Chronic actinic dermatitis (overview) L57.1

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

actinic dermatitis; actinic reticuloid; Actinic reticuloid; CAD; Chronic actinic dermatitis; Chronic photosensitive dermatitis; Light eczema; Persistent light reaction; Photosensitive dermatitis; Photosensitive eczema; Reticuloid actinic

History
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Hawk and Magnus, 1979

Definition
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Relatively rare, eminently chronic, very itchy or burning, therapy-resistant, eczematous skin disease in light-exposed areas which can be provoked at the beginning of the disease by UV-rays (UVB), in the further course also by UVA or by normal daylight (unspecific).

The triggering photoallergen is in many cases no longer detectable.

There is a seasonal dependency with intensified skin symptoms in the summer months.

Classification
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The term "chronic actinic dermatitis", in short CAD, is considered as an umbrella term (or is also used synonymously) for various light dermatoses already described above.

These include:

Etiopathogenesis
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The pathomechanism of the disease is unclear. It is assumed that a photoinduced antigen leads to a delayed-type hypersensitivity reaction, analogous to allergic contact dermatitis.

However, less exogenous allergens but rather endogenous photoreactive autoantigens are suspected, which are formed by electromagnetic irradiation.

The triggering action spectrum usually lies in the UVB and UVA range; less frequently and, if persistent for several years, also in visible light.

Manifestation
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Men in middle and old age are particularly affected. Ratio m:w=10:1

Localization
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Predilection sites are the entire face, neck and back of the hand. The retroauricular region remains free (DD Airborne Contact Dermatitis), as does the chin shadow. If the disease is very severe, the entire integument can be affected (very rare), because even the smallest UV/daylight doses are sufficient to trigger and maintain a photoallergic reaction.

Clinical features
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S.a. under the individual clinical pictures.

Mostly large-area, massively itching, also painful, chronic eczematous, scaly skin changes with considerable lichenification and distinct inflammatory infiltration of the skin appear, which leads to a leather-like increase in the consistency of the lesional skin. The skin lesions are clearly demarcated from the unexposed skin, whereby this transition is not sharply linear but irregularly loosened. Dermatitic scattering phenomena may also occur in skin areas covered by clothing.

The skin changes persist for months after low UV exposure, may subside in winter and then exacerbate and persist again in spring after brief UV exposure.

After a number of years, this rhythm is lost and the eczematous skin changes persist throughout the year, with an additional worsening of the chronic eczema condition occurring during the light-rich season.

Facies leontina as the maximum expression of chronic actinic dermatitis (so-called actinic reticuloid) in the facial area is possible.

Histology
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Picture of a chronic, lichenified dermatitis with partly psoriasiform acanthosis, prolongation of the reteleasts, hyperkeratosis with parakeratotic parts, perivascular, partly also diffuse, very dense, predominantly lymphocytic infiltrate in the upper dermis with slight to distinct dermal fibrosis (depending on the duration of the eczema reaction). Mostly proliferation of wall-thickened capillaries in the infiltrate zone. Focally very differently pronounced epidermotropy with spongiosis(depending on the degree of acuity of the eczema reaction). In case of a very dense epidermotropic infiltrate, the differential diagnosis is a cutaneous T-cell lymphoma of the mycosis fungoides type.

Differential diagnosis
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Clinical:

  • Contact Allergic Dermatitis: especially the aerogenic contact allergic eczema is important for differentiation. Here an analogous clinical picture may be present. The connection between the triggering contact principle and the skin changes must be investigated anamnestically.
  • Photoaggravated atopic dermatitis Deterioration of eczematous skin symptoms in previously known extrinsic atopic dermatitis under UV (mostly UVA) or sunlight exposure. A diganostic auxiliary sign in differentiation from aerogenic contact allergic eczema is the remaining chin (chin shadow) and retroauricular region.
  • Actinic reticuloid: no real differential diagnosis, since the actinic reticuloid is considered the (maximum) variant of chronic actinic dermatitis.
  • Acute dermatitis solaris: acute event with painful dermatitis sharply limited to the site of exposure (no marginal scattering phenomena). The clinical relation to the triggering situation is usually clear.

Histological:

  • Lymphomatoid contact dermatitis: quite analogous histological picture with acanthosis, band-shaped lmyphoid cell infiltrate, epidermotropism: clinic excludes this DD.
  • Mycosis fungoides (also other T-cell lymphomas): depending on the stage of the disease an analogous histological picture may appear. In most cases, however, a clear cell polymorphism is to be expected. Clonality studies are useful for differentiation. Finally, the summarizing evaluation of clinic and histology is decisive.
  • Atopic dermatitis: UV-triggered atopic eczema may show an analogous histological pattern.

