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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Dermatitis accounts for about 30% of all illnesses in the workplace; the prevalence of skin diseases caused by chemicals in the environment is unknown.

A thorough exposure history is the most important element in accurate diagnosis of skin lesions.

In some cases, skin lesions are a diagnostic clue to the presence of systemic toxicity.

This monograph is one in a series of self-instructional publications designed to increase the primary care provider’s knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 45 for more information about continuing medical education credits and continuing education units.

Guest Contributor:

Alan H.Hall, MD

Guest Editor:

Daniel J.Hogan, MD

Peer Reviewers:

John Ambre, MD, PhD; Charles Becker, MD; Jonathan Borak, MD;

Joseph Cannella, MD; Howard Kipen, MD, MPH;

Richard J.Jackson, MD, MPH; Jonathan Rodnick, MD;

Brian A.Wummer, MD

Reviewed by the American Academy of Dermatology

U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES

Public Health Service

Agency for Toxic Substances and Disease Registry

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Unlike most organs, the skin is in constant contact with the external environment. The skin ensures the body’s integrity by preserving internal fluids and electrolytes, maintaining thermoregulation, and protecting against physical injury and entry of harmful agents. Because the skin has such a prominent and protective role, many factors affect it adversely, including mechanical agents (friction, vibration, pressure, and trauma); physical agents (heat, cold, and radiation); biologic agents (plants, insects, animals, and microbes); and a variety of chemical agents.

The large number of chemicals in the home and workplace and the accidental and intentional releases to air, water, and soil potentially allow ever-increasing contact with chemicals in the environment. Dermatitis from chemical exposures in the workplace accounts for about 30% of all reported occupational illness; the prevalence of skin lesions due to chemicals encountered outside the workplace (i.e., environmental exposures) may never be known.

Seven common skin conditions that can have environmental etiologies are presented in this monograph. Accurate diagnoses and identification of etiologies are necessary, not only to properly treat skin diseases, but also to prevent future occurrence of disease or exposure.

Familiarity with the vocabulary of dermatology is helpful in understanding this specialized topic. A glossary of terms begins on page 42.

Answers begin on page 39.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Page 820ShareCite

Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

A husband and wife consult you because of skin rashes that have developed since they began renovating a recently purchased older home. They have no history of skin problems.

The man complains of severe itching of the hands and an erythematous rash with papules and excoriations on the arms and lower legs. This rash began during the time he was placing new insulation in the attic.

The woman complains of a rash with redness and a small amount of blistering on the hands and wrists. There is mild itching, and some painful fissures have formed on the fingertips. The rash developed over a period of several days, beginning with only erythema while she was using a commercial paint-stripping product to remove old paint from interior trim. Although she wore rubber gloves, some of the stripping compound came in contact with her skin by running down into the gloves from the wrist area and through small holes in the fingers.

(1a) What is the most likely cause of the husband’s rash? How could this be confirmed?

_________________________________________________________________

_________________________________________________________________

(1b) What are the most likely causes of the woman’s rash?

_________________________________________________________________

_________________________________________________________________

(1c) How would you treat the skin lesions experienced by these patients?

_________________________________________________________________

_________________________________________________________________

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Description

❑ More than 90% of skin lesions caused in the workplace are contact dermatitis.

❑ Lesions of irritant contact dermatitis are localized and the symptoms are generally less severe than those of allergic contact dermatitis.

In the occupational exposure setting, the most common skin lesions (greater than 90%) are dermatitis due to either contact irritation or contact allergy, with irritant contact dermatitis being reported more frequently.

Irritant contact dermatitis caused by chronic exposure to mild irritants typically begins with erythema and progresses to eczema with exudative vesicles and papules, most often limited to the area of direct contact. Itching, stinging, and burning sensations may be noted—especially with stronger irritants—but are generally not as severe as symptoms of patients who have allergic contact dermatitis. (For a discussion of allergic contact dermatitis, see page 9.)

After days to weeks of chronic irritant exposure, the skin may become lichenified. Painful fissures may develop, along with hyperpigmentation, crusts, and scales. When contact with the offending irritant is discontinued, the rash usually resolves spontaneously in 1 to 3 weeks. Irritant contact dermatitis rarely spreads to areas of the body remote from the site(s) of direct contact.

Cutaneous hardening can develop when patients with irritant contact dermatitis have daily exposure to irritating substances. The skin becomes tough and resistant at the sites of contact, allowing further exposure to the irritant but without reaction. If exposure ceases, however, this protective adaptation is lost rapidly.

Pathophysiology

❑ Irritant contact dermatitis is caused by direct action of irritants on the skin.

