eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Contact Dermatitis

Author: Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Contributor Information and Disclosures

Updated: Dec 4, 2007

Introduction

Background

Contact dermatitis can be subdivided on etiologic grounds into the following types: irritant contact dermatitis, allergic contact dermatitis, photo contact dermatitis, contact urticaria, and reactions to pharmacologically active agents.

Allergic contact dermatitis in childhood was considered rare until recently. However, reports of this condition are increasing, which may reflect an increased incidence, more frequent patch testing of children, or both.1 Allergen exposure in children has also likely changed over time. Allergic contact dermatitis may affect as many as 20% of the pediatric population, occurs less frequently in the first few months of life, and increases in prevalence with increasing age. In the adolescent age group, females have significantly higher rates of allergic contact dermatitis on the face. This is likely explained by increased exposures to nickel in piercings and to preservative and fragrance chemicals in cosmetic products.1

Once diagnosed, most cases of contact dermatitis are self-limited or are easily treated. However, morbidity from contact dermatitis depends on its cause and the possibility of avoiding repeated or continued exposure. Unless the diagnosis of contact dermatitis is considered and appropriate history is obtained, a correct diagnosis is rarely made. As a result, the patient may have chronic or recurrent episodes of dermatitis.

A comprehensive review of the topic of contact dermatitis is beyond the scope of this article. Several major textbooks are dedicated to this subject. One of the more comprehensive textbooks on this subject is Fisher's Contact Dermatitis.2 It contains over 1100 pages discussing contact dermatitis associated with numerous products, occupations, hobbies, and other environmental sources. In addition, new contactants are created in an industrial society and are reported in the literature on a daily basis.

Pathophysiology

Irritant contact dermatitis

Irritant contact dermatitis is a condition caused by direct injury of the skin. An irritant is any agent capable of producing cell damage in any individual if applied for sufficient time and in sufficient concentration.

Immunologic processes are not involved, and dermatitis occurs without prior sensitization. Irritants cause damage by breaking or removing the protective layers of the upper epidermis. They denature keratin, remove lipids, and alter the water-holding capacity of the skin. This leads to damage of the underlying living cells of the epidermis.

Irritant contact dermatitis consists of a spectrum of disease that ranges from a mild dryness, redness, or chapping to various types of eczematous dermatitis or an acute caustic burn. The severity of dermatitis produced by an irritant depends on the type of exposure, vehicle, and individual propensity. Normal, dry, or thick skin is more resistant to irritant effects than moist, macerated, or thin skin. Cumulative irritant dermatitis most commonly affects thin exposed skin, such as the backs of the hands, the webspaces of the fingers, or the face and eyelids.

Allergic contact dermatitis

Allergic contact dermatitis is a type IV hypersensitivity reaction only affecting previously sensitized individuals. A common example of allergic contact dermatitis is rhus dermatitis, the allergic reaction to plants, such as poison ivy, poison oak, and poison sumac. The 2 distinct phases in a type IV hypersensitivity reaction are the induction (ie, sensitization) phase and the elicitation phase.

During the induction phase, an allergen, or hapten, penetrates the epidermis, where it is picked up and processed by an antigen-presenting cell. Most allergens in contact dermatitis are of low molecular weight and require minimal processing. However, many have a complicated structure and are significantly altered by the antigen-presenting cell. Antigen-presenting cells include Langerhans cells, dermal dendrocytes, and macrophages. The processed antigen is presented to T lymphocytes, which undergo blastogenesis in the regional lymph nodes. One subset of these T cells differentiates into memory cells, whereas others become effector T lymphocytes that are released into the blood stream.

The elicitation phase occurs when the sensitized individual again is exposed to the antigen. The antigen penetrates the epidermis and is picked up and processed by an antigen-presenting cell. The processed antigen is presented to the circulating effector T lymphocytes that, in turn, produce lymphokines. These lymphokines mediate the inflammatory response that is characteristic of an allergic contact dermatitis. The elicitation phase requires several hours to develop, and, as a result, symptoms of allergic contact dermatitis usually develop hours to days following exposure. Once acquired, contact sensitivity tends to persist. The degree of sensitivity may decline unless boosted by repeated exposure, but with a high initial level of sensitivity, it may remain demonstrable throughout life.

