Contact dermatitis

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Contact dermatitis

  1. 1. Contact dermatitis<br />Boonthorn<br />23 June 2010<br />
  2. 2. Definition<br />Classification<br />Epidemiology<br />Pathology & Pathophysiology<br />Clinical presentation & Differential diagnosis<br />Investigation<br />Special exposure associated with CD<br />management<br />Outline <br />
  3. 3. Common inflammatory skin disorder<br />Most common recognized as eczematous inflammation<br />Allergic or irritant skin reaction caused by an external agent<br />Definition<br />J Allergy ClinImmunol 2010;125:S138-49.<br />Allergy 2009:64:1669-1714.<br />
  4. 4. Allergic contact dermatitis (ACD) (20%)<br />inflammation caused by allergen-specific T lymphocytes. rapid development of dermatitis occurs following re-exposure to low concentrations of allergen, not cause lesions in non-sensitized individuals<br />Irritant contact dermatitis (ICD) (80%)<br />develop following prolonged and repeated exposure to irritants<br />inflammatory cells have role in development of dermatitis<br />allergen-specific lymphocytes not involved in pathogenesis <br />prior sensitization is not necessary<br />Classification <br />www.worldallergy.org<br />
  5. 5. In U.S. (2004)<br />overall prevalence rate 24,400 /100,000 people<br />Cohort population-based studies in Europe<br />prevalence rates 0.7% - 18.6% for ACD<br />Incidence of OCD in other countries 1.3 - 19 cases per 10,000<br />All age groups are affected with slight female preponderance<br />prevalence increases with age<br />decreased prevalence in patients >70 years<br />Epidemiology <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  6. 6. Pathology <br />epidermal hyperplasia with spongiosis and mounds of parakeratosis.<br />There is superficial, perivascular infiltrate of lymphocytes and eosinophils with exocytosis<br />
  7. 7. inflammation in epidermis and superficial dermis<br />Acute<br />superficial perivascular infiltration with lymphocytes, monocytes and small number of eosinophils<br />increased intercellular spaces between keratinocytes (spongiosis):predominant histologic feature of CD<br />Chronic <br />thickening of epidermis, irregular elongation of the rete ridges and vertical thickening of collagen of papillary dermis <br />Pathology <br />WWW.worldallergy.org<br />
  8. 8. ACD<br />prototype of type IV cell-mediated hypersensitivity reaction<br />ICD <br />nonimmunologic, multifactorial, direct tissue reaction<br />T cells activated by nonimmune, irritant, or innate mechanisms release proinflammatory cytokines<br />dose-dependent inflammation <br />ACD and ICD frequently overlap because many allergens at high enough oncentrationscan also act as irritants<br />Pathophysiology<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  9. 9. Pathophysiology (ACD) <br />Allergy 2009: 64: 1699–1714.<br />
  10. 10. Pathophysiology (ACD)<br />Allergy 2009: 64: 1699–1714.<br />
  11. 11. Keratinocytes play key role in development of both ACD and ICD<br />synthesize and release pro-inflammatory cytokines, in particular interleukins IL-1, 6 and 8, TNF-α and GM-CSF<br />These cytokines play important part in recruitment and homing of inflammatory cells and can be induced and released from keratinocytes by both irritants and allergens<br />role of keratinocyte<br />
  12. 12. Langerhans cells are primary APCs of epidermis<br />cell surface expression of CD1a and presence of intracytoplasmicBirbeckgranules<br />process protein Ag by cleaving them into peptides and present fragments in peptide-binding groove of their surface located MHC class II<br />Hapten-conjugated LC migrate to local LN where they present allergen to T lymphocytes<br />T lymphocytes must then home to inflamed skin <br />Antigen presentation: The role of Langerhanscell<br />
  13. 13. Homing is process whereby circulating cells migrate to relevant sites<br />This process relies on linkage between adhesion molecules expressed on endothelial cells and their ligands expressed on lymphocytes<br />homing receptor on T lymphocytes probably "cutaneous lymphocyte antigen" (CLA), ligandfor E-selectin<br />Additional adhesion molecule <br />ICAM-1 interacts with LFA-1<br />VCAM-1 interacts with VLA-4<br />Homing of T lymphocytes<br />
  14. 14. Classic presentation <br />pruritic, eczematous plaque localized to site of allergen exposure<br />redness, edema,papules, vesiculation, weeping, crusting<br />Geometric or linear patterns or involvement of unusual focal skin areas, eg. earlobes, or weight-bearing areas of feet may suggest contact cause<br />Chronic ACD (i.e. nickel and fragrances) can be insidious and present as localized lichenification or with more generalized reactions<br />Clinical presentation<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006<br />