Irritant substances cause dermatitis by direct chemical action (i.e., nonimmune-mediated) on contacted components of the skin. Irritants may be acidic substances, which coagulate skin proteins, or alkaline substances, which remove surface lipids. Both types of substances may cause drying and cracking of the skin. Epidermal necrosis with separation of the epidermis from the underlying dermis results in formation of vesicles that contain mainly polymorphonuclear (PMN) leukocytes. Vesicles and bullae with both PMN leukocytes and lymphocytes occur in the upper portion of the dermis.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Common Etiologies

Almost any substance can be a contact irritant (Table 1), although some substances, such as some alcohols, oils, and glycols cause irritant contact dermatitis in only a small percentage of exposed persons. In contrast, strong irritants, such as concentrated mineral acids, alkalies, and amines, cause chemical burns or irritant contact dermatitis in almost everyone exposed. Mild to moderate irritants (e.g., dilute acids, organic hydrocarbon solvents, and some detergents) generally produce irritant dermatitis in only a small percentage of persons after a single contact but will cause a reaction in nearly everyone after prolonged or repeated exposure.

Table 1. Common irritants in the home and workplace*

Home

Workplace

*Adapted from Robert M.Adams, Occupational skin disease, 2nd edition. Philadelphia: W.B.Saunders Co., 1990.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

The young are generally more susceptible to irritant contact dermatitis than adults are because the threshold for skin irritation is low in children, particularly infants. Irritation reactivity gradually lessens after about 8 years of age. During play, children are likely to have skin contact with soils containing hazardous substances or with wooden playground structures that may have been treated with irritating chemicals such as arsenate and pentachlorophenol. The occurrence of skin problems is also common in the elderly. Besides age, personal factors that predispose persons to irritant contact dermatitis include genetic constitution and previous episodes of eczema.

Environmental and physical factors influence the skin’s susceptibility to irritant contact dermatitis. Susceptibility is often enhanced by wet work and conditions such as cold and windy weather, low relative humidity, and high temperatures that cause sweating. Some anatomic regions are more sensitive than others. Friction and lacerations or other mechanical skin injury may facilitate the development of irritant contact dermatitis. Occlusion by protective equipment such as gloves provides a humid environment, minimizing evaporation and making the stratum corneum more permeable to chemical substances that come in contact with the skin.

Diagnosis

❑ Onset of irritant contact dermatitis tends to be insidious.

Irritant contact dermatitis is often difficult to differentiate from allergic contact dermatitis. Routine skin biopsy generally is not helpful because the histologic appearance of irritant and allergic contact dermatitis is similar. However, unlike allergic contact dermatitis, irritant contact dermatitis tends to localize at the exposed area and to cause mild itching and more erythema than vesiculation. The onset of irritant contact dermatitis is insidious rather than explosive. Patch testing by, or in consultation with, a dermatologist may be necessary to reach a diagnosis or to exclude allergic contact dermatitis. If fibrous glass is the suspected irritant, skin scrapings suspended in a few drops of 10% potassium hydroxide and examined under a light microscope at low power may reveal glass fibers.

Treatment

❑ Removal from exposure is the most important step in treating irritant contact dermatitis.

The most important step in treatment is to remove the patient, at least temporarily, from further exposure to the offending agent. Substituting less irritating chemicals for the offending substance and correctly using protective materials, such as gloves and barrier creams, may help reduce exposure. During healing, the skin should be protected from other insults such as frequent washing, trauma, wind, and rapid changes in temperature.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

❑ Topical corticosteroids may be useful in cases of irritant contact dermatitis.

Treatment for acute vesicular irritant contact dermatitis includes topical application of wet dressings for 15 to 20 minutes, 3 to 6 times daily. Domeboro’s solution (diluted 1:40) or Burow’s solution may be used to soak the dressings. Dressings should be discontinued after 2 to 3 days to avoid drying the skin.

Topical application of corticosteroid preparations may be efficacious. A low-potency corticosteroid should be used for mild to moderate skin conditions, with progression to more potent corticosteroids as required (Table 2). Some over-the-counter and prescription topical medications or their excipients can further irritate the skin or provoke allergic contact dermatitis. Administering mild sedatives and antihistamines to relieve itching may also be beneficial.

Clinical signs of secondary bacterial infection include increased erythema and tenderness; development of a yellow, crusting, or purulent exudate; and occasionally, formation of small pustules around the edges of the dermatitis. Infection with monilia has an appearance similar to bacterial infection, except that the exudate is usually white. Infection may be difficult to recognize initially because the serous exudate and erythema of the dermatitis can obscure the signs. Obtaining samples of the exudate for culture and sensitivity before initiating topical or systemic antibiotic therapy is generally advisable.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Table 2. Groups of topical corticosteroid products, in order of decreasing potency*

Drug

Trade Name

% Concentration

Group 1

Betamethasone dipropionate

Diprolene

0.05

Halbertasol propionate

Ultravate

0.05

Clobetasol propionate

Temovate

0.05

Diflorasone diacetate

Psorcon

0.05

Group II

Amcinonide

Cyclocort

0.1

Betamethasone dipropionate

Diprosone

0.05

Desoximetasone

Topicort

0.25

Diflorasone diacetate

Florone, Maxiflor

0.05

Fluocinolone acetonide

Synalar-HP

0.2

Fluocinonide

Lidex

0.05

Halcinonide

Halog

0.1

Triamcinolone acetonide

Aristocort, Kenalog, etc.

