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. 2017 Oct 9;2017(10):CD005069. doi: 10.1002/14651858.CD005069.pub3

Interventions for polymorphic light eruption

Tsui Chin Ling 1,✉, Robert S Dawe 2, Elizabeth Gardener 3, Lesley E Rhodes 1,4
PMCID: PMC6485352

Abstract

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:

To assess the effects of interventions in the prophylaxis and treatment of polymorphic light eruption.

Background

Description of the condition

Polymorphic Light Eruption (PLE) (also known as polymorphous light eruption and benign summer light eruption) is a recurrent, itchy skin eruption occurring on exposed skin sites after sun exposure, which heals without scarring within 14 days (Hawk 1999). The presenting skin eruption is most commonly spots and blisters but may also take other forms, including plaques (raised patches), large blisters, eczematous areas and bruising. It often presents in a cyclical fashion, beginning in spring and fading by autumn. Sun exposure of between 30 minutes to several hours is required to trigger PLE, with the rash appearing several minutes to hours later.

'Hereditary' PLE, first described in Amerindians, is now recognised to be actinic prurigo, a separate entity, and is not considered in this review. Another condition, 'juvenile spring eruption', sometimes considered to be a variant of PLE in children, is also excluded from this review as it behaves and is treated differently.

Epidemiology

PLE, the most common photosensitivity disorder in white people, is estimated to affect 11%‐21% of the population in temperate climates (Morison 1982; Pao 1994; Ros 1986). The prevalence of PLE appears to rise with increasing distance from the equator. Pao et al found that the prevalence is 5.2% in Perth (latitude 32 degrees), 3.6% in Ballarat (37.5 degrees) and 14.8% in London (51.5 degrees). PLE is rarely reported in tropical countries. The precise explanation for the higher prevalence in temperate climates is likely to be the greater proportion of long wave (UVA) to short wave ultraviolet light (UVB) with increasing distance from the equator (Farr 1989; Pao 1994), since UVB is an effective suppressor of the immune response in the skin whereas UVA may more commonly provoke the rash.

Mechanisms

The disorder is almost certainly a delayed‐type hypersensitivity immunological reaction (Norris 1989a) with evidence of impairment of ultraviolet‐induced suppression of the immune response in the skin (Kolgen 1999; Palmer 2004; van de Pas 2004). A positive family history is present in 10%‐63% of cases (Jansen 1979; Morison 1982; Pao 1994; Ros 1986). It is likely that the underlying cause may be a combination of environmental and genetic factors (McGregor 2000; Millard 2000).

Impact

For the majority of people with PLE, the disease is mild and self‐limiting and quickly settles within a few days with sun avoidance. The proportion of people with PLE who seek medical attention is estimated to be less than 26% (Morison 1982; Pao 1994; Ros 1986), although this still represents a very large number of people, considering PLE may affect up to 21% of the population.

Description of the intervention

Therapies for PLE may be preventive or suppressive, and their application depends on the severity of the disease, availability of equipment, and the patient's preference. Oral and topical corticosteroids and prophylactic phototherapy are commonly used for PLE, and there is an array of other treatments that have also been used (Ling 2003). The most common are:

Sun avoidance, sunscreen application

Preventive management is routinely advocated by sun avoidance between 11 a.m. and 3 p.m., use of protective clothing, and application of sunscreen. However, for more severe PLE sufferers, this is rarely adequate. Previous studies have demonstrated that photosensitive people only apply approximately a quarter of the thickness of cream used under the manufacturers' test conditions and that certain exposed body sites (ears, temples, posterior and lateral neck) are often missed (Azurdia 1999). In addition, people can become allergic to sunscreen ingredients. Sunscreen agents are now the commonest cause of positive photopatch tests (BPG Workgroup 1997). Furthermore, sunscreens protect against UVB but less well against UVA. Since UVB tends to inhibit the occurrence of PLE and UVA tends to provoke the rash, the application of sunscreen may, paradoxically, make the rash more likely to occur.

