Prurigo actinic L56.4

Hutchinson 1878; Haxthausen 1918; Fox 1939; Escalona 1959; Lopez-Gonzales 1961;

Rare, chronic, idiopathic photodermatosis leading to scarring, especially in children and adolescents, with the development of prurigo and eczema-like skin changes that occur preferentially in areas exposed to light. Considered by some authors to be a special form of polymorphic light dermatosis . It can severely impair the quality of life

.

Two forms are distinguished by some authors:

• Non-American actinic prurigo with partial symptoms of atopic dermatitis, polymorphic light dermatosis, hydroa vacciniforme and persistent light reaction.
• American (hereditary) actinic prurigo occurring in Indians in North and Latin America. There it is called "hereditary polymorphic light dermatosis" or "familial actinic prurigo".

Immediately after radiation exposure, development of an early urticarial phase. This slowly changes into a persistent, lichenified dermatitis. Subsequently, or overlapping, the typical pruriginous skin changes develop in the light-exposed areas, as well as scattered reactions. Mostly a year-round course with worsening in summer. Conjunctivitis and cheilitis of the lower lip have been described.

Papular efflorescence: acanthosis, focal spongiosis; epidermotropic lympho-histiocytic, perivascular infiltrate. Eosinophilia is possible. A follicular cheilitis in the lip biopsy supports the diagnosis.

Polymorphic light dermatosis; atopic eczema; porphyria; lupus erythematosus; airborn contact dermatitis; photoallergic eczema or phototoxic dermatitis; chronic actinic dermatitis;

Physical, in particular textile light protection. See below for photoprotective agents.

Topical corticosteroids are helpful in the acute stage.

In severe, therapy-resistant cases, immunosuppressive treatment with azathioprine 100 mg/day or with glucocorticoids such as prednisolone (e.g. Solu-Decortin H) 40-60 mg/day.

Thalidomide 200 mg/day ( off-label use) and cyclosporine (3mg/kgKG) appear to be effective.

Individual case reports have reported good success with baricitinib, a JAK-1/2 inhibitor (4mg/day) and dupilumab (Gli-Lianes J et al. 2024).

1. Arrese JE et al (2001) Effectors of inflammation in actinic prurigo. J Am Acad Dermatol 44: 957-961
2. Escalona PE, Magana LM (1959) Dermatologfaia: Io esencial para el estudiante, 2nd edn, Mexico, pp. 174-178
3. Fox H (1939) Diseases of the skin in Oklahoma Indians. Arch Dermatol 40: 544-546

• Gil-Lianes J et al (2024) Complete response of actinic prurigo to oral baricitinib. JDDG 22: 837-839

1. Hutchinson J (1878) Summer prurigo, prurigo aestivalis, seu prurigo adolescentium, seu acne-prurigo.Medical Times and Gazette (London) 1: 161
2. Hojyo-Tomoka MT et al. (2003) Diagnosis and treatment of actinic prurigo. Dermatol Ther 16: 40-44
3. Kuno Y et al. (2003) Actinic prurigo: a 10 years follow-up study by questionnaire. Br J Dermatol 149(Suppl 64): 48-49
4. Lane PR et al (1992) Actinic prurigo: Clinical features and prognosis. J Am Acad Dermatol 26: 683-692
5. Millard TP et al. (2001) A candidate gene analysis of three related photosensitivity disorders: cutaneous lupus erythematosus, polymorphic light eruption and actinic prurigo. Br J Dermatol 145: 229-236
6. Neumann NJ et al (2004) Actinic prurigo. JDDG 2: 373-375
7. Umana A et al. (2002) Lymphocyte subtypes and adhesion molecules in actinic prurigo: observations with cyclosporin A. Int J Dermatol 41: 139-145