Polymorphous Light Eruption Treatment & Management

  • Author: Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jul 27, 2011
 

Medical Care

Prophylactic therapy (eg, avoiding sunlight, wearing protective clothing, using sunscreen) remains a key factor in the care of patients with polymorphous light eruption (PMLE). Sunscreens with high sun protection factor (SPF) values are not protective against UV-A–induced PMLE. Systemic vitamin C and vitamin E do not prevent photoprovocation test reactions in persons with PMLE.

In a randomized, double-blinded, placebo-controlled clinical study by Hadshiew et al, the efficacy of a new topical formulation was compared with a broad-spectrum sunscreen.[26] The new product contained 0.25% alpha-glucosylrutin (a natural, modified flavonoid) and 1% tocopheryl acetate (vitamin E). Thirty patients with a history of PMLE were pretreated with the formulations 30 minutes prior to daily photoprovocation with UV-A irradiation of 60-100 J/cm2 to the upper arms.

The authors found a statistically significant difference (P < .001) between the antioxidant-containing formulations and placebo and between the sunscreen-only formulation. Only a single patient treated with the new antioxidant UV-protective gel formulation developed clinical signs of PMLE in the area treated. In comparison, 62.1% of the placebo-treated areas and 41.3% of the sunscreen-only treated areas showed mild-to-moderate signs of PMLE. The authors suggested that combining a potent antioxidant with a broad-spectrum sunscreen is far more effective in preventing PMLE than sunscreen alone. Also see Sunscreens and Photoprotection.

Gruber-Wackernagle et al evaluated the preventive effect of a cream containing calcipotriol (an analog of calcitriol, 1,25-dihydroxyvitamin D3) in a randomized double-blinded placebo-controlled intraindividual half-body trial.[27] Thirteen patients with PMLE applied cream (calcipotriol or placebo) topically to symmetrically located pairs of test areas twice daily for 7 days before photoprovocation with solar-simulated UV radiation was begun.

The authors used a specific PMLE test score based on affected area, skin infiltration, and pruritus to rate symptom severity at 48, 72, and 144 h after the first photoprovocation exposure. They found pretreatment with calcipotriol, compared with placebo, significantly reduced PMLE symptoms on average by 32% (P=0.0022) over the time series, suggesting a possible benefit from prophylactic use of topical 1,25-dihydroxyvitamin D3 analogs in patients with PMLE.[27] However, this does not change the standard of care for PMLE.

Jeanmougin et al studied the effectiveness 0.25% alpha-glucosyl-rutin, 1% vitamin E, and a broad-spectrum highly UVA–protective sunscreen (SPF 15; persistent pigmentation darkening 6) under real solar exposure conditions in the spring and summer.[28] The cream was applied every 2 hours after the first summer exposure. No topical or systemic treatments to prevent PMLE were used; dermatologists checked patients after the summer was over and interviewed them.

In this study, 52 of 54 patients finished study, and 67% of patients had no eruptions, 19% had minor eruptions, and 13% had severe eruptions of PMLE.[28] Pruritus, which had been present in all patients the year preceding the study, was not observed in 69% of patients and was unbearable for only 3 patients (compared with 27 patients before the study preparation was used).The dermatologic assessment was that global efficacy was approximately 80%, with inadequate results in 10% of cases; specifically, it was deemed excellent for 35 patients and good for 7 patients.

DeLeo et al reported that sunscreen with 4 UVA filters (ie, ecamsule 3%, octocrylene 10%, avobenzone 2%, and titanium dioxide 5%) was more effective for preventing PMLE flares than a sunscreen with a triad of UVA blockers.[29] Other studies support the use of UVA blockers to help prevent PMLE.[30]

