| Allergic contact dermatitis |
|
Illustration of allergic contact dermatitis
|
| Classification and external resources |
| ICD-10 |
L23 |
| ICD-9-CM |
691.8 |
| DiseasesDB |
29435 |
| MeSH |
D017449 |
Allergic contact dermatitis (ACD) is a form of contact dermatitis that is the manifestation of an allergic response caused by contact with a substance; the other type being irritant contact dermatitis (ICD).
Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans.[1] 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 on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.
Contents
- 1 Signs and symptoms
- 2 Cause
- 3 Mechanism
- 4 Diagnosis
- 5 Treatment
- 6 References
Signs and symptoms
The symptoms of allergic contact dermatitis are very similar to the ones caused by irritant contact dermatitis, which makes the first even harder to diagnose. The first sign of allergic contact dermatitis is the presence of the rash or skin lesion at the site of exposure.[2] Depending on the type of allergen causing it, the rash can ooze, drain or crust and it can become raw, scaled or thickened. Also, it is possible that the skin lesion does not take the form of a rash but it may include papules, blisters, vesicles or even a simple red area. The main difference between the rash caused by allergic contact dermatitis and the one caused by irritant contact dermatitis is that the first one tends to be confined to the area where the trigger touched the skin, whereas in the second case, the rash is more likely to be more widespread on the skin.[3] Another characteristic of the allergic contact dermatitis rash is that it usually appears after a day or two after exposure to the allergen, unlike irritant contact dermatitis that appears immediately after the contact with the trigger.
Other symptoms may include itching, skin redness or inflammation, localized swelling and the area may become more tender or warmer. If left untreated, the skin may darken and become leathery and cracked.[4] Pain can also be present.
The symptoms of allergic contact may persist for as long as one month before resolving completely. Once an individual has developed a skin reaction to a certain substance it is most likely that they will have it for the rest of their life, and the symptoms will reappear when in contact with the allergen.
Cause
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 and dental materials
- Balsam of Peru (Myroxylon pereirae) – used in food and drink for flavoring, in perfumes and toiletries for fragrance, and in medicine and pharmaceutical items for healing properties; derived from tree resin.[5][6][7] It may also be a component of artificial vanilla and/or cinnamon flavorings.[5]
- Chromium – used in the tanning of leather. Also a component of uncured cement/mortar, facial cosmetics and some bar soaps.
- Oily coating from plants of Toxicodendron genus – poison ivy, poison oak, and poison sumac.
- Sap from certain species of mangrove and agave
- Thiomersal – mercury compound used in local antiseptics and in vaccines
- Neomycin – topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap, and pet food. Found by itself, or in Neosporin or Triple Antibiotic
- Fragrance mix – group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes, and dental products [8]
- Formaldehyde – preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products, and fabric finishes. Often released into products by the use of formaldehyde releasers such as imidazolidinyl urea, diazolidinyl urea, Quaternium-15, DMDM Hydantoin, and 2-bromo-2-nitropropane-1,3-diol.
- 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 – 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).[9]
- 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
- Isothiazolinone/Methylisothiazolinone/Methylchloroisothiazolinone – preservative used in many personal care, household, and commercial products.
- Soluble salts of platinum – see platinosis
Mechanism
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.[10] As it involves a cell-mediated allergic response, ACD is termed a Type IV delayed hypersensitivity reaction, making it an exception in the usage of the designation "allergic," which otherwise usually refers to type I hypersensitivity reactions.
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 other 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.[11] 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.
White et al. have suggested that there appears to be a threshold to the mechanisms of allergic sensitisation by ACD-associated allergens (1986).[12] 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.
Memory Response
Once an individual is sensitized to an allergen, future contacts with the allergen can trigger a reaction, commonly known as a memory response, in the original site of sensitization. So for example if a person has an allergic contact dermatitis on the eyelids, say from use of makeup, touching the contact allergen with the fingers can trigger an allergic reaction on the eyelids.
This is due to local skin memory T-cells, which remain in the original sensitization site. In a similar fashion, cytotoxic T lymphocytes patrol an area of skin and play an important role in controlling both the reactivation of viruses (such as the "cold sore" virus) and in limiting its replication when reactivated.[13] Memory response, or "Retest Reactivity", usually takes 2 to 3 days after coming in contact with the allergen, and can persist for 2 to 4 weeks.
Diagnosis
Diagnosing allergic contact dermatitis is primarily based on physical exam and medical history. In some cases doctors can establish an accurate diagnosis based on the symptoms that the patient experiences and on the rash's appearance. In the case of a single episode of allergic contact dermatitis, this is all that is necessary. Chronic and/or intermittent rashes which are not readily explained by history and physical exam often will benefit from further testing.
A patch test (contact delayed hypersensitivity allergy test)[14] is a commonly used examination to determine the exact cause of an allergic contact dermatitis. According to the American Academy of Allergy, Asthma, and Immunology, "patch testing is the gold standard for contact allergen identification".[2]
The patch test consists of applying small quantities of potential allergens to small patches and which are then placed on the skin.[15] After two days, they are removed and if a skin reaction occurred to one of the substances applied, a raised bump will be noticeable underneath the patch. The tests are again read at 72 or 96 hours after application.
