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Contact Dermatitis Part One Andrews: Chapter 6, pages 91115 Bolognia: Pages 215286


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Title: Contact Dermatitis Part One Andrews: Chapter 6, pages 91115 Bolognia: Pages 215286

Contact Dermatitis Part OneAndrews Chapter 6,
pages 91-115Bolognia Pages 215-286
  • Patrick Keehan, D.O.
  • 7/31/07

Irritant contact dermatitis (ICD)
  • Accounts for approximately 80 of all contact
  • ICD is the result of a local toxic effect when
    the skin comes in contact with irritant chemicals
    such as soaps, solvents, acids, or alkalis
  • This 37-year-old woman developed a contact
    irritant dermatitis from obsessive-compulsive
    hand washing 20-30 times a day.

Introduction to Irritant Contact Dermatitis
  • ICD is a cutaneous inflammation resulting from a
    direct cytotoxic effect of a chemical or physical
  • Constitutes nearly 80 of occupational contact
    dermatitis (OCD)
  • OCD is a matter of public health importance,
    contributing to combined direct and indirect
    annual costs (in the USA) of up to 1 billion
    when accounting for medical costs, workers
    compensation, and lost time from work

Epidemiology of ICD
  • The US Bureau of Labor Statistics data show that
    occupational skin diseases accounted for 10 to
    15 of all occupational illnesses
  • High-risk occupations with frequent irritant
    exposure in caterers, furniture industry workers,
    hospital workers, hairdressers, chemical industry
    workers, dry cleaners, metal workers, florists,
    and warehouse workers

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

  • Bilateral shoe irritant dermatitis resulting from
    chronic occlusive footwear

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

Practicing dentist with moderately severe
irritant hand dermatitis from chronic exposure to
disinfecting solutions and antiseptics. The
results of patch testing, latex challenge
testing, and RAST testing were negative.
Pathogenesis of ICD
  • Denaturation of epidermal keratins
  • Disruption of the permeability barrier
  • Damage to cell membranes
  • Direct cytotoxic effects

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Acute Irritant Contact Dermatitis
  • Commonly seen in occupational accidents
  • Irritant reaction reaches its peak quickly,
    within minutes to hours after exposure
  • Symptoms include stinging, burning, and soreness
  • Physical signs include erythema, edema, bullae,
    and possibly necrosis
  • Lesions restricted to the area where the irritant
    or toxicant damaged the tissue
  • Sharply demarcated borders and asymmetry points
    to an exogenous cause
  • Most frequent irritants are acids and alkaline

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Acute Delayed Irritant Contact Dermatitis
  • Delayed inflammatory response characteristic of
    certain irritants such as anthralin, benzalkonium
    chloride, and ethylene oxide
  • Visible inflammation is not seen until 8 to 24
    hours after exposure
  • Symptoms are more frequently burning rather than
  • Sensitivity to touch and water are elicited
  • This form of ICD is commonly seen during
    diagnostic patch testing

Irritant Reaction Irritant Contact Dermatitis
  • Type of subclinical irritant dermatitis in
    individuals exposed to wet chemical environments
    such as hairdressers, caters, or metalworkers
  • Characterized by scaling, redness, vesicles,
    pustules, and erosions
  • Often begins under occlusive jewelry and then
    spreads over the fingers to the hands and
  • May simulate dyshidrotic dermatitis

Cumulative Irritant Contact Dermatitis
  • Consequence of multiple sub-threshold skin
    insults, without sufficient time between them for
    complete barrier function repair
  • In contrast to acute ICD, the lesions of chronic
    ICD are less sharply demarcated
  • Itching and pain due to fissures of
    hyperkeratotic skin are symptoms of chronic ICD
  • Skin findings include lichenification,
    hyperkeratosis, xerosis, erythema, and vesicles

Asteatotic Dermatitis
  • Exsiccation eczematid ICD
  • Seen mainly during the winter months in elderly
    individuals who frequently bath without
  • Skin appears dry with ichthyosiform scale and
    patches of eczema craquele

