1. Consultant, Section of Dermatology The Medical City Hospital
ECZEMAS
Cecilia T. Roxas-Rosete, FPDS
Consultant, Section of Dermatology
The Medical City Hospital

2. ECZEMA Inflammatory Skin Disorder
Greek word ek – zeo “to boil or bubble over”

3. Tiny bubbles in between epidermal cells under the microscope.

4. Erythema Papules Vesicles Pustules Oozing Crusts Scales Regression
This is an algorithmn showing the evolution of skin lesions in CD and even all other eczemas in general. Almost all lesions of CD start w/ erythema or redness of the skin due to dilatation of dermal blood vessels. When the cause is eliminated early, the disease takes a subacute course, the erythema subsides & is superseded by fine scaling which persists for some time b4 healing. However, if the cause persists, it goes through all these stages the first one being the acute stage characterized by the formation of tiny papulovesicles.
Scales
Regression
Progression
Healing
Chronic eczema

5. A PEODG and SP Dermatology Exclusive
Acute Eczema
In severe case, these tiny papulovesicles coalesced or form into groups forming large blisters or bullae. These in turn may form 2dary bacterial infection leading to pustule formation & some cellulitic inflammation.
Series 2007
A PEODG and SP Dermatology Exclusive

6. When these vesicles, bullae & pustules rupture, they produce areas of denudation & erosion. Solidification of the exudates forms crusting which gets sloughed off after sometime to form fine scaling before healing.

7. A PEODG and SP Dermatology Exclusive
Chronic Eczema
However, if the cause becomes too persistent, the disorder progresses to chronic eczema characterized by extreme dryness, coarseness & lichenification or thickening of the skin 2dary to constant rubbing or scratching.
Series 2007
A PEODG and SP Dermatology Exclusive

9. EPIDEMIOLOGY
Atopic dermatitis (AD) is a chronically relapsing skin disorder that arises most commonly during early infancy, childhood or adolescence
Usually begins before age 6 months
Remits spontaneously in 65% of affected children before age 10 years

10. EPIDEMIOLOGY:
STAGES
Infantile – 2 months to 2 yrs.
Childhood – 2 to 10 yrs.
Adulthood

11. ETIOLOGY & PATHOGENESIS
Unknown
Triggered by an interplay of factors
Genetic
Immunologic
Environmental

12. Hanifin &Rajka’s Diagnostic Criteria for Atopic Dermatitis Must have > 3 major criteria & > 3 minor criteria
Major Criteria:
Pruritus
Personal or family history of atopic disorders (asthma, atopic eczema, allergic rhinitis)
Chronic or chronically relapsing course
Typical distribution and morphology
> infants: facial and extensor involvement
> children & adults: flexural lichenification and linearity

18. Hanifin & Rajka’s Diagnostic Criteria for Atopic Dermatitis
Minor Criteria:
Xerosis
Icthyosis/keratosis pilaris/palmar hyperlinearity
Type I skin test reactivity
Elevated serum IgE
Early age at onset
Tendency to skin infection (Staph aureus & HS I)
Hand / foot dermatitis

23. Hanifin & Rajka’s Diagnostic Criteria for Atopic Dermatitis
Minor Criteria:
Nipple eczema
Cheilitis / conjunctivitis / keratoconus / ant. subscapular cataracts
Dennie-Morgan fold
Orbital darkening
Pityriasis alba

28. Hanifin & Rajka’s Diagnostic Criteria for Atopic Dermatitis
Minor Criteria:
Itch when sweating
Intolerance to wool and lipid solvents
Food intolerance
Perifollicular accentuation
White dermographism / delayed blanching
Course influenced by environmental/emotional factors

31. Triggering Factors in Atopic Dermatitis
Contact irritants and allergens
Aeroallergens – house dust mites,pollens and molds
Foods – egg, milk, peanuts, fish, wheat and shellfish
Microbial organisms – Staph. aureus, URTI, Candida
Hormones
Stress
Climate

32. SEBORRHEIC DERMATITIS
common chronic skin disorder
infants / adults
often assoc with increased sebum production (seborrhea) of face & scalp
2-5% of the population
affects males > females
often assoc with HIV (85%), parkinsonism

