Detail description about atopic dermatitis

1. ECZEMA

2.  Den :- An inflammatory skin reaction.
o clearly superficial form
o early is erythematous ,papulovesicular, oozing &crusting
o
o later, red purple,scaly,lichenified &pigmmented with
inflammatory cell infiltrates.
o non sharp margination .
o hist spongiosis, with varying degrees of acanthosis and
superficial peri vascular lymphohistiocytic infiltrate.
o Eczema ≈ ‘Dermatitis’

3. Classification
 Eczema Large proportion of all skin diseases
 Difficulty of classification
 controversial nomenclature
 precise cause in many cases unknown
 multiple factors implicated
 2 or more forms in the same p’t simultaneous or
consecutive

4. convenient classification into exogenous & endogenous
-Exogenous clearly defined external trigger
Endogenous processes originating within the body
mediate
- Both internal/external factors – in some
eg. – Hand eczema -- primarily endogenous ,
-- aggravated by irritants (detergents)

5. Exogenous eczemas
o Irritant dermatitis
o
o Allergic contact dermatitis
o Photoallergic contact dermatitis
o phototoxic d’ts
o Eczematous polymorphic light eruption
o
o Dermatophytide.
o Post-traumatic eczema.

6. Endogenous eczemas
o AD,SD.
o
o Asteatotic eczema
o Discoid eczema.
o lichenoid dermatitis.
o Pityriasis alba.
o Hand eczema.
o
o Juvenile plantar dermatosis.
o Metabolic or eczema associated with SD
o Eczematous drug eruptions.

7. Stages of eczema :- three stages
o acute
o subacute
o chronic
- Each represent a stage in the evolution of dynamic
inflammatory process
- Clinically may start at any stage & evolve into
another
- Most eczematous diseases, if left alone
(neither irritated, scratched nor medicated),
resolve in time without complication

9. Acute stage Spongiosis -> intercellular epidermal
edema/vesiculation
Subacute stage ↓spogiosis & vesiculation variable
lymphocytic infiltration
 hyperkeratosis  LICHENIFICATION
Chronic stage hyperkeratosis ,parakeratosis acanthosis
no cellular invasion of epidermis
Recovery :- uncomplicated eczema
no 2⁰ changes gradually revert to normal
Modified by- infection
- trauma of rub
- scratching

10. Eczema and age
 AD commonest in <5yrs
 perioral eczema common in atopic children

 hand eczema – common in atopic children
 some specific patterns almost restricted to children
o lichen striatus
o juvenile plantar drmatosis
o SD of infancy
o napkin dermatitis
o discoid/dyshidrotic - less common

11. Elderly
- discoid eczema – commonest in male/winter
asteatotic eczema
irritant hand eczema – factory workers
↓ with advancing age
pompholyx/atopic eczema – uncommon in elderly

12.  Pathophysiology :
o Eczema – exact cause unknown
o Involve – dry, sensitive skin
o alteration in immune system
o - genetic factors
- aggravating factors
Skin physiology :-
o Eczematous conditions primarily affect the SC
o SC -> 15% water + 85% lipids (ceramide, FFAs,
Cholesterol)
o Lipids regulate natural water loss from skin

13. Ceramides ↓ by – sunburn, harsh soap, cosmetics,
env’tal factors (skin damage)
↓
↑ water loss
↓
Drying skin (Xerosis)
↓
Irritated itchy skin
↓
Continuous cycle of itching
= ITCH-SCRATCH-ITCH CYCLE

14. opruritus  scratching  release of inflammatory
products (ILs)  further itching  scratch &
inflammation  chafing & cracking of skin  ↑risk of
bacterial invasion/infection  add.
oInflammation/drying  into cycle
o Persistent scratch -> impact on ql. of life
o sleep disruption
o
o Breaking cycle -> identify trigger -> ~ Mgt