Traumatic Irritant Contact Dermatitis
  • May develop after acute skin trauma, such as
    burns, lacerations, or acute ICD
  • Patients should be asked if they have cleansed
    with strong soaps or detergents
  • Characterized by eczematous lesions most commonly
    on the hands, that persist
  • Healing is delayed with redness, infiltration,
    scale, and fissuring in the affected areas

Pustular and Acneform Irritant Contact Dermatitis
  • Result to certain irritants such as metals,
    croton oil, mineral oils, tars, greases, cutting
    and metal working fluids, and naphthalenes
  • Should be considered in conditions in which
    folliculitis or acneform lesions develop in
    setting outside of typical acne
  • Pustules are sterile and transient
  • Milia may develop in response to occlusive
    clothing, adhesive tape, ultraviolet and infrared

Chloracne. Note heavy involvement of
retroauricular skin with comedones and cysts
Subjective or Sensory Irritant Contact Dermatitis
  • Reports of stinging or burning in the absence of
    visible cutaneous signs of irritation
  • Response to irritants such as lactic or sorbic

Airborne Irritant Contact Dermatitis
  • Develops on irritant-exposed skin of the face and
    periorbital regions
  • Often simulates photoallergic reactions
  • Involvement of the upper eyelids, philtrum, and
    submental regions help to differentiate from
    photoallergic reaction

Frictional Irritant Contact Dermatitis
  • Results from repeated low-grade frictional trauma
  • Plays adjuvant role in ACD and ICD
  • Characterized by hyperkeratosis, acanthosis, and
    lichenification, often progressing to hardening,
    thickening, and increased toughness

9 year old girl demonstrates a lichenified
hyperpigmented round plaque on the top of her
thumb produced by chronic thumb sucking.
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

  • Inorganic and organic acids can be corrosive to
    the skin
  • Cause epidermal damage via protein denaturation
    and cytotoxicity
  • Symptoms include erythema, vesication, and
  • Hydrofluoric and sulfuric acid can cause the most
    severe burns
  • Hydrofluoric acid, used in the semiconductor
    industry, is able to penetrate intact skin with
    subsequent dissociation in deeper tissues and
    resultant liquefactive necrosis

  • Chromic acid causes ulcerations known as chrome
    holes and often perforates the nasal septum
  • Chemical burns and irritant dermatitis from
    nitric acid can cause a distinctive yellow
  • In general, organic acids are less irritating
    than inorganic acids
  • Formic acid has the greatest corrosive potential
    of the organic acids

Examples of chrome holes
  • Strong Alkalis include sodium, ammonium,
    potassium hydroxide, sodium and potassium
    carbonate, and calcium oxide
  • Found in soaps, detergents, bleaches, ammonia
    preparations, lye, drain pipe cleaner, toilet
    bowl cleansers, and oven cleaner
  • Often more painful and damaging than acids
  • No vesicles. Necrotic skin that appears dark
    brown then black, ultimately becomes hard, dry,
    and cracked
  • Alkalis disrupt barrier lips and denature
    proteins with subsequent fatty acid saponification

  • Cement mixed with water can cause ulcerative
    damage due to alkalinity
  • Changes appear 8 to 12 hours after exposure
  • Chronic irritant cement dermatitis may also
    develop over months to years
  • Can accompany allergic contact dermatitis

Hand dermatitis due to contact with cement
Metal Salts
  • Include arsenic trioxide, beryllium compounds,
    calcium oxide, copper salts, inorganic mercury,
    thimerosal, and selenium
  • Signs ranging from ulceration to folliculitis

  • Act mainly by dissolving the intercellular lipid
    barrier of the epidermis
  • Prolonged skin contact can result in severe burns
    and well as systemic toxicity
  • Examples include turpentine, benzene, toluene,
    xylene, carbon tetrachloride, gasoline, and