Photo contact dermatitis

With photo contact dermatitis, irradiation of certain substances by light results in the transformation of the substance into an allergen (photoallergic) or an irritant (phototoxic). This transformation is usually wavelength specific for any individual substance. Dermatitis may develop following exposure to only UV-A, UV-B, or white light.

Contact urticaria

Contact urticaria may be defined as a wheal-and-flare reaction that occurs after topical exposure to an agent. It may be immunologic, nonimmunologic, or of unknown mechanism. The immunologic type may be severe, with associated anaphylaxis. Nonimmunologic contact urticaria is the most common and is caused by agents that directly stimulate the release of vasoactive substances from mast cells. Other forms of urticaria may mimic contact urticaria and include cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.

Reactions to pharmacologically active agents

Contact reactions occur to pharmacologically active agents in some plants, most commonly plants in the family Urticaceae. Stinging nettles are in this family and are densely covered with coarse stinging hairs. The hairs consist of a tiny capillary tube with a small bladderlike base. Pressure on the bladderlike base injects fluid containing histamine, acetylcholine, and serotonin into the skin. The result is a typical triple response with itching noted in seconds and pruritus that lasts a few hours. Most stings are benign and require little or no therapy.

Frequency

United States

Contact dermatitis is exceedingly common, accounting for 4-7% of all dermatologic consultations, and is consistently among the top 10 causes for patient visits in primary care clinics. Each year, 10-50 million Americans develop an allergic rash after contact with poison ivy, poison sumac, or poison oak.

Incidence of contact dermatitis in the pediatric age group is debated, but allergic contact dermatitis affects approximately 20% of all children at some time. Approximately 20-35% of healthy children react to one or more allergens on standard patch tests. Among worker's compensation claims for dermatologic conditions, 90% are due to contact dermatitis. Children of parents who experience contact dermatitis are 60% more likely to have positive patch test results.

International

The most common environmental allergens appear to be the same in Europe and the United States. Allergens such as benzocaine, neomycin, and lanolin are common in all countries. However, each country has a small number of locally unique topical medications, which are a source of allergens. Rhus dermatitis is extremely common in the United States but virtually nonexistent in Europe. The level of sensitivity to a specific allergen in a population changes over time. Some allergens come and go, and the perceived incidence of sensitivity to an individual substance depends on many variables.

Mortality/Morbidity

Most cases of contact dermatitis are easily treated. However, morbidity from contact dermatitis depends on its cause and the possibility of avoiding repeated or continued exposures. Some ubiquitous allergens, such as rubber or nickel, are impossible to completely avoid. Exposure can be reduced with careful instruction, but occult exposures may produce chronic or recurrent symptoms.

In a study of the prevalence of dermatitis of the hands, half of patients had experienced dermatitis for more than 5 years.3 Relapses and chronicity are due not only to reexposure to allergens and irritants but also to other contributory mechanisms. The barrier function of the skin is impaired for months or even years after significant dermatitis. Recovery may be prevented by exposure to irritants or allergens in concentrations that are tolerated by normal skin.

Overzealous use of cleansers and antiseptics or use of various popular or herbal remedies, or both, may also prolong the course of dermatitis. Latex allergy is common among dentists and surgeons. In rare cases, this may have a significant impact on their medical practice. Anaphylaxis and death can occur following epidermal exposure to some antigens. Antigens such as latex rarely produce an immunoglobulin E (IgE)–mediated immediate hypersensitivity reaction that results in anaphylactic shock.

Race

Contact dermatitis is thought to affect whites more frequently than people of other races. People with fair skin and red hair are the most vulnerable.

Sex

  • Both allergic and irritant reactions are twice as common in females as in males.
  • Nickel is the most frequent contact allergen in females older than 8 years. In one study, reactions to nickel sulfate occurred in 16% of children but occurred in 25% of girls aged 14-15 years and in only 4.5% of boys aged 6-13 years.4

Age

Contact dermatitis is most common during adulthood, but it affects people of all ages. The type of contact dermatitis is frequently age related. Infants are most likely to have irritant contact dermatitis in the diaper area. Toddlers and older children become increasingly exposed to poison ivy, poison oak, and poison sumac. Adolescents are more likely to develop irritant reactions from excessive exposure to soaps and allergic reactions to nickel and to preservatives in creams and lotions. The recent trend of piercing ears in infants and body piercing by adolescents can be expected to lower the average age at which nickel allergy occurs.