15. Immune system - Eczematous skin lesions –
o ↑ IgE level (≈ 80% atopics)/studies
o ↑ cytokine production
o acute (< 3 ds)  IL-4, IL-13
o chronic (> 2wks)  IL-2, IFN- , IL-12
o roles in - inflammation, erythema, oedema
o ( X-ics of eczema)
o Th-cells in skin disorders/immune response
o Th2  stimulated by IL-4, IL-5, IL-13 over expressed
in acute lesions down regulation of Th1
associated with atopic conditions

16. Genetic factors
o certain ILs (IL-3,4,5,13) linked to atopic disease
o on specific chromosomes (5q31,5q32,5q33,11q13)
o
o way for newer AD Rxs to focus on inhibiting
o cytokine production (topical immunomodulators)
o children with both parents atopic
o  70% chance of atopy
o  other family members (? twins) at high risk
o on going confirmation of genes inv’d in atopy
o identify p’ts at high risk

17. Aggravating factors
- irritants -> affect skin when in contact (longer
time/large qt)
- allergens -> immune Rxn on exposure (small amount
exposure)
- emotion
- environmental factors
- bacterial

19. Food allergies – most common type of allergen
o a third of children with AD
o eggs, milk, soy, peanuts, wheat
o ≈ 90% of food allergies in children
o can affect -> whole body
o -> skin Rxn (itching )
o -> GI effects (abdominal pain)
o -> URT Sxs (congestion, sneezing,..)
o -> LR Sxs (asthma-like Sxs )
o Gold standard for Dx -> (placebo food + food in question)

20. Current treatment for food allergies
-> avoidance/elimination diet
-> immunotherapy
-small amount of allergen extract
 ↑tolerance to offending allergen
 improve Sxs of other atopic conditions
 protect against anaphylaxis

21. Env’tal/physiological/microbial factors
 potential triggers in trigger eczema
- changes in weather/climate
- stressors (job, family related, etc…)
-> in stressor exacerbated conditions
- relaxation techniques
- behavioral modifications
- life style changes, … are helpful

22. ~ Bacterial infection – flares of the disease
- S. aureus -> normally inhabits skin of eczema p’ts
-> potential to invade dry/cracked skin
-> inflammation/injury to the area
-> ↑IgE/cytokines to help fight infection
↓
initiate acute attack of eczema
-> need of AB mgt in microbial flares

24. Introduction
Atopy -term used for allergic conditions such as allergic
rhinitis, asthma or AD
Atopos- unusual
- chronically relapsing skin disease
- during early infancy & childhood
- ↑ed IgE level, family Hx of atopy
- No single distinguishing feature or lab test

25. Epidemiology
o Prevalence in children15-20%, 1-3% in adult
o F:M ≈ 1.3:1
o Affects all race
o Typically begins during infancy
o In 50% -in the 1st year of life
o 30%- B/n age 1-5
o in 80% - before age 5
o - 50-80% of AD pts develop allergic rhinitis or asthma later

26. Etiopathogenesis multifactorial
o Complex interaction- genetic, environmental &
immunologic
o Environmental factors- critical for disease expression
o exposure to allergens, irritants, bacteria, and hard water
o socioeconomic status
o large family size
o Hygiene hypothesis→ allergic disease might be prevented
by infection in early childhood

27. Genetics
o Family Hx of AD is common
o Strong maternal influence
o Skin barrier/epidermal differentiation gene & immune
response/host defense gene
o Filaggrin, epidermal barrier protein- major predisposing
factor
Defective skin barrier
o Results in transepidermal water loss & entry of allergens,
chemicals → skin inflammatory response

28. It results due to :
o downregulation of cornified envelop genes
o ↓ ceramide level
o ↑endogenous proteolytic enzymes
o enhanced transepidermal water loss
o Damage- also due to exogenous proteases
o /house dust mite & S. aureus/

29. Clinical feature
o Intense pruritus- more prominent feature
o Scratching follows
o exposure to allergen
o change in humidity
o low concentration of irritants
o excessive sweating