Professional paint and crayon illustrator with
bilateral palmar dermatitis secondary to repeated
contact with paint solvents. Extensive patch
testing excluded allergic contact dermatitis
Detergents and Cleansers
  • Include any surface active agent (surfactant)
    that concentrates at the oil-water interfaces and
    has both emulsifying and cleansing properties
  • Found in skin cleansers, cosmetics, and household
    cleaning products
  • Surfactants cause protein denaturation of the
    stratum corneum, impairing barrier function
  • Anionic detergents such as alkyl sulfates and
    alkyl carboxylate salts are the most irritating

  • Include, alcohols, aldehydes, phenolic compounds,
    halogenated compounds, surfactants, dyes,
    oxidizing agents, and mercury compounds
  • Weak toxic agents that can cause chronic ICD

Practicing dentist with moderately severe
irritant hand dermatitis from chronic exposure to
disinfecting solutions and antiseptics. The
results of patch testing, latex challenge
testing, and RAST testing were negative.
  • Three categories thermoplastics, thermosettings,
  • Skin damage is attributed to monomer ingredients,
    hardeners, and stabilizers
  • Final hardened plastic product is generally
    considered inert

  • Agriculture, fishing, catering, and food
  • Often work without gloves, in damp working
    conditions with frequent hand washing
  • Mechanical, thermal, and climatic factors
  • Nearly 100 of exposed persons in food handling
    and fishing professions may be affected by
    chronic irritant hand dermatitis

  • Ubiquitous skin irritant
  • Tropical immersion foot, seen during Vietnam War
  • Hairdressers, hospital cleaners, cannery workers,
  • Irritancy of water is exacerbated by occlusion

9 year old is an habitual hand washer who
develops a contact irritant dermatitis every
winter. At times she washes over 10 times a day.
Fabric/man-made vitreous fibers
  • Fibers larger than 3.5 µm in diameter cause the
    highly pruritic contact dermatitis caused by
  • Erythematous papules with superimposed
    excoriations on neck and dorsal hands
  • Wool and rough clothing cause dermatitis in
    atopic individuals

Fiberglass dermatitis
Differential Diagnosis
  • Allergic and ICD, especially in chronic stage
    appear similar by clinical appearance, histology,
    and immunohistology
  • Look identical with erythema, papules, xerosis,
    scaling, and lichenification with sharp borders
  • ICD has remained a diagnosis of exclusion when
    dermatitis is not explained by positive patch
    test to a known allergen
  • More frequent complaint of burning and stinging
    with ICD in contrast to pruritus in ACD

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  • Avoidance of causative irritants at home or in
    the workplace is the primary TX
  • Engineering controls to reduce exposure in the
  • Shielding and personal protection such as gloves
    and special clothing
  • Pre-exposure protection by protective creams,
    removal of irritants by mild cleaning agents, and
    enhancement of barrier function generation by
    emollients and moisturizers
  • Emphasizing personal and occupational hygiene
  • Establishing educational programs to increase
    awareness in the workplace

Treatment of Chemical Burns
  • Initial tx irrigation with large volumes of
    water, if chemical is insoluble in water a soap
    solution may be used
  • High pressure water to be avoided to prevent
  • 2.5 calcium gluconate gel used to treat
    hydrofluoric acid burns, immediate application of
    a weak acid such as vinegar, lemon juice, or 0.5
    hydrochloric acid will lessen the effect of
    alkali burns
  • Ulcerated areas should be managed with
    antibacterial creams or ointments to prevent
    secondary infection
  • Frequent evaluation is required because ulcers
    may progress over several days
  • Excision, debridement and/or grafting may speed
  • Monitoring of blood, liver, and kidney function
    may be needed when exposed to chemicals with
    potential for systemic toxicity such as
    hydrofluoric acid, phenolic compounds, chromic
    acid, and gasoline

