Dermatitis and Eczema

Dermatitis and eczema Professor Danka Švecová MD, PhD, Dept.of Dermatovenerology Faculty of Medicine, Comenius University Dermatitis and Eczema Definition • The form of epidermal intolerance reaction • Noncontagious inflammatory dermatoses • Acute case – exudative – inflammatory skin changes – redness, swelling, vesicles, oozing, crusts, itching • Chronic case – proliferative inflammatory processes – redness, epidermal thickening (acanthosis), scaling, lichenification, itching • Origin of the disease – exogenous or endogenous - toxic or allergic - noxious factors : known or unknown Dermatitis and Eczema Classification • Irritant contact dermatitis: acute and chronic • Allergic contact dermatitis (eczema): acute and chronic • Dyshidrotic dermatitis (eczema) • Atopic dermatitis (eczema) • Nummular (microbial) dermatitis (eczema) • Seborrheic dermatitis Acute irritant contact dermatitis It results from the exposure of the skin to external agents that overwhelm the normal skin barrier function • External agents → simply highly toxic →or repeated exposures to agents of low toxicity (washing hands many times daily) →or variety of predisposing intrinsic factors (atopy, ichthyosis) Epidemiology far more common than allergic contact dermatitis; toxic substances - in many work places, the home, the garden, in a variety of hobbies Acute irritant contact dermatitis Etiopathogenesis toxic reaction – tissue necrosis from a concentrated acid or base solution – damaging effect in minutes; less noxious agents – damage of the skin protective barrier Acute irritant contact dermatitis Exogenous factors – type of irritant (chemical structure, pH), amount of irritant reaching skin (solubility, concentration, vehicle, duration and type of exposure), body region, body temperature, mechanical factors (pressure, rubbing, abrasion), climatic factors (temperature, humidity, wind) Endogenous factors – individual susceptibility towards irritant, sensitive skin in general, atopy and especially atopic dermatitis, lack of hardening, racial factors, sensitivity to UV radiation, age Acute irritant contact dermatitis Clincal findings skin damage is sharply localized to the areas of contact, distant spread does not occur; lesions are asymmetrical, history is often easy; erythema and edema; blisters→usually superficial, rapidly becoming erosions→ weeping erythematous erosions→ dried secretions→ crusts, sheding of crusts, scales→ appearance of new epidermis beneath→residual erythema Acute irritant contact dermatitis Course and prognosis self-limiting, when the toxic agent is removed, the acute skin inflammation regresses DifDg allergic contact dermatitis, erysipelas, phototoxic reaction, acute systemic lupus erythematosus and dermatomyositis, various forms of physical injury Therapy systemic usually none is needed, only serious condition→ systemic corticosteroids reduce erythema and swelling, pain medication. Topical therapy below. Cumulative irritant contact dermatitis Cumulative exposures to irritanting and drying substances such as water, cutting oils, chemicals, cement, tars; the back of the hands and forearms housewives are at risk (repeated exposure to water, soaps, soiled diapers) Cumulative irritant contact dermatitis Etiopathogenesis the crucial factor –repeated exposure to low-grade irritation defense mechanism of the skin is broken down → toxic substances may penetrate deeper Buffering capacity pH about 5.7(acid mantle), buffering both acidic and basic solutions to a limited extent Water-binding capacity str.corneum- natural moisturizing factors consist of aminoacid, sugars and lipids. A lack of lipids (ceramide) → decreased water binding and drying out Skin lipid in sebum, also from keratinocytes; sweating determines the dilution of the film; also antimicrobial properties; repeated contact with soap and detergens removes the film faster than the body can restore it →dry skin Individual factors: drynees of the skin, particular risk → atopy and ichthyosis Cumulative irritant contact dermatitis Common irritants associated with various occupations: • Chemicals – alkali and acid solutions rapidly exhaust the skin´s limited buffering capacity • Detergents – soaps, syntetic detergents (syndets), lipid solvents, other cleansing agents remove the lipids and water-soluble substances • Organic solvents – acetone, alkohols, benzene, benzol, toluene, carbon tetrachloride, many others • Physical agents – contact with sand, dust, fabrics, paper →can be very drying; wool – in atopic diathesis, UV radiation- drying effect (immunosupressive effect, epidermal thickening stimulation) • Body secretions – urine, stool, saliva, sweat, secretion from a wound, Dermatitis surrounding an abrasion or injury is often irritant nor infectious Cumulative irritant contact dermatitis