30. Pruritus
o Worse at night
o Results in prurigo papules, lichenification, eczematous skin lesions
Acute skin lesions
o Intensely pruritus
o Erythematous papules excoriation
o Vessicle, oozing( serous exudate)
Subacute
o Erythematous excoriated papule, scaling
Chronic
o - lichenification, fibrotic papules( prurigo papules)

31. - Distribution of lesions
Infants:
o Symmetric lesions over cheeks, forehead, scalp, trunk,
and the extensor surfaces
o Lesions may extensively involve the flexural surfaces,
sparing only the diaper area.
o Scalp involvement may be severe enough to cause
alopecia

33. Children
o Symmetric lesions on wrists, ankles, and flexor areas of
the extremities
o Generalized eruptions also may occur
Adults
o primarily involves the flexor areas .
o Axillary, groin, and intergluteal involvement is
uncommon and should raise suspicion of another
diagnosis

36. Other features Of AD
Ichthyosis vulgaris
o Observed in one third of
patients
o polygonal fishlike scales
on the lower legs

37.  Palmar hyperlinearity

38. Keratosis pilaris
o - horny follicular
papules on the
extensor surfaces of
the upper arms,
buttocks & anterior
thighs

39. Associated feature
o Facial erythema
o Perioral pallor
o
o Infraorbital fold (Dennie-
Morgan line)
o Dry skin
o Pityriasis alba

40. Lab investigation
o Not needed routinely
o Serum IgE level ↑ed in 70-80% of pts
o Peripheral blood eosinophilia

42. Complications
Ocular
o - keratoconjunctivitis
o keratoconus- conical deformity of cornea from chronic
rubbing
Infections
o Superficial fungal infection
o staph aureus- 90% of AD skin lesion
o pts with severe AD even without overt infection shows
clinical response to cbn of antistaph agents + topical
steroid

43. o Recurrent viral
infection- eczema
herpeticum
o Multiple, itchy
vesiculopustular lesion
in a disseminated
pattern
o Vesicles are umblicated,
hemorhagic, crusted

44. Hand dermatitis
o non-specific irritant dermatitis
o Frequent wetting & washing with harsh soap &
detergents
Exfoliating dermatitis
o Extensive skin involvement
o redness, scaling, weeping, crusting
o Due to superinfection
o Withdrawal of systemic steroid may be a precipitating
factor

45. Rx---goals of treatment :
o reduce itching
o “ inflammation of the skin
o moisturize the skin
o prevent infection
o It incorporates
o skin hydration
o pharmacologic
o identification & elimination of flare factors

46. General preventive measures for flare-ups
o Avoid contact with irritants
o Practice good skin care techniques
o Do not use harsh soaps
o short fingernails, as scratching may contribute to an
infection
o Use moisturizers at least once a day

47. Cutaneous hydration
o Aggressive Rx with emollients
o Lukewarm soaking bath, application of an occlusive
emollients to retain moisture give sxic relief
o Restore & preserve the stratum corneum barrier
o Topical therapy to replace abn lipid, improve skin
hydration & ↓skin barrier dysfunction

48. o Hydration by bath or wet dressing promote
transepidermal penetration of topical steroid
o Dressing – serve as a barrier from persistent scratching
o Wet dressing- severely affected or chronically involved
area refractory to Rx
o maceration

49. Topical steroids
o Mainstay of Rx for acute flare-ups
o Low potency- used for face, groin & axillae
o Also for infants
o Oint –generally more potent than creams
o Should be avoided in open, oozing or intertrigenous
o Daily/twice daily use
o For up to 4 wks- safe & effective

50. Long term use of steroids
○ Local
o Atrophy
o Striae
o Telangiectasia
o Worsening of acne
○ Systemic
o hypothalamic-pituitary-adrenal axis

51. Topical calcineurin inhibitors
/tacrolimus & pimecrolimus/
o Inhibit calcineurin in the skin
o Blocks early T cell activation & release of cytokines
o Second line Rx
o Should not be used in those ‹2 years of age &
immunosuppressed
o Local skin irritation
o sunprotection