Chronic ICD Treatment
  • Treatment goal is to restore normal epidermal
    barrier function
  • Topical corticosteroids frequently used
  • Systemic corticosteroids although helpful in
    reducing inflammation, are not useful in
    treatment of chronic ICD unless offending
    contactants are avoided
  • PUVA and Grenz ray considered for chronic
    dermatitis that does not respond to other tx
  • Hyperkeratotic palmoplantar dermatitis from
    frictional or chronic ICD may benefit from the
    adjunctive use of systemic retinoids such as

Allergic contact dermatitis (ACD)
  • ACD accounts for approximately 20 of all contact
  • ACD is a type IV, delayed or cell-mediated immune
    reaction that is elicited when the skin comes in
    contact with a chemical to which an individual
    has been previously sensitized
  • Synonyms include contact dermatitis and contact
  • Allergic contact dermatitis. Linear s streaks
    seen with ACD to poison ivy.

  • Key Features
  • ACD is a pruritic, eczematous reaction
  • Acute ACD and many cases of chronic ACD are well
    demarcated and located to the site of contact
    with the allergen
  • Prototypic reactions are ACD due to poison ivy
    and nickel
  • Patch testing remains the gold standard for
    accurate and consistent diagnosis

This healthy adolescent developed an intensely
pruritic vesiculobullous allergic contact
dermatitis from hair dye.
  • Classic picture of ACD is a well-demarcated
    erythematous vesicular and/or scaly patch or
    plaque with well defined margins corresponding to
    the area of contact
  • Chronic allergic contact dermatitis leading to
    hand dermatitis. This golfer wore one leather
    glove and had positive patch tests to potassium
    dichromate and a piece of his glove. Courtesy of
    Kalman Watsky, M.D.

  • Allergic contact dermatitis to leather shoes.
    Note the correspondence to sites of exposure.
    Courtesy of Yale Residents Slide Collection.
  • Mercaptobenzothiazole (MBT) is the most common
    cause of allergic shoe dermatitis

  • Because ICD and ACD are not always discernable
    clinically, patch testing is required to help
    identify an allergen or exclude an allergy to a
    suspected allergen.
  • Allergic contact dermatitis. Chronic hand
    dermatitis due to ACD to mercaptobenzothiazole
    found in rubber gloves

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 vocations play an important role
  • Allergens differ from region to region, e.g.
    preservatives used in personal care products can
    vary based on government legislation

Pathogenesis of ACD
  • ACD is a type IV hypersensitivity response
  • Lesions appear in acute ACD within 24 to 96 hours
    of exposure
  • Requires prior sensitization to the chemical in
  • Subsequent re-exposure of individual leads to
    allergen being presented to a primed T-cell
    milieu leading to release of numerous cytokines
    and chemotactic factors leading to the clinical
    picture of eczema
  • Once sensitized a low concentration of causative
    chemical elicits a response

  • Induction of contact hypersensitivity.
    Application of contact allergens (Ag) induces the
    release of cytokines by keratinocytes, Langerhans
    cells and other cells within the skin. These
    cytokines in turn activate Langerhans cells which
    uptake the antigen and emigrate into the regional
    lymph nodes. During this process, the Langerhans
    cells mature into dendritic cells. In addition,
    the antigen is processed, re-expressed on the
    surface and finally presented to naïve T cells in
    the regional lymph node. Upon appropriate antigen
    presentation, T cells bearing the appropriate T
    cell receptor clonally expand and become effector
    T cells. These alter their migratory behavior due
    to the expression of specific surface molecules
    like CLA. Effector T cells recirculate into the
    periphery where they may later meet the antigen
    again. Ag, antigen KC, keratinocyte.

  • Elicitation of contact hypersensitivity.
    Application of contact allergens (Ag) into a
    sensitized individual causes the release of
    cytokines by keratinocytes and Langerhans cells.
    These cytokines induce the expression of adhesion
    molecules and activation of endothelial cells
    which ultimately attracts leukocytes to the site
    of antigen application. Among these cells, T
    effector cells are present which are now
    activated upon antigen presentation either by
    resident cells or by infiltrating Langerhans
    cells. Antigen-specific T cell activation again
    induces the release of cytokines by T cells. This
    causes the attraction of other inflammatory cells
    including granulocytes and macrophages which
    ultimately cause the clinical manifestation of
    contact dermatitis. Ag, antigen DDC, dermal
    dendritic cell KC, keratinocyte CLA, cutaneous
    lymphocyte antigen.

