Allergic and irritant contact dermatitis

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Information about Allergic and irritant contact dermatitis
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Published on February 19, 2014

Author: daulatramdhaked

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Description

Allergic and irritant contact dermatitis

INTRODUCTION • CD defined as an inflammatory process affecting skin • Induced by contact with chemical, physical and/or biotic agents in environment, • Causes lesions of skin, mucosa and semi-mucosa by means of allergic and irritant pathogenic mechanisms . • Allergic form generally starts at age of 2-3 years (sometimes as early as six months) because of progressive exposure to sensitizing agents and immaturity of CMI, • Irritant contact dermatitis may develop from birth. • CD grows in frequency with age.

Epidemiology of ICD • Clinical manifestations of ICD are determined by: – Properties of the irritating substance – Host factors – Environmental factors including concentration, mechanical pressure, temperature, humidity, pH, and duration of contact – Cold alone may also reduce the plasticity of the horny layer, with consequent cracking of the stratum corneum – Occlusion, excessive humidity, and maceration increase percutaneous absorption of water-soluble substances

Epidemiology of ICD • Important predisposing characteristics of the individual include: – Age, race, sex, pre-existing skin disease, anatomic region exposed, and sebaceous activity – Both infants and elderly are affected more by ICD because of their less robust epidermal layer – Patients with darkly pigmented skin seem to be more resistant to irritant reactions – Other skin disease such as active atopic dermatitis may predispose an individual to develop ICD – The most commonly affected sites are exposed areas such as the hands and the face, with hand involvement in approximately 80% of patients and face involvement in 10%

Pathogenesis of ICD • Denaturation of epidermal keratins • Disruption of the permeability barrier • Damage to cell membranes • Direct cytotoxic effects

Pathology of ICD • Variable mix of inflammation, necrosis of epidermal keratinocytes, and mild spongiosis • Combination of an upper dermal perivascular infiltrate of lymphocytes with minimal extension of inflammatory cells into the overlying epidermis, and widely scattered necrotic keratinocytes is most typical picture • True features of interface dermatitis are absent, and spongiosis should be focal or absent • Over time additional histologic findings include acanthosis with mild hypergranulosis and hyperkeratosis

Epidemiology of ACD • Affects the old and young, individuals of all races, and both sexes • Differences in genders usually based on exposure patterns, such as nickel allergy being seen more frequently in women, presumably due to greater exposure to jewelry • Occupations and avocations play an important role • Allergens differ from region to region, e.g. preservatives used in personal care products can vary based on government legislation

ACD: Causes: • M/C agents are plants of Toxicodendron genus – eg : poison ivy, poison oak, poison sumac • Other common agents – – – – – – – – – – – – Nickel sulfate (various metal alloys) Sunscreens Potassium dichromate (cements, household cleaners), Chromate (leather products) Lanolin (emollients) Formaldehyde Ethylenediamine (dyes, medications) Mercaptobenzothiazole (rubbers) Thiram (fungicides) Paraphenylenediamine (Hair dyes, Henna, photographic chemicals) Balsam of peru (fragrnce) CAPB (COCOAMIDOPROPYL BETAINE) (shampoos, bath products, and eye and facial cleaners)

PATHOGENESIS TWO PHASES • Sensitization phase – Hapten penetrates skin -> – Biochemically transformed by epidermal enzymatic processes -> – Conjugated with a carrier protein to become immunogenic -> – Captured by antigen presenting cells (APCs), particularly Langherans cells -> – Processed, bound to class II MHC molecules, and exposed on cell surface -> – Cytokines produced by keratinocytes and APCs -> – Langherans cells migrate towards locoregional lymph nodes -> – Specific effector and memory T lymphocytes selected and clonally proliferated -> – Enter bloodstream and reaches to skin and subject is sensitized to hapten.

