Allergic Contact Dermatitis

Article Author:
Patrick Murphy
Article Author (Archived):
Joanna Hooten
Article Editor:
William Gossman
Updated:
7/26/2019 10:01:37 PM
PubMed Link:
Allergic Contact Dermatitis

Introduction

Allergic contact dermatitis (ACD) is a type 4 or delayed-type, hypersensitivity response (DTH) by an individual’s immune system to a small molecule (less than 500 daltons), or hapten, that contacts a sensitized individual’s skin.[1] The initial or induction phase of ACD occurs when the hapten combines with a protein to form a complex that leads to the expansion of an allergen-specific T cell population; the name for this process is sensitization. During the elicitation phase, re-exposure to the antigen leads to the development of dermatitis.[2] ACD accounts for 20% of contact dermatoses, and allergens differ greatly based upon geography, personal habits and hobbies, and often, the types of preservatives that are legally permissible, such as quaternium-15 in the United States but not Europe.[3]

Etiology

Allergic contact dermatitis is an inflammatory disease of the skin that is caused by a type 4 hypersensitivity reaction. It results from the contact of an offending chemical or antigen with the skin.[4] Morphology and location of the dermatitis are often the best indicators of the offending agent. For instance, when found around the wrist, it may indicate an allergic response to a bracelet or watchband.

Poison ivy is a common cause of ACD and presents as linear streaks where the plant comes into contact with the skin.

Nickel is another common cause of ACD and presents as dermatitis where necklaces and earrings containing nickel are worn.

Rubber gloves are also a common cause of chronic dermatitis.

Other agents include hair dyes, textile chemicals, preservatives, fragrances, sunscreens, and photoallergens.

Epidemiology

Allergic contact dermatitis is an inflammatory disease of the skin that is common in the general population. It is the most common type of occupational skin disease.[5]

The disorder is more common in women than in men. In the elderly, the condition often correlates with topical medications.

Pathophysiology

The pathophysiology of allergic contact dermatitis begins with the contact of the allergen to the skin. The allergen penetrates that stratum corneum and is taken up by Langerhans cells.[6] The antigens subsequently undergo processing by these cells and get displayed on their surface. As part of the skin's normal immunity, Langerhans cells migrate towards regional lymph nodes. The antigens taken up by the Langerhans cells come in contact with the adjacent T-lymphocytes.[7] Because of the process of clonal expansion as well as cytokine-induced proliferation, antigen-specific T lymphocytes get created. These lymphocytes may then traverse through the blood and into the epidermis. This process collectively is known as the sensitization phase of allergic contact dermatitis.[8] The elicitation phase is what occurs after reexposure to the antigen takes place. The Langerhans cells containing the antigen interacts with the antigen-specific T-lymphocytes for that antigen, which triggers a cytokine-induced proliferation process.[9] This proliferation, in turn, creates a localized inflammatory response.

Histopathology

The diagnosis of allergic contact dermatitis is usually established by a combination of history and physical, clinical presentation, and a positive patch test. If further evaluation is required, a skin biopsy of an affected area of skin will typically demonstrate spongiosis, although the literature has described alternate histopathologic findings.[10]

Toxicokinetics

The intensity of the inflammatory response in allergic contact dermatitis is dependent on both the sensitizing ability of the allergen and the concentration of the allergen present. Poison ivy is an example of a strong sensitizer that can create an intense inflammatory response, even in small concentrations.[11]

History and Physical

Obtain a thorough history of occupation, hobbies,  medications, lifestyle, use of fragrances, and perfumes.

Allergic contact dermatitis can present on physical exam as acute or chronic. Acute ACD characteristically presents as an erythematous, eczematous, or vesicular dermatitis. Although ACD may present with a localized, well-demarcated skin eruption, it can also be more widespread. For example, rinse-off products such as shampoo or body wash may come into contact with many parts of the body, leading to a more diffuse presentation.[12] Additionally, in cases where the patient systemically consumes an allergen, a more diffuse cutaneous reaction may occur. Chronic ACD more commonly presents with lichenification, fissuring, and scale.[13]

Evaluation

A good clinical evaluation of allergic contact dermatitis involves a detailed history and physical. The morphology and location of the dermatitis is often the best indicator of the offending agent. Patch testing can be performed to help confirm the diagnosis. If the diagnosis is still not certain, a skin biopsy usually demonstrates spongiosis.[14]

One should always rule of tinea as a cause of dermatitis.

Patch testing can help determine the allergen and avoid future exposure. While patch testing is easy to perform, the test is over-utilized, leading to higher costs for the patient.

Treatment / Management

 The most definitive treatment of allergic contact dermatitis (ACD) is the identification and removal of the offending agent. Acute allergic contact dermatitis is also treatable with topical or oral corticosteroids.  Oral antihistamines may help with pruritus in some cases.  If ACD involves a delicate area such as skin folds or eyelids, topical calcineurin inhibitors or PDE4 inhibitors may also be effective.  Upon identification of the allergen, strict avoidance is necessary to prevent a recurrence.[4]

Hydrocortisone can be used to relieve the itching. Also, cool water and wet soaks help relieve symptoms. Vesicles should not be ruptured as there is a risk of infection. Use of moisturizers is a recommended adjunct.