0.5

Group III

Betamethasone benzoate

Benisone, Uticort

0.025

Betamethasone valerate

Betatrex, Beta-Val

0.1

Desoximetasone

Topicort LP

0.05

Flurandrenolide

Cordran

0.025

Hydrocortisone valerate

Westcort

0.2

Triamcinolone acetonide

Aristocort, Kenalog, etc.

0.1

Group IV

Betamethasone valerate

Valisone, Reduced Strength

0.01

Clocortolone pivalate

Cloderm

0.1

Fluocinolone acetonide

Fluonid, Flurosyn, Synalar, etc.

0.025

Flurandrenolide

Cordran SP

0.025

Triamcinolone acetonide

Aristocort, Kenalog, Triacet

0.025

Group V

Alclometasone dipropionate

Aclovate

0.05

Desonide

DesOwen, Tridesilon

0.05

Fluocinolone acetonide

Fluonid, Synalar

0.01

Group VI

Dexamethasone

Aeroseb-Dex, Decaderm

0.01–0.1

Hydrocortisone

(generic, over-the-counter)

0.25–2.5

Methylprednisolone acetate

Medrol

0.25–1.0

Adapted from RC Cornell and RB Stoughton. The use of topical steroids in psoriasis. Dermatol Clin 1984;2:397–409.

*No significant difference exists among agents in a group. These products come in various forms (i.e., creams, gels, lotions, solutions, and ointments), although some products are not available in all forms.

Use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

You are consulted by a 44-year-old male office worker who has a chief complaint of a rash on his hands and wrists. His company recently relocated from a building where each employee had a private office to an older, renovated building with large bay areas. New wallboard was placed, the area was painted, and new carpet was laid just before the move. Employees now work in cubicles; the patient’s cubicle is located in an interior area with no windows. A copying machine is adjacent to his work area.

Since the move, many of the patient’s coworkers have been complaining of unpleasant odors, a feeling of fatigue or excessive tiredness, and mild irritation of the eyes, nose, and throat. They associate these symptoms with working in the new area. Although the patient has not noted such symptoms, he does complain of the increased noise and distraction in the new work area; he feels that his rash is somehow related to the new location.

The rash began 5 days ago with itching and redness. It then developed weeping and raised, vesicular lesions that spread from the initial location on the hands to the volar surfaces of the wrists. The patient states that he has a history of reaction to poison ivy, which produces a similar rash, but he has not been in an infested area for the past 2 months. He has no direct contact with industrial cleaning agents or carbonless copy paper in his work. He does have contact with chemicals through his woodworking hobby. He recently built an end table from exotic Japanese woods and has been applying a varnish that a friend brought from Japan.

(2a) Could the patient’s rash be due to airborne allergens or irritants in the new office location?

_________________________________________________________________

_________________________________________________________________

(2b) Could the rash be related to his woodworking hobby?

_________________________________________________________________

_________________________________________________________________

(2c) What is the most effective treatment for this patient?

_________________________________________________________________

_________________________________________________________________

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Description

❑ About 30% of occupational skin disorders are allergic contact dermatitis.

❑ In sensitized persons, inflammation begins about 12 hours after exposure to an allergen.

Although contact allergens produce sensitization in only a small percentage of exposed persons, allergic contact dermatitis constitutes about 30% of the skin disorders found in the workplace. Once a person has been sensitized to an offending substance, further exposure may result in relatively rapid development of local inflammation with erythema, papule formation, induration, and weeping vesiculation. Inflammation usually begins about 12 hours after exposure; intensity peaks in 50 hours or more. The rash may spread locally around the margins of the original site or to distant sites that did not have contact with the allergen. Potentially, the entire skin surface could become involved (a condition known as erythroderma or exfoliative dermatitis).

Pathophysiology

❑ Cross-reactivity with antigenically similar substances can occur with allergic contact dermatitis.

❑ The clinical and histologic appearances of allergic and irritant contact dermatitis are similar.

Allergic contact dermatitis results from a true allergic (i.e., cell-mediated) sensitization to the offending substance. Cross-reactivity with antigenically similar substances may occur. Initially, during the refractory period, the patient may be exposed without developing a reaction. During the induction phase, which may last from 4 days to several weeks (usually about 14 to 21 days), the development of complete allergic sensitization occurs as the allergen comes in contact with the skin. After the skin is fully sensitized, further contact with the allergen may result in rapid and severe dermal manifestations. When no further contact with the allergen occurs, the patient is in the period of persistence of sensitivity. The level of sensitivity can decrease over time, but sensitization may be lifelong.

Most allergens that cause allergic contact dermatitis have molecular weights of less than 500 daltons. The allergens are haptens rather than complete antigens; they must penetrate the skin and combine with endogenous proteins to form full antigens. Langerhans cells play a key role in then presenting the antigen to T lymphocytes, thereby activating the T cells. The sensitized T cells proliferate in the paracortical regions of the lymph nodes and produce effector and memory lymphocytes that remain in the general circulation. On subsequent contact with the complete antigen, the effector cells release lymphokines that may result in rapid and severe, local inflammation.

