This is the current release of the guideline.

Contact dermatitis (CD)

Note: Contact dermatitis (CD) encompasses all adverse cutaneous reactions that result from the direct contact of an exogenous agent (a "foreign" molecule, ultraviolet light, or temperature) to the surface of the skin or mucous membranes.

To ensure that contact dermatitis (CD) patients benefit from the best available diagnostic and therapeutic applications by consultant allergists/clinical immunologists

Patients with contact dermatitis

Diagnosis

1. Patient history and physical examination
2. Patch tests
3. Differential diagnosis
4. Assessment of exposure
   • Occupational
   • Plant dermatitis
   • Cosmetics
   • Medicinal
   • Allergic contact cheilitis (ACC)
   • Contact dermatitis (CD) due to surgical implant devices
   • Systemic CD
   • Concurrent exposure to irritants and contactant allergens

Management

1. Avoidance of contact with the offending agent(s)
2. Skin hydration with moisturizers and emollients
3. Topical corticosteroids
4. Systemic corticosteroids
5. Topical T-cell selective inhibitors of inflammatory cytokines
6. Topical, and occasionally systemic, antibiotics should be used for secondary infections of acute contact dermatitis (ACD) or irritant contact dermatitis (ICD)
7. Phototherapy with or without psoralen
8. Referral to dermatologist
9. Hospitalization (and transfer to burns unit)
10. Prevention
    • Surveillance programs in high risk industries
    • Emollients, moisturizers, and/or barrier creams

Objective evidence for major content listings was obtained by searching PubMed MEDLINE.

Not stated

Ia Evidence from meta-analysis of randomized controlled trials

Ib Evidence from at least one randomized controlled trial

IIa Evidence from at least one controlled study without randomization

IIb Evidence from at least one other type of quasi-experimental study

III Evidence from nonexperimental descriptive studies, such as comparative studies, correlation studies, and case-control studies

IV Evidence from expert committee reports, opinions or clinical experiences of respected authorities, or both

LB Evidence from laboratory-based studies

Wherever possible, references were selected according to the following priority scale: (1) meta-analyses; (2) randomized controlled trials; (3) controlled trials without randomization; (4) other quasi-experimental studies; (5) nonexperimental descriptive studies, such as comparative, correlation, or case-controlled studies; (6) committee reports or opinions, clinical experience of respected authorities, or both; and (7) laboratory-based studies.

This guideline was developed by the Joint Task Force on Practice Parameters, which has published 20 practice parameters for the field of allergy/immunology (see list of publications). The 3 national allergy and immunology societies—the American College of Allergy, Asthma and Immunology (ACAAI) the American Academy of Allergy, Asthma and Immunology (AAAAI), and the Joint Council of Allergy, Asthma and Immunology (JCAAI)—have given the Joint Task Force the responsibility for both creating new and updating existing parameters.

A formal cost analysis was not performed and published cost analyses were not reviewed.

The working draft of the Practice Parameter was then reviewed by a number of experts on contact dermatitis (CD) selected by the supporting organizations. This document therefore represents an evidence-based, broadly accepted, consensus opinion.

This practice parameter includes an algorithm on the diagnosis and management of food allergy accompanied by annotations (numbered to correspond with the algorithm). Guideline recommendations are presented in the form of summary statements. After each statement is a letter in parentheses that indicates the strength of the recommendation. Categories of evidence (Ia, Ib, IIa, IIb, III, IV, LB) and strength of recommendations (A-F) are defined at the end of the "Major Recommendations" field.