52. Infections
- Antistaphylococcal Abcs
- Antiviral Rx for herpes infection
acyclovir 400mg TID X 10 days or 200mg QID
IV Rx in severe cases
- Dermatophytes infection or IgE Abs against
Malassezia
may benefit topical or systemic antifungal

53. pruritus
o Reduce skin inflammation & xerosis- sxic relief
o Inhaled or food allergens should be eliminated
o Antihistamine- minimal effect
o give Sxic relief by tranquilizing & sedating effect
o
o use of sedating antihistamines can be beneficiary in
those with:
▫ allergic rhinitis
▫ sleep disturbance
▫ Urticaria

54. Other therapies
o Natural sunlight-might be beneficiary
o Phototherapy using UVB, UVA or PUVA
o For severe cases
 UVB- immunosuppressive effect by blocking APCs/LC/ & altered keratinocyte cytokine
prodn
 UVA- targets epidermal LC& eosinophils

55. Systemic Rx
For severe & resistant disease
o Systemic steroids- acute control, short term
o - Clinical improvement ass with severe rebound flare up
o Cyclosporine - Severe AD refractory to Rx
o Methotrexate- recalcitrant dse
o Azathioprine- Antinflammatory & antiproliferative
o Mycophenolate mofetil

56. Prognosis
o natural Hx- not known
o tends to be severe & persistent in young children
o Spontaneous resolution – after age 5 in 40-60% of pts
affected during infancy
o AD disappear in 20% of children followed from infancy
to adolescence but 65% less severe

57. Predictive factor for poor prognosis :
o widespread AD during childhood
o Associated allergic rhinitis & asthma
o family Hx of AD
o early age of onset
o only child
o very high serum IgE level

58. CONTACT DERMATITIS

59. Definition
 A dermatitis caused by substances coming in contact
with the skin
 It has two major categories
1- ICD
2-ACD

60.  Cutaneous inflammatory response resulting from a
direct effect of a chemical of physical agent
 The most common form of OCD
 Accounts 70-80% of CD

61. Etiology and Pathogenesis
 Immunological memory cells aren’t involved
 No prior sensitization
 Many chemicals that penetrate the skin can alter or
damage the cells
 Occurs when the repair capacity of the skin is
exhausted
 Penetration of the chemical excites an inflammatory
response
 Strong irritants induce a clinical rxn in almost all
individuals

62.  Four interrelated mzm have been associated with ICD
 Removal of surface lipid and water holding substances
 Damage to the cell membrane
 Epidermal keratin denaturation
 Direct cytotoxic effect

63. Predisposing Factor
Sex
 Women more frequently report skin disease than men
Increased exposure rather than inherent gender difference
Age
 Age related skin change can alter the responsiveness to
irritants
Premature neonates and infants are more affected
Skin Site
 Thickness of the stratum corneum
Atopic dermatitis
 Lowered threshold for skin irritation
• Impaired skin barrier function
• Slower healing process

64. Exogenous factor
Chemical properties of the irritant
 PH ,Concentration ,Molecular size ,Solubility
Characteristic of the exposure
 Amount ,Concentration ,Duration,Type of contact
,Simultaneous exposure with other irritant
Environmental factor
 Low humidity ,Cold temperature
Mechanical factor
 Pressure, friction ,Abrasion

65. Irritant reaction
 Present as an acute monomorphic rxn
 Scaling, erythema, vesicles or erosions
 Common on the dorsum of the hand
 Exposure to wet work
 Can result in cumulative ICD with prolonged exposure

67.  Commonly seen in occupational accidents
 Exposure to single potent irritant
 Rxn occur within mints to hrs of exposure
 Burning, stinging and soreness
 Erythema, edema, bulla and necrosis
 Lesion is restricted to the area of contact with sharply
demarcated border