For severe cases, topical immunomodulators like tacrolimus may be beneficial. Some patients may benefit from phototherapy using UV A plus psoralen. Rarely in severe cases, one may need to use immunosuppressive agents like mycophenolate.

In cases of chronic or recalcitrant ACD, patch testing is the gold standard in identifying the causative agent.[6] Successful patch testing requires several components: choice of appropriate chemicals for testing, a positive patch test to relevant allergens, and patient counseling of patch test results. Additionally, the American Contact Dermatitis Society’s Contact Allergen Management Program (CAMP) can be utilized to generate a “safe list” of products that do not contain the patient’s allergens. In the case where allergens are unavoidable, systemic therapy may be necessary.[2]

Differential Diagnosis

Morphologically the clinical presentation of allergic contact dermatitis is very similar to irritant contact dermatitis and atopic dermatitis.[15] Other skin conditions that should be ruled out include drug eruptions, scabies, urticarial bullous pemphigoid, urticaria, psoriasis, seborrheic dermatitis, periorificial dermatitis, and rosacea. 

Treatment Planning

The goal of the treatment of allergic contact dermatitis is to decrease the inflammatory response that is triggered by the type 4 hypersensitivity reaction. Reactions caused by strong sensitizers may require quicker and more aggressive treatment as the intensity of dermatitis will increase. Identifying and removing the allergen is the most effective definitive treatment. Ointment-based moisturizers and steroids are preferred vehicles of treatment as creams contain a variety of chemicals and preservatives.[16]

Toxicity and Side Effect Management

The most important step in the management of allergic contact dermatitis is the removal of the offending agent. Toxicities and adverse effects to monitor are related to the treatment options. It is crucial to control the strength of the topical steroids to appropriate dosages as the most common adverse effect of these medications is thinning of the skin.[16]

Prognosis

This disease process stays with the affected populations throughout their lives. To avoid symptoms, strict avoidance of the allergen needs to be the implemented strategy. Management of the inflammatory response is the essential goal in treatment.[4]

The longer one has ACD, the longer it will take time to resolve.

Complications

Complications associated with allergic contact dermatitis (ACD) involve the inflammatory response.[17] The inflammation subsides with the removal of the allergen. If the allergen consumed systemically, diffuse dermatitis might occur, but this condition is not considered a dermatologic emergency.

Consultations

Unknown causes of allergic contact dermatitis (ACD) may require patch testing, which is best performed by a dermatologist, immunologist, allergist, or physician with clinical experience in analyzing and testing allergic contact dermatitis.

Deterrence and Patient Education

Educating patients on allergic contact dermatitis (ACD) involves assisting the patient in identifying their allergic triggers. Patients must then be provided with practical behavioral modifications to help decrease the inflammatory response of this disease. For instance, in professions that require regular use of rubber gloves, it is essential that patients can identify the natural rubber allergy and choose a glove type that uses a rubber accelerator (i.e., thiurams, carbamates, mercapto compounds) towards which they do not form a reaction.[17]

A diet low in nickel and other minerals has been said to improve symptoms in some patients.

Pearls and Other Issues

Cross-sensitization may occur in the population affected by allergic contact dermatitis (ACD). This process occurs when an antigen that is chemically similar to an antigen that had previously been sensitized by the host triggers a contact dermatitis. Additionally, systemically-induced allergic dermatitis may take place when an individual who already has undergone sensitization to a contact allergen consumes the allergen by another route (inhalation, ingestion, injection).[1]

Enhancing Healthcare Team Outcomes

The pharmacist is in the prime position to educate the patient on prevention. Patients should be told to avoid wearing nickel-containing jewelry, use latex-free gloves, avoid hair dyes and fragrances which trigger dermatitis. Patients should receive education about reading labels on products to ensure that they do not contain the trigger chemicals. Nursing is also in a strong position to provide counsel on these avoidance strategies.

For those who have ACD of the hands, the use of latex-free gloves may help. Also, patients should use mild cleansing agents on the skin and use protective agents like emollients to help minimize symptoms.