Annotations

1. Patient presents with localized or generalized manifestations of an eczematous pruritic dermatitis. Contact dermatitis (CD) is a common skin problem. All age groups are affected with a slight female preponderance. The most common presentation consists of a papulovesicular eruption, which may evolve into a pleomorphic dermatitis with hyperkeratosis, lichenification, fissuring, and scaliness. The lesions may be localized or generalized. Exposure to a putative agent may be evident. If the lesion is associated with exposure to sunlight, a photoallergic CD or a phototoxic reaction is possible. Pruritus is a prominent symptom.
2. Evaluation of history and physical examination consistent with CD (allergic [ACD] vs. irritant [ICD])? The history should elicit the suspicion that CD, either ACD or ICD, is the cause of the symptoms. The site of inflammation must have come in direct contact with the offending agent. Initially, the area may itch, burn, or sting, but as the lesion evolves, pruritus is the major symptom. Identifying the putative agent requires meticulous exploration of the history. Work and hobby history must be carefully reviewed. Careful examination of the skin may yield important clues as to what contactants are involved. This is particularly germane to skin areas, such as eyelids, face, neck, scalp, hair, axillae, lower extremities, and the anogenital region.
3. CD not the likely cause. If CD is not probable based on history and physical examination, many dermatologic and/or systemic diseases should be considered. Additional evaluation should include a skin biopsy interpreted by a dermatopathologist and skin scrapings for the presence of hyphal fragments. For further delineation of the problem, the patient may be referred to a dermatologist.
4. Is the dermatitis active or widespread? Acute vesiculobullous ACD (e.g., Toxicodendron dermatitis) may become widespread within a short time and may also be associated with considerable soft tissue swelling. The evolution of CD caused by other agents is usually more gradual. If the symptoms are disabling or the lesions are widespread, immediate treatment is required. Patch testing should be delayed until the acute phase is resolved because of the potential for worsening of the dermatitis and the possibility of false-positive reactions due to hyperirritability of the skin.
5. Consider diagnostic testing. Patch test result positive? Under ordinary circumstances, patch tests to Toxicodendron are not indicated. For other suspected presentations, patch testing should be offered to confirm the specific agent that is responsible for ACD. Patch testing with appropriate antigens is the gold standard for confirming ACD. Even though this is the best way to identify specific contactants, patients may not desire patch testing, particularly when avoidance of the suspected contactant is effective.

   If the history is consistent with a potential contactant and patch test results to a standard battery of screening allergens (e.g., TRUE Test) are negative, patch testing patients with their own products at nonirritant concentrations may be required. In some cases, contacting the manufacturer of a suspected product may be necessary to identify the ingredient(s) responsible for the ACD. If this is contemplated, toxicity and irritant reactions should be excluded by using suitable controls.

   Patches should be applied to the skin of the back 2.5 cm lateral to the midspinal column. The patches are removed and results read at 48 hours. Patients should be instructed to remove patches from the irritable site(s) before 48 hours should the site of application become uncomfortably pruritic. Since 30% of reactions are negative at 48 hours, additional reading(s) should be performed at 3 or 4 and sometimes 7 days after the initial application, depending on the allergen. Patches are read according to a special scale recommended by the International Contact Dermatitis Research Group. Correct interpretation of the test result is critical, because both false-negative and false-positive test results are possible. Reactions graded as 2+ and 3+ strongly suggest the presence of prior or present sensitization to a contactant. The relevance of these test results should be interpreted by considering historical probability of exposure and the area of involved skin.

