Contact dermatitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[3]

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. 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).^[1] 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.^[2] 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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[3]

There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photo-allergic.

This is the most common form of contact dermatitis. ICD can be caused by either an acute or chronic exposure to a toxic insult. It is caused by either chemical or physical irritants. People who do a lot of wet work (mothers of small children, hairdressers, nurses, chefs) are very prone to developing ICD.

• Chemical irritant contact dermatitis is either acute or chronic, which is usually associated with strong and weak irritants respectively (HSE MS24)^[1]. The following definition is provided by Mathias and Maibach (1978):^[2] 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)^[3] 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, anthroquinones, and (in the case of plant bulbs) irritant calcium oxalate crystals – all of which can cause CICD (Mantle and Lennard, 2001)^[4].

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)^[5]. Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans (Kimble et al 2002)^[6]. 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). ^[7] 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)
• 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
• Fragrance mix – a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products^[8]
• 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
• Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).^[9]

Sometimes termed “photoaggravated”(Bourke et al 2001)^[10], 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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

Irritant contact dermatitis

Irritant contact dermatitis arises from sufficient inflammation due to the release of proinflammatory cytokines from keratinocytes, in response to chemical stimuli. This causes skin barrier disruption, epidermal cellular changes, and cytokine release ^[1]

Irritants can be classified as ^[1]

• Cumulatively toxic (e.g., hand soap causing irritant dermatitis in a hospital employee)
• Subtoxic
• Degenerative
• Toxic (e.g., hydrofluoric acid exposure at a chemical plant).

Allergic contact dermatitis

Allergic contact dermatitis is T-cell mediated inflammation of the skin due to repeated skin exposure to haptens in a sensitized individual.^[1]

Allergic contact dermatitis has two phases.^[1]

• The sensitization phase; antigen-specific effector T cells are induced in the draining lymph nodes by antigen captured cutaneous dendritic cells that migrate from the skin.
• The elicitation phase; effector T cells that are activated in the skin by antigen captured cutaneous dendritic cells and produce various chemical mediators, which create antigen-specific inflammation.

Photo contact dermatitis occurs when an allergen becomes an irritant in the presence of light.^[1]

Contact urticaria usually presents with as a ‘wheal and flare’ reaction after exposure to the offending topical agent. While most cases are mild, anaphylactic reactions can occur. Some common types of contact urticaria include ^[1]

• Exposure to cold
• Dermatographism
• Pressure
• Exercise
• Solar
• Heat
• Cholinergic.

Contact dermatitis can also occur after exposure to plants of the Urticaceae family.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[3]

• Benzoyl Perroxide
• Cosmetics

• Deodrants

• Detergents

• Insecticide sprays

• Jewellery

• Latex

• Poison ivy

• Poison oak

• Poison sumac

• Solvents

Cardiovascular	No underlying causes
Chemical / poisoning	Adhesives, Alcohol, Alkalies, Black mustard poisoning, Buttercup poisoning, Cement (Potassium dichromate), Chromium,Cleaning agents, Cobalt, Cosmetics, Deodrants, Detergents, Ethylene oxide, Ethylenediamine, Eucalyptus oil poisoning, Formaldehyde,Gold, Hair dyes (p-Phenylenediamine), Insecticide sprays, Jewelry, Kerosene, Lanolin, Latex, Leather tanning agents,Mercaptobenzothiazole (rubber), Moisturizers,Nickel, Perfumes, Poison ivy, Poison oak, Poison sumac, p-Phenylenediamine (PPD) in temporary tattoos, Sodium lauryl sulfate, Solvents, Thiram in fungicides, Turpentine, Xylene
Dermatologic	No underlying causes
Drug Side Effect	Benzocaine topical, Benzoyl peroxide, Bexarotene , Clocortolone pivalate, Diazepam, dibucaine, Eflornithine, Fluocinonide, Halcinonide, Hydrochlorothiazide, Hydroquinone, Luliconazole, Mometasone furoate, Mupirocin, Neomycin, Ointments containing NSAIDs,Psoralens, Sertaconazole, Tetracaine, Tiagabine, Thimerosal
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	Balsam of Peru, Calcium oxalate from plants, Cashew nuts,
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	No underlying causes
Musculoskeletal / Ortho	No underlying causes
Neurologic	No underlying causes
Nutritional / Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal / Electrolyte	No underlying causes
Rheum / Immune / Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	Long-term exposure to wet diapers