Clinical

History

When contact dermatitis is suspected, the history must include a detailed list of environmental exposures. Determine whether the patient has had any exposure to materials such as plants, paints, dyes, cleaning solutions, soaps, and protective gear such as eye wear and athletic gloves. Discover if any new products or plants are present in the home or during recreational activities. Query patients regarding hobbies that might be the source of an irritant or allergen. Determine whether the patient is applying any products or treatments to the involved area. If the lesions or symptoms appear to be primarily in exposed areas, determine how much sun exposure has occurred recently. Ask the patient if symptoms improve over weekends or vacations.

  • Irritant contact dermatitis is the most common form of contact dermatitis, but it is mild in most cases. A detailed history may help confirm that an irritant is producing the dermatitis and help to identify that irritant. The history should include the following questions:
    • What is the chief symptom? Mild pruritus or a burning sensation is more common than the intense pruritus usually associated with allergic contact dermatitis.
    • When did the symptoms start? If a suspected irritant is recognized, how long prior to the symptoms did the exposure occur? Symptoms may occur within minutes of the exposure. Mild irritants require prolonged or repeated exposure before inflammation is noted, while strong irritants, such as strong acids and alkalis, can produce an immediate reaction similar to a thermal burn.
    • Is this the first time this has occurred? When symptoms are episodic, an accurate diary of exposures occurring shortly prior to symptoms may help narrow the list of possible irritants.
    • Many substances produce a nonallergic inflammatory reaction. Examples of irritants include acids, alkalis, metal salts, bromine, chlorine (commonly used in hot tubs and swimming pools), hydrocarbons, and harsh soaps or detergents. Soaps and detergents are the most common causes of an irritant reaction, but patients may develop an allergic reaction to perfumes, dyes, lanolin, deodorants, or antiperspirants. Some plants may cause an irritant dermatitis. The history must include exposure to these products.
  • Allergic contact dermatitis is usually more severe and acute in onset than irritant contact dermatitis. Again, a detailed history may help confirm the dermatitis is produced by an allergen and may help to identify that allergen. The history should cover the following areas:
    • What is the chief symptom? Allergic contact dermatitis is frequently very pruritic. Mild pruritus or a burning sensation is more common in irritant contact dermatitis.
    • When did the symptoms start? If a suspected allergen is recognized, how long prior to the symptoms did the exposure occur? Type IV hypersensitivity reactions usually take 6-24 hours to produce symptoms.
    • Has the dermatitis been spreading? Allergic contact dermatitis frequently appears to spread over time. In fact, this represents delayed reactions to the allergens. Heavily contaminated areas may break out first, followed by areas of less exposure. Thick skin may react much later than thin skin or may not react at all. Different sites may have come in contact with the allergen at different times. Gloves and other clothing contaminated with sap from poison ivy may expose the skin days, weeks, or months later. All these factors may produce the false impression that the dermatitis is spreading or is contagious.
    • Is this the first time the symptoms have occurred? When symptoms are episodic, an accurate diary of exposures occurring shortly prior to symptoms may help narrow the list of possible allergens.
    • Many substances can produce an allergic contact dermatitis. The patient's age and the location and appearance of the dermatitis frequently lead the history in a particular direction. For example, if the dermatitis is perioral, the history might include exposure to pacifiers, bubble gum, musical instruments played with a mouthpiece, toothpaste, mouthwashes, lip licking habits, hobbies with mouthpieces (eg, snorkeling, diving), lipstick, lip balms, products applied to treat the symptoms, sucking limes and lying in the sun, and eating foods such as mangos (specifically exposure to the skin rind of the mango). Occasionally, simply asking about some of these possible allergens may stimulate the patient or parent to recall an exposure they had forgotten.
  • Photo contact dermatitis usually occurs on sun-exposed areas (at some clothing-optional beaches or in tanning booths, sun-exposed areas may include most, if not all, of the skin surface). A detailed exposure history, including a detailed history of types and quantity of light exposure, is required. Determine whether the reaction occurred following exposure through window glass or on a cloudy day. This would suggest photo dermatitis related to UV-A light. The history should also include the following questions:
    • What is the chief symptom? Pruritus is the main symptom in photoallergic reactions. Phototoxic reactions produce a primary symptom of burning. Reactions range from sunburns to bullous eczematous dermatitis and usually occur on sun-exposed areas of the body.
    • Many plants can cause a phototoxic response. These include the citrus family (eg, limes), the mulberry family (eg, figs), and the Umbelliferae family (eg, parsnip, celery). Lime juice exposure most commonly occurs when limes are squeezed into beverages. Excess juice dribbles down the arm or neck. Sun exposure of this lime juice on the skin produces linear streaks of dermatitis or hyperpigmentation. Perfumes are also common sources of photo contact dermatitis.
  • Contact urticaria is usually very pruritic and is usually rapid in onset. Because symptoms occur so rapidly following exposure, the etiology for contact urticaria is usually obvious. If the etiology is not apparent, an exposure history may include the following items:
    • Agents that can produce allergic contact urticaria include silk, wool, rubber, animal hair, dander, saliva, serum, seminal fluid, cockroaches, moths, insect stings, milk, eggs, fish, meat, fruits, potatoes, beer, penicillin, neomycin, nickel, formaldehyde, and rubber. Contact urticaria from rubber occurs almost exclusively from the use of rubber gloves.
    • Agents that produce a nonimmunologic contact urticaria include jellyfish, Portuguese man-of-war, balsam of Peru, caterpillar hair, moths, insect stings, benzoic acid, and nettles (plants).
    • Contact reactions to pharmacologically active agents occur most commonly following exposure to plants in the family Urticaceae (eg, stinging nettles). Itching is noted in seconds and lasts a few hours.
    • The exposure history also is important to rule out other forms of urticaria, such as cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.

