AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Background

Polymorphous light eruption (PMLE) is an acquired disease and is the most common of the idiopathic photodermatoses. PMLE is characterized by recurrent, abnormal, delayed reactions to sunlight, ranging from erythematous papules, papulovesicles, and plaques to erythema multiforme–like lesions on sunlight-exposed surfaces. Within any 1 patient, only 1 clinical form is consistently manifested.

Richards et al¹ found that PMLE engenders a substantial psychosocial impact on patients who have the condition. Based on results from the Illness Perception Questionnaire sent to 302 patients and returned by 150 patients, 40% experienced emotional distress linked to PMLE. The psychological impact was related to the predicted consequences of PMLE, whereas health-related variables played a lesser role. Women associated more severe consequences linked to PMLE and were more emotionally distressed than men.

Pathophysiology

The etiology of PMLE is not fully known, and it is likely to be multifactorial. The immunologic pathogenesis of PMLE is supported by the study of timed biopsy samples of PMLE lesions. The CD4 subtype of T cells seen very early after exposure is replaced by CD8 lymphocytes 72 hours after irradiation. In general, findings conform to type IV delayed-type hypersensitivity mechanism.

In some PMLE lesions induced by UV-A, keratinocytes were found to express intercellular adhesion molecule 1 (ICAM-1).^{2, 3} ICAM-1 is absent from normal keratinocytes, but it is known to be strongly induced by interferon gamma. The induction of ICAM-1 on keratinocytes results either from direct effects of UV on the promoter region of the ICAM-1 gene or from indirect effects of interferon gamma produced by activated lymphocytes aggregating in an underlying PMLE.

Intravascular and focal perivascular deposits of fibrin were detected in biopsy samples of PMLE papules. Vascular deposits of C3 and immunoglobulin M (IgM) were noted in a few patients. These findings may suggest that vascular injury with activation of a clotting cascade may play a role in the pathogenesis of PMLE. Repair of ultraviolet-damaged DNA is normal.

The recent demonstration that the female hormone 17beta-estradiol prevents UV radiation–induced suppression of the contact hypersensitivity response caused by the release of immunosuppressive cytokines (interleukin [IL]–10) from keratinocytes might thus explain why the risk of PMLE is higher in females than in males and why the risk decreases in women after menopause.

Neutrophils may play a role in the development of PMLE. Immunohistochemical analysis by Schornagel et al⁴ in 2004 showed a significant decreased neutrophil infiltration in PMLE skin after UV-B irradiation compared with healthy case control subjects (P <.05). ICAM-1 and E-selectin expression on endothelial cells increased in both healthy controls and in the PMLE patients after UV-B irradiation. Chemotactic response towards IL-8 and C5a was not different between PMLE patients and healthy controls. The authors concluded that PMLE is marked by an altered immune response resulting in decreased skin infiltration of neutrophils after UV-B irradiation.

Kölgen et al⁵ noted that the reduced expression of tumor necrosis factor-alpha, IL-4, and IL-10 in the UV-B–irradiated skin of patients with PMLE. The reduction of these cytokines seems linked to a relative neutropenia and is a manifestation of decreased Langerhans cell migration and reduced TH2 skewing. An impairment of these mechanisms underlying UV-B–induced immunosuppression may be important in the pathogenesis of PMLE.⁶

Frequency

United States

PMLE affects about 10% of the US population. This figure is likely to be an underestimate because many patients do not seek medical attention. Many of the photodermatoses were lumped together before their individual pathogeneses were identified. PMLE is now a distinct clinical entity, as are many of the other photodermatoses (eg, solar urticaria, photoallergic dermatitis, hydroa vacciniforme, chronic actinic dermatitis, erythropoietic porphyria, lupus erythematosus).

Reported in 2007, Kerr and Lim⁷ identified 280 patients with photodermatoses. One hundred thirty-five (48%) were African Americans, 110 (40%) were white, and 35 (12%) were patients of other races. They noted a statistically significantly higher proportion of African Americans with PMLE compared with whites.

Benanni et al⁸ noted a low incidence of PMLE in renal transplant recipients.

International

Deng et al⁹ used a questionnaire to survey 4899 residents (49% men and 51% women) of random Chinese villages in Yuan Jiang county (Dai and Hani minorities), Kunming city (Han people and Yi minority), Lijiang county (Naxi minority), and Shangri-La county (Zang minority). The altitudes of these regions were 380 meters, 1870 meters, 2410 meters, and 3280 meters, respectively. The prevalence of PMLE was 32 (0.65%) in 4899 residents and was 3.8 times higher in women compared with men. At higher elevations, the prevalence of PMLE increased. The mean time of sun exposure for PMLE was 6 h/d. The mean duration of PMLE was 5.8 years.

PMLE affects 21% of the population in Sweden.

Mortality/Morbidity

Expression of PMLE may range from an insignificant, mild rash to severe disease affecting the patient's quality of life. Each case should be evaluated individually.

Richards et al¹ found that emotional distress attributable to PMLE occurred in greater than 40% of individuals. Women more than men associated more severe consequences with their PMLE and experienced more emotional distress.

