1/9/14 Allergic Contact Dermatitis

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Allergic Contact Dermatitis

Author: Daniel J Hogan, MD; Chief Editor: William D James, MD more...

Updated: Apr 26, 2013

Practice Essentials

Individuals with allergic contact dermatitis may have persistent or relapsing dermatitis, particularly if the material(s)to which they are allergic is not identified or if they practice inappropriate skin care. The longer an individual hassevere dermatitis, the longer, it is believed, that the dermatitis will take to resolve once the cause is identified.

Essential update: Allergic contact dermatitis caused by non-latex rubber gloves

In a study of surgery personnel in Sweden with occupational allergic contact dermatitis, Pontén et al found

evidence that the condition was caused by 1,3-diphenylguanidine (1,3-DPG) in non-latex rubber gloves.[1] Usingpatch tests, the investigators found that 12 of 16 patients reacted to 1,3-DPG. The 1,3-DPG was present in thegloves worn by the patients in the study, with a higher concentration on the inside of the gloves than on the

outside. In 7 of 8 patients, contact allergy to cetylpyridinium chloride was also found[1]

Signs and symptoms

Acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base.Lichenified pruritic plaques may indicate a chronic form of the condition.

Individuals with allergic contact dermatitis typically develop the condition within a few days of exposure, in areasthat were exposed directly to the allergen. Certain allergens (eg, neomycin), however, penetrate intact skin poorly;in such cases, the onset of dermatitis may be delayed for up to a week following exposure.

Individuals may develop widespread dermatitis from topical medications applied to leg ulcers or from cross-reactingsystemic medications administered intravenously.

Intraoral metal contact allergy may result in mucositis that mimics lichen planus, which has an association withintraoral squamous cell carcinoma.

See Clinical Presentation for more detail.

Diagnosis

Diagnostic studies for allergic contact dermatitis include the following:

Potassium hydroxide preparation and/or fungal culture: To exclude tinea; these tests are often indicated fordermatitis of the hands and feetPatch testing: To identify external chemicals to which the person is allergicRepeat open application test (ROAT): To determine whether a reaction is significant in individuals whodevelop weak or 1+ positive reactions to a chemical

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Dimethylgloxime test: To determine whether a metallic object contains enough nickel to provoke allergicdermatitisSkin biopsy: May help to exclude other disorders, particularly tinea, psoriasis, and cutaneous lymphoma

See Workup for more detail.

Management

The definitive treatment for allergic contact dermatitis is the identification and removal of any potential causalagents; otherwise, the patient is at increased risk for chronic or recurrent dermatitis. Treatments also include thefollowing:

Corticosteroids: Topical corticosteroids are the mainstay of treatment, although acute, severe allergiccontact dermatitis, such as from poison ivy, often needs to be treated with a 2-week course of systemiccorticosteroidsTopical immunomodulators (TIMs): Approved for atopic dermatitis, but they are also prescribed for cases ofallergic contact dermatitis when they offer safety advantages over topical corticosteroidsPhototherapy: Administered to individuals with chronic allergic contact dermatitis that is not controlled wellby topical corticosteroids; these patients may benefit from treatment with a combination of psoralen (aphotosensitizer) and ultraviolet-A (PUVA)Immunosuppressive agents: Chronic immunosuppressive agents are, in rare instances, used to treatrecalcitrant cases of severe, chronic, widespread allergic contact dermatitis or severe hand dermatitis thatprevents a patient from working or performing daily activitiesDisulfiram: Occasionally, an individual who is highly allergic to nickel and has severe vesicular handdermatitis will benefit from treatment with disulfiram (Antabuse); the drug has a chelating effect

See Treatment and Medication for more detail.

Image library

Chronic stasis dermatitis w ith allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis

produces areas of erythema in areas of atrophie blanche and varicose veins.

Background

Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity (allergy) resulting from cutaneous contactwith a specific allergen to which the patient has developed a specific sensitivity. This allergic reaction causesinflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation.

The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis. Contactdermatitis is inflammation of the skin induced by chemicals that directly damage the skin (see Irritant ContactDermatitis) and by specific sensitivity in the case of allergic contact dermatitis.

