Polymorphous Light Eruption
- Author: Noah S Scheinfeld, JD, MD, FAAD; Chief Editor: Dirk M Elston, MD more...
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.
The possibility that a subset of PMLE called benign summer light eruption or BSLE which might be milder and might be more UVA driven has been suggested by an Italian group.
Richards et al 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.
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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.
Some have suggested that glutathione S-transferases (GSTs) act to protect against PMLE, but a study of the isoenzymes of the GST genes GSTM1, GSTT1, and GSTP1 found no protective relationship of these isoenzymes to PMLE.
It is possible that the use of tobacco makes PMLE worse.
In some PMLE lesions induced by UV-A, keratinocytes were found to express intercellular adhesion molecule 1 (ICAM-1).[5, 6] 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.
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). 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. 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.
A study by Koulu et al assessed a total of 48 subjects (24 patients with PMLE and 24 healthy sex-matched and age-matched controls). The study found similar immunosuppression of contact sensitization to diphenylcyclopropenone due to earlier exposure to solar-simulating UV radiation between both groups. However, among patients with PMLE who were immunosuppressed by UV radiation, only one exhibited immunotolerance to the same allergen 10–24 months later (P=0.023). The study concluded that impaired propensity to UV-induced, allergen-specific immunotolerance may promote recurrent PMLE.
It has recently been shown that UV-C can cause PMLE.
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. 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.
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). 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.
A report from India in 2013 notes that PMLE is the most common photodermatitis after chronic actinic dermatitis, while hydroa vacciniforme and solar urticaria are uncommon. Furthermore, this report stated lichenoid PMLE and pin-point papular PMLE are the most common types found in the subcontinent.
Polymorphous light eruption (PMLE) affects all racial skin types. 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. The popular variant can involve the face and seems most common in patients with Fitzpatrick type skin III-VI.[19, 20]
One study of a cohort of 229 patients with photodermatoses reported that 63 (42.2%) were white and 138 (46.6%) were African American and PMLE was present in 54% and 86.2%, respectively, (P < 0.0001); thus, the researchers suggested that PMLE occurs more frequently in African Americans.
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.
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. They noted only 4 required phototherapy treatment.
Guarrera M, Cardo P, Rebora AE, Schena D, Calzavara-Pinton P, Venturini M, et al. Polymorphous light eruption and benign summer light eruption in Italy. Photodermatol Photoimmunol Photomed. 2011 Feb. 1:35-9. [Medline].
Richards HL, Ling TC, Evangelou G, et al. Psychologic distress in polymorphous light eruption and its relationship to patients' beliefs about their condition. J Am Acad Dermatol. 2007 Mar. 56(3):426-31. [Medline].
Zirbs M, Pürner C, Buters JT, Effner R, Weidinger S, Ring J, et al. GSTM1, GSTT1 and GSTP1 gene polymorphism in polymorphous light eruption. J Eur Acad Dermatol Venereol. 2012 Jan 9. [Medline].
Metelitsa AI, Lauzon GJ. Tobacco and the skin. Clin Dermatol. 2010 Jul-Aug. 4:384-90. [Medline].
Norris PG, Barker JN, Allen MH, et al. Adhesion molecule expression in polymorphic light eruption. J Invest Dermatol. 1992 Oct. 99(4):504-8. [Medline].
Stephansson E, Ros AM. Expression of intercellular adhesion molecule-1 (ICAM-1) and OKM5 in UVA- and UVB-induced lesions in patients with lupus erythematosus and polymorphous light eruption. Arch Dermatol Res. 1993. 285(6):328-33. [Medline].
Aubin F. Why is polymorphous light eruption so common in young women?. Arch Dermatol Res. 2004 Oct. 296(5):240-1. [Medline].
Schornagel IJ, Sigurdsson V, Nijhuis EH, Bruijnzeel-Koomen CA, Knol EF. Decreased neutrophil skin infiltration after UVB exposure in patients with polymorphous light eruption. J Invest Dermatol. 2004 Jul. 123(1):202-6. [Medline].
Kolgen W, van Meurs M, Jongsma M, et al. Differential expression of cytokines in UV-B-exposed skin of patients with polymorphous light eruption: correlation with Langerhans cell migration and immunosuppression. Arch Dermatol. 2004 Mar. 140(3):295-302. [Medline].
Wackernagel A, Back B, Quehenberger F, Cerroni L, Kerl H, Wolf P. Langerhans cell resistance, CD11b+ cell influx, and cytokine mRNA expression in skin after UV exposure in patients with polymorphous light eruption as compared with healthy control subjects. J Invest Dermatol. 2004 May. 122(5):1342-4. [Medline].
Koulu LM, Laihia JK, Peltoniemi HH, Jansén CT. UV-induced tolerance to a contact allergen is impaired in polymorphic light eruption. J Invest Dermatol. 2010 Nov. 130(11):2578-82. [Medline].