• Elicitation phase – New contact penetration of skin -> – Substance undergoes chemical changes -> – Recognized and processed by Langherans cells -> – Specific T lymphocytes are recalled at skin level and, together with keratinocytes, release numerous cytokines -> Amplify inflammatory response -> – Give rise to skin damage

Pathology of ACD • ACD is the prototype of spongiotic dermatitis • Acute stage: variable degree of spongiosis with mixed dermal inflammatory infiltrate containing lymphocytes, histiocytes, and variable numbers of eosinophils • Moderate to severe reactions show intraepidermal vesiculation • Subacute to chronic stages have epidermal hyperplasia, often psoriasiform

Regional Sites of Predilection 13

Inflammatory Response in CD: • Acute – Bright red edematous skin – May have clear fluid-filled vesicles or bullae – As lesions break, skin becomes exudative and weeps clear fluid • Subacute – Characterized by the formation of papules instead of vesicles – Additionally, less edema is seen in subacute phase. – Dry scales are sometimes seen in subacute contact dermatitis. • Chronic – Scaling, skin fissuring, and lichenification but only minimal edema. – Excoriations can also be observed in chronic contact dermatitis.

ICD ACD Morphology • Acute ICD includes erythema and edema and sometimes vesicles or bullae, oozing and pustules • Pustules, necrosis or ulceration are rarely seen • Necrosis and ulceration may also be seen with corrosive materials • ACD is mostly characterized by edema, • ICD is mostly characterized by dryness, vesicles and oozing, however, these features roughness, glazed or scalded appearance of the are usually not present in subacute or chronic skin ACD • Chronic ICD may have hyperkeratosis, desquamation, lichenification and fissuring • Chronic ACD may display hyperkeratosis, desquamation, lichenification and fissuring • Lesions are characteristically sharply circumscribed to the contact area • Clinical lesions are more intense in the contact area, but they usually exceed this area and their limits are ill defined • Usually there is absence of distant lesions, but sometimes dermatitis may be generalized, • Dissemination of the dermatitis with distant depending on the nature of the exposure lesions may occur

ICD ACD Symptoms • Symptoms of acute ICD are burning, stinging, prickling, pain and soreness of the skin (pruritus may be present) • Pruritus is the main symptom of ACD Clinical course • Sensitizing exposure(s) is required • Acute ICD may appear after first exposure (at least with strong irritants) • Clinical lesions appear after subsequent challenges with re-presentation of the antigen • In acute ICD, lesions appear rapidly, usually to already primed (memory) T cells within minutes to a few hours after exposure, but delayed reactions can be seen • Lesions usually appear 24–72 h after the last exposure to the causative agent, but they may • Irritant reactions are characterized by the develop as early as 5 h or as late as 7 days after 'decrescendo phenomenon' exposure • The reaction reaches its peak quickly, and then starts to heal • Allergic reactions are characterized by the 'crescendo phenomenon' and the kinetics of resolution may be slower

Differences between Contact Dermatitis Irritant and Allergic IRRITANT ALLERGIC People at risk: everyone Mechanism of response: nonimmunologic a physical and chemical alteration of epidermis Number of exposure required: few to many depends on individual,s ability to maintain an effective epidermal barrier Nature of substance: organic solvent, soaps, acids Concentration of substance required: usually high Evolution: rapid (few hours after exposure) lesions: monomorphical Margination and site: well-defined to site of exposure Investigative procedure: trial of avoidance Management: protection and reduced incidence of exposure Genetically predisposed Delayed hypersensitivity reaction One or several to cause Sensitization low molecular weight hapten (metal, formalin, epoxy,...) May be very low Not so rapid Polymorphical poor-defined, spreading in the periphery, may become generalized Trial of avoidance, patch testing Complete avoidance

ACD and ICD ACD ICD Histology Spongiosis, exocytosis Epidermal necrosis Patch tests Skin immunology Blood immunology Positive (eczema) Presence of activated T cells Presence of specific T cells Negative No activated T cells No specific T cells

