Contact Dermatitis
August 25, 2004

Annie Khuntia
James Baldwin

Background: Contact dermatitis refers to a spectrum of inflammatory skin reactions arising from direct skin exposure to an external agent. It is a common problem which affects patients of all ages. It presents in two forms, irritant and allergic. 80% of all cases are irritant type reactions and the other 20% are of the allergic form.

Both can present in an acute, subacute, or chronic form. Acute dermatitis presents with severe pruritus, erythema, and edema. It can also result in the development of papules, vesicles or bullae. Similarly, chronic dermatitis is characterized by pruritus and erythema. Additionally, chronic changes such as scaling, fissuring, excoriation and lichenification may be apparent. Less commonly, contact dermatitis can present as urticaria, acneiform lesions, or pigmentary changes.

Allergic Contact Dermatitis: Allergic contact dermatitis is an antigen specific, lymphocyte mediated, hypersensitivity reaction. It is classified as a type IV or delayed type hypersensitivity reaction. Unlike classic type IV reactions which are mediated by CD4+ T-cells and occur in the dermis, allergic contact dermatitis occurs in the epidermis and is mediated primarily through CD8+ T-cells with a Th1-type cytokine profile. [1, 2]

There are two phases in the development of allergic contact dermatitis, sensitization and elicitation. During the sensitization phase, haptens or low molecular weight substances (< 500 daltons), penetrate across the stratum corneum layer of the skin into the epidermis. The hapten combines with an epidermal protein to form an immunogen or hapten-carrier complex. When the hapten enters the epidermis it non-specifically activates keratinocytes to release inflammatory cytokines and chemokines. [3] The release of these molecules leads to an influx of activated langerhan cells (LH) and endothelial cells to the site of antigen contact. The process of sensitization begins 1-4 hours after exposure to an antigen. Some antigen-bearing LH cells emigrate from the epidermis via the lymphatics to regional lymph nodes. This process takes about 24 hours. In the regional lymph nodes LH cells interact with antigen-specific T-cells which are activated and proliferate to form effector and memory T-cells. These cells are subsequently released into the circulation and migrate to the dermis where they await reactivation. The whole sensitization process takes approximately 10-14 days. [3]

The elicitation phase occurs upon re-exposure to an already sensitized antigen. During this process, macrophages, dermal dendritic cells and MHC II expressing endothelial cells stimulate antigen-specific memory T-cells in the dermis and peripheral blood. Activation of T-cells results in the production and release of INF g and IL-17 which stimulate keratinocytes in the epidermis. They in turn release additional cytokines enhancing the inflammatory response, resulting in a local inflammatory reaction. The initial elicitation phase in a previously sensitized person occurs over 12-48 hours. Subsequent exposure to antigen shortens the period of latency from contact to the appearance of the rash. This process is called anamnesis.

Allergic contact dermatitis clinically presents with an intensely pruritic rash. It is typically papular and erythematous with indistinct margins distributed in the area of exposure. The papules result from a collection of fluid in the epidermis. Severe cases can result in vesicle formation and serous oozing. The extent of the dermatitis is usually a reflection of the degree of exposure and remote sites may be affected due to transfer of the allergen by hand or other vehicles of spread. [4]

Common Triggers and Distribution: Table 1 and Table 2

Irritant Contact Dermatitis: Irritant contact dermatitis is a non-immunologic process that results from contact with agents that abrade, irritate, or traumatize the skin. It is a dose and time dependent process. The major differences between irritant and allergic contact dermatitis are that irritant dermatitis can occur immediately and does not require prior sensitization. There are an estimated 85,000 chemicals in the world and the majority of these agents when applied to any individuals skin can induce an irritant contact dermatitis. [5] Environmental factors such as wetting, drying, perspiration, or temperature extremes can also cause irritant contact dermatitis.

The pathogenesis of irritant contact dermatitis is secondary to a natural disruption of the skin barrier leading to an increase in transepidermal water loss. The disruption is thought to be secondary to a disorganization of the lipid bilayer in the epidermis. [6] Epidermal keratinocytes which make up the majority of the epidermis are the key effector cells in both the initiation and propagation of contact irritant dermatitis. [7] Production of mediators by keratinocytes results in the infiltration of CD4+ T cells with a Th1 predominance. [8]

Histologically, early on there is intracellular edema of keratinocytes and areas of scattered necrosis found throughout the epidermis. Neutrophils may be seen in the epidermis as well as the lower dermis. Mononuclear cells and eosinophils can also be seen. At later stages the histology is virtually identical to allergic contact dermatitis

Exposure to mild irritants presents with erythema, chapped skin, dryness, and fissuring. Pruritus associated with irritant contact dermatitis can range from mild to severe. Pain is a common symptom when erosions and fissuring are present. Severe cases can present with edema, serous oozing, and extreme tenderness. [4] Clinical presentation is usually restricted to the skin site directly in contact with the offending agent and there is little extension beyond the site of contact. Hands are the usual site of irritant contact dermatitis, with the webs of the fingers being the first area affected. The face, especially the thin skin around the eyes is also commonly affected.