6. Initial management. If presenting symptoms are severe or lesions are generalized, palliative methods to control the itching and skin hydration should be instituted. Cold compresses, colloidal baths, and emollients may be helpful. Antihistamines may partially control pruritus. The mainstay of treatment is topical corticosteroid (TCs). Traditionally, treatment begins with high-potency corticosteroids that may be switched to medium- or even lower-potency preparations as symptoms improve. For unusually severe or widespread ACD, systemic corticosteroids may be required. If the history is suggestive of a particular contactant, avoidance should be started immediately at this stage of treatment. Rarely, CD may be secondarily infected with staphylococcal or streptococcal bacteria, which ultimately may act as super-antigens. Systemic antibiotics should be used if this is suspected. Since topical irritants such as detergents are known to augment the effects of contact allergens, they should be avoided.
7. Avoidance of proven contact allergens. Known contact allergens should be avoided. Patients therefore should be given complete instructions on how to avoid allergens that were detected by patch tests. This is often difficult for cosmetics, since many of the contact allergens are used in all cosmetic products even though they are purported to be nonallergenic. There are also specific circumstances where ingestion of a cross-reacting food or drug could lead to a serious systemic flare of the ACD. OCD may require counseling for not only the worker but also the responsible industrial health professional. Material safety data sheets may provide clues regarding the offending agent. Sometimes a work site visit may be helpful in determining whether a worker can continue to work in a particular job or work site.
8. Perform additional patch tests. If test results to standard sets of validated contact allergens are negative, it may be necessary to obtain expanded patch test kits that contain the relevant contact allergens in certain occupations or activities. At times it also may be necessary to prepare customized test reagents. Indeed, this is most productive if cosmetics are suspected. Once the suspected product produces a positive patch test result, further tests for the active or inert ingredients in the preparation can then be done. In some cases, especially with substances causing CD around the eyelids or other areas of thin skin, an open application test may be helpful. This involves applying the patch to more sensitive skin areas, such as antecubital fossae or behind the ear. Repetitive challenges are then applied to the same site daily for 1 to 2 weeks.
9. If screening and additional test results are negative, the probable diagnosis is ICD. ICD is generally a multifactorial response that occurs after contact with a substance that chemically abrades, physically irritates, or damages the skin. It is usually a direct cytotoxic reaction produced by a wide variety of agents and by contributory physical factors that include scrubbing, washing, overhydration, perspiration, and temperature extremes. The inflammatory reaction that results from these irritants is dose dependent. The evolution and resolution of ICD are less predictable than ACD.
10. Management of ICD. Although palliative relief after use of skin hydrating and emollient agents may be helpful, avoidance of the involved irritants should be implemented whenever this is possible. The use of topical or systemic corticosteroids does not appear to offer as much relief in ICD as in ACD.
11. Management successful? If there is complete clearance of ACD, the patient is less likely to have a recurrence provided there is avoidance of the proven contact allergen. In occupational settings, however, clearance rates vary between 18% and 40%. Partial improvement ranges from 70% to 84%. Rarely, some workers continue to have persistent, ongoing dermatitis despite removal of exposure at work.
12. Follow-up after initial successful treatment. Prevention of skin dryness in patients with a proven diagnosis of CD can be attempted with the long-term use of emollients and moisturizers. The efficacy of protective barrier creams is debatable. Unfortunately, none of these secondary measures appears to be effective, especially after large amounts of exposure to skin irritants. If symptoms recur, further treatment options in Annotation 15 may be considered.
13. Is diagnosis of CD correct? If no improvement in symptoms or appearance of the lesions is evident, reassessment is appropriate at this stage of management. This is essential to prevent further complications, such as superinfection of the skin, excess keratinization, or, rarely, exfoliative dermatitis.
14. Other consultation? A dermatologist's opinion should be sought to determine whether other possible dermatologic or systemic diseases are masquerading as CD. In some cases, there is underlying dermatologic disease with secondary contact sensitization. A dermatologist can be of help in making this judgment. If other diagnostic studies, such as skin biopsy or skin scrapings for dermatophytosis, have not yet been done, the dermatologist may wish to pursue these possibilities.
15. Additional treatment possibilities. Further stepwise treatment options should be considered for recalcitrant CD. Several new immunophilin (calcineurin inhibitors) T-cell suppressants have been approved by the Food and Drug Administration (FDA) for atopic dermatitis. Some early studies indicate that they may also be effective in CD. Thus, a trial of one or both of these topical agents could be considered for refractory CD. If these treatments are unsuccessful, systemic corticosteroids in sufficient doses (1 mg/kg daily) should be considered. For particularly severe treatment failures, phototherapy with or without psoralen may be attempted by physicians experienced in this technique. In the case of widespread CD evolving into generalized exfoliative dermatitis, hospitalization may be required. If large areas of the skin are denuded by the exfoliative process, transfer to a burn unit for appropriate treatment is mandatory.

