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Contact Dermatitis
Guangzhou, China. June 2019
China Medicine Education Association
Prof. Mario Sánchez Borges
Venezuela
Prof. J.A. Ortega Martell
México
Objectives
 Introduction
 Definition
 Epidemiology
 Pathogenesis
 Diagnosis / Diagnostic Criteria / Lab Findings
 Differential Diagnosis / Pediatric Issues
 Treatment
 Summary / Conclusions
Introduction
 Contact Dermatitis (CD):
 Occurs after direct or indirect contact with
substances that are harmful to the skin
 Irritant and allergic contact dermatitis are
the most common forms
 More than 4000 contact irritants and
allergens have been described
Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7.
Introduction
 Contact Dermatitis (CD):
 Should be considered in the differential diagnosis
of any patient presenting with a pruritic skin rash
with erythematous papules, vesicles, or
eczematous rash with crusted lesions.
 Chronic CD is associated with secondary skin
changes such as lichenification, fissuring,
thickening, and scaling.
Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8
Introduction
Contact Dermatitis
Classification
Contact Dermatitis
Irritant Allergic
Contact
Urticaria
Photocontact
Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421
Classification
Definition
 Irritant Contact Dermatitis:
 It does not require prior sensitization, but rather is
caused by direct damage to keratinocytes by an
irritating substance (e.g., an alkaline or acidic chemical).
 This leads to a localized release of
proinflammatory cytokines and the subsequent
development of an eczematous dermatitis
Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421
Definition
Definition
 Allergic Contact Dermatitis:
 Type IV (delayed) hypersensitivity reaction, which
requires a prior sensitization, and elicitation
 Allergic contact dermatitis in children is increasing
 Sensitization to contact allergens may already
begin at an early age
 Patch testing is the gold standard diagnostic test
Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421
Definition
Epidemiology
 The data on prevalence of contact allergy
among children visiting dermatology clinics
vary between 15% and 71%.
 Nevertheless, the true prevalence of
sensitization continues to be grossly
underreported because of deficiencies in
reporting and tracking.
Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7.
Epidemiology
Epidemiology
 The most common contact allergens in
children are:
 metals (nickel, cobalt, and chromate)
 fragrances
 preservatives
 neomycin
 rubber chemicals
 p-tert-butylphenol-formaldehyde resin
de Waard-van der Spek et al. Pediatric Allergy and Immunology 24 (2013) 321–329
Epidemiology
Allergen Common Source of Exposure Positive Rate of Patch Test (%)
Nickel Jewelry, metal items, coins 19.0
Balsam of Peru Fragrances, spices 11.9
Fragrance mix Fragrances 11.5
Quaternium 15 Preservative 10.3
Neomycin Topical antibiotic 10.0
Bacitracin Topical antibiotic 9.2
Formaldehide Preservative 2.0
Cobalt chloride Metal 8.4
Methyldibromoglutaronitrile/
phenoxyethanol
Preservative 5.8
p-Phenylenediamine Permanent hair dye 5.0
Potassium dichromate Metallic salt in wet cement
and leather
4.8
Carba mix Rubber accelerator 3.9
Thiuram mix Rubber accelerator 3.9
Diazolidinylurea Preservative 3.7
2-Bromo-2-nitropropane-1,3-diol Preservative 3.4
Pathogenesis
 Allergic contact dermatitis (ACD) results from a biphasic,
delayed (type IV) hypersensitivity reaction comprising
primary sensitization and secondary elicitation:
Non
Sensitized
Sensitization Elicitation
Allergen
(hapten + carrier)
Allergen
(hapten + carrier)
Pathogenesis
Pathogenesis
 The sensitization phase is characterized by an
exogenous allergen entering the epidermis through
an impaired skin barrier.
 These allergens then bind with selfproteins to
create complete antigens that are taken up and
presented by dendritic cells on the cell surface
with major histocompatibility complexes (MHC).
Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421
Pathogenesis
Pathogenesis
 The elicitation phase occurs upon repeated
exposure to the allergen at which time a clinical
dermatitic response occurs.
 The repeated exposure can occur trans-
epidermally or systemically through ingestion,
inhalation, or intravenous entry.
Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421
Pathogenesis
PathogenesisPathogenesis
Sensitization
phase
Elicitation
phase
Pathogenesis
Direct cutaneous
exposure to
allergens/haptens
(lipophilic molecules
of < 500 Daltons)
Migration and
maturation of
dendritic cells
Dendritic cells
interact with T
lymphocytes
Diffusion of allergens/haptens
into the skin and activation of
sensitized T lymphocytes
(Th1, Tc, Th17, Th22, Th9)
Pathogenesis
Pathogenesis
 APC  Th1  Mf  Inflammation
 APC  Th17  Neu  Inflammation
Pathogenesis
TissueDamage
Pathogenesis
 Tc lymphocyte dependent cell cytotoxicity
 APC  Th1  Tc  Apoptosis, Necrosis
Pathogenesis
Tissue Damage
Diagnosis
 Allergic Contact Dermatitis classically presents as a
localized, erythematous, eczematous eruption,
often with geometric or linear patterns
corresponding to sites of contact with the allergen.
 The location of the reaction can be a useful clue
about the inciting allergen, especially when the
presentation is limited.
Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7.
Diagnosis
Diagnosis
GoldenbergA,etal.JAllergyClinImmunolPract
2015;3:661-7.
Diagnosis
Diagnosis
 Epicutaneous patch testing is the criterion
standard for the diagnosis of ACD:
 Remove patch at 48 Hours
 Interpret Results at 72 and 96 Hours
Diagnosis
Diagnosis
 Patch Testing:
 Panels with common contact allergen components
Diagnosis
DiagnosisDiagnosis
DiagnosisDiagnosis
DiagnosisDiagnosis
Patch TestPatch test
Patch TestPatch test
Patch TestPatch test
Patch TestPatch test
Patch TestPatch test
Differential Diagnosis
 Allergic vs Irritant Contact Dermatitis
Differential Dx
Differential Diagnosis
 Patch test interpretation
Differential Dx
Differential Diagnosis
• Personal or family history of atopy, Early age
of onset, Chronic and recurrent, Dry, scaly,
very pruritic,Typical distribution: Facial in
infancy, Extensors in early childhood, Flexural
areas in adolescents and adults
Atopic
dermatitis
• Distribution in areas with sebaceous glands:
scalp, periauricular, face (medial eyebrows,
glabella, nasolabial folds), presternal trunk,
interscapular ; Distinctive morphology: dull,
yellowish-red, sharply demarcated lesions
covered with greasy-looking scales
Seborrheic
dermatitis
Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8
Differential Dx
Differential Diagnosis
• Small (1-2 mm) vesicles, deep seated on
nonerythematous base “tapioca” like,
Palms, soles, and/or lateral fingers, often
symmetrical; Intensely pruritic and itching
prodrome; Persists for 2 to 3 wk, then
resolves by involution and desquamation
Dyshidrotic
eczema
• Plaques typically have dry, thin, silvery-
white scale, Auspitz sign: removing scale
reveals a smooth, red, glossy membrane
with tiny punctate bleeding
Psoriasis
Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8
Differential Dx
Treatment
 Topical corticosteroids are usually sufficient
 short-term systemic steroids: more severe dermatitis
 antibiotics occassionally needed
 Irritants - avoid while healing
 Avoidance measures
 don’t forget substances that cross-react
 find substitutes for necessary products
 skin protection to prevent repeat exposure
Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8
Treatment
Summary/Conclusions
 Allergic CD common problem in children
 Age-appropriate history is key to dx
 Potential sensitizers are in diapers, hygiene
products, cosmetics, sun blocks, textiles and dyes,
medications, tattoos and sporting accessories
 Patch testing sometimes needed
 Treatment: corticosteroids acutely, and then
avoidance measures
Summary / Conclusions
THANK YOU
Guangzhou, China. June 2019
Questions?

