Protein Contact Dermatitis 

In 1976, Hjorth and Roed-Peterson coined the term protein contact dermatitis (PCD) to refer to an allergic skin reaction induced by proteins of either animal or plant origin.^[1] In 1983, Veien and colleagues defined the following specific criteria for protein contact dermatitis^[2] :

• A chronic dermatitis caused by contact with proteinaceous material
• An acute urticarial or vesicular eruption occurring minutes after contact with the causative protein
• Immediate prick- or scratch-test results that are usually positive
• Patch-test results that are often negative

Four groups of proteins can cause protein contact dermatitis: plant, animal, flour, and proteolytic enzymes (see Etiology). Anecdotally, risk factors for the development of protein contact dermatitis include a history of atopy, chronic irritant dermatitis, and an occupation or hobby involving exposure to one of these protein allergens (see Clinical).

In treatment, avoidance of the particular allergen is of primary importance. Symptomatic relief may be provided with short-term corticosteroids, immunomodulatory agents, or antihistamines (see Treatment).

Go to Irritant Contact Dermatitis, Allergic Contact Dermatitis, and Pediatric Contact Dermatitis for complete information on these topics.

Several theories have been proposed. First, protein contact dermatitis may be a type I immediate hypersensitivity reaction with superimposed irritant contact dermatitis or allergic contact dermatitis. This theory is supported by the observation that flares of urticaria often accompany contact with the causative material.

Second, protein contact dermatitis may be a result of combined type I and type IV delayed hypersensitivity reactions. Negative patch-test results could occur because large protein-based molecules cannot penetrate intact, uninvolved skin. Also possible is that the type I histamine response may block the detection of a type IV response. This is supported by experimentation of chronic dermatophytosis, wherein Trichophyton mentagrophytes induces an immediate type I reaction with no subsequent delayed type IV response. However, when the antihistamine chlorpheniramine is injected, blocking the type I reaction, a positive delayed type IV reaction is uncovered.^[3]

Finally, the pathogenesis of protein contact dermatitis may involve an immunoglobulin E (IgE)–mediated delayed hypersensitivity reaction, similar to that proposed for atopic dermatitis. In atopic dermatitis, IgE-bearing Langerhans cells are proposed to promote systemic expansion of T_H 2 memory T cells, inducing influx of interleukin (IL)–5, IL-4, IL-13, and IL-3. This leads to eosinophilia, an increase in IgE, and the development of mast cells.

A mouse model of protein contact dermatitis induced by natural rubber latex revealed an increase in CD4⁺ CD3⁺ T cells and mast cells and a T_H 2-type response with a strong IgE-mediated response.^[4] Another experimental model of protein contact dermatitis induced the generation of T cells, the infiltration of eosinophils, and the production of IL-4 and IL-5.^[5]

Four groups of proteins can cause protein contact dermatitis.^{[6, 7]} The first group consists of fruits, vegetables, spices, and plants and is most common in kitchen workers, caterers, food vendors, food packers, and gardeners. Protein sources include the following:

• Apple
• Asparagus
• Banana
• Bean
• Carrot
• Chrysanthemum
• Cornstarch
• Mugwort
• Natural rubber latex
• Paprika
• Peach
• Peanut
• Pear
• Shiitake mushroom
• Soy

The second group consists of animal proteins and is observed in slaughterhouse workers, butchers, commercial anglers, cooks, farmers, and veterinarians. Those in contact with animal intestines are most susceptible. Common triggers include the following:

• Blood
• Bovine amniotic fluid
• Cheese
• Cow dander
• Egg yolk
• Maggots
• Meat
• Milk
• Salmon
• Squid
• Worms

The third group is flour-associated protein contact dermatitis, reported primarily in bakers. A generalized dermatitis may be observed in this group, often involving the face. The most common culprits are wheat and rye.

The fourth group is proteolytic enzyme–associated protein contact dermatitis, most common among soap makers, bakers, pharmaceutical workers, and chemical enzyme factory workers. Respiratory symptoms are most common in this group. Reported enzymes include alpha amylase, glucoamylase, and lactase.

The prevalence of protein contact dermatitis, in the United States or internationally, is unknown. In Finland, the total number of occupational skin diseases reported in 2002 was 965, 11.2% (108) of which were cases of contact urticaria and protein contact dermatitis.^[8] A study in Denmark of 144 slaughterhouse workers revealed a cumulative prevalence of 22%, with the highest prevalence amongst those who cleansed the animal gut.^[9]

Race, sex, and age-related demographics

No racial or sexual predilection is known for protein contact dermatitis. Persons of all ages can be affected, but protein contact dermatitis is most common in adulthood.

Avoidance of the allergen should result in clearing of the dermatitis. No cases of death secondary to protein contact dermatitis have been reported. However, morbidity may be significant, including angioedema, gastrointestinal symptoms, rhinoconjunctivitis, and bronchial asthma. These systemic symptoms are more likely to occur if the allergen is ingested.