A 54-year-old woman presents with a 1-day history of a painful pruritic rash on the lower extremity. There are several intact and excoriated bullae on the lower extremity overlying large areas of erythema. The patient states that the rash developed 1 to 2 days after she returned home from her annual family camping trip. She does not have any recollection of being bitten, falling, or injuring herself on her trip. The patient feels fine and is afebrile. She is stable and has no symptoms that would indicate a systemic infection.
A 42-year-old man who is a car mechanic presents with an 8-month history of a waxing and waning rash on his right upper extremity. The patient says that the area is mildly pruritic but is not painful. After questioning from the clinician, he states that he has significant pain in his right elbow secondary to multiple traumas he sustained while playing college football. He mentions that the area is usually covered by a large elbow brace that helps alleviate the pain. The patient has no other dermatologic or medical problems.
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There are two types of dermatitides resulting from substances coming into contact with the skin: allergic contact dermatitis (ACD), which accounts for 20% of contact dermatitis cases, and irritant contact dermatitis (ICD), which accounts for the remaining 80%.1,2 ACD is an acquired delayed-type hypersensitivity reaction, with a response only occurring in people who have already been sensitized to the allergen.1,2 ACD affects a wide range of individuals, including the old and young, all races, and both sexes. There may be some sex-based differences, but this is due more to exposure patterns. For example, nickel allergies occur more frequently in women, likely because women wear more jewelry and are therefore exposed to more nickel.2
In ACD, initial sensitization occurs when an individual first comes into contact with the causative substance.2-5 This initial exposure does not necessarily lead to apparent changes to the skin.1 The allergen enters the skin where it is processed by antigen-presenting cells and is transported to lymph nodes.4 There, the antigen is presented to T cells, causing proliferation of allergen-specific T cells.4 Individuals may be exposed to these allergens for years before they develop hypersensitivity.1 The second phase in the development of ACD is the elicitation phase, in which additional exposure to the allergen leads to the presentation of the substance to primed T cells, resulting in the release of multiple cytokines and chemotactic factors, including interferon-γ, interleukin (IL)-2, and IL-17.2,3,5 The activated T cells cause apoptosis in keratinocytes, leading to a clinical presentation of erythema, edema, vesicles, oozing, and pruritus.2,3 Sensitization is affected by genetic variability, as well as other factors, such as the concentration of the allergen, its vehicle, timing and exposure site, occlusion, age, sex, and race of the patient, and the presence of other skin or systemic disorders.1 After an individual becomes sensitized, only a low concentration of the allergen is necessary to elicit a reaction.2
ACD presents as a well-demarcated pruritic eczematous eruption that can be acute or chronic. Acute stages are characterized by blistering, weeping, and/or edema associated with intense itch, burning, and sometimes pain. Chronic stages demonstrate lichenified, hyperkeratotic, scaly, or fissured plaques.2,3 The reaction is typically localized to the region of skin that contacted the allergen, but wide-spread reactions known as autoeczematization can occur.2 Common areas of involvement include hands, neck, and eyelids.1,5
Histologically, the acute stage of ACD can show a variable degree of spongiosis with a mixed dermal inflammatory infiltrate that contains lymphocytes, histiocytes, and some eosinophils.2 In more moderate and severe reactions, spongiosis leads to intraepidermal vesiculation.2 In the chronic stage, epidermal hyperplasia, often psoriasiform, develops.2 However, it should be noted that the use of topical corticosteroids may alter the histologic findings.2
Some common causes of ACD in the United States include toxicodendrons (poison ivy, oak, or sumac), nickel sulfate, balsam of Peru (Myroxylon pereirae), neomycin, formaldehyde and formaldehyde-releasing preservatives, bacitracin, rubber compounds, and cobalt chloride; currently nickel sulfate is the most common cause.1,2,6
ACD must be differentiated from other types of dermatitides, including ICD, atopic dermatitis, stasis dermatitis, and seborrheic dermatitis, as well as the erythematous form of rosacea.2 Chronic ACD, particularly on the extremities, can be difficult to differentiate from psoriasis. The distribution of the rash, as well as a comprehensive history including time course and exposures, can be useful.2 Atopic dermatitis begins in childhood, displays a chronic course, and frequently occurs in conjunction with allergic rhinitis and asthma. Stasis dermatitis occurs in patients with venous insufficiency and is localized to the lower extremities. Seborrheic dermatitis almost invariably occurs in a seborrheic distribution, involving the scalp, eyebrows, nasolabial folds, and ears, and often is not associated with significant pruritus. Rosacea flares with heat, consumption of spicy foods and alcohol, and exercise, and it can be differentiated from facial ACD by history. Psoriasis classically affects the scalp, knees, elbows, gluteal cleft, and nails; thus, involvement of these areas can help differentiate psoriasis from ACD.
