Allergic versus Contact Dermatitis Julie Sterbank, DO Assistant Clinical Professor Allergy/Immunology MetroHealth Medical Center/Case Western Reserve University
Disclosure I have no financial disclosures or conflict of interests to declare
Objectives 1. Identify key features of allergic contact dermatitis 2. Review the proposed etiology of allergic contact dermatitis 3. Develop a treatment plan pending further investigation and referral to a specialist
Start at the Very Beginning Is the child acutely ill in front of you? Do you need to make an urgent referral for fluids/antibiotics? Is there an actual rash and if so what is the distribution? Do you have urticaria present?
Urticaria Involves a different part of the immune system and depending on exposure can be part of a local reaction to something or potentially something more sinister as a serious widespread reaction Involves cross-linking of IgE antibodies leading to an immediate hypersensitivity reaction
In Contrast..
Allergic Contact Dermatitis Defined Classic presentation of a T-cell mediated, delayed hypersensitivity reaction of the skin in most cases, the reaction is limited to the site of contact
Biggest Clues Morphology - first what are you looking at? History - exposure!! Location of affected area
Acute versus Chronic Acute erythematous vascular pruritic burning stinging Chronic persistence of itch lichenification stinging burning pain
Lichenification
Most Common Distribution Eyes (eyelids) Face Hands Patchy distribution can be from body washes, shampoo, clothing/textile dyse or preservatives Sunscreens can cause photosensitive eruptions
Pathophysiology T-cell mediated so thought to require initial sensitization followed by subsequent re-exposure Previously only thought to include T-cells, however, it involves many more inflammatory cells (Langerhans cells, keratinocytes, CD8/CD4, B-1 cells, NK cells, mast cells, and Tregs) Often thought to involve haptens that penetrate the stratum corneum of the skin some of the most common players include nickel and chromium in North America, poison ivy, poison sumac and poison oak are frequent players
Pathophysiology (Continued) Biopsy often will reveal spongiotic dermatitis Intercellular edema leading to the disruption of intercellular adhesions (result in the formation of vesicles) Usually with lymphocytic infiltration in the superficial layers of the skin Spongiotic dermatitis is also seen in atopic, nummular, dyshydrotic and seborrheic dermatitis
Common Players Latex Protective equipment Eye glasses/safety goggles Soaps/cleansers Resins Acrylics Metals: gold and nickel Fragrances Topical antibiotics Preservatitives Emulsifiers in personal products Hair dyes
How common? 13 to 14 cases per 100,000 20 to 40% of people estimated to be allergic to nickel Up to a third of patients can have positives to patch testing, which may or may not be clinically relevant
Patch Testing Patches are placed for 48 hours First read occurs 48 to 72 hours from initial placement - can help identify irritant versus true delayed hypersensitivity reactions Second read 96 to 130 hours from initial placement - look for true delayed hypersensitivity reactions
What Next????
When you refer, know who you are referring to & what services they provide
Caveat Some Allergy/Immunology practices offer patch testing, others do not Some Dermatology practices offer patch testing, others do not
In the Interim You will never harm someone by recommending sensitive skin care regimens Soap-free Fragrance-free Dye-free
In the Interim (continued) Restore the natural barrier of the skin Use caution with creams, they tend to burn/sting open or severely irritated skin Keep in mind, some people can be sensitive to topical steroids and emollients such as petroleum products but this is relatively uncommon
In the Interim (continued) Be familiar with a few of the different steroids in each class from low potency (e.g. hydrocortisone) to ultra- potency (e.g. clobetasol) Even I don t generally prescribe clobetasol on a regular basis without having patients see Derm
Don t forget Calciuerin inhibitors such as tacrolimus and picrolimus good medicines but often get skipped due to block-box warning and cost in my patient population, often need to see failure with other agents
In the Interim (continued) Keep in mild that topical and oral steroids can blunt patch testing responses Unless patients can identify a particular trigger, often the problem will return (unfortunately)
Take Home Points Know the history and the exposure Identify whether you are looking at urticaria or something else Know who you are referring to and what service you are asking them to provide Restore the skin barrier in the interim
Questions?
References Loden, M Role of topical emollients and moisturizers in the treatment of dry skin barrier Am J Clin Dermatol. 2003;4(11):771-88. Jacob SE, Steele T, Brod B, Crawford GH Dispelling the myths behind pediatric patch testing-experience from our tertiary care patch testing centers Pediatr Dermatol. 2008;25(3):296 Silverberg NB, Licht J, Friedler S, Sethi S, Laude TA Nickel contact hypersensitivity in children. Pediatr Dermatol. 2002;19(2):110 Bruckner AL, Weston WL Allergic contact dermatitis in children: a practical approach to management. Skin Therapy Lett. 2002;7(8):3 Stables GI, Forsyth A, Lever RS Patch testing in children. Contact Dermatitis. 1996;34(5):341.