Many factors can affect the development of allergic contact dermatitis, including characteristics of the allergen itself, patient factors, and environmental conditions. Allergen factors include the physiochemical nature of the allergen (e.g., lipophilicity, solubility, and inherent sensitizing potency), concentration, total dose that comes in contact with the skin, anatomic site of contact, number and frequency of exposures, and occlusion by clothing or gloves.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

The most important predisposing patient factors are a history of irritant contact dermatitis and the presence of an inflammatory skin condition that may promote absorption of the allergen. Irritant dermatitis caused by household cleaning agents on women’s hands may continue as allergic nickel dermatitis (from costume jewelry). In addition, age and genetic predisposition can influence the development of allergic contact dermatitis. Persons who have histories of atopic dermatitis have been reported to havedecreasedrisk of developing allergic dermatitis butincreased riskof developing irritant dermatitis.

Common predisposing environmental factors for allergic contact dermatitis are pressure, friction, heat, and prolonged immersion in water (such as occurs during wet work). Relative humidity, ambient temperature, and season of the year also play roles in development of allergic contact dermatitis.

Common Etiologies

❑ Aromatic compounds with polar or ionic substituents are potent sensitizing agents.

Only several hundred of the thousands of chemicals used are known to cause allergic contact dermatitis. With the exception of nickel, cobalt, and some forms of chromium, most metals do not produce sensitization. Strong inorganic alkalies and acids seldom cause allergic reactions. Although a substance’s sensitization potential cannot be determined from its chemical structure alone, some chemical classes are more likely to cause allergic contact dermatitis (see Table 3). Aromatic compounds with polar or ionic substituents are typically sensitizing agents (e.g.,p -aminophenol and hydroquinone used in photographic film developers).

In addition, chemicals that are structurally similar to the original sensitizing agent may provoke recall of the specifically sensitized lymphocytes, a phenomenon known as cross-sensitization. For example, persons exposed to p-phenylenediamines used in the rubber industry may react to related substances used in photographic developers and dyes. Persons sensitized toRhusplants such as poison ivy or poison oak may be sensitive to cross-reacting substances found in exotic trees and their derivative products (lacquers, varnishes, and oils).

Table 3. Some chemical groups known to cause allergic contact dermatitis

Aromatic amines

Benzothiazoles

Caine-type anesthetics

Ethylenediamine compounds

Halogenated germicides

Hydroxyquinolines

Phenolic compounds

Phenothiazines

Streptomycin group of antibiotics

Thiurams

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Synthetic substances that commonly cause allergic contact dermatitis are rubber products, plastic resins, organic dyes, topical medications, germicidal and biocidal preparations, and various commercial and medication ingredients (Table 4). Natural products can also produce allergic contact dermatitis. Exposure to certain airborne contaminants may also cause allergic contact dermatitis. Airborne contaminants include dichromates in cement dust, rosins used in soldering operations, and sawdust.

Table 4. Common causes of allergic contact dermatitis

Germicides and biocides

Grains

Foods/Spices

Medication/product ingredients

Metals

Organic dyes

Plastic resins

Rhusplants*

Rubber products

Topical medications

*For a more complete listing of plants that cause dermatitis see R.M.Adams, Occupational skin disease, 2nd edition, Philadelphia: W.B.Saunders Co., 1990, p. 507–9.

Diagnosis

❑ Allergic contact dermatitis often spreads to areas remote from the site of contact.

Allergic contact dermatitis is often misdiagnosed as irritant contact dermatitis. Other conditions to consider in the differential diagnosis are atopic dermatitis, pustular eruptions on the palms and soles, psoriasis,Herpes simplexandHerpes zoster,insect bites, parasite infestation such as scabies, fungal infections of the feet with idiopathic vesicular reactions, nummular eczema, drug eruptions, and erythema multiforme.

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Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

❑ The clinical and microscopic appearances of skin lesions due to allergic contact dermatitis are the same as those due to irritant contact dermatitis.

No distinctive features of the lesions facilitate the differentiation of allergic from irritant contact dermatitis. An important diagnostic clue to allergic contact dermatitis is the spread of rash to areas remote from the site of contact; the mucous membranes are usually spared, and the scalp, soles, and palms are often unaffected.

Patch testing (seeDiagnostic Procedures,page 35) may help differentiate allergic from irritant contact dermatitis. Because the histologic appearance of lesions due to allergic or irritant contact dermatitis is the same, routine skin biopsy is not helpful in their differentiation.

Treatment

❑ Treatment for allergic contact dermatitis is identical to that for irritant contact dermatitis.

At present, there are no satisfactory means of desensitizing humans to allergens. The most important step is to remove the patient from exposure to the offending substance. In the workplace, options such as protective clothing and substitute chemicals should be explored. The therapy for allergic contact dermatitis is the same as that for irritant contact dermatitis (seeTreatment, Irritant Contact Dermatitis,page 6).