Therapy
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In the foreground is stringent prophylaxis (see there). Further therapeutic measures; see below reticuloid, actinic.

Internal therapy
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In therapy-resistant cases, systemic immunosuppression with glucocorticoids, azathioprin/cyclosporin A is necessary. An immunosuppressive combination therapy is useful in the early phase of PUVA therapy.

Progression/forecast
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The disease is highly chronic and tends to aggravate the symptoms by increasing light sensitivity as the duration of the disease increases. Thus, minimal exposure to light can lead to long-term eczema reactions in the affected areas.

Prophylaxis
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  • Protection through clothing: Covering the skin with clothing is an effective light protection with few side effects. It should be noted, however, that fabrics vary depending on the fibre, dye and especially the type and size of knitwear and that a considerable proportion of the radiation can penetrate the textile in low-density fabrics.
  • Chemical sunscreens: By absorbing UV light, these substances prevent the primary photochemical reaction in the skin. Added antioxidants additionally reduce the secondary photochemical reactions of the body's own molecules. Mainly in the UV-B range, substances from the substance groups of paraaminobenzoic acid derivatives, salicylates, camphor derivatives, cinnamic acid esters and benzimidazole derivatives absorb. So-called broadband filters such as dibenzoylmethanes and benzophenones absorb both UV-B and UV-A.
  • Physical light stabilizers: Pigments of titanium oxide, iron oxide or also zinc oxide in a particle size of 10-60 nm absorb in the range of UV light, but hardly reflect visible light. They can be used in a wide range of applications. The formation of dangerous radicals can be completely prevented by coating the pigment granules or by doping, a kind of contamination of the crystal lattice.
  • Light-hardening: Photo(chemo)therapy or narrow band UVB in very low dosages (see also reticuloid actinic).

Tables
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Criteria and differentiation for the classification of chronic photosensitive eczematous skin diseases (modified according to mildness)

Diagnosis

Histology

Photosensitivity

Photopatch test

Patch test

Persistent light reaction

Cancellous Dermatitis

UVB, (UVA)

+

+/-

Actinic reticuloid

Mycosis fungoides-like

UVB, UVA, (visible light)

-

+/-

Photoallergic eczema

Cancellous Dermatitis

UVB, (UVA), (visible light)

+/-

+/-

Photoaggraved endogenous eczema

Cancellous Dermatitis

UVA, (UVB)

-

+/-

Test location

Skin region not exposed to light

Test Fields

5 x 5 cm

Radiation sources

UV-A:Fluorescent lamp (Philips TL 09 N, TL 10 R)

Metal halide lamps (340 - 400 nm)

UV-B. Fluorescent lamps (Philips TL 12, 285 - 350 nm)

Visible light: Slide projector

Radiation doses

UV-A. 1.0, 10, 30 J/cm2

UV-B: 0.5, 1.0, 1.5 times MED

Visible light: 30J/cm2

Reading

24, 48, 72 h after irradiation

Literature
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  1. Bhari N et al (2017) Tacrolimus 0.1% ointment applied under occlusion using cling film clears chronic
    actinic dermatitis resistant to systemic treatment.Int J Dermatol 56:e139-e141.
  2. Dawe RS (2003) Diagnosis and treatment of chronic actinic dermatitis. Dermatol Ther 16: 45-51
  3. Lehmann P et al (2011) Light dermatoses: Diagnostics and overview. Dt Ärztebl 108: 135-141
  4. Ling TC et al (2003) Treatment of polymorphic light eruption. Photodermatol Photoimmunol Photomed 19: 217-227
  5. Mang R et al (2003) Sun protection during holidays. dermatologist 54: 498-505
  6. McCall CO (2003) Treatment of chronic actinic dermatitis with tacrolimus ointment. J Am Acad Dermatol 49: 775
  7. O'Gorman SM et al (2014) Photoaggravated disorders. Dermatol Clin 32:385-398
  8. Paek SYet al (2014) Chronic actinic dermatitis. Dermatol Clin 32:355-361
  9. Wolf C et al (1988) The syndrome of chronic actinic dermatitis. Dermatologist 39: 635-641
  10. Yap LM et al (2003) Chronic actinic dermatitis: A retrospective analysis of 44 cases referred to an Australian photobiology clinic. Australas J Dermatol 44: 256-262

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 29.10.2020