Summary Statements

Clinical Background

1. CD is a common skin disorder seen by allergists and dermatologists and can present with a spectrum of morphologic cutaneous reactions. (C)

Pathophysiology of CD

2. The inflammatory lesions of CD may result from either allergic (ACD) or nonallergic, irritant (ICD) mechanisms. Factors that affect a response to the contact agent include the agent itself, the patient, the type and degree of exposure, and the environment. (A)
3. Tissue reactions to contactants are attributable primarily to cellular immune (delayed hypersensitivity) mechanisms, except for contact urticaria. (A)
4. ICD is usually the result of nonimmunologic, direct tissue reaction and yet may at times be difficult to differentiate from ACD. (A)
5. Spongiosis is the predominant histologic feature of CD. (A)

Susceptibility and Genetics of CD

6. Age- and sex-specific, but not race-specific, differences in patch test responses have been observed in several large patch test surveys. (B)
7. In recent years, several cytokine gene polymorphisms have been described, but their functional significance is not yet clear. (A)

Clinical Diagnosis of ACD

Historical Features

8. The diagnosis of ACD is suspected from the clinical presentation of the rash, which then must be supported by a history of exposure to a putative agent and subsequently confirmed by patch testing whenever this is possible. (C)

Physical Examination

9. Location. The skin site of the dermatitis is important in the diagnosis of ACD, because the area of predominant involvement and the regional distribution of the lesions often reflect the area of contact with the allergen.(A)
10. Eyelids. ACD is a common cause of eyelid dermatitis induced not only by locally applied cosmetics but also by agents applied to other parts of the body (e.g., nail polish) that may come into contact with the eyelids. (A)
11. Face. Cosmetics (including vehicles and preservatives) and fragrances are the most common sensitizers of the facial skin. (B)
12. Scalp. Paraphenylenediamine is a common sensitizer of scalp skin. (B)
13. Hands. Hand dermatitis is extremely common (10% of women and 4.5% of men, aged 30–40 years). In this location, ICD and ACD are often indistinguishable. (B)
14. Neck. Vehicles, preservatives, drippings from permanent wave preparations, hair dyes, shampoos, conditioners, fragrances, and nickel in jewelry may produce ICD or ACD on the neck. (A)
15. Axilla. Contact to topically applied agents may involve the entire axillary vault, whereas allergy due to clothing leachates usually spares the apex of the vault. (B)
16. Lower extremities. Drug- or excipient- induced ACD of the lower extremities often occurs in patients with chronic stasis dermatitis due to increased exposure to topical medications. Less commonly, other sensitizing agents, such as shaving agents, moisturizers, and, rarely, stocking materials or dyes, should be considered. (B)
17. Anogenital region. Topical medications, suppositories, douches, latex condoms and diaphragms, spermaticides, lubricants (used during coitus), sprays, and anogenital cleansers are potential causes of CD in the anogenital area. (B)

Patch Tests

18. Epicutaneously applied patch tests are the standardized diagnostic procedures to confirm ACD. (A)
19. The clinical diagnosis of ACD can be complicated by atopic susceptibility. (B)
20. Although clinical relevance is still evolving with regard to the atopic patch test (APT), several European investigative groups have reported that this test may be an adjunct in the detection of both inhalant and food allergy in atopic dermatitis patients. (B)
21. Patch tests are indicated in any patient with a chronic, pruritic, eczematous, or lichenified dermatitis if underlying or secondary ACD is suspected. (A)
22. Patch test results are affected by oral corticosteroids, TCs, and calcineurin inhibitors but not by oral antihistamines. (A)
23. A screening battery of patch tests is best developed by using standardized sets of allergens previously calibrated with respect to nonirritant concentrations and compatibility with the test vehicle. (A)
24. Reading and interpretation of patch tests should conform to principles developed by the International Contact Dermatitis Research Group and the North American Contact Dermatitis Research Group. (A)
25. A 96-hour reading may be necessary, because 30% of relevant allergens that are negative at the 48-hour reading become positive in 96 hours. (A)
26. Interpretation of patch test results must include the possibilities of false-positive and false negative reactions. (A)
27. Nonstandard and customized patch testing is often required, depending on the patient's exposure history. (C)
28. Several in vitro procedures are being investigated for the diagnosis of ACD. (A)
29. Several other tests are available for (1) identification of allergens, (2) improving the reliability of interpreting test results for leave-on products, or (3) distinguishing CD from morphologically similar diseases. (B)
30. Although systemic ACD after patch testing is rare, reactivation of patch test reactions may occur after oral ingestion of related allergens or even by inhalation of budesonide in patients with sensitization to topical steroids. (B)
31. Patch testing can sensitize a patient who had not been previously sensitized to the contactant being tested, particularly to poison ivy/oak. (B)

