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.

Causes

In North and South America, the most common causes of allergic contact dermatitis are plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Specific plant species that can induce such contact dermatitis include Western Poison Oak, a widespread plant in the western USA. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, detergents, and cleaning products.

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 that is, phototoxic and photoallergic.

Chemical irritant contact dermatitis

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

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.

• Low humidity

In a recent analysis of patient data, low humidity from air conditioning was found to be the most common cause of PICD (Morris-Jones, Rachael et al.) To the lay person a definition of low humidity being a physical irritant can be confusing because low humidity is a deficit (or absence) of an elemental substance, whereas ALL other irritants implicated in contact dermatitis are in concentrations of relative abundance. So the irritant is actually a lack of another substance, namely water vapour. This confusion is further compounded with the use of the term contact implying 'touching' (as is the case with all other forms of PICD) whereas in the case of low humidity PICD there is an absence of contact with water vapour.

• Plants

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).

Butternut squash and Acorn squash have been known to cause an allergic reaction in many individuals, especially in food preparation where the squash skin is cut and exposed to the epidermis. Food handlers and kitchen workers should take precautions to wear rubber or latex gloves when peeling butternut and acorn squash to avoid temporary Butternut squash (Cucurbita moschata) dermatitis. A contact dermatitis reaction to butternut or acorn squash may result in orange and cracked skin, a sensation of "tightness", "roughness" or "rawness". Applying Cortisone cream to the affected area should stop the reaction within 24 hours.

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 III (Kucenic and Belsito, 2002).

Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans (Kimber 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:

• Nickel (nickel sulfate hexahydrate) – metal frequently encountered in jewelry and clasps or buttons on clothing
• Gold (gold sodium thiosulfate) – precious metal often found in jewelry
• Balsam of Peru (Myroxylon pereirae) – a fragrance used in perfumes and skin lotions, derived from tree resin (see also Tolu balsam)
• Chromium – used in tanning
• Thimerosal – a mercury compound used in local antiseptics and in vaccines
• Neomycin – a topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap and pet food. Found by itself, or in Polysporin or Triple Antibiotic
• Fragrance mix – a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products
• Formaldehyde – a preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products and fabric finishes
• Cobalt chloride – metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment
• Bacitracin – a topical antibiotic found by itself, or as Polysporin or Triple Antibiotic
• Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).
• Colophony (Rosin) – Rosin, sap or sawdust typically from spruce or fir trees
• Topical steroid – see steroid allergy
• Photographic developers, especially those containing metol
• Topical anesthetics such as pramoxine or diphenhydramine, after prolonged use

Photocontact Dermatitis

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 (320-400 nm 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.

Symptoms

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:

• Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.
• Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly exposed to the allergen or irritant.
• Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.

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, swimming pools with high chlorine) containing the irritant.

Treatment

Self-care at Home

Immediately after exposure to a known allergen or irritant, wash with soap and cool water to remove or inactivate most of the offending substance. Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by exposure to basic irritants.

• If blistering develops, cold moist compresses applied for 30 minutes 3 times a day can offer relief.
• Calamine lotion and cool colloidal oatmeal baths may relieve itching.
• Oral antihistamines such as diphenhydramine (Benadryl, Ben-Allergin) can also relieve itching.
• For mild cases that cover a relatively small area, hydrocortisone cream in nonprescription strength may be sufficient.
• Avoid scratching, as this can cause secondary infections.
• A barrier cream such as those containing zinc oxide (e.g. Desitin, etc.) may help to protect the skin and retain moisture.

Medical Care

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 or physician assistant. Medical treatment usually consists of lotions, creams, or oral medications.

• Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat inflammation in a localized area. This medication may be applied to your skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.
• Antihistamines. Prescription antihistamines may be given if nonprescription strengths are inadequate.

Prevention

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.

In an industrial setting the employer has a duty of care to the individual worker to provide the correct level of safety equipment to mitigate the exposure to harmful irritants. This can take the form of protective clothing, gloves or barrier cream depending on the working environment.

Summary

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.
 