  15. 15. Differentiation between ICD and ACD<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  16. 16. J Allergy ClinImmunol 2010;125:S138-49.<br />
  17. 17. Exogenous causes of ICD in Occupational Dermatology Clinic, Skin and Cancer Foundation, Australia (total 621 patients over the period 1993–2002)<br />Australasian Journal of Dermatology (2008) 49, 1–11<br />
  18. 18. Differential diagnosis<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006<br />
  19. 19. Differential diagnosis<br />Best practice<br />
  20. 20. Physical examination<br />Current Opinion in Pediatrics 2009, 21:491–498<br />
  21. 21. Patch tests<br />gold standard for identification of contact allergen<br />occlusive patch testing is most common technique<br />Patch testing a patient with active AD more likely to produce “angry back” reaction, resulting in a false-positive reading<br />affected by <br />oral corticosteroids (>20 mg of prednisone per day or its equivalent)<br />cancer chemotherapy, or immunosuppressive drugs<br />Topical corticosteroids should be discontinued for 5 to 7 days before patch testing<br />not affected by antihistamines<br />Investigation <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  22. 22. Sources of allergens<br />T.R.U.E. TEST :not US FDA approved<br />But recommended by CD experts<br />No. of allergens<br />ideal number remains controversial<br />T.R.U.E. Test contains 29 allergens<br />higher false-negative reactions to neomycin, thiurammix, balsam of Peru, fragrance mix, cobalt, and lanolin<br />NACDG series from 65 to 70 allergens<br />use of FDA-certified antigen panel available in US can fully evaluate ~ 25- 30% of ACD<br />Investigation <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  23. 23. Current Opinion in Pediatrics 2006, 18:385–390<br />
  24. 24. applied to upper or middle back areas (2.5 cm lateral to midspinalreference point) free of dermatitis and hair<br />kept in place for 48 hours<br />read 30 minutes after removal of patches <br />second reading should be done 3 to 5 days after initial application <br />Metals , topical antibiotics , topical orticosteroids, and PPD can elicit positive reactions after 7 days<br />Nonstandardized patch tests tested at 1:10 to 1:100 dilutions<br />Patch test technique<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  25. 25. ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006<br />
  26. 26. Repeat open application test (ROAT)<br />Improving reliability of interpreting tests for leave-on products<br />suspected allergens are applied to antecubitalfossa twice daily for 7 days and observed for dermatitis<br />absence of reaction makes CD unlikely<br />If eyelid dermatitis is considered, ROAT can be performed on back of ear<br />dimethyl-glyoximetest for nickel<br />identification of allergens<br />Skin biopsy<br />Distinguishing CD from morphologically similar diseases<br />Investigation <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  27. 27. localized or generalized inflammatory skin disease in contact-sensitized individuals exposed to hapten orally, transcutaneously, intravenously, or by means of inhalation<br />Cause<br />Metal (cobalt, copper, chromium, gold, mercury, nickel, and zinc)<br />Medicationscorticosteroids, antihistamines (diphenhydramine, ethylenediamine, hydroxyzine, and doxepin), miconazole, terbinafine, neomycin,gentamicin, erythromycin, pseudoephedrine, benzocaine, tetracaine, oxycodone, IVIG, aminopenicillins, 5-aminosalicylic acid, naproxen, allopurinol, mitomycinC, 5-FU<br />Herbal medicine<br />Systemic contact dermatitis<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  28. 28. Symmetric drug-related intertriginous and flexural exanthema<br />Criteria for diagnosis :<br />exposure to systemic drug at first or repeated dosing (contact allergens excluded)<br />erythemaof gluteal/perianalarea, V-shaped erythemaof inguinal/perianalarea, or both<br />involvement of at least 1 other intertriginous/flexural localization<br />symmetry of affected areas<br />absence of systemic signs and symptoms<br />Drug induced SCD <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  29. 29. Second most common type of occupational disease<br />In 1999, incidence rate of occupational skin disorders was 49 cases per 100,000<br />most common occupations associated with OCD are health professionals (especially nurses), food processors, beauticians and hairdressers, machinists,andconstruction workers<br />Occupational contact dermatitis<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  30. 30. 