  • Prophylactic phototherapy or photochemotherapy at the beginning of spring for several weeks may prevent flare-ups throughout the summer. PUVA was found to be superior to UV-B in several studies, controlling the outbreaks in 90% of patients.[31] Oral prednisone may be useful in conjunction with phototherapy to avoid eruption during therapy. Narrow-band UV-B (311 nm) may be an acceptable alternative to PUVA. In a study of 25 patients with severe PMLE, both modalities were equally effective.[32] Barolet and Boucher report on the use of light-emitting diode (LED) nonthermal therapy as a prophylactic measure for PMLE.[33]
  • When preventive measures fail and light therapy is ineffective or contraindicated, pharmacologic treatment assumes its role. Topical corticosteroids are useful, as would be expected in many dermatoses associated with lymphocytic skin infiltrate. Tachyphylaxis and skin atrophy limit their use. Antihistamines may help with pruritus. Systemic steroids may be needed to suppress acute flares or extensive generalized eruption. Adverse effects of prolonged systemic steroid use include decreased glucose tolerance, osteoporosis, impaired immunity, and weight gain. Obviously, this treatment can only be offered intermittently and for a short period of time. It may also be considered for patients going on vacation or for those patients experiencing other unavoidable sun exposure.
  • Antimalarials at low doses are sometimes helpful, especially in patients with a large papular variety of PMLE. Beta-carotene, which is effective in erythropoietic protoporphyria, may be an alternative to chloroquine.[34] Oral carotenoid preparation (beta-carotene and canthaxanthin in a daily total dose of 100 mg) was compared to hydroxychloroquine (200 mg qd). Both offered full sun tolerance in an equal but small, percentage of patients, when compared to a placebo.
  • Some authorities believe that vitamin therapy is helpful in the treatment of PMLE. Nicotinamide was successful in 60% of 42 patients treated with 3 g/d orally for 2 weeks.[35] The rationale for its use was the knowledge that it blocks the formation of kynurenic acid, a photosensitizer that may play a role in PMLE. Ahmed et al found that oral vitamin E supplementation (400 IU) and use of sunblock decreased the markers of oxidative stress and lipid peroxidation in patients with PMLE.[36]
  • Azathioprine was reported to be effective in 2 cases of recalcitrant severe disease at 0.8-2.5 mg/kg/d for 3 months.[37] In one patient, the effect lasted up to 4 months after the discontinuation of therapy. However, the limited available data and azathioprine toxicity should necessitate extreme caution in choosing this form of treatment.
  • Interest in the use of thalidomide for a number of dermatoses (eg, Behçet syndrome, cutaneous lupus, porphyria cutanea tarda [PCT], PMLE) is reemerging. The immunomodulatory action on subsets of T cells was proposed. Thalidomide (50-200 mg PO qhs) has reportedly been very effective for Native American patients with PMLE. The most commonly described adverse effects with thalidomide are sedation, constipation, and weight gain.
    • The most serious complications of thalidomide are peripheral neuropathy and teratogenicity. Unfortunately, no recent published controlled trials of this drug being used in the treatment of PMLE are available. Thalidomide is available only to pharmacies and physicians participating in the System for Thalidomide Education and Prescribing Safety (STEPS) program. A new variant of thalidomide is available.
    • Lenalidomide (Revlimid, formerly known as Revimid) is the first of a new class of oral cancer drugs called IMiDs. This immunomodulatory drug is chemically similar to thalidomide. However, it is more powerful in the laboratory. It appears to lack some of the more common adverse effects of thalidomide. Its role in the treatment of PMLE is uncertain.
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Contributor Information and Disclosures
Author

Noah S Scheinfeld, MD, JD, FAAD  Assistant Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, and New York Eye and Ear Infirmary; Private Practice

Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Optigenex Consulting fee Independent contractor

Coauthor(s)

Sophie Shirin, MD  Consulting Staff, Global Dermatology

Sophie Shirin, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Raul Del Rosario, MD  Consulting Staff, Dermatopathology, Mission Hospital at Laguna Beach

Raul Del Rosario, MD is a member of the following medical societies: American Society for Clinical Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Craig A Elmets, MD  Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Palomar Medical Technologies Stock None; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor; UpToDate Salary Employment; Biogen Grant/research funds Independent contractor; Clinuvel Independent contractor; Covan Basilea Pharmaceutical Grant/research funds Independent contractor; ISDIN None Consulting; TenX BIopharma Grant/research funds Independent contractor

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD  Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Dr. Ada Winkielman, to the development and writing of this article.

References

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The face of a patient with polymorphous light eruption. Note the erythema and an indurated plaque.
Close-up view of polymorphous light eruption plaque.
Papular variant of polymorphous light eruption.
Large facial plaques.
Histopathologic features of polymorphous light eruption. Note the tight perivascular lymphocytic infiltrate in the upper dermis.
Close-up view of the perivascular infiltrate.
Photograph of a springtime eruption of polymorphous light eruption in a 6-year-old boy. The eruption has occurred in the spring since the patient was aged 5 years, and it resolves completely with no scarring by mid to late summer. High block sunscreens attenuate but do not prevent the eruption. No itching or pain occurs. Courtesy of Jeremy F. Harrison, FRCA, FFAEM.
 
 
 
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