Contact Dermatitis to Metal 4 pages

Contact Dermatitis to Metal: Case Study


Contact dermatitis on the hands can be caused by a number of distinct mechanisms (Usatine & Riojas, 2010). The type most amenable to treatment is dermatitis caused by environmental irritants. Other possible causes include allergic and atopic dermatitis, each arising from different mechanisms. The patient under consideration here has been diagnosed with contact dermatitis due to metal exposure and is concerned about a possible link between the eczema and rhinitis. This report will examine the pathophysiology of contact dermatitis and whether there could be any relationship between the patient’s dermatitis and rhinitis.

Irritant Contact Dermatitis

Irritant contact dermatitis is caused by exposing the skin to harmful substances (Usatine & Riojas, 2010). A wound or injury can compromise the ability of the skin to maintain an effective barrier against noxious substances, resulting in skin trauma. A single or chronic exposure can lead to local inflammation of the skin and produce a characteristic pattern of thick, scaly lesions on the hands (Alavi, Skotnicki, Sussman, & Sibbald, 2012). Treatment and management is fairly straightforward and involves cleansing the skin, bandaging any wounds or injuries, and preventing future exposures either through avoiding the substance or the use of personal protective gear. Irritant contact dermatitis can lead to the development of allergic contact dermatitis.

Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) results when the immune system has inappropriately reacted to an otherwise benign substance as if it was a harmful agent (Usatine & Riojas, 2010). One of the most important functions of the skin is to distinguish between useful or commensal microbes and those that could potentially harm us (McFadden, Puangpet, Basketter, Dearman, & Kimber, 2013). The skin would not be able to perform this barrier function if not for the immune system, which has evolved an elaborate method for distinguishing between good and bad microbes and reacting appropriately. The immune system also plays a critical role in wound repair, including the growth of new tissue. This system has gone astray when ACD has developed.

Some of the most common allergens that cause contact dermatitis are poison ivy and nickel (Usatine & Riojas, 2010). Statistically, the patient who is the subject of the case study under consideration here would most likely have ACD to nickel, although other metals have been known to cause ACD. A recent meta-analysis of skin patch tests revealed the most common allergen identified was nickel (14.7%), followed by thimerosol (5.0%), cobalt (4.8%), and fragrance (3.4%). However, in most people these substances do not illicit an immune reaction, which begs the question of why ACD occurs.

There are two mechanisms believed to lead to the development of ACD and these include immune activation during wound repair and/or a non-commensal microbe infection (McFadden, Puangpet, Basketter, Dearman, & Kimber, 2013). Regardless of how the metal came into contact with the patient’s immune system the sensitization results in the metal being ‘seen’ as dangerous. Immune tolerance to the metal is therefore lost, theoretically through a process of covalent binding to skin proteins; however exposure to the metal alone is usually insufficient to trigger an immune response. What is needed is a ‘danger’ or ‘pathogen’ signal being presented to the immune system at the same time it exposed to the metal.

The danger signal consists of extracellular matrix proteins released when skin trauma occurs (McFadden, Puangpet, Basketter, Dearman, & Kimber, 2013). These proteins are called danger-associated molecular patterns (DAMPs) and include fibronectin, hyaluronan, cathelicidin, and heparin sulfate. Non-commensal microbes also produce pathogen-associated molecular patterns (PAMPs), including lipopolysaccharide and lipoteichoic acid. Both DAMPs and PAMPs bind to and activate Toll-like receptors (TLR) expressed on the outside of cells and the most relevant to ACD are believed to be TLR2 and TLR4. Although an adaptive, and thus antibody-mediated, immune response is being triggered, the most immediate response is activation of the innate immune system.

When a DAMP binds to TLRs a proinflammatory response is triggered through production of IL-1, TNF-?, IL-6, IL-12, IL-18, IL-23, and interferon-? (McFadden, Puangpet, Basketter, Dearman, & Kimber, 2013). This is a prototypical T. helper-1 (Th1) immune response that is designed to clear intracellular pathogens (Spergel, 2010). The Th1 cells that become embroiled in an immune response begin to produce large amounts of DAMP proteins, thereby generating a positive feedback loop. If the patient is suffering from atopy, however, the severity of the ACD could be reduced and/or the immune response could eventually convert to a Th2, IgE-mediated immune response. A similar series of events can be triggered when an otherwise non-allergenic metal is introduced together with PAMPs.

Allergic Rhinitis

The patient in the current case study is concerned about the possibility that the ACD is somehow connected with their rhinitis. Given the finding that close to 75% of all young children who develop atopic contact dermatitis eventually develop allergic rhinitis (Spergel, 2010), the patients concerns seem reasonable. The patient could be suffering from atopic contact dermatitis, which is very common in atopic patients, and hand involvement is frequently the only manifestation in adults (Alavi, Skotnicki, Sussman, & Sibbald, 2012).

Atopic dermatitis is typically the first manifestation of atopy, often occurring during childhood (Spergel, 2010). This tends to be closely followed by food allergies, asthma, and then rhinitis, which are all expressions of allergies to common allergens like pollen, dust mites, and cat dander. These allergies are a manifestation of an IgE, Th2-mediated immune response that is normally designed to clear the body of parasitic worms, but has instead begun to recognize common allergens that have gained access to the immune system through the skin, gut, and airways. The cytokines involved in this immune response are typically IL-4, IL-5, and IL-13.


The patient in this case study should be told that their allergic rhinitis is probably the result of lifelong allergic disease (atopy). During their childhood they may have developed contact dermatitis and food allergies. Asthma and rhinitis may have developed as they grew into adults. This disease is mediated by the adaptive arm of the immune system relying on IgE and Th2 cells. By contrast, the contact dermatitis to metal is most likely the result of an innate immune response mediated by Th1 and Th17 cells; however, they could have developed a metal allergy more readily because they suffer from atopy. In addition, there is a risk that the metal allergy will switch to an IgE/Th2-mediated response if future, repeated exposures are not prevented.

Allergic rhinitis also develops because the airway epithelium is reacting to the inhalation of allergens (Spergel, 2010). These allergens arrive in the presence of proteases that help degrade the proteins that form tight junctions in the skin and airway epithelium, thereby permitting entry into tissues under active immune surveillance. Without knowing more about how the patient was exposed to the metal, it seems unlikely that the rhinitis in this adult patient developed due to the inhalation of the offending metal unless they are routinely exposed to aerosols containing the metal.


Alavi, A., Skotnicki, S., Sussman, G., & Sibbald, R.G. (2012). Diagnosis and treatment of hand dermatitis. Advances in Skin & Wound Care, 25(8), 371-381.

McFadden, J.P., Puangpet, P., Basketter, D.A., Dearman, R.J., & Kimber, I. (2013). Why does allergic contact dermatitis exist? British Journal of Dermatology, 168(4), 692-699.

Spergel, J.M. (2010). From atopic dermatitis to asthma: The atopic march. Annals of Allergy, Asthma, & Immunology, 105, 99-106.

Usatine, R.P. & Riojas, M. (2010). Diagnosis and management of contact dermatitis. American Family Physician, 82(3), 249-255.



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