Jadassohn first described allergic contact dermatitis in 1895. He developed the patch test to identify the chemicalsto which the patient was allergic. Sulzberger popularized patch testing in the United States in the 1930s. The Finn

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chamber method for patch testing was designed in the 1970s; these chambers consist of small metal cups,typically attached to strips of tape, filled with allergens dispersed in either petrolatum or water. The thin-layer rapiduse epicutaneous (TRUE) test for patch testing became available in the United States in the 1990s.

The importance of specific substances as causes of allergic contact dermatitis varies with the prevalence of thatsubstance in the environment. Mercury compounds once were significant causes of allergic contact dermatitis butrarely are used as topical medications and, currently, are uncommon as a cause of allergic contact dermatitis.Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of allergiccontact dermatitis once Mycolog cream was reformulated to no longer contain this allergen.

A detailed history, both before and after patch testing, is crucial in evaluating individuals with allergic contactdermatitis. Before patch testing, the history identifies potential causes of allergic contact dermatitis and thematerials to which individuals are exposed that should be included in patch testing. After patch testing, the historydetermines the clinical significance of the findings. (See Clinical.)

Topical corticosteroids are the mainstay of treatment, while a variety of symptomatic treatments can provide short-term relief of pruritus. However, the definitive treatment of allergic contact dermatitis is the identification andremoval of any potential causal agents; otherwise, the patient is at increased risk for chronic or recurrentdermatitis. (See Treatment.)

Go to Irritant Contact Dermatitis, Pediatric Contact Dermatitis, and Protein Contact Dermatitis for completeinformation on these topics.

Pathophysiology

Approximately 3000 chemicals are well documented as specific causes of allergic contact dermatitis.

Compounds must be less than 500 d for efficient penetration through the stratum corneum barrier, which is thewater-impermeable outer layer of the skin. Small organic molecules that are chemically reactive (chemicalsensitizers) bind with self-proteins to generate immunogenic neoantigens through a process termed haptenization.Although haptens can penetrate through intact skin, patients with certain disease states that impair barrierfunction (eg, leg ulcers, perianal dermatitis) have an increased risk of sensitization to topically applied medicationsand their vehicle components.

Many patients with atopic dermatitis or allergic contact dermatitis to nickel harbor a defective form of the filaggrin

gene.[2] Filaggrin helps aggregate cytoskeletal proteins that form the cornified cell envelope. In its absence, thebarrier is defective.

Prehaptens are chemicals that are not activated by host proteins, but instead require chemical transformation byoxidative derivatization by ambient or air oxidation to form hydroperoxide. Examples include certain fragrancematerials and dyes used in hair coloring, such as para-phenylenediamine.

Haptens activate Toll-like receptors (TLRs) and activate innate immunity. The importance of hapten-mediatedactivation of innate immunity is highlighted by the clinical observation that the irritancy of chemicals (ie, the abilityof these chemicals to cause grossly visible skin inflammation upon primary exposure) correlates with their abilityto act as contact sensitizers and to induce acute contact dermatitis.

Haptens or haptenated self-proteins are recognized by innate immune mechanisms in the skin, and this leads tothe elaboration of a number of proinflammatory mediators, including interleukin (IL)–1β. As a result, skin-residentdendritic cells (DCs) become activated. There are several populations of DCs. Langerhans cells are the only DCsubtype in the epidermis. Like all skin-resident DCs, Langerhans cells efficiently acquire antigen in the peripheryand migrate to regional lymph nodes where they present antigen to naïve and memory T cells. These DCs, whichmay have been directly haptenated or could have acquired haptenated proteins from their surroundings, migrate toskin-draining lymph nodes where they present peptides from haptenated proteins to activate memory and naïve Tcells.

In the final step, hapten-induced inflammation recruits activated effector T cells back to the initial site of antigenencounter in the skin. The effector T cells release proinflammatory cytokines, such as interferon-γ, and promotethe killing of haptenated cells, resulting in the development of the classic inflammatory rash seen in allergic

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contact dermatitis.