Systemic corticosteroids may be indicated for some patients who have allergic contact dermatitis, especially when large areas of the skin (20% total body surface area or greater) are involved. Short courses of oral corticosteroids, particularly if used for aRhus -induced contact dermatitis, may be given for 2 to 3 weeks (up to 21 days). Corticosteroids administered even for a short period of time should always be delivered in decreasing doses over the course of therapy to prevent adrenal suppression.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

You are consulted by the headmaster of a children’s summer camp because of an outbreak of skin rashes in 20 of the campers. No counselors are affected. On examination, the rashes, which are confined to the hands, wrists, and forearms, consist of discrete linear streaks and patches that are hyperpigmented and do not itch.

One of the staff members speculates that the rashes are caused by contact with an epoxy glue used in building a model. However, only two of the children who have rashes have been involved in this activity. All the affected children had participated in a craft class in which they made lime sachets by puncturing lime skins and inserting sprigs of cloves over the surfaces of the limes. During the class, they also prepared gift cards from recycled paper. While the children attended to these activities, the counselors were engaged in planning an outdoor activity that was to follow the craft session.

(3a) What causes of the children’s dermatitis might be considered, given the rural location and nature of camp activities?

_________________________________________________________________

_________________________________________________________________

_________________________________________________________________

(3b) What treatment would you recommend?

_________________________________________________________________

_________________________________________________________________

_________________________________________________________________

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

Description

❑ Photosensitivity reactions occur mainly on sun-exposed areas of the body.

❑ Photoallergic reactions are immune-mediated responses; phototoxic reactions are not.

Photosensitivity contact dermatitis occurs mainly on sun-exposed areas such as the face, upper chest, posterior portion of the neck, extensor surfaces of the forearms, dorsum of the hands and feet, and anterior surfaces of the lower legs. Areas of the skin normally covered by jewelry and clothing are spared, as are eyelids, areas under the chin, and upper portions of the ears covered by hair. Photosensitivity contact dermatitis may be the result of phototoxicity or photoallergy.

Lesions of phototoxic and photoallergic contact dermatitis resemble those of irritant and allergic contact dermatitis. They have been described as discrete, confluent, polymorphous linear streaks and patches that are macular and nonpruritic. The patient may experience a stinging or burning sensation of the skin, typically beginning shortly after exposure to sunlight and resolving rapidly when the skin is shaded. Lichenification and hyperpigmentation may occur, and the lesions may persist for months or years. In some cases, widespread involvement of the skin develops later. The photoallergic response usually occurs in only a small number of persons who have been previously sensitized to the photoactive agent.

Pathophysiology

❑ Sunlight can cause formation of the agents that result in photosensitivity contact dermatitis.

The mechanisms of photosensitivity contact dermatitis are broadly analogous to the mechanisms of irritant and allergic contact dermatitis except for the added requirement of appropriate ultraviolet (UV) radiation (i.e., wavelengths of 315 to 400 nanometers, known as UV-A). The agent that provokes the irritant or allergic response is formed after its precursor has been exposed to UV-A.

In phototoxicity, the excited state of the agent produced during irradiation is thought to lead to oxidation of cellular components or to allow binding of the agent with nucleic acids. In photoallergy, the initial reaction of the topical agent with UV-A forms either an excited molecule that can bind with protein to form a complete allergen or a product that is itself a strong contact allergen.

Common Etiologies

❑ Many topical products can produce photosensitivity dermatitis.

Many products that cause photosensitivity dermatitis are applied topically. Common examples are lotions containing fragrances; suntanning products with ultraviolet absorbers such as 6-methylcoumarin, homosalicylate, orp -aminobenzoic acid (PABA); and aftershave lotions containing musk ambrette. Germicides in soaps and detergents may also cause photosensitivity dermatitis. A major epidemic of allergic contact dermatitis occurred in Great Britain in 1960 after the introduction of two soaps that contained tetrachlorosalicylanilide, a photoactive antibacterial agent.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

❑ Psoralens, which can cause phototoxic dermatitis, are useful in the treatment of psoriasis.

Certain systemically administered medications have caused photoallergic drug reactions. Examples include nalidixic acid, phenothiazines, sulfonamides, sulfonylureas, tetracyclines, and thiazide diuretics. Pharmacists, nurses, and others who routinely have skin contact with these drugs are prone to photosensitivity dermatitis.

Plants such as celery and citrus fruits have caused phototoxic dermatitis in persons who handle them extensively; farm workers are particularly susceptible. Contact with oil released from lime skins or with coal tar and pitch has resulted in phototoxic dermatitis, especially in lightly pigmented persons.

Psoralens, which are photoactive and can cause phototoxic dermatitis, are also used therapeutically in the treatment of psoriasis. In PUVA (psoralen plus UV-A radiation) treatment, a psoralen is painted on the affected skin or given systemically to patients who are then exposed to UV radiation. The photoadduct that is formed between the psoralen and DNA serves to slow the rate of the psoriatic overgrowth.