• Adhesives

• Alcohol

• Alkalies

• Balsam of Peru

• Benzocaine topical
• Benzoyl peroxide

• Black mustard poisoning

• Buttercup poisoning

• Calcium oxalate from plants

• Cashew nuts

• Cement (Potassium dichromate)

• Chromium

• Cleaning agents

Clocortolone pivalate

• Cobalt

• Cosmetics

• Deodrants

• Detergents

• Diazepam

• Eflornithine

• Ethylene oxide

• Ethylenediamine

• Eucalyptus oil poisoning

• Fluticasone (cream/lotion)

• Formaldehyde

• Gold

• Hair dyes (p-Phenylenediamine)

• Hydrochlorothiazide

• Insecticide sprays

• Jewelry

• Kerosene

• Lanolin

• Latex

• Leather tanning agents

• Long-term exposure to wet diapers

• Mercaptobenzothiazole (rubber)

• Moisturizers

• Neomycin

• Nickel

• Ointments containing NSAIDs

• Perfumes

• Poison ivy

• Poison oak

• Poison sumac

• p-Phenylenediamine (PPD) in temporary tattoos

• Psoralens

• Sodium lauryl sulfate

• Solvents

• Tetracaine

• Thimerosal

• Thiram in fungicides

• Tiagabine

• Turpentine

• Xylene

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD

Females, infants, elderly, and individuals with atopic tendencies are more susceptible to irritant contact dermatitis. It is reported that up to 80% of cases of occupational dermatitis are irritant contact dermatitis.^[1]

All individuals are at risk of developing allergic contact dermatitis. Risk factors for allergic contact dermatitis include age, occupation, and history of atopic dermatitis.

Overall contact dermatitis is most common in people with red hair and fair skin. Women are more likely to develop contact dermatitis because of the use of jewelry and fragrances.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[3], Ogechukwu Hannah Nnabude, MD

Bacterial skin infections may occur.

Contact dermatitis usually clears up without complications in 2 or 3 weeks. However, it may return if the substance or material that caused it cannot be found or avoided.You may need to change your job or job habits if the disorder is caused by occupational exposure.

The prognosis of patients with contact dermatitis depends on the cause and lifestyle. Isolated cases usually resolve if the offending agent exposure is discontinued. Those who do not remain compliant and continue to wear jewelry with metal or are exposed to plants because of lifestyle generally tend to have a chronic course. Relapses are very common. In healthcare, latex allergy is a very common form of contact dermatitis and can have an impact on clinical practice. Cases of anaphylaxis are reported all the time.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Sumanth Khadke, MD[2]

In general, diagnosis (plural diagnoses) has two distinct dictionary definitions. The first definition is “the recognition of a disease or condition by its outward signs and symptoms”, while the second definition is “the analysis of the underlying physiological/biochemical cause(s) of a disease or condition”.

Diagnosis covers a broad spectrum, or spectra, of testing in some form of analysis; collective reasoning using such tests is called the method of diagnostics, leading then to the results of those tests by ideal (ethics) would then be considered a diagnosis, but not necessarily the correct one.

In medicine, diagnosis or diagnostics is the process of identifying a medical condition or disease by its signs, symptoms, and from the results of various diagnostic procedures. The conclusion reached through this process is called a diagnosis. The term “diagnostic criteria” designates the combination of symptoms which allows the doctor to ascertain the diagnosis of the respective disease.

Typically, someone with abnormal symptoms will consult a physician, who will then obtain a history of the patient‘s illness and examine him for signs of disease. The physician will formulate a hypothesis of likely diagnoses and in many cases will obtain further testing to confirm or clarify the diagnosis before providing treatment.

