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CHRONIC ACTINIC DERMATITIS
1
DEFINITION:
It is a common eczematous photodermatosis
i.e., an itchy, inflammatory skin disorder
caused due to sun exposure persisting for
long term.
2
3
ETIOLOGY:
Action Spectrum- UVA, UVB, Visible light.
PREDISPOSING CONDITIONS:
 Allergic contact dermatitis
 Drug induced photosensitivity
 Endogenous eczema
 Air borne contact dermatitis
 HIV Infection
 Photoaged and aged skin.
4
PATHOGENESIS:
 Presence of predominantly CD8+ cytotoxic
suppressor cells results in developing
CAD from pre existing disorders.
 CAD may develop as delayed type of
hypersensitivity reaction during initial
localized photo allergic reaction to a
normal skin altered to become antigenic
by light or hapten binding to endogenous
carrier protein through UVA dependent
covalent photochemical reaction. DNA is
the prime target.
5
DNA of normal
skin cells
Altered to
become an
antigen
Delayed type of
Hypersensitivity
reaction
UV
Radiation
CLINICAL FEATURES:
 Itchy, confluent eczematous patches seen
over photo exposed sites
 Often a sharp border at the edge of
clothing
 Sparing of upper eyelids, retroauricular
and submental region, finger webs, depth
of skin creases.
 Erythematous plaques with shiny infiltrated
papules may develop.
 Lichenification over period of time.
6
7
8
VARIANTS:
 Actinic Reticuloid
 Persistent light reactors
 Photosensitivity Dermatitis and Eczema
DIAGNOSIS:
Based on
 Clinical examination
 Histology-chronic eczema with or without
lymphoma like changes.
 Photobiologic- reduction in MED of UVB, UVA
on normal skin.
DIFFERENTIAL DIAGNOSIS
9
10
INVESTIGATIONS:
 Histopathology:
 In mild cases- chronic eczema, acanthosis and
spongiosis are seen.
 In severe CAD Pautrier like microabcesses
seen in epidermis.
 An upper dermal dense lymphocytic
perivascular infiltration seen.
 Eosinophils, macrophages, plasma cells may
be present.
 In Actinic Reticuloid it resembles T cell
lymphoma except mitotic figures are less
frequent.
11
12
 PHOTO TESTING:
Photo provocation is performed on uninvolved
skin. An eczematous response to UVB in majority
and to UVA,VR in less patients.
The MED of UVB is reduced in 70% & UVA in
33% of patients.
 PATCH TEST and PHOTOPATCH
TEST:
To detect allergens like oleoresins, compositae
sunscreens etc.
 Blood tests:
Circulating Antinuclear antibodies. CD8+ sezary
cells in the absence of malignancy.
13
14
 TREATMENT:
 Absolute photoprotection .
 Usage of broad spectrum sunscreens.
 Topical steroids in mild cases.
 Topical use of Tacrolimus.
 In moderate to severe cases:
Azathioprine- 1.5 to 2.5 mg/kg/day
Cyclosporine- 3.5 to 5 mg/kg/day
 PUVA therapy
15

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Chronic actinic dermatitis

  • 2. DEFINITION: It is a common eczematous photodermatosis i.e., an itchy, inflammatory skin disorder caused due to sun exposure persisting for long term. 2
  • 3. 3 ETIOLOGY: Action Spectrum- UVA, UVB, Visible light. PREDISPOSING CONDITIONS:  Allergic contact dermatitis  Drug induced photosensitivity  Endogenous eczema  Air borne contact dermatitis  HIV Infection  Photoaged and aged skin.
  • 4. 4 PATHOGENESIS:  Presence of predominantly CD8+ cytotoxic suppressor cells results in developing CAD from pre existing disorders.  CAD may develop as delayed type of hypersensitivity reaction during initial localized photo allergic reaction to a normal skin altered to become antigenic by light or hapten binding to endogenous carrier protein through UVA dependent covalent photochemical reaction. DNA is the prime target.
  • 5. 5 DNA of normal skin cells Altered to become an antigen Delayed type of Hypersensitivity reaction UV Radiation
  • 6. CLINICAL FEATURES:  Itchy, confluent eczematous patches seen over photo exposed sites  Often a sharp border at the edge of clothing  Sparing of upper eyelids, retroauricular and submental region, finger webs, depth of skin creases.  Erythematous plaques with shiny infiltrated papules may develop.  Lichenification over period of time. 6
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  • 8. 8 VARIANTS:  Actinic Reticuloid  Persistent light reactors  Photosensitivity Dermatitis and Eczema DIAGNOSIS: Based on  Clinical examination  Histology-chronic eczema with or without lymphoma like changes.  Photobiologic- reduction in MED of UVB, UVA on normal skin.
  • 10. 10 INVESTIGATIONS:  Histopathology:  In mild cases- chronic eczema, acanthosis and spongiosis are seen.  In severe CAD Pautrier like microabcesses seen in epidermis.  An upper dermal dense lymphocytic perivascular infiltration seen.  Eosinophils, macrophages, plasma cells may be present.  In Actinic Reticuloid it resembles T cell lymphoma except mitotic figures are less frequent.
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  • 12. 12  PHOTO TESTING: Photo provocation is performed on uninvolved skin. An eczematous response to UVB in majority and to UVA,VR in less patients. The MED of UVB is reduced in 70% & UVA in 33% of patients.  PATCH TEST and PHOTOPATCH TEST: To detect allergens like oleoresins, compositae sunscreens etc.  Blood tests: Circulating Antinuclear antibodies. CD8+ sezary cells in the absence of malignancy.
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  • 14. 14  TREATMENT:  Absolute photoprotection .  Usage of broad spectrum sunscreens.  Topical steroids in mild cases.  Topical use of Tacrolimus.  In moderate to severe cases: Azathioprine- 1.5 to 2.5 mg/kg/day Cyclosporine- 3.5 to 5 mg/kg/day  PUVA therapy
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