Diagnosis

❑ A thorough drug history will usually rule out photoallergic drug reactions.

Photoallergy from chemical contact must be differentiated from polymorphous light eruption, systemic lupus erythematosus, pellagra, dermatomyositis, porphyria, allergic contact dermatitis and photoallergic drug reaction. A thorough history of medication treatment will usually rule out photoallergic drug reaction.

Photopatch testing may be useful in confirming the diagnosis, but results of photopatch testing are often difficult to interpret and are best left to dermatologists with specialized equipment and knowledge in this field.

Treatment

❑ Treatment for phototoxic and photoallergic dermatitis is the same as that for irritant and allergic contact dermatitis.

The treatment for phototoxic or photoallergic dermatitis is the same as the treatment for irritant and allergic contact dermatitis (see pages 6 and 13). Identifying the offending agent and counseling the patient to avoid further exposure to it are the most important interventions. When the photosensitizing agent cannot be avoided, limiting sunlight exposure and wearing protective clothing, such as hats, gloves, long-sleeved garments, socks, and shoes, may help. Sunscreens may be used if reaction or cross-sensitivity between the causative agent and components in the sunscreen is not a possibility.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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A 42-year-old man consults you because of a persistent skin condition that he feels resembles the cosmetically displeasing acne he had as a teenager. His present skin condition consists of pale yellowish, cystic lesions and comedones localized on the face, below and lateral to the eyes, and behind the ears. Similar lesions are present on the cheeks, forehead, and neck; a few are present on the buttocks, where, according to the patient, he never had lesions with his prior affliction. He also complains of moderately severe itching.

History reveals no changes in diet, and the patient is not taking medications. For the last 15 years, the patient has worked for a local utility company. His most recent job duties have included replacing the heat exchange fluids in transformers. He first noted the rash about a month ago; he is not certain whether the rash appeared before or after he began this activity.

(4a) Is the skin condition described by the patient consistent with a reactivation of acne vulgaris? What other causes should be considered?

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(4b) What therapy would you recommend?

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Description

❑ Chloracne is rare and is usually due to occupational exposure to chloracnegenic agents.

❑ Chloracne may be an indication of systemic toxicity.

Environmental acne is a variety of acne venenata typically caused by industrial chemicals. It may result from contact with petroleum and its derivatives (oil acne), coal tar products (coa-tar-pitch acne), and halogenated aromatic hydrocarbons (chloracne). Environmental acne may also be caused by certain physical, mechanical, and biologic agents. Although the occurrence of chloracne is rare (probably fewer than 4000 cases worldwide), it is of great concern because it is an extremely refractory acne and because it may be indicative of systemic toxicity by a highly toxic chemical.

The lesions of chloracne consist of straw-colored cysts, numerous comedones, milia, and papules. The lesions are located on the face (especially at “crow’s feet” and below and to the outside of the eyes [malar crescent]), neck, earlobes, shoulders, abdomen, legs, buttocks, and genitalia. The nose is often spared. With severe chloracne, all the follicles in an area may be involved, resulting in a rather bizarre “pebbled” appearance. Pruritus is common and occurs in about 50% of chloracne cases.

Pathophysiology

❑ Chloracne is often refractory to treatment.

Onset of disease is typically delayed 2 to 4 weeks after exposure to a chloracnegenic agent. The first changes are a thickening of the follicular epithelium, development of comedones, and a slow disappearance of the sebaceous glands as they are replaced by keratinous cysts. Initially, inflammation is uncommon; inflammatory lesions with larger cysts and abscesses are later developments. Severe scarring may occur. Increased fragility of the skin, hypertrichosis, widespread follicular hyperkeratosis, or hyperpigmentation may develop. A brownish discoloration of the nails, swollen eyelids, and conjunctivitis or discharge may be present in some patients.

With no additional exposure, the disease will first progress, then regress over a 4- to 6-month period. A few cases of chloracne have persisted for 30 years or more after contact with the chloracnegenic agent has ceased.

Common Etiologies

❑ Chlorinated aromatic hydrocarbons cause chloracne.

Many chlorinated aromatic hydrocarbon compounds used in the workplace can cause chloracne. These compounds include chlorinated naphthalenes, polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), dioxins, polychlorinated dibenzofurans, pentachlorophenol, azobenzenes, and azoxybenzenes. (SeeCase Studies in Environmental Medicine: Polychlorinated Biphenyl (PCB) Toxicity, Case Studies in Environmental Medicine: Dioxin Toxicity, and Case Studiies in Environmental Medicine: Pentachlorophenol Toxicity .)

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Diagnosis

❑ Chloracne must be differentiated from other more common acnes.

Chloracne must be differentiated from oil acne or folliculitis due to exposure to grease and oils; acne vulgaris; acne cosmetica from heavy cosmetic use; acne mechanica from local pressure and friction; acne medicamentosa from medications such as corticosteroids, hormonal preparations, phenytoin, iodides (e.g., in kelp tablets), bromides and solar elastosis with comedones.