Type of irritation Acute ICD Onset and type of exposure Acute; often single exposure to strong irritant Delayed onset of clinical lesions: 8–24 h or Acute-delayed ICD longer after exposure; induced by special irritants Develops in weeks; often seen in individuals Irritant reaction involved in wet work and appears after multiple exposures Develops in months to years; multiple exposures to different agents; often weak Cumulative ICD irritants, capable of inducing a reaction only after repetitive exposure Develops in months to years; multiple Traumiterative ICD exposure to a single agent Develops in weeks to months after skin Traumatic ICD trauma Develops in weeks to months by repetitive Friction ICD microtrauma Develops in weeks to months; exposure to Pustular and special agents (comedogenic-pustulogens), acneiform CD frequently occurs with occlusion Exsiccation Develops in weeks; multiple exposure Clinical characteristics Erythema, edema, weeping, vesicles, bullae, necrosis, burning, pain Erythema, papules, vesicles, bullae Erythema, papules, dryness, scaling; it may resolve or, with continued exposure, may progress to a full-blown ICD Erythema, papules, dryness, scaling, fissuring, lichenification. Burning, itching, soreness Erythema, papules, dryness, scaling, fissuring, lichenification Erythema, papules, dryness, scaling, fissuring, lichenification, callus Erythema, papules, dryness, scaling, lichenification Papules, pustules, comedones Dryness, scaling, fissuring, itching,

Irritant Contact Dermatitis Acute Irritant Contact Dermatitis • Burning, stinging, painful sensations can occur immediately within seconds after exposure or may be delayed up to 24 hour LESION Erythema with a dull, nonglistening surface  vesiculation (blister formation)  erosion  crusting  shedding of crusts and scaling or erythema  necrosis  shedding of necrotic tissue  ulceration  healing 22

Irritant Contact Dermatitis Acute Irritant Contact Dermatitis 23

Irritant Contact Dermatitis Acute Irritant Contact Dermatitis 24

Irritant Contact Dermatitis Chronic Irritant Contact Dermatitis • Prolonged and repeated exposures of the skin to irritants results to a chronic disturbance of the barrier function, subsequently, elicit a chronic inflammatory response. • Stinging and itching, pain as fissures develop LESION Dryness  chapping  erythema  hyperkeratosis and scaling  fissures and crusting • Lichenification, vesicles, pustules, and erosions 25

Irritant Contact Dermatitis Chronic Irritant Contact Dermatitis 26

Allergic Contact Dermatitis Acute Allergic Contact Dermatitis • Well-demarcated erythema and edema on which are superimposed closely spaced, nonumbilicated vesicles, and/or papules LESION: Erythema Papules vesicles erosions crusts scaling. 27

Allergic Contact Dermatitis Acute Allergic Contact Dermatitis 28

Allergic Contact Dermatitis Acute Allergic Contact Dermatitis 29

Allergic Contact Dermatitis Chronic Allergic Contact Dermatitis • Plaques of lichenification (thickening of the epidermis with deepening of the skin lines in parallel or rhomboidal pattern), scaling with satellite, small, firm, rounded or flat-topped papules, excoriations, erythema, and pigmentation LESION Papules scaling lichenification excoriations 30

Allergic Contact Dermatitis Chronic Allergic Contact Dermatitis 31

Allergic Contact Dermatitis Chronic Allergic Contact Dermatitis 32

ICD & ACD • Differentiation is often difficult in clinical setting, • Deciding whether dermatitis primarily depends on irritancy or allergy is not always straightforward. • No pathognomic clinical signs and symptoms can unambiguously discriminate between ACD and ICD. • Diagnosis of CD depends on: – Patient history, – Clinical examination, – Exposure assessment (including hazard identification, estimation of dermal exposure and risk characterization), – Analysis of all predisposing and contributory factors, – Comprehensive diagnostic testing.

Clinical characteristics of the dermatitis • Characteristics of initial lesions and clinical evolution • Time of onset and possible relationship with exposure to allergens or irritants • Dermatitis area corresponding to exposure site • Dermatitis morphology suggesting specific contactants

History of occupational exposure • Job description; occupational gestures and characteristics of working milieu • Potential allergens and irritants in working environment • Characteristics of exposure: dose, frequency and site • Concomitant exposure factors: temperature, humidity, occlusion, friction, and so on. • Time relationship to occupation; effect of holidays and time off work • Personal protective measures at work (gloves, masks and barrier creams) • Other workers similarly affected?