33. Etiology – Inflammatory Rx to yeast (Pityrosporum Ovale)
Sites: Face, ears, scalp, upper trunk
Infants – Cradle Cap
Adults – Dandruff (scalp, eyebrows)
Skin: “greasy” yellowish scales on a red base

34. Seborrheic Dermatitis

38. Nummular Eczema discrete coin-shaped pruritic lesion
erythematous, vesicular, crusted patches
assoc with emotional stress
sites – legs, arms, dorsum of hands

41. Dyshidrotic eczema

44. Lichen simplex chronicus

45. CONTACT DERMATITIS
Any pruritic skin disorder that results when a particular substance comes in contact with the skin
Inflammation of the skin with spongiosis or intercellular edema of the epidermis
A common cause of occupational disability
A form of extrinsic eczema
Contact dermatitis is a pruritic skin disorder that results when a particular substance comes in contact with the skin. In general, CD is a form of an eczema particularly the extrinsic kind caused by external factors rather than by endogenous factors or those that come intrinsically from within our body.The word eczema comes from the Greek word “ek-zeo” which means to boil or bubble over suggesting the reactive inflammatory nature of this skin disorder. If you take a skin biopsy of a lesion of contact dermatitis, what you see would be histologic findings of spongiosis or intercellular edema of the epidermis which would look literarily like NSP …

46. Contact Dermatitis: Prevalence
General population: 1.5% - 5.4%
Important cause of disability in occupational and personal life
Accounts for about 20% of all dermatological consultations
Accounts for majority of all occupational skin diseases
The prevalence of CD in the general population has been variously estimated at between 1.5% and 5.4%. It is an important cause of disability in both occupational and personal life since they are very recurrent especially if the cause has not been identified which is the situation in majority of cases.

47. 2 Types (Contact Dermatitis)
Irritant CD – Skin reaction resulting from exposure to an offending agent.
- immediate Rx
- Acids, alkali, detergents
2. Allergic CD – results from repeated exposure to an allergen or compound due to DELAYED hypersensitivity RX
days

48. IRRITANT CONTACT DERMATITIS
Severity of the reaction is related to the amount and duration of exposure to the irritant.
Most cases are acute in onset - symptoms develop within seconds of exposure.
Prolonged exposure to a low-level irritant (soap, water) can lead to chronic ICD.
Most common site: hand.
Irritants maybe mild & strong. Mild irritants such as soap & detergents seem to gradually overwhelm the barrier of the skin & its repair function causing cumulative irritant reactions over time. Naturally,occupations at high risk for this type of low-level irritancy would be those whose work entails frequent handwashing like housewives, laundrywomen, medical professionals like us doctors, nurses & dentists & those in the food industry like the chefs, waitresses & bartenders.

49. Irritant Contact Dermatitis: Mild Irritant (Acute)
This is a clinical picture of ICD caused by a mild irritant which is Papaya soap. Prolonged and frequent exposure to alkaline based detergents result to disruption of the epidermal lipid layer leading to an increase in TEWL and eventually to skin dryness as you can see in this picture.

50. Irritant Contact Dermatitis: Mild Irritant (Chronic)
In time, frequent and cumulative recurrences of these skin irritations lead to the chronic phase of ICD showing aside from dry scaling the characteristic feature of chronic eczemas which is lichenification.

51. Irritant Contact Dermatitis: Strong irritant
Severe irritants are those which produce strong skin reactions following just with the 1st application such as strong acids like sulfuric acid or strong alkalis like phenol. They are sometimes called cauterants since the reaction could be clinically similar to either 1st to 2nd degree burn showing erythema, blisters and erosions as you could see with this patient.

52. ALLERGIC CONTACT DERMATITIS (ACD)
Due to repeated exposure to a substance to which the individual is sensitized
A cell-mediated type IV delayed hypersensitivity reaction
ACD on the other hand is due to delayed or cell-mediated type hypersensitivity. There is a previous sensitization to the allergen meaning the patient’s skin should have been previously exposed to the allergen for many times in the past before an allergic rxn could take place.

