eMedicine Specialties > Dermatology > Photo-Related Diseases

Polymorphous Light Eruption: Treatment & Medication

Author: Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice
Coauthor(s): Sophie Shirin, MD, Consulting Staff, Global Dermatology; Raul Del Rosario, MD, Consulting Staff, Surgical Pathology and Dermatopathology, South Coast Medical
Contributor Information and Disclosures

Updated: Oct 23, 2009

Treatment

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.20 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.

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.21 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.21 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.22 Other studies support the use of UVA blockers to help prevent PMLE.23

  • 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.24 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.25 Barolet and Boucher report on the use of light-emitting diode (LED) nonthermal therapy as a prophylactic measure for PMLE.26
  • 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.27 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.28 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.29
  • Azathioprine was reported to be effective in 2 cases of recalcitrant severe disease at 0.8-2.5 mg/kg/d for 3 months.30 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 lupusporphyria 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.

Medication

The goals of pharmacotherapy for polymorphous light eruption (PMLE) are to reduce morbidity and to prevent complications.

Antimalarials

These agents may have immunomodulatory effects.


Hydroxychloroquine (Plaquenil)

Inhibits chemotaxis of eosinophils, locomotion of neutrophils, and impairs complement-dependent antigen-antibody reactions.
Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Adult

200-400 mg/d PO in divided doses

Pediatric

10 mg base/kg PO initially, followed by 5 mg/kg at 6, 24, 48 h

Cimetidine increases levels; kaolin and magnesium trisilicate decrease levels; increases digoxin levels; do not administer chloroquine and hydroxychloroquine together (retinal toxicity)

Absolute: Documented hypersensitivity, retinopathy from any cause.
Relative: Pregnancy, breastfeeding, retinal and visual-field changes, severe blood dyscrasias, psoriasis, G-6-PD deficiency (caution advocated, but routine G-6-PD screening not recommended; associated with hemolysis, but not in usual dosage range), significant hepatic dysfunction, myasthenia gravis, significant neurologic disease, long-term therapy in children (Physicians Desk Reference lists as contraindication; main concern is overdose/toxicity; chronic toxicity risk, however, is thought to be no greater than in adults; neither drug available as a syr; crush tab and mask bitter taste in jam, applesauce, or other food)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; not recommended for long-term use in children; perform baseline and periodic (6 mo) ophthalmologic examinations; test periodically for muscle weakness

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.


Prednisone (Deltasone, Meticorten, Orasone)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocyte and antibody production.

Adult

0.05-2 mg/kg/d PO divided bid/qid; not to exceed 80 mg qd or divided bid/qid; individualize according to severity of disease, patient response, and weight; taper over 1-2 wk as symptoms resolve

Pediatric

4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve

Ketoconazole, erythromycin, clarithromycin, estrogens, and birth control pills increase levels; aminoglutethimide, phenytoin, phenobarbital, rifampin, cholestyramine, and ephedrine decrease levels; increases levels of potassium-depleting diuretics (potentiates potassium loss and digitalis toxicity) and cyclosporine; decreases levels of isoniazid, insulin (resistance is induced), and salicylates; monitor anticoagulant therapy and theophylline levels

Absolute: Systemic fungal infection, herpes simplex keratitis, documented hypersensitivity (usually with corticotropin; occasionally with IV preparations)
Relative: Hypertension, active TB, CHF, prior psychosis, positive intermediate purified protein derivative test result, glaucoma, severe depression, diabetes mellitus, active peptic ulcer disease, cataracts, osteoporosis, recent bowel anastomosis, pregnancy

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid vaccination if patient on high doses of steroids; avoid exposure to chickenpox and measles; may exacerbate diabetes, high blood pressure, osteoporosis, peptic ulcer disease, and tuberculosis; abrupt discontinuation of glucocorticoids may cause adrenal crisis

Immunomodulators

These agents modify the activity of key factors in the immune system.


Thalidomide (Thalomid)

Drug only supplied to pharmacies participating in STEPS program. Immunomodulatory agent that may suppress excessive production of TNF-alpha and may down-regulate selected cell surface adhesion molecules involved in leukocyte migration.

Adult

50-200 mg PO hs

Pediatric

Not established

May increase sedation of alcohol, barbiturates, chlorpromazine, and reserpine; because of teratogenic effects, women must use 2 additional methods of contraception or abstain from intercourse

Documented hypersensitivity; pregnancy

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Perform pregnancy test within 24-h period prior to initiating therapy (weekly during the first month, followed by monthly tests in women with regular menstrual cycles or q2wk in women with irregular menstrual cycles); bradycardia may occur; use protective measures (eg, sunscreens, protective clothing) against exposure to sunlight or UV light (eg, tanning beds); prescribing physician must enter STEPS program established by manufacturer

Vitamins

These agents are essential for normal DNA synthesis and cell function.


Beta-carotene

May provide a limited level of photoprotection. Causes yellowing of skin (carotenoderma). Any photoprotection afforded will increase slowly after drug is commenced over 4- to 6-wk period. When discontinued, skin color and benefit fade over several weeks.

Adult

30-300 mg PO qd

Pediatric

30-150 mg PO qd

Coadministration with vitamin A may result in additive toxic effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with renal or hepatic impairment; may increase risk for lung cancer in heavy smokers; may cause orange stools and diarrhea or loose stools at onset of therapy that tends to resolve with continued use


Nicotinamide (Vitamin B-3)

Source of niacin used in tissue respiration, lipid metabolism, and glycogenolysis.

Adult

3 g/d PO used in a study quoted; 20 mg/d represents 100% RDA

Pediatric

Not established

Cutaneous vasodilation may be a problem if high-dose used with peripheral dilators, such as nitroglycerin; taking aspirin 30-60 min before first dose of the day may help alleviate prostaglandin-mediated adverse effects of niacin (eg, flushing, itching); clonidine may inhibit niacin-induced flushing

Documented hypersensitivity; active liver disease or unexplained, significant increases in AST and ALT levels; large doses of niacin, especially when administered in a sustained-release form (associated with severe hepatotoxicity); peptic ulcer disease (can reactivate ulcers)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in gallbladder disease or diabetes and those predisposed to gout; monitor blood glucose level; may elevate uric acid levels

More on Polymorphous Light Eruption

Overview: Polymorphous Light Eruption
Differential Diagnoses & Workup: Polymorphous Light Eruption
Treatment & Medication: Polymorphous Light Eruption
Follow-up: Polymorphous Light Eruption
Multimedia: Polymorphous Light Eruption
References

References

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Further Reading

Keywords

polymorphous light eruption, polymorphic light eruption, PLE, PMLE rash, idiopathic photodermatosis, reaction to sunlight, ultraviolet radiation exposure, UV-R exposure, erythema multiforme–like lesions

Contributor Information and Disclosures

Author

Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, 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, Surgical Pathology and Dermatopathology, South Coast Medical
Raul Del Rosario, MD is a member of the following medical societies: American Society for Clinical Pathology
Disclosure: Nothing to disclose.

Medical Editor

Craig A Elmets, MD, Director of Dermatology, Departments of Dermatology, Pathology, and Environmental Health Sciences; Professor, The Kirklin Clinic, University of Alabama at Birmingham
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; Amgen Consulting fee Review panel membership; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University 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.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, 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 Honoraria Consulting; Centocor Honoraria Consulting; Medicis Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

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 None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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