69.  Due to delayed inflammatory response
 The rxn is acute but signs appear after
8-24hrs or more after exposure
 Clinically similar with acute ICD
 The presentation simulates ACD

70.  The most frequent type of ICD
 A result of multiple sub threshold insult
 Due to different stimuli or repeated exposure of one
agent
 No sufficient time for complete restoration of the skin
barrier function
 Slowly developing over weeks to years
 Lesions are less sharply demarcated

71.  Extensive and frequent exposure to irritant may result
in hardening or adaptation
 Hardened skin appear coarser and lichenified
 Resistant for further irritation
 Brief period away from exposure may lower the
resistance for re-exposure

73.  No reliable confirmatory test for ICD
 History of exposure to a known irritant
 Clinical appearance
 Anatomic distribution
 Exclusion of ACD
Patch test
 Measurement of TEWL
 Microbiologic examination
 Skin biopsy

74.  Successful management of ICD requires
 Identification of susceptible individuals
 Appropriate career advice
 Identification of potential irritants and complicating
factors in the working env’t
 Advice about irritant management and protection
 Advice on use of barrier creams and after work emollients
 Treatment of any dermatitis/inflammation
 Investigation of the cause of persistence

75.  Topical steroid
 Calcineurine inhibitor
 Phototherapy
 Systemic drugs
• Azathioprine, cyclosporine
 Antibiotics

76. Prognosis
 Good if the irritant identified and avoided
 The prognosis for chronic ICD is guarded and may be
worse than ACD
• Atopic background
• Lack of knowledge
• Delayed diagnosis and treatment

77.  Accounts 20% of contact dermatitis
 A delayed type of hypersensitivity response to
exogenous agents
 Previous exposure is needed
 The rxn is specific to a specific agent or to a group of
similar chemical
 All area of skin that are in contact with the allergen
will develop the rash

78.  Most contact allergens are haptens
 Simple chemicals that needs binding to protein to
form complete antigen
 The MHC class 2 on APCs act as the binding site
 The antigenicity of the hapten is dependent on
 The nature of the antigenic determinant
 The type of binding of the hapten with the carrier
protein
 Variety of unknown factor


79. To develop ACD
 Genetically susceptible individual should have
biologically significant and repeated contact with the
allergen
 Sensitization Phase
 Elicitation Phase
 Commonly occur within 48-72hrs of exposure to a
specific allergens
 Vary from few hrs to many days depending on
• Degree of sensitivity
• Penetration
• Other unknown factors

80. Eczematous response
 The dominant symptom is itching
 The primary signs in the acute cases
• Erythema
• Swelling
• Papules
 papulovesicles Continued exposure to the allergen
 Dryness
 Scaly
 Lichenification
 Fissuring

81.  In chronic cases difficult to distinguish from ICD and
etiology may be mixed
 Distribution of the lesion may give a clue to the
diagnosis
 Site of involvement suggest a specific cause or range of
possible allergens
 Palms, soles and scalp are relatively resistant to ACD

88. Systemic manifestation
 Relatively uncommon and poorly understood
 Occur in topically sensitized and systemically exposed
individual
 Extensive, bizarre appearing dermatitis and
erythroderma can occur
 Pts can have metabolic effect and secondary infection

89. Generalized dermatitis
 Systemic exposure
 Follow topical exposure to allergens
• Nickel
• Formaldehyde
• Balsam of peru
• Natural and synthetic rubber

91.  Largely a clinical diagnosis aided with patch testing
 Repeat open application test
 Dimethylgloxime
 Microbiologic exam.
 Biopsy

92. Symptomatic treatment
 Drying agents for oozing lesion
• Topical aluminum sulfate, calcium acetate
 Emollients for chronic casesTopical steroid
 Short course systemic steroid
 Topical immunomodulators
 Immunosupressive drugs
 PUVA

93. Prevention
 Identification of the allergen
 Advice the pt to avoid the allergen and cross reacting
chemicals

94. THANK YOU