Keratinocytes are crucial for the development of allergic contact dermatitis. They constitute the vast majority ofcells in the epidermis and form the anatomic barrier of the skin. Keratinocytes express most TLRs, and this allowsthem to respond to TLR4-triggering haptens, such as nickel. Keratinocytes are also a source of IL-10, animmunosuppressive cytokine that limits the extent of contact hypersensitivity

The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such aspoison ivy. Some individuals develop specific sensitivity to allergens following years of chronic low-grade exposure;for example, sensitivity to chromate in cement can eventually develop in individuals with chronic irritant contactdermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, allergiccontact dermatitis develops within hours to several days of exposure.

CD4+ CCR10+ memory T cells persist in the dermis after clinical resolution of allergic contact dermatitis.

Etiology

Approximately 25 chemicals appear to be responsible for as many as one half of all cases of allergic contactdermatitis. These include nickel, preservatives, dyes, and fragrances.

Poison ivy

Poison ivy (Toxicodendron radicans) is the classic example of acute allergic contact dermatitis in North America.Allergic contact dermatitis from poison ivy is characterized by linear streaks of acute dermatitis that develop whereplant parts have been in direct contact with the skin.

Nickel

Nickel is the leading cause of allergic contact dermatitis in the world. The incidence of nickel allergic contactdermatitis in North America is increasing; in contrast, new regulations in Europe have resulted in a decreasing

prevalence of nickel allergy in young and middle-aged women.[3, 4]

Allergic contact dermatitis to nickel typically is manifested by dermatitis at the sites where earrings or necklaces(see the image below) containing nickel are worn or where metal objects (including the keypads of some cell

phones[5] ) containing nickel are in contact with the skin.

Nickel may be considered a possible occupational allergen. Workers in whom nickel may be an occupationalallergen primarily include hairdressers, retail clerks, caterers, domestic cleaners, and metalworkers. Individualsallergic to nickel occasionally may develop vesicles on the sides of the fingers (dyshidrotic hand eczema orpompholyx) from nickel in the diet.

Allergic contact dermatitis to nickel in a necklace.

Rubber gloves

Allergy to 1 or more chemicals in rubber gloves is suggested in any individual with chronic hand dermatitis whowears them, unless patch testing demonstrates otherwise. Allergic contact dermatitis to chemicals in rubbergloves typically occurs maximally on the dorsal aspects of the hand. Usually, a cutoff of dermatitis occurs on theforearms where skin is no longer in contact with the gloves. Individuals allergic to chemicals in rubber gloves maydevelop dermatitis from other exposures to the chemicals (eg, under elastic waistbands).

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Hair dye and temporary tattoos

p-Phenylenediamine (PPD) is a frequent component of and sensitizer in permanent hair dye products and

temporary henna tattoos[6] ; exposure in to it in hair dye products may cause acute dermatitis with severe facialedema. Severe local reactions from PPD may occur in black henna tattoos in adults and children. Epidemiologicdata indicate that the median prevalence of positive patch test reactions to PPD among dermatitis patients is

4.3% (increasing) in Asia, 4% (plateau) in Europe, and 6.2% (decreasing) in North America.[7]

Textiles

Individuals allergic to dyes and permanent press and wash-and-wear chemicals added to textiles typically developdermatitis on the trunk, which occurs maximally on the lateral sides of the trunk but spares the vault of the axillae.Primary lesions may be small follicular papules or may be extensive plaques.

Individuals in whom this allergic contact dermatitis is suspected should be tested with a series of textilechemicals, particularly if routine patch testing reveals no allergy to formaldehyde. New clothing is most likely toprovoke allergic contact dermatitis, since most allergens decrease in concentration in clothing following repeatedwashings.

Preservatives

Preservative chemicals added to cosmetics, moisturizers, and topical medications are major causes of allergiccontact dermatitis (see the image below). The risk of allergic contact dermatitis appears to be highest toquaternium-15, followed by allergic contact dermatitis to isothiazolinones. Kathon CG ismethylchloroisothiazolinone in combination with methylisothiazolinone.

Methylisothiazolinone is now used as an individual preservative and may be a significant allergen.[8]

Although parabens are among the most widely used preservatives, they are not a frequent cause of allergiccontact dermatitis.

Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing w as negative to the active ingredients in the

sunscreen.