Diagnosis

Diagnosis is obtained during an upper GI endoscopy where biopsies are taken of the esophagus. At the time of endoscopy, ridges or furrows may be seen in the esophagus wall. Presence of white exudates in esophagus is also suggestive of the diagnosis. Sometimes, multiple rings may occur in the esophagus, leading to the term "corrugated esophagus" or "feline esophagus" due to the similarity in the rings of the cat esophagus. A high number of eosinophils are seen on microscopic examination of the biopsy specimens.

Eosinophilic esophagitis may be present even if the esophagus appears, initially, to be normal. This is why the biopsy samples are important to making the diagnosis of EE. A high number of eosinophils(> 15 per high power field) throughout the length of the esophagus suggests the diagnosis of EE.

Skin testing can help identify which foods might contribute to this disease, but often skin testing implicates foods that are not involved. Common allergens of EE patients are cow's milk, soy, egg, fish and wheat.

Treatment

Treatment strategies include dietary modification, medical therapy, and mechanical dilatation of the esophagus. The initial approach to the disorder is often allergy evaluation as described above in an attempt to identify the allergens in the diet or environment. If the offending agent is found, the diet is modified so that these allergens are eliminated. There are cases, especially in children, where there are multiple food allergies involved. Some patients require an elemental diet through the use of a specialty formula. Sticking to this diet and drinking the required amount of formula can be difficult. The use of feeding tubes in these situations is often required.

Medical therapy begins with acid-inhibition medication. A sizable minority of patients with EE have some reflux component to their condition which warrants such treatment. Proton pump inhibitors are often the first-line medical therapy. EE patients by definition have persistent symptoms even with acid-inhibition therapy. For this reason, alternative medical therapies are often employed. Treatment that targets the inflammation includes swallowed corticosteroids such as fluticasone, leukotriene modifiers like montelukast, and anti-interleukins such as the anti-IL-5 monoclonal antibody mepolizumab. To swallow the medications, you must do so with a small amount of water. Swallowing these medications can cause yeast infections in the throat so beware of this method. Other drugs attempt to halt the allergic response; these include antihistamines such as loratadine. Patients with severe symptoms despite these interventions may require oral corticosteroids such as methylprednisolone.

Mechanical dilatation may be considered in severe cases of EE that have progressed to esophageal stricture or severe stenosis. Dilatation is accomplished by passing dilators through the mouth and down the esophagus to gently expand its diameter. As the esophagus of patients with EE is rather thin and delicate, care is taken not to perforate the esophagus by overzealous dilatation.

Bullous (blisters) disorders

There are three main types of bullous (blisters) disorders:

• Acantholysis, including pemphigus.
• Pemphigoid, including bullous pemphigoid and gestational pemphigoid.
• Dermatitis herpetiformis, which appears similar to a herpes virus infection, but is not caused by that virus.

Mild allergies like hay fever are highly prevalent in the human population and cause symptoms such as allergic conjunctivitis, itchiness, and runny nose. Allergies can play a major role in conditions such as asthma. In some people, severe allergies to environmental or dietary allergens or to medication may result in life-threatening anaphylactic reactions and potentially death.

A variety of tests now exist to diagnose allergic conditions; these include testing the skin for responses to known allergens or analyzing the blood for the presence and levels of allergen-specific IgE. Treatments for allergies include allergen avoidance, use of anti-histamines, steroids or other oral medications, immunotherapy to desensitize the response to allergen, and targeted therapy.

Signs and symptoms

Many allergens such as dust or pollen are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, and itching and redness of the eyes. Inhaled allergens can also lead to asthmatic symptoms, caused by narrowing of the airways (bronchoconstriction) and increased production of mucus in the lungs, shortness of breath (dyspnea), coughing and wheezing.

Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis.  Insect stings, antibiotics, and certain medicines produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system. Depending of the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered suddenly, or the onset can be delayed. The severity of this type of allergic response often requires injections of epinephrine, sometimes through a device known as the EpiPen or Twinject auto-injector. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a prolonged period of time.

Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema. Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a "wheal and flare" reaction characteristic of hives and angioedema.
 

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