History of nonoccupational exposure • Domestic products: cleansers and detergents • Skin care products, fragrances, nail and hair products • Pharmaceutical products (under prescription and over the counter) • Personal protective measures at home (gloves) • Jewellery and clothing • Homework and hobbies

Variants on exposure • Direct contact with agent • Contact through fomites or contaminated surfaces • Combination of contact with causative agent and sun exposure, resulting in a photocontact or photoaggravated dermatitis • Transfer from other body sites, generally by hands, to more sensitive areas, such as eyelids or neck, resulting in an ectopic dermatitis • Exposure to gases, droplets or particles in atmosphere, which results in airborne dermatitis • Systemic exposure in previously sensitized patients

History of previous dermatitis, atopy and other skin/general diseases • Past contact dermatitis (occupational or not) • Previous patch testing • Other exogenous or endogenous dermatitis: atopic dermatitis, stasis dermatitis, psoriasis and sensitive skin • Mucosal atopy (asthma and rhinoconjunctivitis) • Family history of atopy and other skin diseases

Physical Examination • Rietschel and Fowler proposed the following as primary diagnostic criteria for irritant contact dermatitis: • Macular erythema, hyperkeratosis, or fissuring predominating over vesiculation • Glazed, parched, or scalded appearance of the epidermis • Healing process beginning promptly on withdrawal of exposure to offending agent • Negative results on patch testing that includes all possible allergens

• Minor objective criteria for irritant contact dermatitis include the following: • Sharp circumscription of dermatitis • Evidence of gravitational influence such as a dripping effect • Lower tendency for the dermatitis to spread than in cases of allergic contact dermatitis • Morphologic changes suggesting small differences in concentration or contact time producing large differences in skin damage

Differential Diagnoses: • • • • • • • • • • • • • Insects Bites, Herpes Zoster Cellulitis Herpetic Whitlow, Impetigo , Atopic Dermatitis, Exfoliative Dermatitis Psoriasis Erysipelas Scabies Erythema Multiforme Vulvovaginitis Herpes Simplex

Workup Laboratory Studies: • • • • • • • • • • • • skin tests, where a positive result, expressing as a dermatitis at the site of contact with the chemical, is considered to be synonymous with contact allergy Patch tests (epicutaneous) Open-tests or repeated open tests – ROAT Thin-layer Rapid Use Epicutaneous Test (T.R.U.E. Test) Photopatch Test Provocative Use Test Differentiation between irritation and allergy can therefore be established clinically by: – The systematic use of a positive control for irritation during the tests; – When a reaction is difficult to interpret or there are positive irritation tests: 1) re-test with patch tests for only 24 hours (or 12 hours if the first reaction is strong); 2) carry out a ROAT test.

• immunological tests • shows the existence of allergen-specific T cells in the skin or blood of patients; • Presence of allergen-specific T cells in the skin found in a punch biopsy of ACD lesions or in skin tests • Presence of allergen-specific T cells in patients’ blood

Management for Contact Dermatitis Prevention • Avoid exposure to potential allergen • Avoid repeated and prolonged exposure to irritants • Wear protective clothing • Check skin reactions to cosmetics before applying 45

Management for Contact Dermatitis Treatment for Irritant Contact Dermatitis • Identify and remove the etiologic agent • Wet dressings with gauze soaked in Burow's solution, changed every 2 to 3 hours • Larger vesicles may be drained, but tops should not be removed • Topical class I glucocorticoid preparations • Severe cases: systemic glucocorticoids – Prednisone, 2-week course, 60 mg initially, tapering by steps of 10 mg 46

Management for Contact Dermatitis Treatment for Allergic Contact Dermatitis • Identify and remove the etiologic agent. • Topical glucocorticoid ointments/gels (classes I to III) for early nonbullous lesions • Larger vesicles may be drained, but tops should not be removed • Wet dressings with cloths soaked in Burow's solution changed every 2 to 3 hours • Systemic glucocorticoids: Severe & Exudative lesions – Prednisone, initial 70 mg (adults), tapering by 5 to 10 mg/d over a 1- to 2-week period. 47

• Antihistamines • Emollients: • Emollients may be used as adjuncts to moisturize dry skin in subacute and chronic contact dermatitis. • Urea Both promote hydration and removal of excess keratin in conditions of hyperkeratosis • Barrier creams: • Primary agents for diaper dermatitis. • Zinc oxide paste • Provides relief of minor skin irritations. • Pediatric: Apply to affected area after gentle cleansing and drying, between each diaper change • Camphor and menthol (0.5% each) in emollient base

Thank you. 49

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