Schnuch et al estimated that preservatives found in leave-on topical products varied over 2 orders of magnitude in

relative sensitization risk.[9]

Formaldehyde is a major cause of allergic contact dermatitis (see the image below). Certain preservativechemicals widely used in shampoos, lotions, other moisturizers, and cosmetics are termed formaldehyde

releasers (ie, quaternium-15 [Dowicil 200], imidazolidinyl urea [Germall 115], and isothiazolinones[9] ).

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Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.

Fragrances

Individuals may develop allergy to fragrances. Fragrances are found not only in perfumes, colognes, aftershaves,deodorants, and soaps, but also in numerous other products, often as a mask to camouflage an unpleasant odor.Unscented products may contain fragrance chemicals used as a component of the product and not labeled asfragrance.

Individuals allergic to fragrances should use fragrance-free products. Unfortunately, the exact chemicalsresponsible for a fragrance in a product are not labeled. Four thousand different fragrance molecules are availableto formulate perfumes. The fragrance industry is not required to release the names of ingredients used to composea fragrance in the United States, even when individuals develop allergic contact dermatitis to fragrances found intopical medications.

Deodorants may be the most common cause of allergic contact dermatitis to fragrances because they are appliedto occlude skin that is often abraded by shaving in women.

Massage and physical therapists and geriatric nurses are at higher risk of occupational allergic contact dermatitisto fragrances.

Corticosteroids

In the last decade, it has become clear that some individuals with chronic dermatitis develop allergy to topicalcorticosteroids. Most affected individuals can be treated with some topical corticosteroids, but an individual can beallergic to all topical and systemic corticosteroids. Budesonide and tixocortol pivalate are useful patch testcorticosteroids for identifying individuals allergic to topical corticosteroids.

Neomycin

The risk of allergy to neomycin is related directly to the extent of its use in a population. The risk of allergy toneomycin is much higher when it is used to treat chronic stasis dermatitis and venous ulcers than when it is usedas a topical antibiotic on cuts and abrasions in children. Assume that individuals allergic to neomycin are allergic

to chemically related aminoglycoside antibiotics (eg, gentamicin, tobramycin).[10] Avoid these drugs both topicallyand systemically in individuals allergic to neomycin.

Benzocaine

Avoid topical use of benzocaine. Benzocaine is included in most standard patch test trays. Individuals allergic tobenzocaine may safely use or be injected with lidocaine (Xylocaine), which does not cross-react with benzocaine.

Many individuals complain of adverse reactions to sunscreens, but many of these individuals are not allergic to thesunscreen materials. They may be allergic to preservatives in these products or may have nonspecific cutaneousirritation from these products.

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Photoallergy

Occasionally, individuals develop photoallergic contact dermatitis. Allergic contact dermatitis may be accentuatedby ultraviolet (UV) light, or patients may develop an allergic reaction only when a chemical is present on the skinand when the skin is exposed sufficiently to ultraviolet light A (UV-A; 320-400 nm).

Epidemiology

United States statistics

The National Health and Nutrition Examination Survey (NHANES) estimated the prevalence of contact dermatitis tobe 13.6 cases per 1000 population, using physical examinations by dermatologists of a selected sample ofpatients. NHANES underreported the prevalence compared with the physical examination findings.

The National Ambulatory Medical Care Survey conducted in 1995 estimated 8.4 million outpatient visits toAmerican physicians for contact dermatitis. This was the second most frequent dermatologic diagnosis. Of officevisits to dermatologists, 9% are for dermatitis. At a student health center dermatology clinic, 3.1% of patientspresented for allergic contact dermatitis, and 2.3% presented for irritant contact dermatitis.

The TRUE test Web site can provide accurate basic information on common allergens. The Contact AllergenManagement Program is provided as a service to the American Contact Dermatitis Society (ACDS) members andis particularly valuable for allergens found in topical skin care products. The Contact Allergen ReplacementDatabase (CARD) contains more than 8100 known ingredients cataloged in more than 5500 commercial skincareproducts and is available as a Smartphone application.

International statistics

A Swedish study found that prevalence of allergic contact dermatitis of the hands was 2.7 cases per 1000population. A Dutch study found that prevalence of allergic contact dermatitis of the hands was 12 cases per 1000population.