53. A PEODG and SP Dermatology Exclusive
Application of contact allergens (Ag)
Release of cytokines by keratinocytes, Langerhans cells and other cells within the skin
Cytokines activate Langerhans cells which uptake the antigen and emigrate into the regional lymph nodes
During this process, the Langerhans cells mature into dendritic cells; the antigen is processed, re-expressed on the surface and finally presented to naïve T cells in the regional lymph node
Upon appropriate antigen presentation, T cells bearing the appropriate T cell receptor clonally expand and become effector T cells.
Effector T cells recirculate into the periphery where they may later meet the antigen again.
This slide seems to be overwhelming but this is just simple diagram explaning the induction of contact hypersensitivity. It all starts naturally with exposure to the allergen. Once the allergen comes in contact with the skin surface, the LC uptakes the allergen and carries it to the regional LN for presentation. After appropriate presentation, the naïve T-cells clonally expand and produce 2 subpopulations of T-cells responsible for sensitization or contact hypersensitivity:Effector T cells with antibodies on their surface , they recognize the specific antigen and initiate the allergic reaction when appropriately challenged. The other group are memory T-cells which remain alive for years and are responsible for the persistence of contact allergy.
Series 2007
A PEODG and SP Dermatology Exclusive

54. Common Allergens In the General Population
NACDG 1998
Nickel
Fragrances
Neomycin
Balsam of Peru
Thimerosal
PCDSG 2000
Nickel
Potassium Dichromate
Fragrance Mix
Cobalt
Paraben Mix
The range of possible substances which may produce ACD is extremely wide. Common allergens in the general population are as follows: nickel which is the commonest allergen among women since this is commonly found in jewelries, hair accessories as well as clothing. Fragrance mixes & volatile oils like Balsam of Peru are found in perfumes & cosmetic products. Potassium dichromate is the commonest among men since they are found in tanned leather products like work gloves, shoes & also in cement.

55. ACD: Nickel
The site of involvement could give us useful clues to the possible allergens like this one which is ACD on the umbilical area due to nickel from a metallic pant’s clip.

56. ACD: Nickel
Chronic ACD again to nickel sulfate in the belt buckle

57. ACD: Nickel
ACD with 2dary infection due to nickel in earrings

58. ACD: Fragrance
ACD on a specific portion of the neck where perfume has been sprayed.

59. ACD: Colorant in Toothpaste
ACD around the mouth due to colorant in toothpaste.

60. ACD: Fragrance in Deodorant
ACD on axillary area due to fragrance in deodorants.

61. Common Occupational Allergens
Rubber accelerating chemicals (thiuram)
Biocides (formaldehydes)
Hairdressing chemicals
Resin – acrylates
Chromates
Plant allergens
Latex
In the workplace, rubber is very common. Allergy is not due to the rubber per se but to its accelerating chemicals like mercaptobenzothiazole & thiuram sulfide. Formaldehyde used in ointments are quite common in the medical industry since it is widely used as preservative due to its antimicrobial properties. Among hairdressers, the most allergenic substance is paraphenylenediamine (PPD) in hair dyes. Acrylates like epoxy resins are most often seen among electrical workers and chromates in cement most often involve construction workers.

62. ACD: Rubber
Almost identical & symmetrical involvement of the feet easily giving away the identity of the allergen which in this case are rubber sandals.

63. ACD due to contact with acrylates
ACD on the tips of the fingers due to contact with acrylates or epoxy resins found in adhesives.
Series 2007
A PEODG and SP Dermatology Exclusive

64. ACD: Chromate
ACD to chromate found in cement.

65. Patch Test
Only objective diagnostic tool for the definitive diagnosis of allergic contact dermatitis
May aid in differentiating ACD from ICD
Patch testing is the only objective diagnostic tool that is available to us in differentiating between ACD and ICD.

66. Patch Test: Technique
Test substances appropriately diluted. Standardized kits available.
The purpose of patch testing is to produce the

68. Some Common Allergens Used in Patch Testing
Nickel - Jewelry
Balsam of Peru - Perfumes, citrus fruits
Dichromate - Cement, leather, matches
Paraphenylenediamine - Hair dyes, clothing
Rubber chemicals - Shoes, clothing, gloves
Colophony - Sticking plasters

69. Some Common Allergens Used in Patch Testing
Benzocaine - Topical anaesthetics
Neomycin - Topical medicaments
Parabens - Preservatives in cosmetics, creams
Epoxy resins - Glues
Formaldehyde - Clothing, cosmetics, paper
Wool alcohol - Lanolin, cosmetics, creams

71. Patch Test: Technique 2. Apply the patch to the upper or mid back.
Leave the patch in place and keep dry for
2 days before removing.