4 of 7 criteria must be positive to conclude OCD<br />clinical appearance is consistent with CD<br />cutaneousirritants or allergens are present in workplace<br />anatomic distribution of dermatitis is consistent with skin exposure to chemicals in course of various job tasks<br />temporal relationship between exposure and onset of symptoms is consistent with CD<br />nonoccupationalexposures are excluded as probable causes of dermatitis<br />dermatitis improves away from work exposure and reexposure causes exacerbation<br />there are positive-reaction and relevant patch tests performed according to established guidelines<br />Occupational contact dermatitis<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  31. 31. Toxicodendron dermatitis (poison ivy) is most common form of ACD and can be readily identified by its streak-like or linear papulovesicularpresentation<br />caused by urushiol, which is found in saps of this plant family<br />Urushiol contained in mango skin,cashewnut oil, ginkgo (female) leaves, Japanese lacquer, and Indian marking ink<br />Plant dermatitis<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  32. 32. Allergic contact dermatitis to poison ivy (toxicodendronradicans). Note the linear lesions induced by contact with branches<br />www.worldallergy.org<br />
  33. 33. Current Opinion in Pediatrics 2006, 18:385–390<br />
  34. 34. Current Opinion in Pediatrics 2009, 21:491–498<br />
  35. 35. Metals<br />Nickel<br />NACDG reported 18.7% of patients evaluated for ACD had positive patch test reaction to nickel<br />Female sensitization to nickel higher because of increased ear piercing<br />1% of nickel allergy have systemic reactions to nickel content of normal diet<br />Foods with higher nickel content include soybean, fig, cocoa, lentil, cashew, nuts, and raspberry<br />SELECTED CONTACT ALLERGENS<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  36. 36. Allergic contact dermatitis to nickel in watchband<br />
  37. 37. Allergic contact dermatitis to nickel in earring<br />
  38. 38. Allergic contact dermatitis to nickel in belt buckle<br />Current Opinion in Pediatrics 2006, 18:385–390<br />
  39. 39. Gold<br />NACDG reported that 389/4101(9.5%) had positive patch test reactions to gold<br />hands (29.6%); face, with seborrheic distribution (19.3%); and eyelids (7.5%)<br />mostly used for fashion appeal, anti-inflammatory medication, used in electroplating industry, part of dental appliances (present with oral symptoms)<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  40. 40. Common allergens in these products include fragrances, preservatives, excipients, glues, and sun blocks<br />Fragrance<br />most common cause of ACD from cosmetics <br />results in positive patch test reactions in 10.4% of patients<br />‘‘unscented’’ and ‘‘Fragrance-free’’<br />Fragrance mix I containsallergensfoundin 15% to 100% of cosmetic products and might detect ~85% of subjects with fragrance allergy<br />positive patch test reaction to fragrance must correlate with distribution of dermatitis and evaluation of clinical relevance, eg. positive ROAT reaction<br />Cosmetics<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  41. 41. Preservatives and excipients<br />Lanolin : common component of consumer products<br />It is weak sensitizer on normal skin but a stronger sensitizer on damaged skin<br />stasis dermatitis, are at higher risk of lanolin sensitivity<br />Cosmetic preservatives <br />Formaldehyde releasers <br />non–formaldehyde releasers : Parabenmost commonly used preservative in cosmetics, as well as in pharmaceutical and industrial products<br />Type I immediate hypersensitivity reactions (contact urticaria) and SCD from ingestion of paraben-containing medications or foods have been reported<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  42. 42. Hair products<br />Second most common cause of cosmetic allergy<br />PPD(Paraphenylenediamine) is most common cause of CD in hairdressers<br />In hair dye users the dermatitis often spares the scalp and usually involves the face near the hairline, eyelids, and neck<br />PPD cross-reacts with COX-2 inhibitor (celecoxib), sunscreens, and antioxidants used in manufacture of rubber products<br />New hair dyes that contain FD&C and D&C dyes have very low levels of cross-reactivity with PPD<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  43. 43. Allergic dermatitis from black leather watch band. Possible allergens include chromates used to tan leather and paraphenylenediaminedye<br />www.worldallergy.org<br />