Race, sex, and age-related demographics

No racial predilection exists for allergic contact dermatitis. Allergic contact dermatitis is more common in womenthan in men. This predominantly is a result of allergy to nickel, which is much more common in women than inmen in most countries.

Allergic contact dermatitis may occur in neonates. In elderly individuals, the development of allergic contactdermatitis may be delayed somewhat, but the dermatitis may be more persistent once developed. Contact allergy

to topical medicaments is more common in persons older than 70 years.[11]

Prognosis

Individuals with allergic contact dermatitis may have persistent or relapsing dermatitis, particularly if the material(s)to which they are allergic is not identified or if they continue to practice skin care that is no longer appropriate (ie,they continue to use harsh chemicals to wash their skin, they do not apply creams with ceramides or blandemollients to protect their skin).

The longer an individual has severe dermatitis, the longer it is believed it will take the dermatitis to resolve once thecause is identified.

Some individuals have persistent dermatitis following allergic contact dermatitis, which appears to be trueespecially in individuals allergic to chrome.

A particular problem is neurodermatitis (lichen simplex chronicus), in which individuals repeatedly rub or scratchan area initially affected by allergic contact dermatitis.

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Mortality

Death from allergic contact dermatitis is rare in the United States. Allergic contact dermatitis to the weed wildfeverfew caused deaths in India when the seeds contaminated wheat shipments to India. This plant then becamewidespread and a primary cause of severe airborne allergic contact dermatitis.

Patient Education

Patients have the best prognosis when they are able to remember the materials to which they are allergic and howto avoid further exposures. Provide patients with as much information as possible concerning the chemical towhich they are allergic, including all known names of the chemical. Web sites, Smartphone applications, standardtextbooks, and the TRUE test kit contain basic information about the chemicals.

Susceptible individuals need to read the list of ingredients before applying cosmetic products to their skin, sincepreservative chemicals are used widely in consumer, medical, and workplace products. The same chemical mayhave different names when used for consumer or industrial purposes.

Provide pamphlets with color pictures of poison ivy to individuals allergic to the plant. The American Academy ofDermatology also has pamphlets on allergic contact dermatitis and hand eczema.

For patient education information, see the Skin, Hair, and Nails Center, as well as Contact Dermatitis.

Contributor Information and DisclosuresAuthorDaniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern UniversityCollege of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academyof Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

Chief EditorWilliam D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director,Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology andSociety for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional ContributorsDonald Belsito, MD Professor of Clinical Dermatology, Department of Dermatology, Columbia UniversityMedical Center

Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy ofDermatology, American Contact Dermatitis Society, Dermatology Foundation, New York County MedicalSociety, New York Dermatological Society, Noah Worcester Dermatological Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine,Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western ReserveUniversity School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha,American Academy of Emergency Medicine, American College of Chest Physicians, American College ofEmergency Physicians, American College of Physicians, American Heart Association, American Thoracic

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Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences,andSociety for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University ofLouisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academyof Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules SteinEye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy ofOphthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department ofMedicine, University of Miami, Leonard M Miller School of Medicine

Mark Louden, MD is a member of the following medical societies: American Academy of Emergency Medicineand American College of Emergency Physicians

Disclosure: Nothing to disclose.

R Scott Lowery, MD Associate Professor of Ophthalmology, Department of Pediatric Ophthalmology andStrabismus, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

R Scott Lowery, MD is a member of the following medical societies: American Academy of Ophthalmology andArkansas Medical Society

Disclosure: Nothing to disclose.

Joshua May, MD Bend Dermatology Clinic

Disclosure: Nothing to disclose.

John A Michael, MD

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of ThomasJefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills EyeInstitute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy ofOphthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association ofOphthalmologists, Cornea Society, Eye Bank Association of America, and International Society of RefractiveSurgery

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon HonorariaSpeaking and teaching; RPS Ownership interest Other; Bausch & Lomb Honoraria Speaking and teaching;Merck Consulting fee Consulting; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas forMedical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology,

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American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

David Todd Schwartz, MD Associate Professor of Emergency Medicine, New York University School ofMedicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center and New YorkUniversity Medical Center

David Todd Schwartz, MD is a member of the following medical societies: American Academy of EmergencyMedicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Bradley D Shy, MD Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center, New YorkUniversity School of Medicine

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University HealthSciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology,Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Jack L Wilson, PhD Distinguished Professor, Department of Anatomy and Neurobiology, University ofTennessee Health Science Center College of Medicine

Jack L Wilson, PhD is a member of the following medical societies: American Association of Anatomists,American Association of Clinical Anatomists, and American Heart Association

Disclosure: Nothing to disclose.