Physical

Many cases of contact dermatitis have a similar appearance regardless of the mechanism or cause of the inflammation. Other than distribution and severity, most cases of acute irritant contact dermatitis appear similar, and the clinical appearance does not suggest the etiologic agent. However, some distributions are highly suggestive of the etiologic agent. For example, pruritic dermatitis of the ear lobes or near the umbilicus almost always is the result of nickel allergy. Inflammatory responses can be categorized into acute, subacute, and chronic phases.

  • In acute contact dermatitis, the skin is bright red and edematous. Clear fluid-filled vesicles or bullae may develop in these areas. As lesions break, they weep clear serum. Yellow crusts form as this serum dries. These may suggest that the area is infected. Although secondary infection can occur, it usually develops over several days and is usually more purulent than the yellow crusts. Most healthy patients do not require antibiotic therapy unless significant purulent drainage is noted or the healing of the wound is not progressing as expected.
  • Subacute contact dermatitis is less edematous and erythematous. Little or no drainage of serum is present. Superficial papules and excoriations are common.
  • Chronic contact dermatitis is characterized by scaling, fissuring, and lichenification with minimal edema. Mild erythema and excoriations are common.
  • The clinical appearance of the dermatitis may suggest the type of contact dermatitis. This may help to narrow the list of possible causes.
    • Irritant contact dermatitis
      • Rash is often localized to the site of exposure.
      • Severity depends on the irritant, concentration, dwell time, site, and condition of the skin.
      • Thick dry skin is the most resistant to the effects of irritants.
      • Maceration makes skin more vulnerable to irritants.
      • Xerosis can predispose to irritant dermatitis.
      • The most common site is the hands.
    • Allergic contact dermatitis: The condition may extend beyond the borders of the region exposed to the allergen. Allergic contact dermatitis is generally much more edematous than irritant contact dermatitis, and vesiculation is more common. Clues by distribution include the following:
      • Scalp and ears - Shampoo, hair spray, hair dyes, earrings, eyeglasses, ear plugs, headphones, telephones, bathing caps, ear drops (Cerumenex)
      • Eyelids - Nail polish (transferred by rubbing), cosmetics, contact lens solution, sport goggles, fragrances, metals, neomycin, oleamidopropyl dimethylamine, tosylamide formaldehyde resin, benzalkonium chloride, other preservatives
      • Face - Airborne allergens (eg, poison ivy from burning leaves, ragweed), cosmetics, sunscreens, nose clips, perfumes
      • Lips - Lip balms, lipstick, toothpaste, mouthwash, bubble gum (ie, rosin, cinnamates), nickel in musical instrument mouthpiece, rubber in snorkeling mouthpiece, cane reed in a clarinet, food (eg, mango skin)
      • Neck - Necklaces, perfumes, aftershave lotion (men or women from contact with someone wearing aftershave), rubber or leather straps
      • Trunk - Topical medication, sunscreens, poison ivy, clothing, undergarments (eg, spandex bras, elastic waistbands), metal belt buckles, dive suits
      • Axilla - Deodorant (axillary vault), clothing (axillary folds)
      • Hands - Soaps and detergents, foods, poison ivy, solvents and oils, cement, metals, topical medications, gloves, athletic tape, rubber additives, innumerable occupational exposures
      • Wrists - Same as hands; watch, watchband, bracelets
      • Genitals - Poison ivy (transferred by hand), rubber condoms, nickel (allergy from a bed-wetting alarm was confused with herpes genitalis and child abuse), feminine hygiene products
      • Anal region - Hemorrhoid preparations (eg, benzocaine, Nupercaine)
      • Lower legs - Topical medication (eg, benzocaine, lanolin, neomycin, paraben), dye in socks, latex/rubber in socks 
      • Feet - Rubber, leather, glues, dyes, or nickel snaps in shoes and sandals; topical medications; swim fins; athletic tape
    • Photo contact dermatitis
      • Phototoxic photo contact dermatitis is essentially a bad sunburn or an allergic reaction to the sun, with a primary symptom of burning.
      • In photoallergic photo contact dermatitis, the primary symptom is of pruritus; this occurs on sun-exposed areas of the body with direct exposure of skin to a photosensitizing agent, and symptoms range from sunburns to eczematous dermatitis or hyperpigmentation. Occasionally, aerosolized contactants may produce a similar clinical appearance.
    • Contact urticaria: Contact urticaria appears as hives or whelps or edematous pale or pink plaques.
    • Contact reactions to pharmacologically active agent: Typical triple response is noted in seconds.