A history of exposure to agents known to cause chloracne and the typical appearance of the rash on physical examination are usually sufficient for diagnosis. Chloracne may be distinguished from acne vulgaris by the distribution of the lesions, age at onset, and morphology. Chloracne lesions typically affect the face, neck, earlobes, shoulders, abdomen, legs, buttocks, and genitalia, whereas lesions of acne vulgaris are found primarily on the face, neck, chest, and back (down to the waist). Chloracne can appear at any age, whereas acne vulgaris is seen most often in patients aged 13 to 26 years. Chloracne lesions consist of straw-colored cysts, numerous comedones, milia, and papules; whereas the lesions of acne vulgaris are typically comedones, papules, pustules, and scars.

Histologic examination of cysts may show typical changes, but the usefulness of biopsy in establishing the diagnosis is questionable. Associated noncutaneous conditions found in some patients who have chloracne include hepatotoxicity, porphyria cutanea tarda, and peripheral neuropathies.

Treatment

❑ Removal from exposure to chloracnegenic agents is the most important treatment for chloracne.

Primary interventions are prevention of exposure to chloracnegenic chemicals and good hygiene because a satisfactory treatment regimen cannot be found in many cases. Administration of oral antibiotics and acne surgery have been of limited success. Retinoic acid (vitamin A) preparations or 13-cis-isoretinoic acid (Accutane) have been successful in carefully selected patients. (Note: Accutane is a known teratogen and should be used cautiously.) Injecting inflamed lesions with dilute triamcinolone, a glucocorticoid, may be helpful, as may dermabrasion for severe scarring.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Fifteen children from a local school are referred by the school nurse for evaluation of skin lesions. The lesions consist of decreased pigmentation in a scattered distribution. Two of the children have histories of itchy, weeping, vesicular rash on the neck and face that cleared before the pigment changes became noticeable. A public health evaluation of the drinking water and food served at the school has not revealed toxic or infectious agents. The school is located near a chemical manufacturing facility, in which the parents of several children work, including the parents of the two children who have histories of vesicular rash.

(5a) Could the nearby manufacturing facility be associated with the decreased pigmentation noted in the children in this case?

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(5b) How could you investigate this possibility?

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(5c) What treatment options are available for persistent hypopigmentation involving large areas of the skin?

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Description

❑ Pigment changes are usually associated with post-inflammatory effects from physical or chemical agents.

A variety of physical and chemical agents may affect the color of the skin. Insults to the skin may cause either increased pigmentation (hyperpigmentation), decreased pigmentation (hypopigmentation), or both in contiguous areas (dyschromia). Inflammation, which may be subclinical and not apparent, usually precedes pigment alterations. Postinflammatory reaction (e.g., to contact dermatitis) is the most common cause of increased pigmentation, although pigment loss may also occur.

Pathophysiology

❑ Hypopigmentation is caused by damage to the melanocyte or through inhibition of melanin synthesis.

❑ Hyperpigmentation is often caused by nonspecific skin damage that leads to melanin or hemosiderin accumulation.

In hypopigmentation, depigmentation probably occurs either by damage to the melanocyte, which leads to cell distortion and death, or through inhibition of melanin synthesis by the offending substance. It may be significant that industrial compounds that cause hypopigmentation (Table 5) are structurally similar to tyrosine, the building block of melanin. In industrially related hypopigmentation (leukoderma), the hands, wrists, and forearms invariably are affected; symmetry is usual. Depigmentation may also appear in body sites remote from the chemical contact (e.g., axillae, genitalia, and torso). The process of depigmentation usually takes 2 to 4 weeks and may require up to 6 months of repeated contact to become visible. The fact that many exposed workers do not lose pigment indicates that host factors are important in susceptibility.

Table 5. Compounds known to cause hypopigmentation

o -Benzylchlorophenol (antiseptic)

p -Butylphenol (used in the manufacture of varnish and lacquer resins, as an antioxidant in soaps, and as a motor oil additive)

p -Cresol (disinfectant)

Hydroquinone and its monoethyl and monobenzyl ethers (used in black-and-white photoprocessing, in skin lighteners, and as antioxidants in synthetic rubbers)

o -Phenylphenol (used as an agricultural fungicide, disinfectant, and in the rubber industry)

Pyrocatechol (topical antiseptic)

p -Tertiary butylcatechol (astringent)

Hyperpigmentation (also known also as melanosis or melanoderma) is due to accumulation of melanin from damaged melanocytes or to deposition of hemosiderin from extravasation of erythrocytes in the dermis. Another possible mechanism is overproduction of melanin by melanocytes in response to the offending agent. Hyperpigmentation is more likely to occur in dark-complexioned persons and can persist for years.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Common Etiologies

The cause of hypopigmentation is contact with alkylphenols (see Table 5, page 24), skin damage due to chemical and thermal burns, or blunt or repeated trauma to the skin. Hyperpigmentation typically follows a bout of dermatitis or other episode of inflammation. Coal tar pitch, creosote, and various aromatic chlorinated hydrocarbons are a few of the compounds that can stimulate overproduction of melanin. UV radiation-induced stimulation of melanin synthesis (tanning) is the most common cause of hyperpigmentation in dark-complexioned persons.