Patch testing is used for patients who have chronic, recurring contact dermatitis.[2] Other tests that may be used to diagnose contact dermatitis and rule out other potential causes of the symptoms include a skin biopsy and culture of the skin lesion.
Treatment
Persons who develop the rash and the other symptoms from a certain trigger are most likely to have it for the rest of their lives and detecting and avoiding the allergen is mandatory in treating the condition and resolving its symptoms.
The first step in treating the condition is applying a damp cloth shortly after the skin problem first shows to make sure that all of the irritant has been removed from the area.[16][clarification needed] In some cases, the best treatment is to do nothing to the area.[2]
In mild to moderate cases, patients may use skin creams containing corticosteroids to reduce the inflammation. These creams should be used carefully and according to the instructions they come with because when overused over longer periods of time they can cause serious skin conditions. Also, calamine lotion and cool oatmeal baths may relieve itching.[17] Over the counter diphenhydramine by mouth is helpful for night time itching.
Usually, severe cases are treated with systemic corticosteroids which may be tapered gradually, with various dosing schedules ranging from a total of 12 – 20 days to prevent the recurrence of the rash as well as a topical corticosteroid.[2] Tacrolimus ointment or pimecrolimus cream can also be used additionally to the corticosteroid creams or instead of these. Oral antihistamines such as diphenhydramine or hydroxyzine may also be used in more severe cases to relieve the intense itching. Topical antihistamines are not advised as there might be a second skin reaction from the lotion itself.
The other symptoms caused by allergic contact dermatitis are generally eased with wet dressings and drying lotions to stop the itching. In most cases however, medication or actual treatment is not required as long as the trigger has been identified and avoided. The discomfort caused by the symptoms may be relieved by wearing smooth-textured clothing to avoid more skin irritation or by avoiding soaps with perfumes and dyes.
Commonly, the symptoms may resolve without treatment in 2 to 4 weeks but specific medication may hasten the healing as long as the trigger is avoided. Also, the condition might become chronic if the allergen is not detected and therefore it is not avoided.
References
- ^ Kimber I, Basketter DA, Gerberick GF, Dearman RJ (2002). "Allergic contact dermatitis". Int. Immunopharmacol. 2 (2–3): 201–11. doi:10.1016/S1567-5769(01)00173-4. PMID 11811925.
- ^ a b c d e "Contact dermatitis". Archived from the original on 15 June 2010. Retrieved 2010-06-16.
- ^ "Contact Dermatitis Symptoms". Retrieved 2010-06-16.
- ^ "Allergic Contact Dermatitis". Archived from the original on 28 June 2010. Retrieved 2010-06-16.
- ^ a b "Balsam of Peru contact allergy". Dermnetnz.org. December 28, 2013. Retrieved March 5, 2014.
- ^ Gottfried Schmalz, Dorthe Arenholt Bindslev (2008). Biocompatibility of Dental Materials. Springer. Retrieved March 5, 2014.
- ^ Thomas P. Habif (2009). Clinical Dermatology. Elsevier Health Sciences. Retrieved March 6, 2014.
- ^ Allergy to fragrance mix at DermNetNZ, http://dermnetnz.org/dermatitis/fragrance-allergy.html
- ^ Mayo Clinic study, http://www.mayoclinic.org/news2006-rst/3268.html
- ^ (Kimble et al. 2002).
- ^ (Kimble et al. 2002)
- ^ White SI, Friedmann PS, Moss C, Simpson JM (1986). "The effect of altering area of application and dose per unit area on sensitization by DNCB". Br. J. Dermatol. 115 (6): 663–8. doi:10.1111/j.1365-2133.1986.tb06646.x. PMID 3801307.
- ^ Iwasaki A (2009). "Local advantage: skin DCs prime, skin memory T cells protect". Nature Immunololgy 10 (5): 451–453. doi:10.1038/ni0509-451. PMC 3662044. PMID 19381136.
- ^ "Contact dermatitis". Archived from the original on 19 June 2010. Retrieved 2010-06-16.
- ^ "Tests and diagnosis". Archived from the original on 19 June 2010. Retrieved 2010-06-16.
- ^ "Allergic Dermatitis Symptoms and Treatment". Archived from the original on 31 May 2010. Retrieved 2010-06-16.