Clinical features of ACD
  • Acute blistering and weeping
  • Chronic lichenified and scaly plaques
  • Patchy and diffuse distributions may be seen with
    body washes and shampoos
  • Acute bullous allergic contact dermatitis due to
    poison ivy. This distribution is seen in patients
    who wear gloves. Courtesy of Yale Residents Slide
  • Chronic allergic contact dermatitis due to
    glutaraldehyde. The patient was an optometrist

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
  • Moderate to severe reactions show intraepidermal
  • Subacute to chronic stages have epidermal
    hyperplasia, often psoriasiform

  • Irregular psoriasiform epidermal hyperplasia with
    slight spongiosis. A The thick compact
    orthokeratotic stratum corneum is due to the
    acral location of the specimen. B Spongiotic,
    vesicular psoriasiform dermatitis due to contact
    dermatitis. The intraepidermal vesiculation is a
    consequence of marked spongiosis. C Spongiotic,
    psoriasiform dermatitis with areas of spongiotic
    microvesiculation within the epidermis. D Higher
    magnification of C showing eosinophils within a
    spongiotic microvesicle at the tip of a rete
    ridge. Eosinophils were also present in the
    dermal infiltrate.

  • Includes many forms of dermatitis ICD, atopic
    dermatitis, stasis dermatitis, and seborrheic
    dermatitis, as well as the erythematous form of
  • Hand and foot ACD need to be distinguished from
    psoriasis and tinea
  • Widespread disease needs to be differentiated
    from other causes of erythoderma, Sezary syndrome

Patch Testing
  • Simple office procedure upon which the diagnosis
    of ACD often rests
  • Although the procedure is simple, deciding when
    and what to test for requires training and
  • Patch testing is underutilized
  • Only 50 of all residency programs in USA have a
  • test center
  • Past surveys show 27 of the responders did no
    patch testing

Patch Testing
  • TRUE Test 23 allergens and a control
  • Other panels include North American Contact
    Dermatitis Group (NACDG) Screening Series, and
    the European Standard Series
  • Other panels are unique to specific occupations
    such as hairdressing tray, dental tray, and
    florist tray

True Test
  • Preimpregnated test that screens for 23 allergens
  • Extending testing beyond these 23 allergens has
    shown to be more beneficial
  • In three studies, extended testing detected
    37-76 more positive reactions, and 47.3 of
    patients had positive reactions only to
    non-screening allergens
  • Additional allergens come in multiuse syringes

Application of TRUE test.
  • Allergens contained within syringes being placed
    by nurse into Finn chambers

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Pre-Patch Testing Questions
  • Exposures both at work and home to understand
    mechanics of the work environment, Materials
    Safety Data Sheets (MSDS) can be helpful for
    workplace exposures
  • Effect of vacations and time away form work or
    home should be ascertained
  • All personal care products should be inventoried
  • All hobbies should be explored

Patch Testing
  • Chemicals brought in by patients should not be
    tested blindly, physician should be aware of the
    chemical ingredients because severe burns or
    ulceration may occur
  • Leave on personal care products such as
    moisturizers and make-up may be tested as is
  • Rinse off products such as soaps or shampoos
    need to be diluted prior to patch testing

Patch Testing
  • Most common site is the upper back
  • Patients should not have a sunburn in test area,
    and should not apply topical corticosteroids to
    the patch test sites for 7 days prior to test
  • Systemic corticosteroids should be avoided for 1
    month prior to testing
  • Patches are applied to back and reinforced with
    Scanpor tape, patient instructed to keep back dry
    and patches secured until second visit at 48 hours
  • Fixing allergens to patient's back using Scanpor