Diagnosis

❑ Hypopigmentation may be the result of environmental exposures or of idiopathic vitiligo.

❑ Skin staining and birthmarks can be misdiagnosed as hyperpigmentation.

Chemically induced hypopigmentation is indistinguishable from idiopathic vitiligo. Vitiligo affects about 1% of the general population and may be associated with autoimmune or endocrine abnormalities. Hypopigmentation must also be differentiated from depigmentation due to tissue destruction by chemical or thermal burns.

Hyperpigmentation should not be confused with birthmarks or direct skin staining or discoloration from contact with substances such as heavy metals (e.g., silver salts), nitrosylated compounds (e.g., nitric acid or dinitrophenol), derivatives of coal distillation (e.g., tar, pitch, and asphalt), and coal dust.

In most cases, the patient’s history and physical examination are sufficient to diagnose cases of pigment alterations. The loss of melanin in light-complexioned persons can be detected by failure of the skin to fluoresce under a Wood’s lamp.

Treatment

❑ Hypopigmented and hyperpigmented areas should be protected from sunlight.

No effective treatment exists to reverse pigment changes. Hypopigmentation may last months to years after contact with the offending substance is discontinued, or it may be permanent. Depigmented skin should be protected from sunlight. Small depigmented areas may be camouflaged with agents such as Covermask, Dy-O-Derm, or Dermablend. Oral administration of psoralens and carefully graded UV radiation exposure (PUVA treatment) may be attempted if hypopigmentation involves large areas of skin.

In patients who have hyperpigmentation, worsening of the condition can be prevented by using sunscreens and covering affected areas

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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with clothing, hats, and gloves. Topical bleaching creams prepared from hydroquinone or its monobenzyl ether must be used cautiously to prevent widespread depigmentation. A preparation consisting of 0.1% hydrophilic tretinoin (Retin-A), 5% hydroquinone, and 0.1% dexamethasone in a hydrophilic ointment has been used in a 5- to 7-week treatment regimen with some success.

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

×

A 35-year-old woman consults you because of episodes of generalized hives that develop about 20 minutes after she uses certain brands of shampoo. The hives are preceded by sensations of itching, burning, and stinging of the skin on the scalp, upper face, and posterior aspect of the neck. The patient also experiences redness and tearing of the eyes, clear rhinorrhea, and nausea. She relates that a similar constellation of symptoms occurred after she applied an over-the-counter topical pain-relieving ointment for sunburn. A mild eczematous rash has been present on her forehead and posterior neck for about 6 weeks.

(6a) What is the most likely cause of the patient’s complaints?

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(6b) What evaluation and testing might be helpful?

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(6c) What treatment will most likely be effective?

_________________________________________________________________

_________________________________________________________________

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Suggested Citation: "Case Study 50: Skin Lesions and Environmental Exposures: Rash Decisions." Institute of Medicine. 1995.Environmental Medicine: Integrating a Missing Element into Medical Education . Washington, DC: The National Academies Press. doi: 10.17226/4795.

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Description

❑ Contact urticaria is a skin reaction that appears immediately after contact with the offending agent.

Contact urticaria is a localized wheal-and-flare response (hives) that develops almost immediately (a few minutes to about 1 hour) after direct contact with the eliciting agent. Many afflicted patients complain of skin sensations such as itching, burning, or tingling. Symptoms typically disappear within 24 hours.

Pathophysiology

❑ Contact urticaria may be due to immunologic-, nonimmunologic-, or uncertain-mediated mechanisms.

❑ Anaphylactic reactions may occur in patients who have contact urticaria syndrome.

Contact urticaria may be mediated by mechanisms classified as immunologic (allergic), nonimmunologic (nonallergic), or uncertain. Nonimmunologic urticaria, the most common type of contact urticaria, is caused by a direct action of the offending substance on the skin vasculature and a nonimmunologic release of vasoactive substances such as bradykinin, histamines, or other inflammatory mediators. The reaction remains localized.

Immunologic contact urticaria is an immediate allergic reaction in persons who have previously become sensitized to the offending agent. Parts of the skin that are remote from the contact site may be affected. The vasoactive effects in the immunologic form of contact urticaria are caused by an IgE-mediated reaction. The resulting erythema and edema are elicited mainly by histamines released from mast cells. Activation of the complement cascade and generation of anaphylatoxins can result in systemic effects (contact urticaria syndrome) in which the typical rash is accompanied by symptoms of asthma, rhinitis, conjunctivitis, orolaryngeal effects (itching and tingling sensations or edema of the lips, tongue, and mouth; or throat irritation), or gastrointestinal signs and symptoms. In rare cases, patients who have contact urticaria syndrome have experienced otherwise unexpla


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