Causes

The causes of contact dermatitis are innumerable and increase daily. The items listed below are some of the more common causes and may help expand the list of possible etiologies, which might need to be researched. Items identified in the history can be further researched either in the medical literature or in one of the extensive textbooks on contact dermatitis.

  • Irritant contact dermatitis
    • Irritant contact dermatitis is a direct local cytotoxic effect of an irritant on the cells of the epidermis, with a subsequent inflammatory response in the dermis.
    • Examples of irritants include acids; alkalis (eg, sodium, potassium, ammonium, calcium hydroxide compounds), which are frequently associated with hand eczemas following exposure to soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, toilet bowl cleaners, or oven cleansers; bromine and chlorine, which are commonly used in hot tubs and swimming pools; and hydrocarbons such as crude petroleum, lubricating oils, and cutting oils. Long-term exposure may cause pruritus, folliculitis, calcifications, or acneiform eruptions. Creosote, asphalt, and other tar products may result in melanoderma. Creosote is a contact irritant, sensitizer, and photosensitizer.
    • Irritant dermatitis from plants usually occurs after exposure to a particular part of the plant, and the degree of toxicity may vary with the season, type of exposure, stage of maturity of the plant, and locality.
    • The spurge plant family includes the most plants capable of producing irritant contact dermatitis and includes the poinsettia, crown-of-thorns, candelabra cactus, and pencil tree. These plants contain a highly irritating white milky sap that may cause erythema, desquamation, and bulla formation. Calcium oxalate is an irritant found in a number of plants, including Dieffenbachia, daffodils, hyacinths, and pineapples.
  • Allergic contact dermatitis
    • This type of dermatitis is an acquired type IV hypersensitivity response generated after exposure to an allergen.
    • Causes include plants of the family Anacardiaceae (eg, poison ivy, poison oak, poison sumac, mango), nickel sulfate (eg, earrings, buckles, zippers, buttons, metal clips, various metal alloys), potassium dichromate (eg, cements, household cleansers, leather, some matches, paints, antirust products), formaldehyde (common preservative in creams), ethylenediamine (eg, dyes, medications), mercaptobenzothiazole (eg, rubber), thiram (eg, fungicides), and paraphenylenediamine (PPD) (eg, hair dyes, photographic chemicals, "black" Henna tattoos).
      • Henna extract has long been used as a stain or dye that produces a temporary tattoo when applied to the skin.
      • Sensitivity to ordinary henna tattoos that are brown in color is rare. However, PPD may be added to henna extract to darken the tattoo and reduce fixation time.
      • PPD in the black henna tattoo mixture is at a significantly higher concentration than is found in commercial hair dye preparations and can induce severe sensitivity to PPD and severe allergic reactions.
    • In almost all studies, nickel is the most common allergen and is even more common in females. Depending on the study population, the most common allergens following nickel are fragrance mix, rubber accelerators, thimerosal, paraphenylenediamine, cobalt, lanolin, and neomycin. 
    • Allergic reaction to topical steroids used to treat eczema is not rare. As with any topical therapy, it may initially be soothing, but if the eczema continues to worsen, the patient may have developed a sensitivity to the active ingredient or a preservative. In patients suspected of having corticosteroid allergy, patch testing confirms allergy in 10%.
    • As mentioned above, harsh soaps most commonly cause an irritant reaction, but allergic reactions to perfumes, dyes, lanolin, deodorants, or antiperspirants can occur.
  • Allergic plant dermatitis
    • The family Anacardiaceae, which includes poison ivy, probably accounts for more cases of allergic contact dermatitis than all other plant families combined. The antigen in these plants is in an oleoresin known as urushiol (you-ROO-shee-ol).