Differential Diagnosis: Table 3

Diagnosis: A good history leads to diagnosis of the causative agent in 10-20% of contact dermatitis cases. An occupational history is important because 20% of cases are due to work exposures ( Table 4 ). Patch testing is the gold standard in the diagnosis of allergic contact dermatitis. It can be used on both children and adults alike. [9] In the United States , Thin-Layer Rapid Use Epicutanteous Test (T.R.U.E) is approved for patch testing. It is composed of 23 standard allergens and a negative control ( Table 5 ). It is placed on the back and then read initially 48 hours after placement and the again at 72-96 hours after placement. [10] Non-standard items such as cosmetics, personal care products, and household products can also be tested, but should be diluted prior to application according to standard protocol. When testing to non-standard items it is important to test several control subjects to rule out an irritant reaction.

The American Contact Dermatitis society has established a grading system for patch testing which is almost universally recognized. Table 6

Treatment: The mainstay of treatment for either form of contact dermatitis is avoidance of the offending agent. Once the offending substance has been identified, it is important to educate patients on the etiology of the dermatitis, triggering agents and irritating factors.

Topical therapy such as cool compresses should be used to help the pruritus. Sedating anti-histamines may decrease itching and help patients sleep. Acute weeping lesions may benefit from drying agents such as topical aluminum sulfate-calcium acetate. [4] Emollients can be used, but it is important that they are non-sensitizing and fragrance-free to minimize additional irritation. Soaps and non-alkaline agents should be avoided because of their drying properties. In extreme cases when there is a secondary infection, oral antibiotics may be required for adequate treatment.

Topical anti-inflammatory agents (Table 7), particularly corticosteroids are the most effective means of treating localized acute, subacute and chronic dermatitis. Low potency agents are recommened for sensitive areas, such as the face, whereas mid to high potency steroids are usually necessary for treatment of thick, lichenified areas. [4] If there is sensitivity to a preservative, preservative free agents should be used.

Systemic corticosteroids can be used in the treatment of acute contact dermatitis, but heir role is limited in subacute and chronic dermatitis. When used, they should be reserved for severe, widespread cases where greater than 10-20% of the body surface area is affected. They should also be administered when there is persistent local irritation despite removal and avoidance of the inciting agent. The usual dose is prednisone orally or IV/IM equivalent at 1-2 mg/kg/day for 3-7 days with a taper over 7-14 days.

Recently, calcineurin inhibitors have emerged as a potential alternative to corticosteroids in the treatment of subacute and chronic forms of allergic contact dermatitis. They are approved for use in patients above the age of 2 for mild to moderate contact dermatitis, but have not found to be as effective as midpotency topical steroids in the treatment of acute contact dermatitis. [11-13] Phototherapy with UVB or PUVA has also been found to be beneficial in refractory cases.

Allergic contact dermatitis can persist 14-28 days after the offending agent has been removed therefore medication use may need to be used for an extended period of time.

 

 

References

1. Grabbe S, Schwarz T: Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity . Immunol Today 1998, 19 (1):37-44.

2. Xu H, DiIulio NA, Fairchild RL: T cell populations primed by hapten sensitization in contact sensitivity are distinguished by polarized patterns of cytokine production: interferon gamma-producing (Tc1) effector CD8+ T cells and interleukin (Il) 4/Il-10-producing (Th2) negative regulatory CD4+ T cells . J Exp Med 1996, 183 (3):1001-1012.

3. Weston WL, Bruckner A: Allergic contact dermatitis . Pediatr Clin North Am 2000, 47 (4):897-907, vii.

4. Peate WE: Occupational skin disease . Am Fam Physician 2002, 66 (6):1025-1032.

5. Beltrani VS, Beltrani VP: Contact dermatitis . Ann Allergy Asthma Immunol 1997, 78 (2):160-173; quiz 174-166.

6. Fartasch M, Schnetz E, Diepgen TL: Characterization of detergent-induced barrier alterations -- effect of barrier cream on irritation . J Investig Dermatol Symp Proc 1998, 3 (2):121-127.

7. Wood LC, Jackson SM, Elias PM, Grunfeld C, Feingold KR: Cutaneous barrier perturbation stimulates cytokine production in the epidermis of mice . J Clin Invest 1992, 90 (2):482-487.

8. Hoefakker S, Caubo M, van 't Erve EH, Roggeveen MJ, Boersma WJ, van Joost T, Notten WR, Claassen E: In vivo cytokine profiles in allergic and irritant contact dermatitis . Contact Dermatitis 1995, 33 (4):258-266.

9. Bruckner AL, Weston WL: Allergic contact dermatitis in children: a practical approach to management . Skin Therapy Lett 2002, 7 (8):3-5.

10. Fischer TI, Maibach HI: The thin layer rapid use epicutaneous test (TRUE-test), a new patch test method with high accuracy . Br J Dermatol 1985, 112 (1):63-68.

11. Nasr IS: Topical tacrolimus in dermatology . Clin Exp Dermatol 2000, 25 (3):250-254.

12. Lauerma AI, Maibach HI, Granlund H, Erkko P, Kartamaa M, Stubb S: Inhibition of contact allergy reactions by topical FK506 . Lancet 1992, 340 (8818):556.

13. Gupta AK, Chow M: Pimecrolimus: a review . J Eur Acad Dermatol Venereol 2003, 17 (5):493-503.

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