Race

PMLE affects all racial skin types, but it is more common in fair-skinned individuals with skin types I-IV than in other individuals. Overall, family history is positive for PMLE in about 15% of the patients. However, Native Americans have a hereditary form of PMLE with apparent autosomal dominant inheritance; 75% reveal disease in a family member.¹⁰

Sex

PMLE affects females 2-3 times more often than males. However, these data may be skewed because women are more likely to seek medical attention for cosmetic problems than males.

Age

PMLE usually has an onset in the first 3 decades of life. Men seem to have later onset of the disease than women.

Naleway et al¹¹ reviewed records of 124 patients diagnosed with PMLE and found most were women and that the mean age of PMLE onset was 37.8 years. They noted only 4 required phototherapy treatment.

CLINICAL

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

History

PMLE tends to manifest in the spring. In addition, PMLE is a recurrent condition and patients state they have had the eruption before and that it went away as time passed.

• Sunlight is clearly the primary etiologic factor.
• • The eruption of PMLE typically occurs in spring or, rarely, in winter following ultraviolet radiation exposure reflected from snow.
  • Typically, the lesions of PMLE first erupt at the onset of a vacation in a sunny place or at a high altitude and disappear by the time the patient returns home.
  • The eruption decreases in severity as the summer progresses.
• The onset of the disease is sudden. The accompanying rash is pruritic and, in some instances, painful.
• • Thirty minutes to several hours of exposure are required to trigger the eruption.
  • Sun-exposed skin, especially that normally covered in winter (eg, upper chest, arms), is primarily affected, but autosensitization may lead to a generalized involvement.
  • The rash appears within hours to days of exposure, and it subsides over the next 1-7 days without scarring.
  • Most patients have associated pruritus, but some patients describe stinging and pain.
• Occasionally, patients experience systemic flulike symptoms after sun exposure.
• Unless severe and particularly bothersome, many patients do not visit a physician for PMLE rash. It is often discovered incidentally.
• Jansén¹² traced the natural history of chronic PMLE in 138 people, 85 of whom were female. Their mean age was 26.4 years. The length of time in the study was 10.5 years. In 57% of cases, the PMLE happened in a rapid fashion. It started in a small photoexposed area in 88% of cases, and extended to a greater area each year. Light sensitivity tended to increase with each subsequent year. The patients’ threshold tolerance to solar radiation occurred 30 minutes after exposure in £60% of patients. In 50% of patients, yearly hardening phenomena  occurred. Ocular and oral involvement occurred in 46% and 49% of the patients, respectively. About 66% patients experienced some general symptoms after solar radiation exposure.

Physical

As the name implies, clinical manifestations of the disease vary. Many different morphologies may appear on sun-exposed areas, but, usually only one morphology dominates in a given individual.

• Papules (greatest incidence), plaques, papulovesicles, and erythema multiforme–like lesions are the most common morphologies.
• • Photosensitive erythema multiforme and erythema multiforme–like PMLE can be difficult to distinguish clinically.
  • Combined morphological types of lesions, while uncommon, do occur. For example, the small papular variety may coalesce to form an eczematous type and large papular lesions may produce plaques or assume an annular configuration.
• Sun-exposed skin, especially that normally covered in winter (eg, upper chest, arms), is affected primarily, but autosensitization may lead to a generalized involvement.
• Cheilitis is uncommon in patients in the United States. In such patients, the rare diagnosis of actinic prurigo is a more likely cause of the inflammatory photosensitivity disorder. Cheilitis often occurs in the tropics and, when this is the case, can be the only manifestation of the PMLE. That is, it can manifest without involvement of the extremities, face, or torso. In the case of photosensitive cheilitis, PMLE must be distinguished from chronic actinic cheilitis and the eczematous cheilitis produced by photosensitizing agents.
• In African Americans, a variant of PMLE with pinpoint papules (1-2 mm) can be observed on sun-exposed areas, sparing the face and flexural surfaces.¹³

Causes

Although most authorities now consider UV-A light as the causative factor in PMLE eruption, UV-B, or even visible light, may be responsible in some individuals

DIFFERENTIALS

Section 4 of 11  

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• Follow-up
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Some physicians regard actinic prurigo as a distinct photodermatosis, and other physicians consider it an insidiously developing, markedly excoriated variant of PMLE. Actinic prurigo is characterized by a high incidence of atopy and family predisposition. It is likely to involve the covered skin.

Chronic actinic dermatitis is a term that encompasses several syndromes previously considered separate entities (ie, actinic reticuloid, persistent light reactivity, photosensitive eczema, photosensitivity dermatitis), but, now, they are considered to be variants of the same condition. Clinically, lesions are usually more eczematous and infiltrated than in PMLE and involve mostly exposed skin, but they may generalize to erythroderma. The actinic reticuloid form of chronic actinic dermatitis has a histologic pattern that resembles cutaneous lymphoma, with CD8⁺ cells predominating. The minimal erythema dose (MED) to UV-B, and sometimes UV-A, is reduced.

