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Contact dermatitis is a term for a skin reaction resulting from exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight.
Additional recommended knowledge
Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis). Unlike contact urticaria, in which a rash appears within minutes of exposure and fades away within minutes to hours, contact dermatitis takes days to fade away. Even then, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant. Contact dermatitis results in large, burning, and itchy rashes, and these can take anywhere from several days to weeks to heal. Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.
In North/South America, the most common causes of allergic contact dermatitis are plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, nickel, detergents, and cleaning products and rubbers.
Types of contact dermatitis
There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.
Chemical irritant contact dermatitis
is either acute or chronic, which is usually associated with strong and weak irritants respectively (HSE MS24). The following definition is provided by Mathias and Maibach (1978): a nonimmunologic local inflammatory reaction characterized by erythema, edema, or corrosion following single or repeated application of a chemical substance to an identical cutaneous site.
The mechanism of action varies between toxins. Detergents, surfactants, extremes of pH, and organic solvents all have the common effect of directly affecting the barrier properties of the epidermis. These effects include removing fat emulsion, inflicting cellular damage on the epithelium, and increasing the transepidermal water loss by damaging the horny layer water-binding mechanisms and damaging the DNA, which causes the layer to thin. Strong concentrations of irritants cause an acute effect, but this is not as common as the accumulative, chronic effect of irritants whose deleterious effects build up with subsequent doses (ESCD 2006).
Common chemical irritants implicated include solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); alkalies (drain cleaners, strong soap with lye residues).
Physical irritant contact dermatitis
is a less researched form of ICD (Maurice-Jones et al) due to its various mechanisms of action and a lack of a test for its diagnosis. A complete patient history combined with negative allergic patch testing is usually necessary to reach a correct diagnosis. The simplest form of PICD results from prolonged rubbing, although the diversity of implicated irritants is far wider. Examples include paper friction, fiberglass, and scratchy clothing.
Many plants cause ICD by directly irritating the skin. Some plants act through their spines or irritant hairs. Some plant such as the buttercup, spurge, and daisy act by chemical means. The sap of these plants contains a number of alkaloids, glycosides, saponins, anthraquinones, and (in the case of plant bulbs) irritant calcium oxalate crystals - all of which can cause CICD (Mantle and Lennard, 2001).
Allergic Contact Dermatitis
This condition is the manifestation of an allergic response caused by contact with a substance. A list of common allergens is shown in Table 1 (Kucenic and Belsito, 2002).
Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans (Kimble et al 2002). By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres around the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.
ACD arises as a result of two essential stages: an induction phase, which primes and sensitizes the immune system for an allergic response, and an elicitation phase, in which this response is triggered (Kimble et al 2002). As such, ACD is termed a Type IV delayed hypersensitivity reaction involving a cell-mediated allergic response. Contact allergens are essentially soluble haptens (low in molecular weight) and, as such, have the physico-chemical properties that allow them to cross the stratum corneum of the skin. They can only cause their response as part of a complete antigen, involving their association with epidermal proteins forming hapten-protein conjugates. This, in turn, requires them to be protein-reactive.
The conjugate formed is then recognized as a foreign body by the Langerhans cells (LCs) (and in some cases Dendritic cells (DCs)), which then internalize the protein; transport it via the lymphatic system to the regional lymph nodes; and present the antigen to T-lymphocytes. This process is controlled by cytokines and chemokines - with tumor necrosis factor alpha (TNF-α) and certain members of the interleukin family (1, 13 and 18) - and their action serves either to promote or to inhibit the mobilization and migration of these LCs. (Kimble et al 2002) As the LCs are transported to the lymph nodes, they become differentiated and transform into DCs, which are immunostimulatory in nature.
Once within the lymph glands, the differentiated DCs present the allergenic epitope associated with the allergen to T lymphocytes. These T cells then divide and differentiate, clonally multiplying so that if the allergen is experienced again by the individual, these T cells will respond more quickly and more aggressively.
Kimbe et al (2002) explore the complexities of ACD's immunological reaction in short: It appears that there are two major phenotypes of cytokine production (although there exists a gradient of subsets in between), and these are termed T-helper 1 and 2 (Th1 and Th2). Although these cells initially differentiate from a common stem cell, they develop with time as the immune system matures. Th1 phenotypes are characterised by their focus on Interleukin and Interferon, while Th2 cells action is centred more around the regulation of IgE by cytokines. The CD4 and CD8 T lymphocyte subsets also have been found to contribute to differential cytokine regulation, with CD4 having been shown to produce high levels of IL-4 and IL10 while solely CD8 cells are associated with low levels of IFN?. These two cell subtypes are also closely associated with the cell matrix interactions essential for the pathogenesis of ACD.
White et al have suggested that there appears to be a threshold to the mechanisms of allergic sensitisation by ACD-associated allergens (1986).  This is thought to be linked to the level at which the toxin induces the up-regulation of the required mandatory cytokines and chemokines. It has also been proposed that the vehicle in which the allergen reaches the skin could take some responsibility in the sensitisation of the epidermis by both assisting the percutaneous penetration and causing some form of trauma and mobilization of cytokines itself.
Common allergens implicated include the following:
Sometimes termed "photoaggravated"(Bourke et al 2001), and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320-400nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which are left uncovered by clothing. The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema and vitiligo.
Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.
Allergic dermatitis is usually confined to the area where the trigger actually touched the skin, whereas irritant dermatitis may be more widespread on the skin. Symptoms of both forms include the following:
While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub) containing the irritant.
Self-care at Home
- Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by exposure to basic irritants [phenol etc.].
If the rash does not improve or continues to spread after 2-3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.
Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names.
The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis (Reitschel 1997). Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish (Rietschel, 1997), and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one. It is important to remember, therefore, that the distinction between the types of contact dermatitis is often blurred, with, for example, certain immunological mechanisms also being involved in a case of irritant contact dermatitis.
other follicular disorders: Hypertrichosis (Hirsutism) - Acne vulgaris - Rosacea (Perioral dermatitis, Rhinophyma) - follicular cysts (Epidermoid cyst, Sebaceous cyst, Steatocystoma multiplex) - Pseudofolliculitis barbae - Hidradenitis suppurativasweat disorders: eccrine (Miliaria, Anhidrosis) - apocrine (Body odor, Chromhidrosis, Fox-Fordyce disease)
|Other||pigmentation (Vitiligo, Melasma, Freckle, Café au lait spot, Lentigo/Liver spot) - Seborrheic keratosis - Acanthosis nigricans - Callus - Pyoderma gangrenosum - Bedsore - Keloid - Granuloma annulare - Necrobiosis lipoidica - Granuloma faciale - Lupus erythematosus - Morphea - Calcinosis cutis - Sclerodactyly - Ainhum - Livedoid vasculitis|
|see also congenital (Q80-Q84, 757)|