Differential Diagnosis of CD

32. The differential diagnosis for CD is influenced by many factors, such as clinical appearance of the lesions, distribution of the dermatitis, and associated systemic manifestations. (B)

Special Exposures Associated With CD

Occupational Contact Disease (OCD)

33. OCD is an inflammatory cutaneous disease caused or aggravated by workplace exposure. (B)
34. There are 7 generally acceptable criteria for establishing causation and aggravation of OCD. (C)
35. The most common occupations associated with OCD are health professionals (especially nurses), food processors, beauticians and hairdressers, machinists, and construction workers. (A)
36. Among health professionals, ACD may occur as part of the spectrum of immunoreactivity to natural rubber latex (NRL) in latex gloves. (A)

Plant Dermatitis

37. ACD from exposure to plants is the result of specific cell-mediated hypersensitivity induced by previous contact with that family of plants. (A)
38. Toxicodendron (Rhus) dermatitis (poison ivy, poison oak, and poison sumac) is caused by urushiol, which is found in the saps of this plant family. (A)
39. Sesquiterpene lactones and tuliposides are large, diverse groups of chemicals found in several plant families that cause ACD in florists, bulb growers, and others working in the floral industry. (A)
40. Seasonal recurrence of ACD on exposed skin surfaces may be due to airborne pollen. (B)
41. Since there are not standardized test antigens for all plants, the incidence of sensitivity in the general population is largely unknown but is likely to be much more common than currently recognized. (D)

Cosmetics

42. Cosmetics and personal hygiene products contain a variety of potential allergens that are common causes of CD, which can occasionally manifest in sites distant from the original application of the product. (B)
43. Although routinely used cosmetics and personal care products contain considerable numbers of chemical ingredients, the most common causes are due to a few important chemical classes. (B)
44. Fragrances are among the most common causes of CD in the United States. (A)
45. Preservatives and antibacterials are present in most aqueous-based cosmetics and personal hygiene products to prevent rancidity and microbial contamination. (A)
46. Formulation excipients other than preservatives and fragrances are typically defined as inert substances that serve to solubilize, emulsify, sequester, thicken, foam, lubricate, or color the active component in a product. They can be responsible for ACD or, when used in higher concentrations, can act as irritants. (A)
47. Hair products are second only to skin care products as the most common cause of cosmetic allergy. Cocamidopropyl betaine, paraphenylenediamine, and glycerol thioglycolate have been reported to cause ACD from hair products. (A)
48. Allergy to acrylics in nails can present locally at the distal digit or ectopically on the eyelids and face. (A)
49. Sunblocks or sunscreens, common causes of photoallergic ACD, are frequently present in cosmetics such as moisturizers, "night" creams, lip and hair preparations, and foundations. (A)

Medicinal CD

50. CD commonly develops after exposure to topical medications, including lanolin, para-aminobenzoic acid, "caine" derivatives, antibiotics, antihistamines, iodochlorhydroxyquin, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids. (A)
51. ACD due to TCs may occur in up to 5% of patients presenting with suspected CD. (A)
52. Topical NSAID preparations that are generally available in over-the-counter preparations can frequently induce ACD. (B)
53. Drug APTs are being investigated as possible diagnostic adjuncts for mixed (T_H1 and T_H2) allergic cutaneous drug reactions. (C)