Clinical findings the chronic changes of lichenification, scaling, fissuring. Also acute changes may be seen – erythema, swelling, blisters, crusts Chronic irritant hand contact dermatitis The cause is rarely monofactorial; at risk: housewives, hairdressers, nurses, other health- care workers; workers in the building trades (cement, mortar), machinists (cutting oils, harsh cleansers) janitors, cleaners, printers, fishermen, butchers, barbers, gardners,florists, automobile and truck mechanics, masseurs, bakers, cooks, dental technicians Clinical findings back of the hands, dorsal aspects of the forearms; inflammatory changes – erythema, swelling, crusting; lesions → asymetric and diffuse, not sharply bordered, lichenification, fissuring; also acute changes- blisters, crusts; pruritus – common Chronic irritant hand contact dermatitis Course and prognosis improvement on weekends and during vacations; difficult to avoid exposure →persistent disease DifDg allergic contact dermatitis, psoriasis, tinea manuum, atopic dermatitis, dyshidrotic dermatitis Therapy avoidance of noxious substance, protective creams, gloves- mainstay of prophylaxis, topical corticosteroids Chronic irritant contact dermatitis Hyperkeratotic palmoplantar dermatitis ordinary dermatitis with underlying tendency or genetic predisposition to keratinization abnormalities on the palms and soles Allergic contact dermatitis Epidemiology incidence in the general population 1-10%, equally common in men and women, although hand dermatitis is more common in women Allergic contact dermatitis Etiopathogenesis Gell and Coombs type IV delayed hypersensitivity reaction Induction phase (afferent limb) sensitizing molecule is often a hapten, must be bound to a skin or serum protein to form a complete antigen. The antigen is taken up by the antigen-processing cells (Langerhans cells- with their dendrites they form a network of interacting cells able to identify bacteria, foreign antigens). LC present antigen to the immune system (Tcells in peripheral lymph node). Both effector and suppressor T cells may be formed → modulating the immune reaction. Sensitized cells are able to identify allergen and they migrate back to the skin where they serve for a potentional re-exposure. Memory cells. Allergic contact dermatitis Elicitation phase (efferent limb) re-exposition to the antigen, even very small amounts are able to trigger a delayed immune response, usually 24 -48 h are required, sometimes only 4-8 h; the sensitized allergen- specific helper Tcells (Th2 group) identify the allergen via receptors and become activated secreting a whole palette of cytokines, that call in other cells needed for the inflammatory response. Reactions →outside the initial area of contact (secretion of cytokines and circulation of responsive lymphocytes in bloodstream) Acute allergic contact dermatitis Clinical findings develops after 24-48h, initial lesions are limited to the contact area, dissemination may occur typical lesions: small red macules and pintop-like papules and vesicules on erythematous base; sweling , blisters, pruritus, lesions tendency to coalesce forming a patch with most pronounced in its centre; vesicles → erosions → crusting →scaling involve the centre of the patch surrounded with a ring of papules with red periphery – indistinctive border Evolutive polymorphism DifDg acute irritant contact dermatitis, erysipelas, acute systemic lupus erythematosus, dermatomyositis Acute allergic contact dermatitis Stadium erythematous et oedematous Acute allergic contact dermatitis Stadium vesiculous et bullous Acute allergic contact dermatitis Stadium madidans Acute allergic contact dermatitis Chronic allergic contact dermatitis It can evolve from acute allergic contact dermatitis, or creep up subtly with no acute phase or appear on top of chronic irritant contact dermatitis; widespread allergens: nickel, formaldehyde, fragrances, preservatives → very difficult to avoid them; Clinical findings symetrical patterns, less sharp border and distant spread, lichenification, skin relief: fine reddish brown rhoimboid net, linear excoriation, crusts . Chronic allergic contact dermatitis DifDg according to the body regions: scalp-psoriasis, seborrheic dermatitis; external ears –psoriasis, seborrheic dermatitis, chronic irritation (swimmer´s ear from moisture); eyelid –atopic dermatitis, rosacea; lips- lick cheilitis or lip chewing especially in atopic patients; hands- chronic irritant contact dermatitis, atopic dermatitis, psoriasis, tinea manuum; fingertips-atopic dermatitis,dyshidrotic dermatitis, nipples- atopic dermatitis, Paget disease; Chronic allergic contact dermatitis DifDg according to the body regions: leg- stasis dermatitis, psoriasis, nummular dermatitis; genitalia –atopic

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