    • In poison ivy and poison oak, the antigen in urushiol is pentadecylcatechol. Slight molecular variations in catechols may result in large variations in the degree of antigenicity. Poison ivy and poison oak sap contains a near maximal percentage of the most allergenic catechols.
    • Uninjured plants do not induce dermatitis. The plant must be injured or bruised before the oleoresin containing the urushiol can contact the skin. Smoke from burning plants may cause a severe dermatitis. All parts of the plant are antigenic, and under controlled conditions, more than 70% of the population in the United States reacts to the urushiol in poison ivy and oak.
    • The plant family Anacardiaceae contains other species that also contain urushiol and cross-react with poison ivy. Mango contact dermatitis develops most commonly in the perioral region and on the hands and results from exposure to the peel, not the juice. Poison sumac is highly antigenic, resulting in severe contact dermatitis in sensitized patients.
  • Photo contact dermatitis
    • Symptoms occur as a result of direct exposure of skin to a photosensitizing agent followed by direct sun exposure.
    • Many plants are known to cause a phototoxic response. These include the citrus family (eg, limes), the mulberry family (eg, figs), and the Umbelliferae family (eg, parsnip, celery). Lime juice exposure is most common when limes are squeezed into beverages. Excess juice dribbles down the arm or neck. Sun exposure of this lime juice produces linear streaks of dermatitis or hyperpigmentation. Perfumes also are common sources of photo contact dermatitis.
  • Contact urticaria
    • Agents that can produce allergic contact urticaria include silk, wool, rubber, animal hair, dander, saliva, serum, seminal fluid, cockroaches, moths, insect stings, milk, eggs, fish, meat, fruits, potatoes, beer, penicillin, neomycin, nickel, formaldehyde, and rubber.
    • Contact urticaria from rubber occurs almost exclusively from the use of rubber gloves. Nonimmunologic contact urticaria results in local edema and erythema. It is more common than the immunologic mechanism.
    • Agents that produce nonimmunologic contact urticaria include jellyfish; Portuguese man-of-war; balsam of Peru; caterpillar hair; moths; insect stings; benzoic, sorbic, cinnamic, or nicotinic acid; and nettles (plants). In one report, 18 out of 20 children aged 1-4 years developed perioral contact urticaria after smearing food around their mouths.5 This was traced to sorbic acid and benzoic acid in a salad dressing.
    • Contact urticaria must be distinguished from environmentally associated urticaria, including cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.
  • Contact reactions to pharmacologically active agents: Most of these reactions are produced by plants in the family Urticaceae (eg, stinging nettles).

More on Contact Dermatitis

Overview: Contact Dermatitis
Differential Diagnoses & Workup: Contact Dermatitis
Treatment & Medication: Contact Dermatitis
Follow-up: Contact Dermatitis
Multimedia: Contact Dermatitis
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

contact dermatitis, allergic contact dermatitis, ACD, dermatitis venenata, contact eczema, rhus dermatitis, poison ivy, poison oak, poison sumac, irritant contact dermatitis, ICD, primary irritant dermatitis, photo contact dermatitis, photoallergic contact dermatitis, phototoxic contact dermatitis, berloque dermatitis, contact urticaria, hives, whelps, eczematous dermatitis, acute caustic burn, cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, exercise-induced urticaria, latex allergy, sunburn, nickel allergy, hyperpigmentation, folliculitis, melanoderma, Umbelliferae family

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Contributor Information and Disclosures

Author

Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society
Disclosure: Nothing to disclose.

Medical Editor

Kevin P Connelly, DO, Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University; Medical Director, Paws for Health Pet Visitation Program
Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation

Managing Editor

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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