References

1. Pontén A, Hamnerius N, Bruze M, Hansson C, Persson C, Svedman C, et al. Occupational allergiccontact dermatitis caused by sterile non-latex protective gloves: clinical investigation and chemicalanalyses. Contact Dermatitis. Feb 2013;68(2):103-10. [Medline].

2. Novak N, Baurecht H, Schäfer T, Rodriguez E, Wagenpfeil S, Klopp N, et al. Loss-of-function mutations inthe filaggrin gene and allergic contact sensitization to nickel. J Invest Dermatol. Jun 2008;128(6):1430-5.[Medline].

3. Lu LK, Warshaw EM, Dunnick CA. Prevention of nickel allergy: the case for regulation?. Dermatol Clin.Apr 2009;27(2):155-61, vi-vii. [Medline].

4. Thyssen JP, Linneberg A, Menné T, Nielsen NH, Johansen JD. Contact allergy to allergens of the TRUE-test (panels 1 and 2) has decreased modestly in the general population. Br J Dermatol. Nov2009;161(5):1124-9. [Medline].

5. Moennich JN, Zirwas M, Jacob SE. Nickel-induced facial dermatitis: adolescents beware of the cellphone. Cutis. Oct 2009;84(4):199-200. [Medline].

6. Jacob SE, Zapolanski T, Chayavichitsilp P, Connelly EA, Eichenfield LF. p-Phenylenediamine in blackhenna tattoos: a practice in need of policy in children. Arch Pediatr Adolesc Med. Aug 2008;162(8):790-2.[Medline].

7. Thyssen JP, White JM. Epidemiological data on consumer allergy to p-phenylenediamine. ContactDermatitis. Dec 2008;59(6):327-43. [Medline].

1/9/14 Allergic Contact Dermatitis

emedicine.medscape.com/article/1049216-overview#showall 11/12

8. Lundov MD, Krongaard T, Menné TL, Johansen JD. Methylisothiazolinone contact allergy: a review. Br JDermatol. Dec 2011;165(6):1178-82. [Medline].

9. Schnuch A, Mildau G, Kratz EM, Uter W. Risk of sensitization to preservatives estimated on the basis ofpatch test data and exposure, according to a sample of 3541 leave-on products. Contact Dermatitis. Sep2011;65(3):167-74. [Medline].

10. Guin JD, Phillips D. Erythroderma from systemic contact dermatitis: a complication of systemicgentamicin in a patient with contact allergy to neomycin. Cutis. Jun 1989;43(6):564-7. [Medline].

11. Green CM, Holden CR, Gawkrodger DJ. Contact allergy to topical medicaments becomes more commonwith advancing age: an age-stratified study. Contact Dermatitis. Apr 2007;56(4):229-31. [Medline].

12. Assier-Bonnet H, Revuz J. [Topical neomycin: risks and benefits. Plea for withdrawal]. Ann DermatolVenereol. 1997;124(10):721-5. [Medline].

13. Gönül M, Gül U. Detection of contact hypersensitivity to corticosteroids in allergic contact dermatitispatients who do not respond to topical corticosteroids. Contact Dermatitis. Aug 2005;53(2):67-70.[Medline].

14. Cohen LM, Cohen JL. Erythema multiforme associated with contact dermatitis to poison ivy: three casesand a review of the literature. Cutis. Sep 1998;62(3):139-42. [Medline].

15. Cohen DE, Brancaccio R, Andersen D, Belsito DV. Utility of a standard allergen series alone in theevaluation of allergic contact dermatitis: a retrospective study of 732 patients. J Am Acad Dermatol. Jun1997;36(6 Pt 1):914-8. [Medline].