Patch Testing
  • When the patient returns in 48 hours the patches
    need to be inspected to ensure that the testing
    technique is adequate
  • As patches are removed their sites of
    application should be marked in order to
    identify the locations of particular allergens

Patch Test Scoring
  • A positive patch test reaction to nickel. This is
    an example of a 3 reaction

Patch Testing
  • Patient again asked to keep back dry until second
    reading, done from 72 hours to 1 week after the
    initial application of the patches
  • This delayed reading is necessary due to patch
    test responses to some allergens such as gold
    having a delayed reaction

Repeat Open Application Test (ROAT)
  • Poor mans patch test
  • Patient applies the product in question to the
    same location (where there is not dermatitis),
    e.g. antecubital fossa, BID for 1-2 weeks
  • If dermatitis develops, it can be concluded that
    the patient is reacting to the product
  • Downside to this approach is that individual
    problem ingredients are not identified

Treatment and Patient Education
  • Once allergens are positively identified, patient
    should be given written information on all of
    these chemicals
  • Patient should be instructed on how to read
    labels on old or new products to avoid future

Treatment of ACD
  • Involves identification of causative allergens
  • Clear the dermatitis with topical, or if
    necessary systemic corticosteroids
  • Complete and prolonged clearing can take up to 6
    weeks or more, even when allergens are being

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  • 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
  • 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
  • Eyelid dermatitis from metal eyelash curlers can
    be seen
  • Photos from

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
  • Co-reactivity is commonly seen with neomycin and

13 year old boy developed an itchy allergic
contact dermatitis from a topical antibiotic.
Balsam of Peru
  • Naturally occurring fragrance material
  • Wood extract derived from Myroxolon balsamum tree
  • Prior to introduction of fragrance mix in the
    1970s, balsam of Peru was used to screen for
    fragrance allergy
  • Capable of identifying 50 of those allergic to
  • Seen in those with allergies to spices, in
    particular cloves, Jamaican pepper, and cinnamon
  • Patients with a positive reaction need to avoid
    fragrances, occasionally spices, and other
    sources such as colas, tobacco, wines, and

Fragrance Mix
  • Contains eight different components cinnamic
    etoh, cinnamic aldehyde, hydroxycitronellal,
    isoeugenol, eugenol, oak moss absolute,
    alpha-amyl cinnamic aldehyde, and geraniol
  • Detects 70-80 of fragrance allergies
  • Patients need to read product labels and avoid
    anything that lists a fragrance, is labeled
    unscented, or has an obvious scent
  • Patients need to look for fragrance-free
  • ACD to fragrance found in cologne. A Patient with
    ACD to fragrance found in his cologne. B Patient
    after avoidance of fragrances and his cologne.

  • Thimerosal is a combination of thiosalicylic acid
    and ethylmercuric chloride, and is used as a
  • Most sensitization may be due to its use as a
    preservative in vaccines
  • Other exposures include contact lens solution,
    otic and opthalmic solutions, antiseptics, and
  • Positive reactions are common, relevance is low
    and therefore routine testing to this allergen
    should be reconsidered
  • False-positive intradermal testing (PPD) can
    occur if the material is preserved with thimerosal

  • NACDG found a positive rate of 9.5
  • NACDC found 90 of gold-allergic patients were
    women, and there was a higher rate of nickel
    (33.5) and cobalt allergy (18) in this group
  • Most common clinical picture is hand, facial, or
    eyelid dermatitis
  • Systemic reactions to gold in patients whom it
    was used to tx RA, SLE, or pemphigus.
  • Cutaneous findings of lichen planus-like
    reactions to pityriasis rosea-like reactions and
    papular eruptions with systemic reactions