74. Patch Test: Technique 3. Read tests:
a) The same day that patches are removed
b) One additional reading 3, 4, or 7 days after test initially applied

76. Patch Test: Technique Grade test reactions according to intensity:
0 = no reaction
doubtful = minimal erythema
(+) = erythema w/ papules
(++) = erythema,papules,vesicles
(+++) = erythema, bullae

77. (++) REACTION

78. (+++) REACTION

80. Patch Test: Technique
5. Relate relevance of positive reactions to clinical dermatitis cautiously. Careful history and review of skin exposures must establish significance

86. Photocontact eczema
Require exposure to sunlight following topical application of certain chemicals
Long wave UVA – action spectrum
Topical photosensitizers – PPD in hair dyes, PABA esters in sunscreening agents, halogenated salicylates in soaps and cosmetics & topical sulfonamides
Topical photoirritants – psoralens in perfumes

89. PSORIASIS Cecilia Roxas-Rosete, MD, FPDS
Consultant, Section of Dermatology
The Medical City Hospital

90. Psoriasis EPIDEMIOLOGY Age of onset: 20 to 50 y/o Sex: M=F
Heredity: Polygenic
Pathogenesis: Alteration of the cell kinetics of keratinocytes

91. Psoriasis PHYSICAL FINDINGS Psoriasis Vulgaris Most common
Erythematous well-defined papules & plaques with large amounts of silvery white scales
Sites: scalp, elbows,knees, lumbar area

92. Psoriasis

93. Psoriasis
Auspitz Sign

94. Psoriasis

95. Psoriasis

96. Psoriasis

97. Psoriasis

98. Psoriasis

99. Psoriasis Physical Findings Eruptive (Guttate) Psoriasis
0.5cm-1.0cm lesions
Young adults
Streptococcal throat infection

100. Psoriasis
PHYSICAL FINDINGS
Psoriasis geographica
‘land map”

101. Psoriasis PHYSICAL FINDINGS Annular Psoriasis
Partial central clearing resulting in ring-like lesions

102. Psoriasis PHYSICAL FINDINGS Psoriasis inversa Flexural psoriasis
Localized in skin folds

103. Psoriasis PHYSICAL FINDINGS Psoriatic Erythroderma
(Exfoliative Dermatitis)
All body sites
Prominent erythema
May represent generalized Koebner’s phenomenon

104. Psoriasis PHYSICAL FINDINGS Pustular Psoriasis
Pustular psoriasis of von Zumbusch
Pus are sterile

105. Psoriasis TRIGGER FACTORS A. Physical trauma: Koebner’s Phenomenon
various traumatic insult to skin
30%-50% of psoriasis patients give history of koebner’s

106. Psoriasis
Koebner’s Phenomenon

107. Psoriasis TRIGGER FACTORS B. Infection
15%-76% report history of infection
E.g. Streptococcal throat infection
- guttate psoriasis
HIV
- 2.5% develop psoriasis

108. Psoriasis TRIGGER FACTORS C. Stress 30%-40% adult cases
90% in children

109. Psoriasis TRIGGER FACTORS D. Drugs
Corticosteroids – may cause flare-ups
Lithium
Beta-Adrenergic blockers, ACE inhibitors
Anitmalarials
Aspirin

110. Psoriasis SYSTEMIC ASSOCIATIONS
Psoriatic arthropathy is the only recognized non-cutaneous manifestation
Classified as one of the seronegative spondyloarthropathies

111. Psoriasis
SYSTEMIC ASSOCIATIONS
Psoriatic Arthritis

112. Psoriasis
SYSTEMIC ASSOCIATIONS
Arthritis mutilans – 5%

113. Psoriasis SYSTEMIC ASSOCIATIONS
Genetically determined autoimmune disease – 5%-8%
(+) HLA-B27 linkage in 20% of psoriatic arthropathies
frequency of ulcerative colitis in psoriasis patients

114. Psoriasis SYSTEMIC ASSOCIATIONS Metabolic syndrome:
> heart disease (high blood pressure)
> stroke
> diabetes (insulin resistance)
> excessive body fat around waist (obesity)
> dyslipidemia ( low HDL,
high triglyceride)

115. THANK YOU