ACD is most commonly diagnosed clinically, but patch testing is sometimes necessary for diagnosis or to elucidate causative agents.1,2 Suspected allergens are applied to uninflamed skin, commonly the back, using individually prepared patches or by a set of commercially available premade patches called the thin-layer rapid-use epicutaneous (TRUE) test.1 The TRUE test is more convenient to use but is limited in that it only screens for 35 allergens.2-4 Patches are removed after 48 hours, and results are read in 72 hours.1 A positive reaction is usually indicated by erythematous papules and vesicles with edema and are graded based on severity.1 Other diagnostic tools for ACD include the provocative use test and the photopatch test.1
Treatment for ACD includes educating the patient to read labels and avoid exposure to the allergen to prevent future reactions.2 The dermatitis is treated with topical corticosteroids or systemic corticosteroids, if necessary.1,2 It may take 6 or more weeks for complete clearing, even if the patient practices avoidance.2 Narrow-band ultraviolet (UV) B phototherapy or psoralen plus UVA (PUVA) treatments may help some patients with chronic ACD.3
The patient in our case had likely been exposed to poison ivy, a common plant in the area in which she was camping. Due to the extensive nature of the rash, the patient was treated with a 15-day prednisone taper, which quickly led the resolution of her rash.
Irritant contact dermatitis (ICD) is a localized, nonimmunologically initiated inflammatory reaction that occurs in most individuals who contact a substance.1,2 Clinical presentation includes erythema, scaling, edema, vesiculation, and erosions; chronic cases lead to lichenification, hyperkeratosis, and fissures.2
In ICD, a reaction occurs in any individual if the concentration of the irritant substance is sufficiently high or repetitive.1 The severity and timing of the reaction depends on many factors, including the concentration and type of toxic substance, duration of exposure, and condition of the skin at exposure.1 Furthermore, a reaction can occur on the first exposure and usually occurs within minutes, or a few hours at most.1
ICD is the most common form of occupational skin disease and is estimated to represent 70% to 80% of all occupational skin disorders.2 Infants and the elderly often are more affected by ICD and develop more severe symptoms due to a weakened epidermal barrier.2 The hands and the face are the most commonly affected areas in ICD.2 A history of atopic dermatitis correlates with a 13.5-times greater risk of developing occupational dermatitis.2
Although the exact cellular mechanisms leading to ICD are unknown, there is evidence that activated keratinocytes may act as signal transducers and may be key immunoregulators in the process.2 Cytokines such as IL-1a, IL-1b, and tumor necrosis factor-a upregulate intercellular adhesion molecule-1 expression, promoting the inflammatory response.2,7
There are several other effects that have been associated with ICD and may play a role in its mechanism. These include denaturation of epidermal keratins, disturbance of the permeability barrier, cell membrane injury, and direct cytotoxic effects, which vary with different irritants.2 Additionally, the mechanisms appear to differ between acute ICD and chronic ICD. In the acute phase, there is direct cytotoxic damage to keratinocytes; in the chronic phase, the stratum corneum’s role as a barrier is altered, leading to loss of cohesion of corneocytes, desquamation, and increased transepidermal water loss.2 Histologically, the pathology of ICD includes mild spongiosis, necrosis of epidermal keratinocytes, and inflammatory infiltrate.2 Over time, acanthosis with mild hypergranulosis and hyperkeratosis develops.2
There are many substances that can cause ICD. Alkalis, found in soaps, detergents, and bleaches, are common culprits, as are acids.1,2 Hydrofluoric acid and sulfuric acid tend to cause the most severe burns, whereas organic acids tend to be less irritating.2 However, there are many other acids that can cause a reaction, including nitric acid, hydrofluoric acid, oxalic acid, phenol (carbolic acid), and chromic acid.1 ICD from alkalis and acids are colloquially referred to as “burns.” Detergents, present in skin cleansers, cosmetics, and household cleaning products, frequently cause chronic ICD.2