Allergic Contact Cheilitis (ACC)

54. ACC is a common form of ACD, because the epithelium of the lips is similar to the skin. (C)
55. Allergic contact mucositis may be a cause of recurrent oral ulcerations. (B)
56. Cinnamon and peppermint flavorings are probably the most common causes of allergic stomatitis from dentifrices and chewing gum. (B)

CD Due to Surgical Implant Devices

57. CD to surgical implants is at times suspected, but definitive association of the reaction with the implant material is only rarely documented. (D)

Systemic CD

58. Allergic systemic CD is a generalized ACD rash from systemic administration of a drug, chemical, or food to which the patient previously experienced ACD. (A)

Concurrent Exposure to Irritants and Contactant Allergens

59. Simultaneous exposure to allergens and irritants may produce both additive and synergistic ACD responses due to their interaction. (A)
60. The role of detergents in hand dermatitis is a reflection of their ability to disrupt the skin barrier. (A)

ACD in Children

61. ACD is a significant clinical problem in children. (A)

Management and Prognosis of ACD

Acute Treatment

62. The identification and avoidance of contact with the offending agent(s) are key to the success of ACD treatment. (A)
63. Topical palliative treatment may offer transient relief during the acute phases of ACD and ICD. (C)
64. TCs are first-line treatment for localized forms of ACD. (A)
65. Systemic corticosteroid therapy offers relief within 12 to 24 hours. (A)
66. Although TCs have been advocated for the treatment of ICD, several recent studies demonstrated that they are ineffective in suppressing experimental ICD induced by known irritants. (A)
67. Several topical T-cell selective inhibitors of inflammatory cytokines have been used successfully in treatment of atopic dermatitis, but their efficacy in ACD or ICD has not been established. (A)
68. Topical, and occasionally systemic, antibiotics should be used for secondary infections of ACD or ICD. (D)
69. Although antihistamines have been used for relief of pruritus associated with ACD, they are generally ineffective for this indication. (D)
70. Several nonspecific alternative treatment modalities are available for immunosuppression and/or long-term, refractory ACD. (C)
71. Patients should be instructed carefully about the causes and future risks of potential exposures to specific contactants. (D)

Prevention

Primary Prevention

72. In high-risk industries and professions, preventive surveillance programs are possible, especially for apprentices or newly hired workers. (A)

Secondary Prevention

73. Once the diagnosis of ACD or ICD is established, emollients, moisturizers, and/or barrier creams may be instituted as secondary prevention strategies for continued exposure. (C)

Prognosis

74. Long-term prognosis of ACD or ICD has only been adequately investigated in OCD. (C)
75. Persistent ACD has an appreciable effect on quality of life. (C)

Definitions:

Category of Evidence

Ia Evidence from meta-analysis of randomized controlled trials

Ib Evidence from at least one randomized controlled trial

IIa Evidence from at least one controlled study without randomization

IIb Evidence from at least one other type of quasi-experimental study

III Evidence from nonexperimental descriptive studies, such as comparative studies, correlation studies, and case-controlled studies

IV Evidence from expert committee reports, the opinions or clinical experiences of respected authorities, or both

LB Evidence from laboratory-based studies

Strength of Recommendation

1. Directly based on category I evidence
2. Directly based on category II evidence or extrapolated recommendation from category I evidence
3. Directly based on category III evidence or extrapolated recommendation from category I or II evidence
4. Directly based on category IV evidence or extrapolated recommendation from category I, II, or III evidence
5. Directly based on category LB evidence
6. Based on consensus of the Joint Task Force on Practice Parameters

None provided

The type of supporting evidence is identified and graded for each summary statement (see "Major Recommendations" field).