  • Is a ubiquitous, colorless gas found in the
    workplace, cosmetics, medications, textiles,
    paints, cigarette smoke, paper, and formaldehyde
    resins in plastic bottles
  • Commonly seen in association with
    formaldehyde-releasing preservatives, such as
    quarternuim-15 imidazolidinyl urea, diazolidinyl
    urea, DMDM hydantoin, 2-bromo-2-nitropropane-1-3,d
    iol, and tris(hydroxymethyl)nitromethane
  • ICD is most common, ACD, contact urticaria, and
    mucous membrane irritation can occur
  • Textile dermatitis due to formaldehyde resins in
    wash-and-wear and wrinkle resistant clothes
  • Another source of formaldehyde is
    formaldehyde-free products that are packaged in
    containers coated with formaldehyde resins
  • So widespread that avoidance is difficult and
    clinical relevance should be determined

  • 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 dermatitis due toquaternium-15 in a
  • Metal that is used in association with other
    metals to add hardness and strength
  • Frequently combined with nickel, chromium,
    molybdenum, and tungsten
  • 80 of individuals with a cobalt sensitivity have
    a co-sensitivity to chromate (more common in men)
    or nickel (more common in women)
  • Exposure through jewelry snaps, buttons, tools,
    cosmetics, hair dyes, joint replacements,
    ceramics, enamel, cement, paints, and resins
  • Used in blue tatoos

  • Topical antibiotic with activity against
    Gram-positive bacteria and spirochetes
  • Commonly used in combination with other
    antibiotics such as neomycin and with
  • In addition to ACD, also rarely causes
    anaphylaxis and contact urticaria

Chronic ulcerations on the lower extremity are
particularly likely to develop allergic contact
dermatitis. This eruption resulted from
sensitization to bacitracin.
  • Have been shown to cause ACD in anywhere from
    0.2 to 5.98
  • It is suspected that ACD to these agents is
    underdiagnosed, due to insufficient testing
  • Clinical scenarios that should raise suspicion
    include chronic dermatitis, failure to clear
    with corticosteroids, and exacerbations of
    dermatitis after use of corticosteroids
  • Tixocortol-21-pivalate (for Group A) and
    budesonide (for Group D) used for screening, with
    91.3 of corticosteroid allergic reactions
  • Complicates patch test interpretation, due to
    edge effect (first reading may have erythema only
    at the rim of the Finn chamber)

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Systemic Contact Dermatitis
  • Systemic exposure to a chemical may result in a
    diffuse dermatitis
  • Patient has had a prior contact allergy and then
    becomes exposed through a systemic route, such as
    injection, oral, intravenous, or intranasal
  • One of most common examples is patient with
    ethylenediamine allergy and subsequent reaction
    to aminophylline

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Airborne Contact Dermatitis
  • Airborne allergens result in several different
    reactions including ICD and ACD
  • PhotoACD, photoICD, phototoxicity, and
    photoallergy to systemic medications clinically
    resemble airborne contact dermatitis
  • Ragweed dermatitis is a classic example
  • Clinically, lichenified and dry skin located in
    the exposed portions of the skin face, V of the
    neck, arms and legs
  • Most common causative agents are plants, natural
    resins, woods, plastics, rubbers, glues, metals,
    pharmaceutical chemicals, insecticides and

  • Airborne contact dermatitis. Example of the
    airborne contact dermatitis pattern seen in a
    patient allergic to sesquiterpene lactones. Note
    involvement on the anterior neck, which would not
    be expected if this were a photodermatitis.
    Courtesy of Dirk Elston, M.D.