Topical and oral steroids

Topical steroids are widely used for mild episodes of PLE. An immediate short course of oral prednisolone considerably reduces the severity of itch and rash in people who suffer from occasional, severe attacks of PLE on vacation (Patel 2000). However, some people may take several holidays per year and the side effects of repeated courses of prednisolone must be considered.

Phototherapy (therapy with ultraviolet radiation only), photochemotherapy (therapy with ultraviolet radiation and psoralen sensitiser medication)

Psoralen‐UVA (PUVA), narrow‐band (NBUVB) or broadband UVB (BBUVB) phototherapy is currently the mainstay of treatment for more severe PLE. A course may also be administered in early spring as a preventive treatment to induce skin tolerance for more severe PLE. The mechanisms by which phototherapy induces subsequent protection from the sun are likely to be through cutaneous immunosuppression (Krutmann 1999). The carcinogenic potential of PUVA is well known (Stern 1988). In people treated with PUVA for psoriasis the incidence of skin cancer (squamous cell carcinoma and melanoma) is significantly increased and this risk persists (Stern 1998), and indeed continues to increase, with the passage of time after treatment (Stern 2001). BBUVB is also associated with increased photocarcinogenicity in people with psoriasis (Pasker‐de Jong 1999), and animal studies suggest that NBUVB may be associated with twice this risk (Gibbs 1995). Thus, the risk of skin cancer and also the time, cost and inconvenience involved in the treatment, have to be weighed against the benefits of ultraviolet therapy. However, in the lower doses used as a prophylactic treatment for PLE, the carcinogenic risks are anticipated to be lower (no long term follow up data are available).

Other anti‐inflammatory agents and immunomodulators that have been used include:

Why it is important to do this review

There are many reported treatments for PLE. Sun protection, corticosteroids and desensitisation phototherapy appear to be the current mainstay of treatment, with immunomodulator agents as second‐line treatment. In all treatments, the therapeutic benefits need to be weighed against the potential side effects. In addition, ultraviolet therapy with or without sensitiser medication (i.e. photochemotherapy and phototherapy respectively) require comparison to establish the most efficacious methodology with the best side effect profile.

Objectives

To assess the effects of interventions in the prophylaxis and treatment of polymorphic light eruption.

Methods

Criteria for considering studies for this review

Types of studies

All randomised controlled trials (RCTs) that evaluate the effectiveness of both topical and systemic interventions for polymorphic light eruption will be considered.

Types of participants

Any individual who has been diagnosed by a dermatologist as having polymorphic light eruption, polymorphous light eruption, or benign summer light eruption. 'Hereditary PLE' (actinic prurigo), and juvenile spring eruption will not be considered in this review.

Types of interventions

Interventions to be assessed in this review include:

First line

  1. behavioural (clothing, environmental, and topical sunscreen, i.e. sunlight protection measures);

  2. corticosteroids (topical and oral).

Second line

  1. phototherapies (broad‐band and narrow‐band ultraviolet B, broad‐band ultraviolet A, ultraviolet A1);

  2. psoralen‐photochemotherapy (8‐MOP + UVA, oral trimethoxpsoralen + UVA, topical trioxsalen + UVA);

  3. systemic immunosuppressants;

  4. other possible immunomodulators and anti‐inflammatory agents (nicotinamide, live attenuated E. coli extract, dead E. coli extract, dietary fish oil, beta‐carotene, antioxidants, and others).

Types of outcome measures

Primary outcomes

(a) participant global self assessment (b) improvement in Quality of Life questionnaires

Secondary outcomes

(a) the decrease in the severity of subjective symptoms of pruritus and rash (b) duration of remission of PLE episodes (c) the speed of resolution of an established episode of PLE (d) the increase in sun tolerance, i.e. time spent in the sun (e) severe adverse events i.e. sufficient to require withdrawal of treatment. (f) minor adverse events, for example mild skin irritation not sufficient to require withdrawal of treatment

Search methods for identification of studies

Electronic searches

Relevant trials will be identified from:

  • the Cochrane Skin Group Specialised Register, which contains the results of a comprehensive programme of ongoing handsearching of dermatological journals and conference proceedings, and the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (last update);

  • MEDLINE (from 2003) and EMBASE (from 2003) ‐ see Appendix 1;

  • the metaRegister of Controlled Trials, which includes the UK NHS National Research Register (www.controlled‐trials.com), will be searched for ongoing trials.