Medical tests commonly performed are measuring blood pressure, checking the pulse rate, listening to the heart with a stethoscope, urine tests, fecal tests, saliva tests, blood tests, medical imaging, electrocardiogram, hydrogen breath test and occasionally biopsy.

The word diagnosis is derived from the Greek words dia which means “by”, and gnosis which means “knowledge”. The verb is diagnose and a person diagnosing could be considered a diagnostician.

A physician‘s job is to know the human body and its functions in terms of normality (homeostasis). The four cornerstones of diagnostic medicine, each essential for understanding homeostasis, are: anatomy (the structure of the human body), physiology (how the body works), pathology (what can go wrong with the anatomy and physiology) and psychology (thought and behavior). Once the doctor knows what is normal and can measure the patient’s current condition against those norms, she or he can then determine the patient’s particular departure from homeostasis and the degree of departure. This is called the diagnosis. Once a diagnosis has been reached, the doctor is able to propose a management plan, which will include treatment as well as plans for follow-up. From this point on, in addition to treating the patient’s condition, the doctor educates the patient about the causes, progression, outcomes, and possible treatments of his ailments, as well as providing advice for maintaining health.

It should be noted however, that medical diagnosis in psychology or psychiatry is problematic. Apart from the fact that there are differing theoretical views toward mental conditions and that there are few “lab” tests available for various major disorders (e.g., clinical depression), a causal analysis with respect to symptomatology and disorder/disease is not always possible. As a result, most if not all mental conditions, function as both symptoms as well as disorders. There are often functional descriptions provided for psychological disorders and these are vulnerable to circular reasoning due to the etiological fuzziness inherent of these diagnostic categories. (BDG, 2006)

Diagnosis is a fluid process in which the physician responds to information garnered from the patient and others, from a physical examination of the patient, and from medical tests performed upon the patient.

The doctor should consider the patient in his ‘well’ context rather than simply as a walking medical condition. This entails assessing the socio-political context of the patient (family, work, stress, beliefs), in addition to the patient’s physical body, as this often offers vital clues to the patient’s condition and its management.

The process of diagnosis begins when the patient consults the doctor and presents a set of complaints (the symptoms). If the patient is unconscious, this condition is the de facto complaint. The doctor then obtains further information from the patient himself (and from those who know him, if present) about the patient’s symptoms, his previous state of health, living conditions, and so forth.

Rather than consider the myriad diseases that could afflict the patient, the physician narrows down the possibilities to the illnesses likely to account for the apparent symptoms, making a list of only those conditions that could account for what is wrong with the patient. These are generally ranked in order of probability.

The doctor then conducts a physical examination of the patient, studies the patient’s medical record, and asks further questions as he goes, in an effort to rule out as many of the potential conditions as possible. When the list is narrowed down to a single condition, this is called the differential diagnosis, and provides the basis for a hypothesis of what is ailing the patient.

Unless the physician is certain of the condition present, further medical tests are performed or scheduled (such as medical imaging), in part to confirm or disprove the diagnosis but also to document the patient’s status to keep the patient’s medical history up to date. Consultations with other physicians and specialists in the field may be sought. If unexpected findings are made during this process, the initial hypothesis may be ruled out and the physician must then consider other hypotheses.

Despite all of these complexities, most patient consultations are relatively brief, because many diseases are obvious, or the physician’s experience may enable him to recognize the condition quickly. Another factor is that the decision trees used for most diagnostic hypothesis testing are relatively short.

Once the physician has completed the diagnosis, he explains the prognosis to the patient and proposes a treatment plan which includes therapy and follow-up (further consultations and tests to monitor the condition and the progress of the treatment, if needed), usually according to the guideline provided by the medical field on the treatment of the particular illness.

Treatment itself may indicate a need for review of the diagnosis if there is a failure to respond to treatments that would normally work.

