Contact dermatitis

Contact dermatitisBoonthorn

23 June 2010

Definition Classification Epidemiology Pathology & Pathophysiology Clinical presentation & Differential diagnosis Investigation Special exposure associated with CD management

Outline

Common inflammatory skin disorder Most common recognized as eczematous

inflammation Allergic or irritant skin reaction caused by

an external agent

Definition

J Allergy Clin Immunol 2010;125:S138-49.Allergy 2009:64:1669-1714.

Allergic contact dermatitis (ACD) (20%)◦ inflammation caused by allergen-specific T

lymphocytes. rapid development of dermatitis occurs following re-exposure to low concentrations of allergen, not cause lesions in non-sensitized individuals

Irritant contact dermatitis (ICD) (80%)◦ develop following prolonged and repeated exposure to

irritants◦ inflammatory cells have role in development of

dermatitis◦ allergen-specific lymphocytes not involved in

pathogenesis ◦ prior sensitization is not necessary

Classification

www.worldallergy.org

In U.S. (2004)◦ overall prevalence rate 24,400 /100,000 people

Cohort population-based studies in Europe◦ prevalence rates 0.7% - 18.6% for ACD

Incidence of OCD in other countries 1.3 - 19 cases per 10,000

All age groups are affected with slight female preponderance

prevalence increases with age decreased prevalence in patients >70 years

Epidemiology

J Allergy Clin Immunol 2010;125:S138-49.

Pathology epidermal hyperplasia

with spongiosis and mounds of parakeratosis.

There is superficial, perivascular infiltrate of lymphocytes and eosinophils with exocytosis

inflammation in epidermis and superficial dermis

Acute◦ superficial perivascular infiltration with lymphocytes,

monocytes and small number of eosinophils◦ increased intercellular spaces between keratinocytes

(spongiosis): predominant histologic feature of CD Chronic

◦ thickening of epidermis, irregular elongation of the rete ridges and vertical thickening of collagen of papillary dermis

Pathology

WWW.worldallergy.org

ACD ◦ prototype of type IV cell-mediated hypersensitivity

reaction ICD

◦ nonimmunologic, multifactorial, direct tissue reaction

◦ T cells activated by nonimmune, irritant, or innate mechanisms release proinflammatory cytokines

◦ dose-dependent inflammation ACD and ICD frequently overlap because

many allergens at high enough oncentrations can also act as irritants

Pathophysiology


Pathophysiology (ACD)

Allergy 2009: 64: 1699–1714.

Pathophysiology (ACD)

Allergy 2009: 64: 1699–1714.

Keratinocytes play key role in development of both ACD and ICD

synthesize and release pro-inflammatory cytokines, in particular interleukins IL-1, 6 and 8, TNF-α and GM-CSF

These cytokines play important part in recruitment and homing of inflammatory cells and can be induced and released from keratinocytes by both irritants and allergens

role of keratinocyte

Langerhans cells are primary APCs of epidermis cell surface expression of CD1a and presence of

intracytoplasmic Birbeck granules process protein Ag by cleaving them into peptides

and present fragments in peptide-binding groove of their surface located MHC class II

Hapten-conjugated LC migrate to local LN where they present allergen to T lymphocytes

T lymphocytes must then home to inflamed skin

Antigen presentation: The role of Langerhans cell

Homing is process whereby circulating cells migrate to relevant sites

This process relies on linkage between adhesion molecules expressed on endothelial cells and their ligands expressed on lymphocytes

homing receptor on T lymphocytes probably "cutaneous lymphocyte antigen" (CLA), ligand for E-selectin

Additional adhesion molecule ◦ ICAM-1 interacts with LFA-1◦ VCAM-1 interacts with VLA-4

Homing of T lymphocytes

Classic presentation ◦ pruritic, eczematous plaque localized to site of allergen

exposure◦ redness, edema,papules, vesiculation, weeping,

crusting Geometric or linear patterns or involvement of

unusual focal skin areas, eg. earlobes, or weight-bearing areas of feet may suggest contact cause