Searching other resources

References from published studies

The bibliographies will be scanned for possible references to RCTs.

Unpublished literature

Unpublished and on‐going trials will be identified by correspondence with authors.

Conference proceedings

The abstracts from the International Research Workshops on photodermatology and major dermatology conference proceedings over the last five years will be scanned for further RCTs.

Adverse effects

A search will be made for adverse effects of drugs used for polymorphic light eruption.

Other

No language restrictions will be imposed and translations will be sought where necessary.

Data collection and analysis

Selection of studies

Titles and abstracts identified from the searches will be checked by one reviewer (TL). If it is clear that the study does not refer to a randomised controlled trial on polymorphic light eruption, it will be excluded. Two reviewers (TL, LR) will independently assess each study to determine whether it meets the pre‐defined selection criteria. Any differences will be resolved through discussion with the review team. Excluded studies will be stated.

Data extraction and management

This will be performed independently by two reviewers (TL, LR) and differences resolved by a third team member (RD). Any missing data will be obtained from the authors where possible. A data collection form will be developed and piloted in order to summarise the trials. Data will be checked and entered by one reviewer (TL).

Assessment of risk of bias in included studies

The assessment of risk of bias will include an evaluation of the following components for each included study, since there is some evidence that these are associated with biased estimates of treatment effect (Juni 2001): (a) the method of generation of the randomisation sequence; (b) the method of allocation concealment ‐ it will be considered 'adequate' if the assignment cannot be foreseen; (c) who was blinded/not blinded (participants, clinicians, outcome assessors); (d) how many participants were lost to follow up in each arm, and whether participants were analysed in the groups to which they were originally randomised (intention to treat).

In addition the assessment will also include: (e) degree of certainty that the participants have PLE; (f) baseline assessment of the participants for age, sex, duration, clinical severity of PLE and response to previous therapies; (g) aims, interventions (including drug doses and duration of treatment) and outcome measures clearly defined; (h) use and appropriateness of statistical analyses.

The information will be recorded in a table of quality criteria and a description of the quality of each study will be given based on a summary of these components.

Measures of treatment effect

A pooled treatment effect (using a random effects model) will be calculated across trials.

Dichotomous outcomes

Dichotomous outcomes such as occurrence of severe adverse events and occurrence of minor adverse events will be expressed as odds ratio (OR) and 95% confidence intervals (CI). The result will also be expressed as number needed to treat (NNT), where appropriate, with a 95% CI and the baseline risk to which it applies.

Scales and Continuous outcomes

Where appropriate, scales and continuous outcomes will be expressed as weighted mean difference (WMD and 95% CI). When different scales are used to measure the same outcome (for example, quality of life) the scores will be standardised by dividing the reported difference in means between the groups by the overall standard deviation of outcome.

The participant rated global assessment will be the primary outcome measure if available. The data will be dichotomised, where possible, into the proportion of people reporting improvement/no improvement. If this outcome is not available, the medical practitioner global rating will be used. Both measures will be taken into account where both are available. No attempt will be made to combine these measures, as they are often not well correlated.

Time to event outcomes

Time to event outcomes such as time to resolution will be summarised using the log hazard ratio and its variance. If these are not provided in the trial report they will be estimated from other summary statistics presented, such as p‐value or test statistic from log‐rank test, or from survival curves. Techniques suggested in Parmar 1998 will be used.

Subgroup analysis and investigation of heterogeneity

Heterogeneity will be assessed using I2. If substantial heterogeneity (I2 > 50%) exists between studies for the primary outcome, reasons for heterogeneity, such as disease severity, dosage and duration of treatment, will be explored. Further subgroup analysis will be performed where adequate information is given. Sensitivity analyses may also be conducted to examine the effects of excluding poor quality studies, and studies in which major imbalances in baseline characteristics (such as disease severity) were present.