Enhancing patient outcomes is the interprofessional healthcare team's number one priority. Physicians will prescribe treatment when necessary and would do well to verify agent selection and strength with the pharmacist. Nursing is in a position to monitor for compliance and also spot adverse events from treatments like topical steroids. Patients with allergic contact dermatitis must have strict return precautions and information on the natural progression of the disease. Patients should not simply receive treatment and sent out the door with a prescription. It is crucial to tailor the treatment to the patient, and the body part affected. Patients also need to have a follow-up with a specialist and continued education. It is vital to utilize nurses and ancillary staff to help communicate in a way that the patient understands. Patients should also have continuous monitoring and follow up with their primary care physician who can help coordinate care. In this collaborative environment, the entire interprofessional healthcare team can direct therapy to its optimal result. [Level V]



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References

[1] Luckett-Chastain LR,Gipson JR,Gillaspy AF,Gallucci RM, Transcriptional profiling of irritant contact dermatitis (ICD) in a mouse model identifies specific patterns of gene expression and immune-regulation. Toxicology. 2018 Aug 29     [PubMed PMID: 30171875]
[2] Jaulent C,Dereure O,Raison-Peyron N, Contact dermatitis to polyacrylamide/C13-4 isoparaffin/laureth-7 mix in an emollient cream for atopic skin. Contact dermatitis. 2019 Jan 25;     [PubMed PMID: 30684286]
[3] Lazzarini R,Mendonça RF,Hafner MFS, Allergic contact dermatitis to shoes: contribution of a specific series to the diagnosis. Anais brasileiros de dermatologia. 2018 Sep-Oct     [PubMed PMID: 30156619]
[4] Nguyen HL,Yiannias JA, Contact Dermatitis to Medications and Skin Products. Clinical reviews in allergy     [PubMed PMID: 30145645]
[5] Özçelik S,Kulaç İ,Yazıcı M,Öcal E, Distribution of childhood skin diseases according to age and gender, a single institution experience. Turk pediatri arsivi. 2018 Jun     [PubMed PMID: 30116131]
[6] Simonsen AB,Foss-Skiftesvik MH,Thyssen JP,Deleuran M,Mortz CG,Zachariae C,Skov L,Osterballe M,Funding A,Avnstorp C,Andersen BL,Vissing S,Danielsen A,Dufour N,Nielsen NH,Thormann H,Sommerlund M,Johansen JD, Contact allergy in Danish children: Current trends. Contact dermatitis. 2018 Aug 9     [PubMed PMID: 30094861]
[7] Ameri AH,Moradi Tuchayi S,Zaalberg A,Park JH,Ngo KH,Li T,Lopez E,Colonna M,Lee RT,Mino-Kenudson M,Demehri S, IL-33/regulatory T cell axis triggers the development of a tumor-promoting immune environment in chronic inflammation. Proceedings of the National Academy of Sciences of the United States of America. 2019 Jan 29;     [PubMed PMID: 30696763]
[8] Bil W,van der Bent SAS,Spiekstra SW,Nazmi K,Rustemeyer T,Gibbs S, Comparison of the skin sensitization potential of 3 red and 2 black tattoo inks using interleukin-18 as a biomarker in a reconstructed human skin model. Contact dermatitis. 2018 Aug 22     [PubMed PMID: 30136287]
[9] Bock S,Said A,Müller G,Schäfer-Korting M,Zoschke C,Weindl G, Characterization of reconstructed human skin containing Langerhans cells to monitor molecular events in skin sensitization. Toxicology in vitro : an international journal published in association with BIBRA. 2018 Feb     [PubMed PMID: 28941582]
[10] Esser PR,Martin SF, Pathomechanisms of Contact Sensitization. Current allergy and asthma reports. 2017 Nov 11     [PubMed PMID: 29129023]
[11] Signore RJ, Prevention of poison ivy dermatitis with oral homeopathic Rhus toxicodendron. Dermatology online journal. 2017 Jan 15     [PubMed PMID: 28329482]
[12] Snyder M,Turrentine JE,Cruz PD Jr, Photocontact Dermatitis and Its Clinical Mimics: an Overview for the Allergist. Clinical reviews in allergy     [PubMed PMID: 29951786]
[13] Coenraads PJ,Aberer W,Cristaudo A,Diepgen T,Holden C,Koch L,Schuttelaar ML,Weisshaar E,Fuchs A,Schlotmann K,Goebel C,Blömeke B,Krasteva M, The Allergy Alert Test: Introduction of a Protocol Suitable to Provide an Alert Signal in p-Phenylenediamine-Allergic Hair Dye Users. Dermatitis : contact, atopic, occupational, drug. 2018 Aug 9     [PubMed PMID: 30096055]
[14] Nicholson P,Brinsley J,Farooque S,Wakelin S, Patch testing with meropenem following a severe cutaneous adverse drug reaction. Contact dermatitis. 2018 Aug 29     [PubMed PMID: 30156311]
[15] Li L,Wang Y,Wang X,Tao Y,Bao K,Hua Y,Jiang G,Hong M, Formononetin attenuated allergic diseases through inhibition of epithelial-derived cytokines by regulating E-cadherin. Clinical immunology (Orlando, Fla.). 2018 Oct     [PubMed PMID: 30077805]
[16] Choi FD,Juhasz ML,Atanaskova Mesinkovska N, Topical Ketoconazole: A Systematic Review of Current Dermatological Applications and Future Developments. The Journal of dermatological treatment. 2019 Jan 22;     [PubMed PMID: 30668185]
[17] Lampel HP,Powell HB, Occupational and Hand Dermatitis: a Practical Approach. Clinical reviews in allergy     [PubMed PMID: 30171459]