Allergic Contact Dermatitis

Article Author:
Patrick Murphy
Article Author (Archived):
Joanna Hooten
Article Editor:
Amber Atwater
Updated:
6/23/2019 10:49:49 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 (< 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; this process is known as 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 (ACD) is an inflammatory disease of the skin that is caused by a type 4 hypersensitivity reaction. It results from 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.

Epidemiology

Allergic contact dermatitis (ACD) 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]

Pathophysiology

The pathophysiology of allergic contact dermatitis (ACD) 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 are subsequently processed by these cells and 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 are 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, in turn, creates a localized inflammatory response.

Histopathology

The diagnosis of allergic contact dermatitis (ACD) 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 alternate histopathologic findings have been described.[10]

Toxicokinetics

The intensity of the inflammatory response in allergic contact dermatitis (ACD) 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

Allergic contact dermatitis (ACD) can present on physical exam as acute or chronic. Acute ACD is typically characterized by 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 an allergen is consumed systemically, 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 (ACD) 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]

Treatment / Management

The most definitive treatment of allergic contact dermatitis (ACD) is the identification and removal of the offending agent. Acute allergic contact dermatitis can also be treated 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.  If the allergen is identified, strict avoidance is necessary to prevent recurrence.[4]

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. In addition, 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 cannot be avoided, systemic therapy may be necessary.[2]

Differential Diagnosis

Morphologically the clinical presentation of allergic contact dermatitis (ACD) 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, periorifical dermatitis and rosacea. 

Treatment Planning

The goal of the treatment of allergic contact dermatitis (ACD) 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 the dermatitis will be increased. 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 (ACD) is the removal of the offending agent. Toxicities and adverse effects to monitor are related to the treatment options. It is important 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 implemented. Management of the inflammatory response is the essential goal in treatment.[4]

Complications

Complications associated 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 may occur, but this condition is not considered a dermatologic emergency.

Consultations

Unknown causes of allergic contact dermatitis (ACD) may require patch testing. This 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 important 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]

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 previously has been sensitized to a contact allergin consumes the allergen by another route (inhalation, ingestion, injection).[1]

Enhancing Healthcare Team Outcomes

Enhancing pt outcomes is a physicians number one priority. It is important that patients with alletgic contact dermatitis are given strict return precations and are advised on the natuarla progression of the diseae. Patients should not simple be treated and sent out the door with a prescription. It is important to tailor the treatemt to the patient and to the body aprt affected. Patients also need to have follow up with a specialist and continued education. It is important to utilize nurses and ancilary staff to help commincate in a way that the patient undersatnds. Patents should also have contined monitoring and follow up with their primary care physicna who can help coordinate care.



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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]