16. Bernstein IL, Li JT, Bernstein DI, Hamilton R, et al. Allergy diagnostic testing: an updated practiceparameter. Part 1. Ann Allergy Asthma Immunol. Mar 2008;100(3 Suppl 3):S15-S66.

17. Bernstein IL, Li JT, Bernstein DI, Hamilton R, et al. Allergy diagnostic testing: an updated practiceparameter. Part 2. Allergy Asthma Immunol. Mar 2008;100(3 Suppl 3):S66-S121.

18. Larkin A, Rietschel RL. The utility of patch tests using larger screening series of allergens. Am J ContactDermat. Sep 1998;9(3):142-5. [Medline].

19. Marks JG, Belsito DV, DeLeo VA, Fowler JF Jr, Fransway AF, Maibach HI, et al. North American ContactDermatitis Group patch test results for the detection of delayed-type hypersensitivity to topical allergens.J Am Acad Dermatol. Jun 1998;38(6 Pt 1):911-8. [Medline].

20. Rajagopalan R, Anderson RT, Sarma S, Kallal J, Retchin C, Jones J, et al. An economic evaluation ofpatch testing in the diagnosis and management of allergic contact dermatitis. Am J Contact Dermat. Sep1998;9(3):149-54. [Medline].

21. Jacobs JJ, Lehé CL, Hasegawa H, Elliott GR, Das PK. Skin irritants and contact sensitizers induceLangerhans cell migration and maturation at irritant concentration. Exp Dermatol. Jun 2006;15(6):432-40.[Medline].

22. Taylor JS, Praditsuwan P, Handel D, Kuffner G. Allergic contact dermatitis from doxepin cream. One-yearpatch test clinic experience. Arch Dermatol. May 1996;132(5):515-8. [Medline].

23. Baeck M, Chemelle JA, Rasse C, Terreux R, Goossens A. C(16) -methyl corticosteroids are far lessallergenic than the non-methylated molecules. Contact Dermatitis. Jun 2011;64(6):305-312. [Medline].

24. Katsarou A, Armenaka M, Vosynioti V, Lagogianni E, Kalogeromitros D, Katsambas A. Tacrolimusointment 0.1% in the treatment of allergic contact eyelid dermatitis. J Eur Acad Dermatol Venereol. Apr2009;23(4):382-7. [Medline].

25. Katsarou A, Makris M, Papagiannaki K, Lagogianni E, Tagka A, Kalogeromitros D. Tacrolimus 0.1% vsmometasone furoate topical treatment in allergic contact hand eczema: a prospective randomized clinicalstudy. Eur J Dermatol. Mar-Apr 2012;22(2):192-6. [Medline].

1/9/14 Allergic Contact Dermatitis

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Medscape Reference © 2011 WebMD, LLC

26. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulsedoses. Indian J Dermatol Venereol Leprol. Jan-Feb 2006;72(1):24-7. [Medline].

27. Shaffer MP, Belsito DV. Allergic contact dermatitis from glutaraldehyde in health-care workers. ContactDermatitis. Sep 2000;43(3):150-6. [Medline].

28. Bråred Christensson J, Andersen KE, Bruze M, et al. Air-oxidized linalool: a frequent cause of fragrancecontact allergy. Contact Dermatitis. Nov 2012;67(5):247-59. [Medline].

29. Kaplan DH, Igyártó BZ, Gaspari AA. Early immune events in the induction of allergic contact dermatitis.Nat Rev Immunol. Jan 13 2012;12(2):114-24. [Medline]. [Full Text].

30. Niklasson IB, Delaine T, Islam MN, Karlsson R, Luthman K, Karlberg AT. Cinnamyl alcohol oxidizesrapidly upon air exposure. Contact Dermatitis. Mar 2013;68(3):129-38. [Medline].

31. Pot LM, Scheitza SM, Coenraads PJ, Blömeke B. Penetration and haptenation of p-phenylenediamine.Contact Dermatitis. Apr 2013;68(4):193-207. [Medline].

32. Thyssen JP, Johansen JD, Linneberg A, Menné T, Engkilde K. The association between contactsensitization and atopic disease by linkage of a clinical database and a nationwide patient registry.Allergy. Sep 2012;67(9):1157-64. [Medline].