  44. 44. CAPB ( Cocoamidopropylbetaine)<br />amphotericsurfactant often found in shampoos, bath products, and eye and facial cleaners<br />CAPB allergy typically presents as eyelid, facial, scalp, and/or neck dermatitis<br />Glycerol thioglycolate<br />active ingredient in permanent wave solution<br />Unlike PPD, thioglycolatesmight remain allergenic in hair long after it has been rinsed out<br />skin eruptions can continue for weeks after application of permanent wave solution<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  45. 45. Antibiotics and antiseptics<br />Neomycin and nitrofurazone are potent sensitizers<br />Neomycin sulfate can cross-sensitize with gentamicin, kanamycin, streptomycin, spectinomycin, tobramycin,andparomomycin<br />Medications<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  46. 46. corticosteroid<br />0.2-6%<br />Patients with worsening of previous dermatitis or initial improvement followed by deterioration of dermatitis after application of corticosteroids should be evaluated <br />Cross-reactivity between groups A and D2 and groups B and D2 also has been reported<br />optimal patch test concentration not worked out for most corticosteroids<br />30% of ACD to corticosteroids be missed if delayed 7-day reading not done<br />Medications<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  47. 47. Current Opinion in Pediatrics 2009, 21:491–498<br />
  48. 48. Allergic contact dermatitis to topical steroid preparation applied to hands. Note massive edema, erythema, and sparing of skin under watch band<br />www.worldallergy.org<br />
  49. 49. use of nickel in biomedical devices,ledto increasing concern about safety in suspected nickel-sensitized patients<br />Presently,highvariability of care <br />no large, evidence-based guidelines<br />10 patients with positive patch test reaction to metal had in-stent restenosis associated with clinical symptoms <br />allergy to metals,plays relevant role in inflammatory fibroproliferativerestenosis<br />CD Due to Surgical Implant Devices<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  50. 50. criteria for diagnosis of cutaneousimplant–induced reaction<br />dermatitis (localized or generalized) appearing after implant surgery<br />persistent dermatitis that is resistant to appropriate therapies<br />positive patch test result proven history to metallic component of implant or to commonly used acrylic glues<br />resolution of dermatitis after removal of implant<br />CD Due to Surgical Implant Devices<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  51. 51. Allergen identification to improve contact avoidance<br />Alternatives and substitutes to cosmetics should be offered to patient to increase compliance<br />supportive care and relief of pruritus, cold compresses with water or saline, Burrow solution , calamine, and colloidal oatmeal baths might help acute oozing lesions<br />Excessive handwashing should be discouraged in hand dermatitis, and nonirritating or sensitizing moisturizers must be used after washing<br />Treatment <br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  52. 52. TC is first-line treatment for ACD<br />For extensive(>20% BSA) and severe CD, systemic corticosteroids might offer faster relief (12-24hr)<br />recommended dose is 0.5 to 1 mg/kg daily for 5 to 7 days, and only if patient is comfortable at that time is dose reduced by 50% for next 5 to 7 days<br />Treatment<br />J Allergy ClinImmunol 2010;125:S138-49.<br />
  53. 53. topical T-cell selective inhibitors <br />efficacy in ACD or ICD not been established<br />antibiotics should be used for secondary infections of ACD or ICD<br />antihistamines have been used for relief of pruritus associated with ACD, generally ineffective <br />diphenhydraminenot be used in patients with ACD to Caladryl and hydroxyzine hydrochloride in ethylenediamine-sensitive patient<br />Other modes of therapy : UV light treatment and immunomodulating agents, eg.MTX,AZA, and MMF<br />Treatment<br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  54. 54. Primary prevention<br />In high-risk industries and professions, preventive surveillance programs are possible, especially for apprentices or newly hired workers<br />Secondary prevention<br />Once diagnosis of ACD or ICD is established, emollients, moisturizers, and/or barrier creams may be instituted <br />Prevention <br />ANNALS OF ALLERGY, ASTHMA & IMMUNOLOGY, VOLUME 97, SEPTEMBER, 2006 <br />
  55. 55. ICD is caused by direct toxicity without prior sensitisation and ACD is delayed hypersensitivity reaction <br />Results in localised burning, stinging, itching, blistering, redness and swelling at area of contact with allergen or irritant. <br />Patch testing may aid identification of offending agent<br />Skin biopsy may also be helpful<br />Treatment involves removal of offending agent, future avoidance of offending agent, topical corticosteroids and/or short course of oral corticosteroids. <br />Conclusion <br />

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