Protein Contact Dermatitis

Protein Contact Dermatitis

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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, 2] In 1983, Veien and colleagues defined the following specific criteria for protein contact dermatitis [3] :

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.

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. [4]

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 TH 2 memory T cells, [5] 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 TH 2-type response with a strong IgE-mediated response. [6] 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. [7]

Four groups of proteins can cause protein contact dermatitis. [8, 9] The first group consists of fruits, vegetables, spices, and plants and is most common in kitchen workers, caterers, food vendors, food packers, and gardeners. [10, 11, 12] 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. [13] 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. [14] A retrospective study from 2006-2014 in a French dermatology and allergy center revealed that only 0.41% of patients with contact dermatitis had positive skin tests with proteins. [15]

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. A history of atopy has been reported in 56-68% of persons with protein contact dermatitis. [15, 16]

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.

Hjorth N, Roed-Petersen J. Occupational protein contact dermatitis in food handlers. Contact Dermatitis. 1976 Feb. 2 (1):28-42. [Medline].

Helaskoski E, Suojalehto H, Kuuliala O, Aalto-Korte K. Occupational contact urticaria and protein contact dermatitis: causes and concomitant airway diseases. Contact Dermatitis. 2017 Dec. 77 (6):390-396. [Medline].

Veien NK, Hattel T, Justesen O, Nørholm A. Causes of eczema in the food industry. Derm Beruf Umwelt. 1983. 31(3):84-6. [Medline].

Jones HE, Reinhardt JH, Rinaldi MG. Immunologic susceptibility to chronic dermatophytosis. Arch Dermatol. 1974 Aug. 110(2):213-20. [Medline].

Rundle CW, Bergman D, Goldenberg A, Jacob SE. Contact dermatitis considerations in atopic dermatitis. Clin Dermatol. 2017 Jul – Aug. 35 (4):367-374. [Medline].

Wang LF, Lin JY, Hsieh KH, Lin RH. Epicutaneous exposure of protein antigen induces a predominant Th2-like response with high IgE production in mice. J Immunol. 1996 Jun 1. 156 (11):4077-82. [Medline].

Lehto M, Koivuluhta M, Wang G, Amghaiab I, Majuri ML, Savolainen K. Epicutaneous natural rubber latex sensitization induces T helper 2-type dermatitis and strong prohevein-specific IgE response. J Invest Dermatol. 2003 Apr. 120(4):633-40. [Medline].

Janssens V, Morren M, Dooms-Goossens A, Degreef H. Protein contact dermatitis: myth or reality?. Br J Dermatol. 1995 Jan. 132(1):1-6. [Medline].

Levin C, Warshaw E. Protein contact dermatitis: allergens, pathogenesis, and management. Dermatitis. 2008 Sep-Oct. 19(5):241-51. [Medline].

Barbaud A, Poreaux C, Penven E, Waton J. Occupational protein contact dermatitis. Eur J Dermatol. 2015 Nov-Dec. 25 (6):527-34. [Medline].

Obtułowicz A, Pirowska M, Wojas-Pelc A. Contact eczema of hands caused by contact with potato protein. Ann Agric Environ Med. 2016 Jun 2. 23 (2):377-8. [Medline].

Lukács J, Schliemann S, Elsner P. Occupational contact urticaria caused by food – a systematic clinical review. Contact Dermatitis. 2016 Oct. 75 (4):195-204. [Medline].

Hannuksela M. Protein Contact Dermatitis. Frosch PJ, Torkil M, Lepoittevin J-P. Contact Dermatitis. 4th. Berlin: Springer; 2006. 345-348.

Hansen KS, Petersen HO. Protein contact dermatitis in slaughterhouse workers. Contact Dermatitis. 1989 Oct. 21(4):221-4. [Medline].

Barbaud A, Poreaux C, Penven E, Waton J. Occupational protein contact dermatitis. Eur J Dermatol. 2015 Nov-Dec. 25 (6):527-34. [Medline].

Vester L, Thyssen JP, Menné T, Johansen JD. Occupational food-related hand dermatoses seen over a 10-year period. Contact Dermatitis. 2012 May. 66 (5):264-70. [Medline].

Pongpairoj K, Ale I, Andersen KE, Bruze M, Diepgen TL, Elsner PU, et al. Proposed ICDRG Classification of the Clinical Presentation of Contact Allergy. Dermatitis. 2016 Sep 7. [Medline].

Kanerva L. Occupational protein contact dermatitis and paronychia from natural rubber latex. J Eur Acad Dermatol Venereol. 2000 Nov. 14 (6):504-6. [Medline].

Warshaw E, Lee G, Storrs FJ. Hand dermatitis: a review of clinical features, therapeutic options, and long-term outcomes. Am J Contact Dermat. 2003 Sep. 14 (3):119-37. [Medline].

Hernández-Bel P, de la Cuadra J, García R, Alegre V. [Protein contact dermatitis: review of 27 cases]. Actas Dermosifiliogr. 2011 Jun. 102 (5):336-43. [Medline].

Mercader P, de la Cuadra-Oyanguren J, Rodriguez-Serna M, Pitarch-Bort G, Fortea-Baixauli JM. Treatment of protein contact dermatitis with topical tacrolimus. Acta Derm Venereol. 2005. 85(6):555-6. [Medline].

Cheryl Levin, MD Resident Physician, Department of Dermatology, University of Minnesota Medical School

Cheryl Levin, MD is a member of the following medical societies: American Academy of Dermatology, Women’s Dermatologic Society, Medical Dermatology Society

Disclosure: Nothing to disclose.

David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: Lilly; Amgen <br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Erin M Warshaw, MD, MS Associate Professor, Clinical Scholar Track and Co-Director of Contact Dermatitis Clinic, Department of Dermatology, University of Minnesota Medical School; Chief of Dermatology, Division of Dermatology, Minneapolis Veterans Affairs Medical Center

Erin M Warshaw, MD, MS is a member of the following medical societies: American Contact Dermatitis Society and Women’s Dermatologic Society

Disclosure: Nothing to disclose.

Protein Contact Dermatitis

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