- ^ "Self-Care at Home". Archived from the original on 15 June 2010. Retrieved 2010-06-16.
|
Dermatitis and eczema (L20–L30, 690–693,698)
|
|
| Atopic dermatitis |
|
|
| Seborrheic dermatitis |
- Pityriasis simplex capillitii
- Cradle cap
|
|
Contact dermatitis
(allergic, irritant) |
- plants: Urushiol-induced contact dermatitis
- African blackwood dermatitis
- Tulip fingers
- other: Abietic acid dermatitis
- Diaper rash
- Airbag dermatitis
- Baboon syndrome
- Contact stomatitis
- Protein contact dermatitis
|
|
| Eczema |
- Autoimmune estrogen dermatitis
- Autoimmune progesterone dermatitis
- Breast eczema
- Ear eczema
- Eyelid dermatitis
- Hand eczema
- Chronic vesiculobullous hand eczema
- Hyperkeratotic hand dermatitis
- Autosensitization dermatitis/Id reaction
- Candidid
- Dermatophytid
- Molluscum dermatitis
- Circumostomy eczema
- Dyshidrosis
- Juvenile plantar dermatosis
- Nummular eczema
- Nutritional deficiency eczema
- Sulzberger–Garbe syndrome
- Xerotic eczema
|
|
Pruritus/Itch/
Prurigo |
- Lichen simplex chronicus/Prurigo nodularis
- by location: Pruritus ani
- Pruritus scroti
- Pruritus vulvae
- Scalp pruritus
- Drug-induced pruritus
- Hydroxyethyl starch-induced pruritus
- Senile pruritus
- Aquagenic pruritus
- Adult blaschkitis
- due to liver disease
- Biliary pruritus
- Cholestatic pruritus
- Prion pruritus
- Prurigo pigmentosa
- Prurigo simplex
- Puncta pruritica
- Uremic pruritus
|
|
| Other |
- substances taken internally: Bromoderma
- Fixed drug reaction
- Nummular dermatitis
- Pityriasis alba
- Papuloerythroderma of Ofuji
|
|
|
Index of skin
|
|
| Description |
- Anatomy
- Physiology
- Development
|
|
| Disease |
- Infections
- Vesiculobullous
- Dermatitis and eczema
- Papulosquamous
- Urticaria and erythema
- Radiation-related
- Pigmentation
- Mucinoses
- Keratosis, ulcer, atrophy, and necrobiosis
- Vasculitis
- Fat
- Neutrophilic and eosinophilic
- Congenital
- Neoplasms and cancer
- nevi and melanomas
- epidermis
- dermis
- Symptoms and signs
- Terminology
|
|
| Treatment |
- Procedures
- Drugs
- antibiotics
- disinfectants
- emollients and protectives
- itch
- psoriasis
- other
- Wound and ulcer
|
|
|
|
Hypersensitivity and autoimmune diseases (279.5–6)
|
|
Type I/allergy/atopy
(IgE) |
| Foreign |
- Atopic eczema
- Allergic urticaria
- Allergic rhinitis (Hay fever)
- Allergic asthma
- Anaphylaxis
- Food allergy
- Milk
- Egg
- Peanut
- Tree nut
- Seafood
- Soy
- Wheat
- Penicillin allergy
|
|
| Autoimmune |
|
|
|
Type II/ADCC
|
| Foreign |
- Hemolytic disease of the newborn
|
|
| Autoimmune |
| Cytotoxic |
- Autoimmune hemolytic anemia
- Idiopathic thrombocytopenic purpura
- Bullous pemphigoid
- Pemphigus vulgaris
- Rheumatic fever
- Goodpasture's syndrome
- Guillain–Barré syndrome
|
|
| "Type V"/receptor |
- Graves' disease
- Myasthenia gravis
- Pernicious anemia
|
|
|
|
Type III
(Immune complex) |
| Foreign |
- Henoch–Schönlein purpura
- Hypersensitivity vasculitis
- Reactive arthritis
- Farmer's lung
- Post-streptococcal glomerulonephritis
- Serum sickness
- Arthus reaction
|
|
| Autoimmune |
- Systemic lupus erythematosus
- Subacute bacterial endocarditis
- Rheumatoid arthritis
|
|
|
Type IV/cell-mediated
(T cells) |
| Foreign |
- Allergic contact dermatitis
- Mantoux test
|
|
| Autoimmune |
- Diabetes mellitus type 1
- Hashimoto's thyroiditis
- Multiple sclerosis
- Coeliac disease
- Giant-cell arteritis
|
|
| GVHD |
- Transfusion-associated graft versus host disease
|
|
|
Unknown/
multiple |
| Foreign |
- Hypersensitivity pneumonitis
- Allergic bronchopulmonary aspergillosis
- Transplant rejection
- Latex allergy (I+IV)
|
|
| Autoimmune |
- Sjögren's syndrome
- Autoimmune hepatitis
- Autoimmune polyendocrine syndrome
- Autoimmune adrenalitis
- Systemic autoimmune disease
|
|
|
|
Index of the immune system
|
|
| Description |
- Physiology
- cells
- autoantigens
- autoantibodies
- complement
- surface antigens
- IG receptors
|
|
| Disease |
- Allergies
- Immunodeficiency
- Immunoproliferative immunoglobulin disorders
- Hypersensitivity and autoimmune disorders
- Neoplasms and cancer
|
|
| Treatment |
- Procedures
- Drugs
- antihistamines
- immunostimulants
- immunosuppressants
- monoclonal antibodies
|
|
|