Cross‐over trials will be analysed using techniques appropriate for paired designs. Non‐randomised controlled studies will be listed but not discussed further. Studies relating to adverse effects will be described qualitatively.

Other

Where there is uncertainty authors will be contacted for clarification. A consumer (ER) will be consulted throughout, particularly for readability and understanding of the final review.

Acknowledgements

The editorial base would like to thank the following people who were external referees for this review: John Hawk (content expert), Andrea Levitt (consumer).

Appendices

Appendix 1. Search strategy for MEDLINE (OVID)

(i) Search strategy to locate RCTs Search terms 1‐29, as given in the Cochrane Handbook (Alderson 2004), Appendix 5b.2 (ii) Search strategy to locate polymorphic light eruption 30. polymorph$ light eruption.mp. 31. benign summer light eruption.mp. 32. eczema solare.mp. 33. summer prurigo.mp. 34. prurigo aestivalis.mp. 35. prurigo adolescentium.mp. 36. acne prurigo.mp. 37. or/30‐36

(iii) Search strategy to locate interventions for polymorphic light eruption 38. (sun protection or photoprotection).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading] 39. behavio?r$.mp. or exp BEHAVIOR/ 40. (sunscreen or sunblock).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading] 41. exp PHOTOTHERAPY/ 42. exp PHOTOCHEMOTHERAPY/ 43. (ultraviolet therapy or UV therapy).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading] 44. exp PUVA Therapy/ 45. UVB.mp. 46. UVA1.mp. 47. desensiti#ation.mp. 48. UV hardening.mp. 49. exp STEROIDS/ 50. exp PREDNISOLONE/ or exp PREDNISOLONE, TOPICAL/ 51. (betacarotene or b‐carotene).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading] 52. exp CAROTENOIDS/ 53. exp ANTIMALARIALS/ 54. (hydroxychloroquine or chloroquine).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading] 55. exp ANTIOXIDANTS/ 56. exp Niacinamide/ 57. exp Immunosuppressive Agents/ 58. exp Cyclosporine/ 59. exp AZATHIOPRINE/ 60. exp DIET/ 61. exp Fish Oils/ 62. exp Fatty Acids, Omega‐3/ 63. exp Escherichia coli/ 64. exp THALIDOMIDE/ 65. exp beta Carotene/ 66. or/38‐65

The results of searches (i), (ii) and (iii) will be combined with the Boolean operator AND.

This is a draft search strategy and will be adapted to include additional search terms where necessary and will be modified for the other databases listed.

What's new

Date Event Description
9 October 2017 Amended The authors have relinquished responsibility for this protocol. It was published some years ago, and Cochrane Skin have decided to withdraw it (Managing Editor, Cochrane Skin).
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History

Protocol first published: Issue 1, 2005

Date Event Description
5 October 2008 Amended Proposed changes to Revman 5 format reviewed and amendments made.
31 July 2008 Amended Converted to new review format.
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Contributions of authors

The following contributions will be made by the reviewers stated: Link with editorial base and coordinate contributions from co‐reviewers (TL) Draft the protocol (TL, LR with contributions from all) Search for trials (TL, RD) Obtain copies of trials (TL) Select which trials to include (TL, LR and RD as arbitrator when necessary) Extract data from trials (TL, LR) Enter data into RevMan (TL) Carry out analysis (TL, EG) Interpret analysis (TL, EG, RD, LR) Draft final review (TL, LR with contribution from all) Update review (TL)

Sources of support

Internal sources

  • University of Manchester, UK.

  • Hope Hospital, Salford, UK.

External sources

  • SUNALL research group, Other.

Declarations of interest

None known.

Notes

The authors have relinquished responsibility for this protocol. It was published some years ago, and Cochrane Skin have decided to withdraw it (Managing Editor, Cochrane Skin).