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Contact dermatitis - Prof. Ortega Martell - Prof. Sánchez-Borges

  • 1. Contact Dermatitis Guangzhou, China. June 2019 China Medicine Education Association Prof. Mario Sánchez Borges Venezuela Prof. J.A. Ortega Martell México
  • 2. Objectives  Introduction  Definition  Epidemiology  Pathogenesis  Diagnosis / Diagnostic Criteria / Lab Findings  Differential Diagnosis / Pediatric Issues  Treatment  Summary / Conclusions
  • 3. Introduction  Contact Dermatitis (CD):  Occurs after direct or indirect contact with substances that are harmful to the skin  Irritant and allergic contact dermatitis are the most common forms  More than 4000 contact irritants and allergens have been described Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7.
  • 4. Introduction  Contact Dermatitis (CD):  Should be considered in the differential diagnosis of any patient presenting with a pruritic skin rash with erythematous papules, vesicles, or eczematous rash with crusted lesions.  Chronic CD is associated with secondary skin changes such as lichenification, fissuring, thickening, and scaling. Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8 Introduction
  • 6. Classification Contact Dermatitis Irritant Allergic Contact Urticaria Photocontact Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421 Classification
  • 7. Definition  Irritant Contact Dermatitis:  It does not require prior sensitization, but rather is caused by direct damage to keratinocytes by an irritating substance (e.g., an alkaline or acidic chemical).  This leads to a localized release of proinflammatory cytokines and the subsequent development of an eczematous dermatitis Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421 Definition
  • 8. Definition  Allergic Contact Dermatitis:  Type IV (delayed) hypersensitivity reaction, which requires a prior sensitization, and elicitation  Allergic contact dermatitis in children is increasing  Sensitization to contact allergens may already begin at an early age  Patch testing is the gold standard diagnostic test Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421 Definition
  • 9. Epidemiology  The data on prevalence of contact allergy among children visiting dermatology clinics vary between 15% and 71%.  Nevertheless, the true prevalence of sensitization continues to be grossly underreported because of deficiencies in reporting and tracking. Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7. Epidemiology
  • 10. Epidemiology  The most common contact allergens in children are:  metals (nickel, cobalt, and chromate)  fragrances  preservatives  neomycin  rubber chemicals  p-tert-butylphenol-formaldehyde resin de Waard-van der Spek et al. Pediatric Allergy and Immunology 24 (2013) 321–329 Epidemiology
  • 11. Allergen Common Source of Exposure Positive Rate of Patch Test (%) Nickel Jewelry, metal items, coins 19.0 Balsam of Peru Fragrances, spices 11.9 Fragrance mix Fragrances 11.5 Quaternium 15 Preservative 10.3 Neomycin Topical antibiotic 10.0 Bacitracin Topical antibiotic 9.2 Formaldehide Preservative 2.0 Cobalt chloride Metal 8.4 Methyldibromoglutaronitrile/ phenoxyethanol Preservative 5.8 p-Phenylenediamine Permanent hair dye 5.0 Potassium dichromate Metallic salt in wet cement and leather 4.8 Carba mix Rubber accelerator 3.9 Thiuram mix Rubber accelerator 3.9 Diazolidinylurea Preservative 3.7 2-Bromo-2-nitropropane-1,3-diol Preservative 3.4
  • 12. Pathogenesis  Allergic contact dermatitis (ACD) results from a biphasic, delayed (type IV) hypersensitivity reaction comprising primary sensitization and secondary elicitation: Non Sensitized Sensitization Elicitation Allergen (hapten + carrier) Allergen (hapten + carrier) Pathogenesis