55-year-old farm worker developed a chronic
allergic contact dermatitis to airborne allergens
(Asteraceae, previously called Compisitae).
Anacardiacea Dermatitis
  • Poison Ivy vine growing up a tree

Anacardiacea ACD
  • Members of the Anacardiaceae cause more contact
    dermatitis that all other plant families combined
  • Most allergenic members belong to the genus
    Toxicodendron, including poison ivy, poison oak,
    and poison sumac
  • Tocicodendron leaves are compound, possessing
    three or more leaflets. Flowers and fruit arise
    in an axillary positions in the angle between the
    leaf and the twig from which it arises
  • Black dots of urushiol often present on leaves
    and fruit

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Anacardiacae Allergens
  • Urushiol derives its name form the Japanese word
    for the sap (kiurushi) of the Japanese lacquer
  • Urushiol contains a mixture of catechols
    (1,2-dihydroxybenzenes) and resorcinols
  • Urushiol self-melanizes on exposure to oxygen
  • Avidly binds to skin but is readily degraded by
  • Poison Ivy

Clinical Features Anacardiacea Dermatitis
  • Damage is generally required for plants to
    release urushiol
  • In late fall plants release urushiol
  • Urushiol may be spread by contaminated clothing,
    dogs, cats, lacquered furniture, sawdust, and
  • Allergen-containing smoke can cause severe
    respiratory tract inflammation, severe
    dermatitis, and even temporary blindness

Clinical Features Anacardiacea Dermatitis
  • After contact with urushiol, a sensitized person
    typically develops and pruritic, erythematous
    eruption within 2 days (4-96 hours) that peaks
    within 1-14 days
  • Dermatitis may last up to 3 weeks after primary
    contact or within hours of secondary contact
  • Streaks of erythema and edematous papules
    typically precede vesicles and bullae
  • Although ACD is the most common cause of streaky,
    vesicular dermatitis, plants may cause this same
    picture by other means e.g. chemical irritant
    dermatitis, or the initial phase of

  • Clinical manifestations of Anacardiaceae
    dermatitis. A Acute, streak-like edematous and
    erythematous dermatitis without vesicles after
    poison ivy brushed across the face. Courtesy of
    Fitzsimons Army Medical Center Dermatology slide
    teaching library. B Acute, streak-like vesicular
    dermatitis after poison ivy (Toxicodendron
    radicans) contact. Courtesy of Fitzsimons Army
    Medical Center Dermatology slide teaching
    library. C Widespread erythema and edema
    associated with intense pruritus after carrying
    logs of the poisonwood tree (Metopium toxiferum)
    of the family Anacardiaceae. D Black-spot
    poison ivy dermatitis note the black
    discoloration in the central portion of the
    edematous plaques due to plant resin.

Clinical Features Anacardiacea Dermatitis
  • Eruption progresses to new areas because of
    variability in antigen concentration and stratum
    corneum/epidermis thickness, not because of
    bullae fluid
  • Over 70 of the US population reacts to poison
    ivy allergens after patch testing, but only 50
    react to plants in the field
  • Only 15 atopic patients are sensitive to poison
  • Uncommonly, eruptions resemble erythema
    multiforme, measles, scarlatina, or urticaria
  • Prolonged postinflammatory hyperpigmentation may
    occur in darkly pigmented individuals

  • Entire body should be washed with copious amounts
    of water as soon as possible after exposure
  • Soap may be used afterwards, but early use of
    soap may expand the area of resin on the body
  • As mentioned before, urushiol is water
    degradable, After 10 minutes only 50 can be
    removed, after 15 minutes only 25 can be
    removed, after 30 minutes only 10 can be
    removed, and after 60 minutes, none of it can be
  • Weepy lesions are best treated with tepid baths,
    wet-to-dry soaks, or bland shake lotions
  • Stringent such as Burows solution (aluminum
    subacetate) works to cool and dry lesions when
    applied as a wet-to-dry dressing
  • Topical antihistamines, anesthetics containing
    benzocaine, and antibiotics should be avoided to
    prevent sensitization

  • Most potent topical corticosteroids only help if
    applied during the earliest stages of the
    outbreak, when vesicles and blisters are not yet
  • Systemic steroids are effective when given at a
    dose of 1-2 mg/kg/day, slowly tapered over 2-3
  • Many patients are referred for a recurrence of
    their poison ivy dermatitis after completing a
    short, 6 day course of oral corticosteroids
  • Oral antihistamines may decrease pruritus