Solvents are another common cause of ICD, responsible for approximately 10% of occupational dermatitis.1 Many different solvents are used in chemical reactions, hydraulic systems, metal refining, dry cleaning, and metal degreasing.2 They function primarily by disrupting the intercellular lipid barrier of the epidermis, which allows for more percutaneous penetration.2 After repeated exposure to solvents, the clinical presentation consists of erythema, scaling and dryness, and eventually eczema on the hands or the hands and face.2 Alcohols and glycols are commonly used as solvents, disinfectants, and in cosmetics, and may cause a reaction.1,2 Other causes of ICD include plastics, food and food additives, water, bodily fluids, airbag dermatitis, metal salts, fiberglass, dusts, capsaicin, tear gas, and chlorinated compounds.1,2
ICD and allergic contact dermatitis (ACD) can appear similar clinically and histologically, especially the chronic types.1,2 A thorough history is extremely important to determine exposure to possible irritants at home or in the workplace.1,2,7 Symptoms of ICD include pain, burning, and stinging.1,2 This is in contrast to the itch that is more frequently observed in allergic reactions, and it can be helpful in distinguishing between ICD and ACD.1 Additionally, diagnosis of ICD is a diagnosis of exclusion when the reaction is unexplained by patch test to an allergen.2
For many, ICD will spontaneously resolve despite continuous exposure due to the hardening effect in which repeated exposure to milder substances leads to the skin becoming more resistant to irritation caused by this substance.1,2,8 Other causes of spontaneous resolution may include increased skin permeability to irritants and changes to remove irritants more quickly, as well as immunologic changes that promote anti-inflammatory reactions to irritants.2 A history of atopy, female sex, and the presence of ACD are indicators of a poor prognosis.2
The main method of treatment is to avoid the irritants at home or in the workplace.1,2 This can include substitution of substances that are nonirritating when possible, or protecting the skin, with the use of gloves or special clothing.1,2 Barrier creams offer an additional method of protection.2,9 Topical corticosteroids are frequently used.1,2,10 Systemic corticosteroids are not useful in treating chronic ICD, unless methods are also taken to avoid the irritants.2 For patients who are nonresponsive to these therapies, other sources of treatment include photochemotherapy (psoralen plus ultraviolet [UV] A [PUVA]) or narrow-band UVB irradiation, as well as systemic retinoids or systemic immunomodulators.2,10
The patient in our case had started using a new large elbow brace to help with his elbow pain, and the ICD was confined to the area under the new elbow brace he had been using. The patient was advised to stop using (or exchange) his elbow brace, which led to the resolution of his rash.
Brigette Mary Lee, BS, is a medical student and Christopher Rizk, MD, is a dermatology resident at Baylor College of Medicine in Houston.
- James W, Berger T, Elston D, Neuhaus I. Andrews’ Diseases of the Skin. 12th ed. Philadelphia, PA: Elsevier; 2016.
- Bolognia J, Jorizzo J, Schaffer J. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012.
- Kostner L, Anzengruber F, Guillod C, Recher M, Schmid-Grendelmeier P, Navarini AA. Allergic contact dermatitis. Immunol Allergy Clin North Am. 2017;37:141-152.
- Fonacier LS, Sher JM. Allergic contact dermatitis. Ann Allergy Asthma Immunol. 2014;113:9-12.
- Ho KK, Campbell KL, Lavergne SN. Contact dermatitis: a comparative and translational review of the literature. Vet Dermatol. 2015;26(5):314-327.
- DeKoven JG, Warshaw EM, Belsito DV, et al. North American Contact Dermatitis Group Patch Test Results: 2013-2014. Dermatitis. 2017;28:33-46.
- Ale IS, Maibach HI. Irritant contact dermatitis. Rev Environ Health. 2014;29:195-206.
- Watkins SA, Maibach HI. The hardening phenomenon in irritant contact dermatitis: an interpretative update. Contact Dermatitis. 2009;60:123-130.
- Hines J, Wilkinson SM, John SM, et al. The three moments of skin cream application: an evidence-based proposal for use of skin creams in the prevention of irritant contact dermatitis in the workplace. J Eur Acad Dermatol Venereol. 2017;31:53-64.
- Cohen DE, Heidary N. Treatment of irritant and allergic contact dermatitis. Dermatol Ther. 2004;17(4):334-340.