Solar urticaria represents an immediate hypersensitivity response to UV radiation. Characteristic whealing may be accompanied by systemic symptoms of faintness, nausea, and bronchospasm.

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Lab Studies

• Laboratory tests are generally performed to rule out other dermatoses, such as erythropoietic protoporphyria or lupus erythematosus. Antinuclear antibody (ANA), anti-Ro (SS-A), and anti-La (SS-B) tests, as well as urine, stool, and blood porphyrin levels, should be obtained.
• The diagnosis of PMLE is usually based on the clinical picture. Normal titers of ANA, as well as normal urine, stool, and blood porphyrin levels, support the diagnosis.

Other Tests

• Results of phototesting are controversial, ranging from an ability to reproduce the eruption by repeat phototesting in 60-100% of patients to an inability to do so except in patients who are very photosensitive. These differences may be explained by a lack of a standardized test procedures, variation in radiation sources used, and imprecision in diagnostic criteria for the disease.
• Perform phototests with UV-A, UV-B, and visible light sources.
• • Determine the MED from these sources. MEDs are normal in PMLE and lowered or abnormal in chronic actinic dermatitis. In solar urticaria, irradiation results in reproduction of the lesion.
  • Perform repetitive light testing; irradiating 3 times the MED to UV-A on the right forearm and 3 times the MED to UV-B on the left forearm for 3 consecutive days. Results are read immediately, at 24 and 72 hours. A delayed reading at 1 week may also be helpful.
  • The test results are often positive in PMLE. A negative result does not exclude the diagnosis.
  • If a lesion (eg, papule, vesicle) develops, biopsy confirmation is suggested.
  • Histologically, a superficial and deep perivascular lymphocytic infiltrate will be apparent with dermal edema.
• Photopatch tests to rule out a photoallergic or airborne contact dermatitis should be performed.
• • Two identical strips of standard photoallergens are placed on the back. One of the two strips is exposed to UV-A radiation 24 hours later. Both the irradiated site and the unirradiated site are read at 24, 48, and 96 hours.
  • A positive reaction at the irradiated site but not at the unirradiated patch test site is diagnostic of a photocontact allergy. Positive reactions at both the irradiated site and the unirradiated site are indicative of a contact allergy.
  • According to Leroy et al¹⁴ in 2002, polychromatic phototesting seems to be more sensitive than UV-A phototesting to assess PMLE, and results suggest UV-B is a key trigger of PMLE.

Histologic Findings

The most striking feature of the biopsy is edema in the upper part of the dermis. Tight, perivascular lymphocytic infiltrate is observed in the upper and mid dermis. When eczematous epidermal changes are present clinically, spongiosis, edema, dyskeratosis, and basal cell vacuolization may be observed. Occasionally, neutrophils and eosinophils may be present in the infiltrate. The dominant cell, however, is the lymphocyte.

TREATMENT

Section 6 of 11  

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• Follow-up
• Acknowledgments
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Medical Care

Prophylactic therapy (eg, avoiding sunlight, wearing protective clothing, using sunscreen) remains a key factor in the care of patients with 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,¹⁵ the efficacy of a new topical formulation was compared with a broad-spectrum sunscreen. 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.

Jeanmougin et al¹⁶ 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. 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,¹⁶ 52 of 54 patients finished study, and 67% of patients had no eruptions, 19% had minor eruptions, and 13% had severe eruptions of PMLE. 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.

• 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.¹⁷ 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.¹⁸
• 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. 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.¹⁹ 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 al²⁰ 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.
• Azathioprine²¹ was reported to be effective in 2 cases of recalcitrant severe disease at 0.8-2.5 mg/kg/d for 3 months. 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.

MEDICATION

Section 7 of 11  

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• Differentials
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• Follow-up
• Acknowledgments
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Antimalarials

These agents may have immunomodulatory effects.

Drug Category: 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.

Drug Category: Immunomodulators

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

Drug Category: Vitamins

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

FOLLOW-UP

Section 8 of 11  

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• Introduction
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• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Deterrence/Prevention

• Avoiding sunlight during the hours of most intense UV irradiation (from 10 am to 2 pm) and wearing protective clothing (eg, hats, gloves, long sleeves) should be emphasized.
  
  
  • Blue denim clothing is particularly beneficial in terms of sun protection.
  • Wide range sunblocks with a high SPF should be applied and reapplied during the day.

Prognosis

• Some patients experience a less severe reaction with each consecutive year, but many patients have reactions that may worsen with time without appropriate treatment.

ACKNOWLEDGMENTS

Section 9 of 11  

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• Acknowledgments
• Multimedia
• References

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

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Media file 1:  The face of a patient with polymorphous light eruption. Note the erythema and an indurated plaque.
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Media file 2:  Close-up view of polymorphous light eruption plaque.
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Media file 3:  Papular variant of polymorphous light eruption.
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Media file 4:  Large facial plaques.
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Media file 5:  Histopathologic features of polymorphous light eruption. Note the tight perivascular lymphocytic infiltrate in the upper dermis.
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Media file 6:  Close-up view of the perivascular infiltrate.
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Media file 7:  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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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

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Article Last Updated: Mar 13, 2008