Chronic ACD (i.e. nickel and fragrances) can be insidious and present as localized lichenification or with more generalized reactions

Clinical presentation

ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006

Differentiation between ICD and ACD



Exogenous causes of ICD in Occupational Dermatology Clinic, Skin and Cancer Foundation, Australia (total 621 patients over the period 1993–2002)

Australasian Journal of Dermatology (2008) 49, 1–11

Differential diagnosis


Condition Differentiating signs/symptoms Patch tests

Atopic dermatitis Lesions are generally symmetrically distributed over flexural areas, less likely to be vesicular, more chronic in nature with seasonal variation, and not sharply delineated.FH is often positive for atopy.

Negative

Nummular eczema Lesions coin-shaped plaques, with pinpoint vesiculation, symmetrically distributed, most commonly on extensor lower extremities

Negative

Dyshidrotic eczema

Dyshidrotic eczema almost exclusively involves palms and soles with little to no involvement of dorsal hands and feet

Negative

Differential diagnosis

Best practice

Physical examination

Current Opinion in Pediatrics 2009, 21:491–498

Patch tests◦ gold standard for identification of contact allergen◦ occlusive patch testing is most common technique

Patch testing a patient with active AD more likely to produce “angry back” reaction, resulting in a false-positive reading

affected by ◦ oral corticosteroids (>20 mg of prednisone per day or its

equivalent)◦ cancer chemotherapy, or immunosuppressive drugs◦ Topical corticosteroids should be discontinued for 5 to 7

days before patch testing not affected by antihistamines

Investigation


Sources of allergens◦ T.R.U.E. TEST :not US FDA approved◦ But recommended by CD experts

No. of allergens◦ ideal number remains controversial◦ T.R.U.E. Test contains 29 allergens

higher false-negative reactions to neomycin, thiuram mix, balsam of Peru, fragrance mix, cobalt, and lanolin

◦ NACDG series from 65 to 70 allergens◦ use of FDA-certified antigen panel available in US

can fully evaluate ~ 25- 30% of ACD

Investigation



applied to upper or middle back areas (2.5 cm lateral to midspinal reference point) free of dermatitis and hair

kept in place for 48 hours read 30 minutes after removal of patches second reading should be done 3 to 5 days after

initial application Metals , topical antibiotics , topical orticosteroids,

and PPD can elicit positive reactions after 7 days Nonstandardized patch tests tested at 1:10 to

1:100 dilutions

Patch test technique



Repeat open application test (ROAT)◦ Improving reliability of interpreting tests for leave-on

products◦ suspected allergens are applied to antecubital fossa

twice daily for 7 days and observed for dermatitis◦ absence of reaction makes CD unlikely◦ If eyelid dermatitis is considered, ROAT can be

performed on back of ear dimethyl-glyoxime test for nickel

◦ identification of allergens Skin biopsy

◦ Distinguishing CD from morphologically similar diseases

Investigation


localized or generalized inflammatory skin disease in contact-sensitized individuals exposed to hapten orally, transcutaneously, intravenously, or by means of inhalation

Cause◦Metal (cobalt, copper, chromium, gold, mercury, nickel, and zinc)

◦ Medications corticosteroids, antihistamines (diphenhydramine, ethylenediamine, hydroxyzine, and doxepin), miconazole, terbinafine, neomycin,gentamicin, erythromycin, pseudoephedrine, benzocaine, tetracaine, oxycodone, IVIG, aminopenicillins, 5-aminosalicylic acid, naproxen, allopurinol, mitomycin C, 5-FU

◦ Herbal medicine

Systemic contact dermatitis


Symmetric drug-related intertriginous and flexural exanthema

Criteria for diagnosis :◦ exposure to systemic drug at first or repeated

dosing (contact allergens excluded)◦ erythema of gluteal/perianal area, V-shaped

erythema of inguinal/perianal area, or both◦ involvement of at least 1 other

intertriginous/flexural localization◦ symmetry of affected areas◦ absence of systemic signs and symptoms

