eMedicine Specialties > Dermatology > Photo-Related Diseases
Polymorphous Light Eruption
Updated: Oct 23, 2009
Introduction
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 al found that PMLE engenders a substantial psychosocial impact on patients who have the condition.1 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.
The face of a patient with polymorphous light eruption. Note the erythema and an indurated plaque.
Close-up view of polymorphous light eruption plaque.
Pathophysiology
The etiology of polymorphous light eruption (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 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.4
Neutrophils may play a role in the development of PMLE. Immunohistochemical analysis by Schornagel et al in 2004 showed a significant decreased neutrophil infiltration in PMLE skin after UV-B irradiation compared with healthy case control subjects (P <.05).5 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 al 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.6 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.7
Frequency
United States
Polymorphous light eruption (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 Lim identified 280 patients with photodermatoses.8 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 al noted a low incidence of PMLE in renal transplant recipients,9 and Hönigsmann reports a prevalence of 10-20% in the United States and Western Europe.10
International
Deng et al 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).11 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 polymorphous light eruption (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 al found that emotional distress attributable to PMLE occurred in greater than 40% of individuals.1 Women more than men associated more severe consequences with their PMLE and experienced more emotional distress.
Race
Polymorphous light eruption (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.12
Sex
Polymorphous light eruption (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
Polymorphous light eruption (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 al 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.13 They noted only 4 required phototherapy treatment.
Clinical
History
Polymorphous light eruption (PMLE) tends to manifest in the spring.14 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 for PMLE.
- 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.
- Jansén traced the natural history of chronic PMLE in 138 people, 85 of whom were female.15 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 polymorphous light eruption (PMLE) 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.
Papular variant of polymorphous light eruption.
Large facial plaques.
- 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.16
Causes
Although most authorities now consider UV-A light as the causative factor in polymorphous light eruption (PMLE) eruption, UV-B, or even visible light, may be responsible in some individuals
Differential Diagnoses
Contact Dermatitis, Allergic
Lupus Erythematosus, Subacute Cutaneous
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 polymorphous light eruption (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
Laboratory Studies
- In polymorphous light eruption (PMLE), 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.17
- 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 in polymorphous light eruption (PMLE) patients 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.18 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 al 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.19
Histologic Findings
The most striking feature of the biopsy specimen from a patient with polymorphous light eruption (PMLE) 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.
Histopathologic features of polymorphous light eruption. Note the tight perivascular lymphocytic infiltrate in the upper dermis.
Close-up view of the perivascular infiltrate.
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 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
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.
Dosing
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
Interactions
Cimetidine increases levels; kaolin and magnesium trisilicate decrease levels; increases digoxin levels; do not administer chloroquine and hydroxychloroquine together (retinal toxicity)
Contraindications
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)
Precautions
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.
Dosing
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
Interactions
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
Contraindications
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
Precautions
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.
Dosing
Adult
50-200 mg PO hs
Pediatric
Not established
Interactions
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
Contraindications
Documented hypersensitivity; pregnancy
Precautions
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.
Dosing
Adult
30-300 mg PO qd
Pediatric
30-150 mg PO qd
Interactions
Coadministration with vitamin A may result in additive toxic effects
Contraindications
Documented hypersensitivity
Precautions
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.
Dosing
Adult
3 g/d PO used in a study quoted; 20 mg/d represents 100% RDA
Pediatric
Not established
Interactions
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
Contraindications
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)
Precautions
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
Follow-up
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 to polymorphous light eruption (PMLE) patients.
- 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 polymorphous light eruption (PMLE) patients experience a less severe reaction with each consecutive year, but many patients have reactions that may worsen with time without appropriate treatment.
Multimedia
Media file 1: The face of a patient with polymorphous light eruption. Note the erythema and an indurated plaque.
Media file 2: Close-up view of polymorphous light eruption plaque.
Media file 3: Papular variant of polymorphous light eruption.
Media file 4: Large facial plaques.
Media file 5: Histopathologic features of polymorphous light eruption. Note the tight perivascular lymphocytic infiltrate in the upper dermis.
Media file 6: Close-up view of the perivascular infiltrate.
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.
References
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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.