Appropriate management of patients with and at risk for contact dermatitis

Although antihistamines generally are not effective for pruritus, they are commonly used. Anecdotally, sedation from more soporific antihistamines may offer some degree of palliation. However, oral diphenhydramine (Benadryl) may be contraindicated in patients with contact dermatitis (CD) to Caladryl (diphenhydramine in a calamine base). The same caveat applies to administration of hydroxyzine hydrochloride (Atarax) in an ethylenediamine-sensitive patient.

This is a complete and comprehensive document according to current scientific standards. Medicine is a constantly changing discipline, and not all recommendations will be appropriate for all patients. Because this document incorporates the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official American Academy of Allergy, Asthma, and Immunology (AAAAI) or American College of Allergy, Asthma, and Immunology (ACAAI) interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

An implementation strategy was not provided.

Not applicable: The guideline was not adapted from another source.

These parameters were developed by the Joint Task Force on Practice Parameters representing the American Academy of Allergy, Asthma and Immunology; and the American College of Allergy, Asthma and Immunology.

Joint Task Force on Practice Parameters

Authors: Vincent S. Beltrani, MD; I. Leonard Bernstein, MD; David E. Cohen, MD; Luz Fonacier, MD

Co-Editors: Vincent S. Beltrani, MD, Associate Clinical Professor, Department of Dermatology, Columbia University, New York, NY, Visiting Professor, Department of Medicine, Division of Allergy & Rheumatology, University of Medicine & Dentistry of NJ, Newark, NJ; I. Leonard Bernstein, MD, Clinical Professor of Medicine and Environmental Health, Division of Immunology, Department of Internal Medicine, Co-Director, Allergy Research Laboratory, University of Cincinnati College of Medicine, Cincinnati, OH; David E. Cohen, MD, MPH, Director of Allergic, Occupational and Environmental Dermatology, Associate Professor, New York University School of Medicine, Clinical Instructor of Environmental Sciences, Columbia University School of Public Health, New York, NY; Luz Fonacier, MD, Associate Professor of Clinical Medicine, SUNY at Stony Brook, Head of Allergy, Winthrop University Hospital, Mineola, NY

Reviewers: Richard A. Nicklas, MD, Clinical Professor of Medicine, George Washington Medical Center, Washington, DC; Jay M. Portnoy, MD, Chief, Section of Allergy, Asthma & Immunology, The Children's Mercy Hospital, Professor of Pediatrics, University of Missouri-Kansas City School of Medicine, Kansas City, MO; Joann Blessing-Moore, MD, Clinical Associate Professor of Medicine and Pediatrics, Stanford University Medical Center, Department of Immunology, Palo Alto, CA; David A. Khan, MD, Associate Professor of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX; David M. Lang, MD, Head, Allergy/Immunology Section, Division of Medicine, Director, Allergy and Immunology Fellowship Training Program, Cleveland Clinic Foundation, Cleveland, OH; John Oppenheimer, MD, Department of Internal Medicine, New Jersey Medical School, Pulmonary and Allergy Associates, Morristown, NJ; Sheldon L. Spector, MD, Clinical Professor of Medicine, UCLA School of Medicine, Los Angeles, CA; Stephen A. Tilles, MD, Clinical Professor of Medicine, University of Washington School of Medicine, Redmond, WA; Dana V. Wallace, MD, Assistant Clinical Professor, Nova Southeastern University, Davie, FL

Not stated

This is the current release of the guideline.

Electronic copies: Available in Portable Document Format (PDF) from the Joint Council of Allergy, Asthma, and Immunology (JCAAI) Web site .

Print copies: Available from JCAAI, 50 N. Brockway, Ste 3-3 Palatine, IL 60067.

A sample patch test report and instruction sheet for patients are available in the appendix of the original guideline document .

None available

This NGC summary was completed by ECRI Institute on May 27, 2009. The updated information was verified by the guideline developer on July 9, 2009.

This NGC summary is based on the original guideline, which is subject to the guideline developer's copyright restrictions. This copyrighted material may only be used personally and may not be distributed further. All rights reserved. [Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol 2006 Sep;97(3 Suppl 2):S1-38.]