The history of medical diagnosis began in earnest from the enlightened days of Hippocrates in ancient Greece but is far from perfect despite the enormous bounty of information made available by medical research including the sequencing of the human genome. The practice of diagnosis continues to be dominated by theories set down in the early 1900s.

Over two thousand years ago, Hippocrates recorded the association between disease and heredity. In similar fashion, Pythagoras noted the association between metabolism and heredity (allergy to Fava beans). The medical community, however, has only recently acknowledged the importance of genetics and its relevance to mainstream medicine.

The ideals of William Osler who transformed the practice of medicine in the early 1900s were based on the principles of the diagnosis and treatment of disease. According to Osler, the functions of a physician were to be able to identify disease and its manifestations, understand its mechanisms, how it may be prevented and how it may be cured. For his medical students he believed that the best textbook was the patient himself – analysis of morbid anatomy and pathology were the keys. The Oslerian ideal continues today, as the basis of the Doctor’s strategy is, “What disease does this patient have and what is the best way for treatment?” The emphasis is on the classification of the disease in order to use the remedies available for its effects to be reversed or ameliorated. The human being in question is representative of a class of people with this type of disease whereas the biological individuality of this person is not given any great weight.

The successor to William Osler as Regius Professor at Oxford was Archibald Garrod. Garrod echoed the observations of his Greek counterparts of two millennia ago, …our chemical individualities are due to our chemical merits as well as our chemical shortcomings; and it is more nearly true to say that the factors which confer upon us our predispositions to and immunities from various mishaps which are spoken of as diseases, are inherent in our very chemical structure; and even in the molecular groupings which confer upon us our individualities, and which went into the making of the chromosomes from which we sprang. Considering that the time that he formulated these ideas were the early 1900’s, and the knowledge of DNA encoding genes that in turn encoded proteins responsible for bodily structure and functions not being discovered until some fifty years later it took some time before medicine could fully appreciate the fundamental importance of his concept of diagnosis.

Whereas Osler laid the founding principles by which medicine should be practiced, Garrod placed these principles in a greater context of a chemical individuality that is inherited and is subject to the mechanisms of evolutionary selection. The Oslerian ideal of medical practice continues to dominate medical philosophy today. The patient is a collective of symptoms to be characterized and analyzed algorithmically in order to draw a diagnosis and subsequently produce a strategy of treatment. Medicine is about problems based solutions. In keeping with this philosophy, today’s pathology reports provide a momentary snapshot of the patient’s biochemical profile, highlighting the end result of the disease process.

Garrod’s conception of biological individuality was confirmed with the advent of the sequencing of the human genome. Finally the subtle relationship between inheritance, individuality and environment became apparent via the variations detected in DNA. In each patient’s DNA lies a script for how their bodies will change and become ill as well as how they will handle the assaults of the environment from the beginning of their life to its end. It is hoped that by knowing a patient’s genes that the biological strengths and weaknesses in respect to these assaults will be revealed and disease processes can be predicted before they have the opportunity to manifest. Although knowledge in this area is far from complete, there are already medical interventions based on this. More importantly, the physician, forewarned with this knowledge can guide the patient towards appropriate lifestyle changes to anticipate and mitigate disease processes.

• GPnotebook web site GPnotebook is a British medical database for GPs that provides an immediate reference resource for clinicians worldwide. The database consists of over 30,000 pages of information.
• Free 24/7 DRG & ICD-9-CM lookup powered by Flash Code at icd9coding.com
• Differential Diagnosis
• Merck Manual of Diagnosis and Therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Sumanth Khadke, MD[2], Ogechukwu Hannah Nnabude, MD

Compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment. ^{[1] [2]}

High-potency topical corticosteroids, e.g. clobetasol propionate 0.05% cream, may be used to reduce the inflammation. ^[3] As a general rule, high-potency corticosteroids should not be used on thin skin, e.g. face, genitals, intertriginous areas, to avoid the risk of skin atrophy. Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2] Aditya Govindavarjhulla, M.B.B.S. [3]

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