  • 13. Pathogenesis  The sensitization phase is characterized by an exogenous allergen entering the epidermis through an impaired skin barrier.  These allergens then bind with selfproteins to create complete antigens that are taken up and presented by dendritic cells on the cell surface with major histocompatibility complexes (MHC). Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421 Pathogenesis
  • 14. Pathogenesis  The elicitation phase occurs upon repeated exposure to the allergen at which time a clinical dermatitic response occurs.  The repeated exposure can occur trans- epidermally or systemically through ingestion, inhalation, or intravenous entry. Admani S, Jacob SE. Curr Allergy Asthma Rep (2014) 14:421 Pathogenesis
  • 16. Pathogenesis Direct cutaneous exposure to allergens/haptens (lipophilic molecules of < 500 Daltons) Migration and maturation of dendritic cells Dendritic cells interact with T lymphocytes Diffusion of allergens/haptens into the skin and activation of sensitized T lymphocytes (Th1, Tc, Th17, Th22, Th9) Pathogenesis
  • 17. Pathogenesis  APC  Th1  Mf  Inflammation  APC  Th17  Neu  Inflammation Pathogenesis TissueDamage
  • 18. Pathogenesis  Tc lymphocyte dependent cell cytotoxicity  APC  Th1  Tc  Apoptosis, Necrosis Pathogenesis Tissue Damage
  • 19. Diagnosis  Allergic Contact Dermatitis classically presents as a localized, erythematous, eczematous eruption, often with geometric or linear patterns corresponding to sites of contact with the allergen.  The location of the reaction can be a useful clue about the inciting allergen, especially when the presentation is limited. Goldenberg A, et al. J Allergy Clin Immunol Pract 2015;3:661-7. Diagnosis
  • 21. Diagnosis  Epicutaneous patch testing is the criterion standard for the diagnosis of ACD:  Remove patch at 48 Hours  Interpret Results at 72 and 96 Hours Diagnosis
  • 22. Diagnosis  Patch Testing:  Panels with common contact allergen components Diagnosis
  • 31. Differential Diagnosis  Allergic vs Irritant Contact Dermatitis Differential Dx
  • 32. Differential Diagnosis  Patch test interpretation Differential Dx
  • 33. Differential Diagnosis • Personal or family history of atopy, Early age of onset, Chronic and recurrent, Dry, scaly, very pruritic,Typical distribution: Facial in infancy, Extensors in early childhood, Flexural areas in adolescents and adults Atopic dermatitis • Distribution in areas with sebaceous glands: scalp, periauricular, face (medial eyebrows, glabella, nasolabial folds), presternal trunk, interscapular ; Distinctive morphology: dull, yellowish-red, sharply demarcated lesions covered with greasy-looking scales Seborrheic dermatitis Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8 Differential Dx
  • 34. Differential Diagnosis • Small (1-2 mm) vesicles, deep seated on nonerythematous base “tapioca” like, Palms, soles, and/or lateral fingers, often symmetrical; Intensely pruritic and itching prodrome; Persists for 2 to 3 wk, then resolves by involution and desquamation Dyshidrotic eczema • Plaques typically have dry, thin, silvery- white scale, Auspitz sign: removing scale reveals a smooth, red, glossy membrane with tiny punctate bleeding Psoriasis Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8 Differential Dx
  • 35. Treatment  Topical corticosteroids are usually sufficient  short-term systemic steroids: more severe dermatitis  antibiotics occassionally needed  Irritants - avoid while healing  Avoidance measures  don’t forget substances that cross-react  find substitutes for necessary products  skin protection to prevent repeat exposure Bernstein D. J Allergy Clin Immunol Pract 2015;3:652-8 Treatment
  • 36. Summary/Conclusions  Allergic CD common problem in children  Age-appropriate history is key to dx  Potential sensitizers are in diapers, hygiene products, cosmetics, sun blocks, textiles and dyes, medications, tattoos and sporting accessories  Patch testing sometimes needed  Treatment: corticosteroids acutely, and then avoidance measures Summary / Conclusions