergic dermatoses IgE-Mediated Non-IgE Mediated B. Immunologic Spectrum Oral Allergy Syndrome AnaphylaxisUrticaria Allergic Rhinitis Acute Bronchospasm Protein-Induced Enterocolitis Protein-Induced Enteropathy Eosinophilic proctitis Dermatitis herpetiformis Food-induced Pulmonary Hemosiderosis

TYPES OF DERMATITIS 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. 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 NickelJewelry, foods Benzocaineanesthetics Fragrance perfumes, personal care products Mercaptomixrubber gloves Black rubber mixrubber gloves PPDblack hair dye Potassium dichromate leather, spackling, detergents Cinammic aldehydefragrance, toothpaste Quaternium 15 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.

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 Water Skin cleansers Industrial cleaning agents Acids and alkalis Oils and organic solvents Oxidizing and reducing agents Plants Animal products COMMON IRRITANTS

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. Infantile Phase ( 0-2 years ) Childhood Phase ( 2-12 years ) Adult Phase (puberty onwards) Clinical Phases

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) ChemicalStressAutoimmune 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 Physical urticaria Ordinary chronic urticaria Urticarial vasculitis Contact urticaria Schnitzler’s syndrome Autoimmune urticaria Idiopathic chronic urticaria

Physical urticaria Physical urticaria Cholinergic: Reaction to body heat, such as when exercising or after a hot shower Dermatographic: Reaction when skin is scratched (very common)

Delayed Pressure Urticaria Delayed Pressure Urticaria : reaction to standing for long periods, bra-straps, elastic bands on undergarments, belts Physical urticaria

Solar urticaria Solar urticaria : Reaction to direct sunlight (rare, though more common in those with fair skin) urticaria 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

Contact urticaria Urticaria Pigmentosa (mastocytosis)

Skin Prick Test (SPT) SpecificSensitive Simple to perform Rapid (result in 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, DESLORATIDINDoxepin 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 Zafilukast, Montelukast

Thank you for your attention!