Withdrawn from publication for reasons stated in the review

References

Additional references

  1. Alderson P, Green S, Higgins JPT (eds). Cochrane Reviewers’ Handbook 4.2.1 [updated December 2003]. The Cochrane Library, Issue 1. Chichester, UK: John Wiley & Sons, Ltd, 2004. [Google Scholar]
  2. Azurdia RM, Pagliaro JA, Diffey BL, Rhodes LE. Sunscreen application by photosensitive patients is inadequate for protection. British Journal of Dermatology 1999;140(2):255‐8. [DOI] [PubMed] [Google Scholar]
  3. Birt AR, Davis RA. Hereditary polymorphic light eruption of American Indians. International Journal of Dermatology 1975;14(2):105‐11. [DOI] [PubMed] [Google Scholar]
  4. British Photodermatology Group. Photopatch testing ‐ methods and indications. British Journal of Dermatology 1997;136(3):371‐6. [PubMed] [Google Scholar]
  5. Corbett MF, Hawk JLM, Herxheimer A. Controlled therapeutic trials in polymorphic light eruption. British Journal of Dermatology 1982;107:571‐81. [DOI] [PubMed] [Google Scholar]
  6. Farr PM, Diffey BL. Adverse effects of sunscreens in photosensitive patients. Lancet 1989;1(8635):429‐31. [DOI] [PubMed] [Google Scholar]
  7. Gibbs NK, Traynor NJ, MacKie RM, Campbell I, Johnson BE, Ferguson J. Phototumorigenic potential of broad‐band (280‐340nm) and narrow‐band (310‐313nm) phototherapy sources cannot be predicted by their edematogenic potential in hairless mouse skin. Journal of Investigative Dermatology 1995;104:359‐63. [DOI] [PubMed] [Google Scholar]
  8. Hadshiew I, Stab F, Untiedt S, Bohnsack K, Rippke F, Holzle E. Effects of topically applied antioxidants in experimentally provoked polymorphous light eruption. Dermatology 1997;195:362‐8. [DOI] [PubMed] [Google Scholar]
  9. Hawk JL. Photodermatology. Arnold, 1999. [Google Scholar]
  10. Jansen CT. The natural history of polymorphous light eruptions. Archives of Dermatology 1979;115(2):165‐9. [PubMed] [Google Scholar]
  11. Jansen CT. Oral carotenoid treatment in polymorphous light eruption: a cross‐over comparison with oxychloroquine and placebo. Photodermatology 1985;2(3):166‐9. [PubMed] [Google Scholar]
  12. Juni P, Altman DG, Egger M. Assessing the quality of controlled clinical trials. British Medical Journal 2001;323:42‐6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Kolgen W, Weelden H, Hengst S. CD11b+ cells and ultraviolet‐B‐resistant CD1a+ cells in skin of patients with polymorphous light eruption. Journal of Investigative Dermatology 1999;113(1):4‐10. [DOI] [PubMed] [Google Scholar]
  14. Krutmann J, Morita A. Mechanisms of ultraviolet (UV) B and UVA phototherapy. Journal of Investigative Dermatology Symposium Proceedings 1999;4(1):70‐2. [DOI] [PubMed] [Google Scholar]
  15. Ling TC, Gibbs NK, Rhodes LE. Treatment of polymorphic light eruption. Photodermatology Photoimmunology Photomedicine 2003;19:217‐27. [DOI] [PubMed] [Google Scholar]
  16. McGregor JM, Grabczynska S, Vaughan R, Hawk JL, Lewis CM. Genetic modelling of abnormal photosensitivity in families with polymorphic light eruption and actinic prurigo. Journal of Investigative Dermatology 2000;115:471‐6. [DOI] [PubMed] [Google Scholar]
  17. Millard TP, Bataille V, Snieder H, Spector TD, McGregor JM. The heritability of polymorphic light eruption. Journal of Investigative Dermatology 2000;115(3):467‐70. [DOI] [PubMed] [Google Scholar]
  18. Morison WL, Stern RS. Polymorphous light eruption: a common reaction uncommonly recognized. Acta Dermato Venereologica 1982;62(3):237‐40. [PubMed] [Google Scholar]