Drug induced SCD


Second most common type of occupational disease

In 1999, incidence rate of occupational skin disorders was 49 cases per 100,000

most common occupations associated with OCD are health professionals (especially nurses), food processors, beauticians and hairdressers, machinists,and construction workers

Occupational contact dermatitis


4 of 7 criteria must be positive to conclude OCD◦ clinical appearance is consistent with CD◦ cutaneous irritants or allergens are present in workplace◦ anatomic distribution of dermatitis is consistent with skin

exposure to chemicals in course of various job tasks◦ temporal relationship between exposure and onset of

symptoms is consistent with CD◦ nonoccupational exposures are excluded as probable

causes of dermatitis◦ dermatitis improves away from work exposure and

reexposure causes exacerbation◦ there are positive-reaction and relevant patch tests

performed according to established guidelines

Occupational contact dermatitis


Toxicodendron dermatitis (poison ivy) is most common form of ACD and can be readily identified by its streak-like or linear papulovesicular presentation

caused by urushiol, which is found in saps of this plant family

Urushiol contained in mango skin,cashew nut oil, ginkgo (female) leaves, Japanese lacquer, and Indian marking ink

Plant dermatitis


Allergic contact dermatitis to poison ivy (toxicodendron radicans). Note the linear lesions induced by contact with branches




Metals Nickel

◦ NACDG reported 18.7% of patients evaluated for ACD had positive patch test reaction to nickel

◦ Female sensitization to nickel higher because of increased ear piercing

◦ 1% of nickel allergy have systemic reactions to nickel content of normal diet

◦ Foods with higher nickel content include soybean, fig, cocoa, lentil, cashew, nuts, and raspberry

SELECTED CONTACT ALLERGENS


Allergic contact dermatitis to nickel in watchband

Allergic contact dermatitis to nickel in earring

Allergic contact dermatitis to nickel in belt buckle


Gold NACDG reported that 389/4101(9.5%) had

positive patch test reactions to gold hands (29.6%); face, with seborrheic

distribution (19.3%); and eyelids (7.5%) mostly used for fashion appeal, anti-

inflammatory medication, used in electroplating industry, part of dental appliances (present with oral symptoms)


Common allergens in these products include fragrances, preservatives, excipients, glues, and sun blocks

Fragrance most common cause of ACD from cosmetics results in positive patch test reactions in 10.4% of patients ‘‘unscented’’ and ‘‘Fragrance-free’’ Fragrance mix I contains allergens found in 15% to 100% of

cosmetic products and might detect ~85% of subjects with fragrance allergy

positive patch test reaction to fragrance must correlate with distribution of dermatitis and evaluation of clinical relevance, eg. positive ROAT reaction

Cosmetics


Preservatives and excipients Lanolin : common component of consumer products It is weak sensitizer on normal skin but a stronger

sensitizer on damaged skin stasis dermatitis, are at higher risk of lanolin sensitivity Cosmetic preservatives

◦ Formaldehyde releasers ◦ non–formaldehyde releasers : Paraben most commonly used

preservative in cosmetics, as well as in pharmaceutical and industrial products

Type I immediate hypersensitivity reactions (contact urticaria) and SCD from ingestion of paraben-containing medications or foods have been reported


Hair products Second most common cause of cosmetic allergy PPD (Paraphenylenediamine) is most common

cause of CD in hairdressers In hair dye users the dermatitis often spares the

scalp and usually involves the face near the hairline, eyelids, and neck

PPD cross-reacts with COX-2 inhibitor (celecoxib), sunscreens, and antioxidants used in manufacture of rubber products

New hair dyes that contain FD&C and D&C dyes have very low levels of cross-reactivity with PPD


Allergic dermatitis from black leather watch band. Possible allergens include chromates used to tan leather and paraphenylenediamine dye


