Polymorphic light dermatosis

Last Updated: 2020-11-19

Author(s): -

  • Bateman 1817
  • Hutchinson 1878
  • Rasch 1900
  • Hausmann und Haxthausen 1929

Sun allergy, light eczema, polymorphic light eruption, PMLE, Prurigo aestivalis, summer prurigo, lupus erythematosus-like light dermatosis, eczema solare

Most frequent light dermatosis, which is characterized by its severe itching. The appearance is monomorphic within the type of PLD (see below: papules, vesicles, plaques, cocardial lesions, etc.).

  • Prevalence (depending on data situation) up to 20%.
  • Seasonal accumulation March - June (exception: during holidays in warm countries)
  • Independent of age
  • Women : Men = 9:1
  • More common among Caucasians, but also possible among Africans.
  • Family accumulation in at least 20%.
  • Triggered by sunlight, exact etiology is not known.
  • Probably a genetic disposition plays a role.
  • Proinflammatory cytokines are induced by UVA (sometimes also UVB) radiation.
  • A cell-mediated immunological reaction of the delayed type occurs through previously unknown photo-induced antigens.
  • Disruption of UV-induced immunosuppression.

Only in sun-exposed areas, individual predilection sites are described.

The skin symptoms are polymorphic and can often be divided into different types.

Classification 

  • Papular type
  • Hemorrhagic type
  • Plaque type
  • Erythema exudative multiforme type
  • Papules (Acne aestivalis Hjorth)
  • Erythema-exsudative-multiform-type type
  • Papulo-vesicular type
  • Ictus type
  • Vesiculo-bullous type
  • Lichenoid type (described in the colored population)
  • Special forms: family variant, found in Indians. Juvenile spring eruption (especially ear helices, hands or nose in young men and children in spring).
  • The first symptoms appear hours to days later. However, a manifestation is also possible after several days (cumulative dose). Often there is a familiarisation effect (hardening). In most cases there is a pronounced itching.
  • Typical medical history
  • Time course (continuous? intermittent? Depending on the season? Age of first manifestation? - e.g. Hidroa vacciniformia or spring perniosis), duration of efflorescence? Medication intake? Family history?
  • Do skin changes also occur behind glass? Indication of triggers by UV-A.
  • Do they occur outdoors, but not behind glass? Indication of triggers by UV-B.
  • In room light? Triggered by visible light.
  • After which exposure period do the efflorescences occur?
  • Light diagnostics

    • light staircase
  • Photo provocation 

    • MED is mostly normal
    • UVA provocation more effective than UVB
    • Photopatch test
  • Biopsy if necessary

  • Laboratory
    • ANAs (to search for lupus erythematosus) (if necessary, plasma fluorescence scan in case of justified suspicion of porphyria).

Different patterns depending on the type. In most cases, cuff-shaped, perivascular lymphohistiocytic cell infiltrates are visible over the entire dermis. In addition, subepidermal oedema, exocytosis and spongiosis can occur.

  • Regular UV hardening in spring (costly)
  • Sun protection, sufficient in the trigger light spectrum
  • Under light-care, the patient heals independently without residuals.
  • Chronic recurrent course.

General measures

  • Light protection!
  • Sun cream SPF 50 incl. UVA protection (note declaration)
  • Light-hardening, if necessary (UVA-hardening is best)

 

Topical Therapy

  • Mometasone furoate cream / solution / ointment 

     

  • Anithistamines
    • Levocetirizine p.o. 5 mg 1x daily
    • Desloratadine  p.o. 5 mg 1x daily
    • Fexofenadine p.o. 180 mg 1x daily
  • Glucocorticoids (in exceptional cases with particularly severe symptoms)
    • Prednisolone p.o. 25-100 mg 1x daily
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  2. Murphy GM, Hawk JLM, Magnus IA. Hydroxychloroquine in polymorphic light eruption: a controlled trial with drug and visual sensitivity monitoring. Br J Dermatol 1987;116:379-86.
  3. Wolf P, Soyer HP, Fink-Puches R, Huff JC, Kerl H. Recurrent post-herpetic erythema multiforme mimicking polymorphic light and juvenile spring eruption: report of two cases in young boys. Br J Dermatol 1994;131:364-7.
  4. Grabczynska, McGregor, Kondeatis, Vaughan, Hawk. Actinic prurigo and polymorphic light eruption: common pathogenesis and the importance of HLA-DR4/DRB1*0407. British Journal of Dermatology 1999;140:232-6.
  5. McGregor JM, Grabczynska S, Hawk JLM, Vaughan R, Lewis CM. Genetic Modeling of Abnormal Photosensitivity in Families with Polymorphic Light Eruption and Actinic Prurigo. Journal of Investigative Dermatology 2000;115:471-6.
  6. Das S, Lloyd JJ, Walshaw D, Farr PM. Provocation testing in polymorphic light eruption using fluorescent ultraviolet (UV) A and UVB lamps. Br J Dermatol 2004;151:1066-70.
  7. Palmer RA, Friedmann PS. Ultraviolet Radiation Causes Less Immunosuppression in Patients with Polymorphic Light Eruption Than in Controls. Journal of Investigative Dermatology 2004;122:291-4.
  8. Richards HL, Ling TC, Evangelou G, Brooke RCC, Fortune DG, Rhodes LE. Evidence of high levels of anxiety and depression in polymorphic light eruption and their association with clinical and demographic variables. British Journal of Dermatology 2008;159:439-44.
  9. Lebwohl, Mark. Treatment of Skin Disease: Comprehensive Therapeutic Strategies. Elsevier, 2014. Print.