  19. Murphy GM, Hawk JL, Magnus IA. Hydroxychloroquine in polymorphic light eruption: a controlled trial with drug and visual sensitivity monitoring. British Journal of Dermatology 1987;116:379‐86. [DOI] [PubMed] [Google Scholar]
  20. Neumann R, Rappold E, Pohl‐Markl H. Treatment of polymorphous light eruption with nicotinamide: a pilot study. British Journal of Dermatology 1986;115(1):77‐80. [DOI] [PubMed] [Google Scholar]
  21. Norris PG, Morris J, McGibbon DM, Chu AC, Hawk JLM. Polymorphic light eruption: an immunopathological study of evolving lesion. British Journal of Dermatology 1989;120:173‐183. [DOI] [PubMed] [Google Scholar]
  22. Norris PG, Hawk JLM. Successful treatment of severe polymorphous light eruption with azathioprine. Archives of Dermatology 1989;125(10):1377‐9. [PubMed] [Google Scholar]
  23. Palmer RA, Friedmann PS. Ultraviolet radiation causes less immunosuppression in patients with polymorphic light eruption than in controls. Journal of Investigative Dermatology 2004;122(2):291‐4. [DOI] [PubMed] [Google Scholar]
  24. Pao C, Norris PG, Corbett M, Hawk JLM. Polymorphic light eruption: prevalence in Australia and England. British Journal of Dermatology 1994;130:62‐4. [DOI] [PubMed] [Google Scholar]
  25. Parmar MK, Torri V, Stewart L. Extracting summary statistics to perform meta‐analyses of the published literature for survival endpoints. Statistics in Medicine 1998;17:2815‐34. [DOI] [PubMed] [Google Scholar]
  26. Pasker‐de Jong PCM, Wielink G, Valk PGM, Wilt GJ. Treatment with UVB for psoriasis and nonmelanoma skin cancer. Archives of Dermatology 1999;135:834‐40. [DOI] [PubMed] [Google Scholar]
  27. Patel DC, Bellaney GJ, Seed PT, McGregor JM, Hawk JL. Efficacy of short‐course oral prednisolone in polymorphic light eruption: a randomized controlled trial. British Journal of Dermatology 2000;143(4):828‐31. [DOI] [PubMed] [Google Scholar]
  28. Przybilla B, Heppeler M, Ruzicka T. Preventive effect of an E. coli‐filtrate (Colibiogen) in polymorphous light eruption. British Journal of Dermatology 1989;121(2):229‐33. [DOI] [PubMed] [Google Scholar]
  29. Rhodes LE, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal and ultraviolet B‐generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. Journal of Investigative Dermatology 1995;105(4):532‐5. [DOI] [PubMed] [Google Scholar]
  30. Ros AM, Wennersten G. Current aspects of polymorphous light eruptions in Sweden. Photodermatology 1986;3(5):298‐302. [PubMed] [Google Scholar]
  31. Shipley DRV, Hewitt JB. light eruption treated with Cyclosporin. British Journal of Dermatology 2001;144:446‐7. [DOI] [PubMed] [Google Scholar]
  32. Stern RS, Lange R. Non‐melanoma skin cancer occurring in patients treated with PUVA five to ten years after first treatment. Journal of Investigative Dermatology 1988;91(2):120‐4. [DOI] [PubMed] [Google Scholar]
  33. Stern RS, Liebman EJ, Vakeva L. Oral psoralen and ultraviolet‐A light (PUVA) treatment of psoriasis and skin cancer. PUVA Follow‐up Study. Journal of National Cancer Institute 1998;90(17):1278‐84. [DOI] [PubMed] [Google Scholar]
  34. Stern RS. The risk of melanoma in association with long‐term exposure to PUVA. Journal of the American Academy of Dermatology 2001;44(5):755‐61. [DOI] [PubMed] [Google Scholar]
  35. Pas CB, Kelly DA, Seed PT, Young AR, Hawk JL, Walker SL. Ultraviolet‐radiation‐induced erythema and suppression of contact hypersensitivity responses in patients with polymorphic light eruption. Journal of Investigative Dermatology 2004;122(2):295‐9. [DOI] [PubMed] [Google Scholar]

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