CAPB ( Cocoamidopropyl betaine )◦ amphoteric surfactant often found in shampoos,

bath products, and eye and facial cleaners◦ CAPB allergy typically presents as eyelid, facial,

scalp, and/or neck dermatitis Glycerol thioglycolate

◦ active ingredient in permanent wave solution◦ Unlike PPD, thioglycolates might remain allergenic

in hair long after it has been rinsed out◦ skin eruptions can continue for weeks after

application of permanent wave solution


Antibiotics and antiseptics Neomycin and nitrofurazone are potent

sensitizers Neomycin sulfate can cross-sensitize with

gentamicin, kanamycin, streptomycin, spectinomycin, tobramycin,and paromomycin

Medications


corticosteroid◦ 0.2-6%◦ Patients with worsening of previous dermatitis or

initial improvement followed by deterioration of dermatitis after application of corticosteroids should be evaluated

◦ Cross-reactivity between groups A and D2 and groups B and D2 also has been reported

◦ optimal patch test concentration not worked out for most corticosteroids

◦ 30% of ACD to corticosteroids be missed if delayed 7-day reading not done

Medications



Allergic contact dermatitis to topical steroid preparation applied to hands. Note massive edema, erythema, and sparing of skin under watch band


use of nickel in biomedical devices,led to increasing concern about safety in suspected nickel-sensitized patients

Presently,high variability of care no large, evidence-based guidelines 10 patients with positive patch test reaction

to metal had in-stent restenosis associated with clinical symptoms

allergy to metals,plays relevant role in inflammatory fibroproliferative restenosis

CD Due to Surgical Implant Devices


criteria for diagnosis of cutaneous implant–induced reaction◦ dermatitis (localized or generalized) appearing

after implant surgery◦ persistent dermatitis that is resistant to

appropriate therapies◦ positive patch test result proven history to

metallic component of implant or to commonly used acrylic glues

◦ resolution of dermatitis after removal of implant

CD Due to Surgical Implant Devices


Allergen identification to improve contact avoidance

Alternatives and substitutes to cosmetics should be offered to patient to increase compliance

supportive care and relief of pruritus, cold compresses with water or saline, Burrow solution , calamine, and colloidal oatmeal baths might help acute oozing lesions

Excessive handwashing should be discouraged in hand dermatitis, and nonirritating or sensitizing moisturizers must be used after washing

Treatment


TC is first-line treatment for ACD For extensive(>20% BSA) and severe CD,

systemic corticosteroids might offer faster relief (12-24hr)

recommended dose is 0.5 to 1 mg/kg daily for 5 to 7 days, and only if patient is comfortable at that time is dose reduced by 50% for next 5 to 7 days

Treatment


topical T-cell selective inhibitors ◦ efficacy in ACD or ICD not been established

antibiotics should be used for secondary infections of ACD or ICD

antihistamines have been used for relief of pruritus associated with ACD, generally ineffective ◦ diphenhydramine not be used in patients with ACD to

Caladryl and hydroxyzine hydrochloride in ethylenediamine-sensitive patient

Other modes of therapy : UV light treatment and immunomodulating agents, eg.MTX,AZA, and MMF

Treatment


Primary prevention◦ In high-risk industries and professions, preventive

surveillance programs are possible, especially for apprentices or newly hired workers

Secondary prevention◦ Once diagnosis of ACD or ICD is established,

emollients, moisturizers, and/or barrier creams may be instituted

Prevention


ICD is caused by direct toxicity without prior sensitisation and ACD is delayed hypersensitivity reaction

Results in localised burning, stinging, itching, blistering, redness and swelling at area of contact with allergen or irritant.

Patch testing may aid identification of offending agent Skin biopsy may also be helpful Treatment involves removal of offending agent, future

avoidance of offending agent, topical corticosteroids and/or short course of oral corticosteroids.

Conclusion

Health & Medicine

Contact dermatitis