Schmutz JL, Trechot P. [Polymorphous light eruption caused by ultraviolet C light]. Ann Dermatol Venereol. 2011 Aug-Sep. 138(8-9):639. [Medline].
Kerr HA, Lim HW. Photodermatoses in African Americans: a retrospective analysis of 135 patients over a 7-year period. J Am Acad Dermatol. 2007 Oct. 57(4):638-43. [Medline].
Benanni B, Bruckner T, Bock M, et al. Low incidence of polymorphous light eruption in renal transplant recipients. Acta Derm Venereol. 2007. 87(4):372-4. [Medline].
Hönigsmann H. Polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2008 Jun. 24(3):155-61. [Medline].
Deng D, Hang Y, Chen H, Li H. Prevalence of photodermatosis in four regions at different altitudes in Yunnan province, China. J Dermatol. 2006 Aug. 33(8):537-40. [Medline].
Sharma VK, Sahni K, Wadhwani AR. Photodermatoses in pigmented skin. Photochem Photobiol Sci. 2013 Jan. 12:65-77. [Medline].
Draelos ZK, Hansen RC. Polymorphic light eruption in pediatric patients with American Indian ancestry. Pediatr Dermatol. 1986 Nov. 3(5):384-9. [Medline].
Chen YA, Lee JY. Clinicopathologic study of solar dermatitis, a pinpoint papular variant of polymorphous light eruption in Taiwan, and review of the literature. J Formos Med Assoc. 2013 Mar. 112(3):125-30. [Medline].
Isedeh P, Lim HW. Polymorphous light eruption presenting as pinhead papular eruption on the face. J Drugs Dermatol. 2013 Nov. 12(11):1285-6. [Medline].
Nakamura M, Henderson M, Jacobsen G, Lim HW. Comparison of photodermatoses in African-Americans and Caucasians: a follow-up study. Photodermatol Photoimmunol Photomed. 2014 Oct. 30(5):231-6. [Medline].
Naleway AL, Greenlee RT, Melski JW. Characteristics of diagnosed polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2006 Aug. 22(4):205-7. [Medline].
Lugovic Mihic L, Bulat V, Situm M, Cavka V, Krolo I. Allergic hypersensitivity skin reactions following sun exposure. Coll Antropol. 2008 Oct. 32 Suppl 2:153-7. [Medline].
Jansen CT. The natural history of polymorphous light eruptions. Arch Dermatol. 1979 Feb. 115(2):165-9. [Medline].
Majoie IM, van Weelden H, Sybesma IM, Coenraads PJ, Sigurdsson V. Polymorphous light eruption-like skin lesions in welders caused by ultraviolet C light. J Am Acad Dermatol. 2010 Jan. 62(1):150-1. [Medline].
Aljasser MI, Lui H, Ball NJ, Kalia S. Persistent polymorphous light eruption after ultraviolet A1 phototherapy. Photodermatol Photoimmunol Photomed. 2013 Feb. 29:52-4. [Medline].
Kontos AP, Cusack CA, Chaffins M, Lim HW. Polymorphous light eruption in African Americans: pinpoint papular variant. Photodermatol Photoimmunol Photomed. 2002 Dec. 18(6):303-6. [Medline].
Chiam LY, Chong WS. Pinpoint papular polymorphous light eruption in Asian skin: a variant in darker-skinned individuals. Photodermatol Photoimmunol Photomed. 2009. 25:71-4. [Medline].
Gronhagen CM, Gunnarsson I, Svenungsson E, Nyberg F. Cutaneous manifestations and serological findings in 260 patients with systemic lupus erythematosus. Lupus. 2010 Sep. 19(10):1187-94. [Medline].
Molina-Ruiz AM, Sanmartín O, Santonja C, Kutzner H, Requena L. Spring and summer eruption of the elbows: A peculiar localized variant of polymorphous light eruption. J Am Acad Dermatol. 68. 2013 Feb:306-12. [Medline].
Balasubramanian P, Jagadeesan S, Sekar L, Thomas J. An interesting observation of polymorphous light eruption occurring on hypopigmented scars. Indian Dermatol Online J. 2015 Jul-Aug. 6 (4):294-6. [Medline].
Totten JE, Brock DM, Schimelpfenig TD, Hopkin JL, Colven RM. Prolonged Exposure Dermatosis: Reporting High Incidence of an Undiagnosed Facial Dermatosis on a Winter Wilderness Expedition. Wilderness Environ Med. 2015 Dec. 26 (4):525-30. [Medline].
Popovic K, Nyberg F, Wahren-Herlenius M, Nyberg F. A serology-based approach combined with clinical examination of 125 Ro/SSA-positive patients to define incidence and prevalence of subacute cutaneous lupus erythematosus. Arthritis Rheum. 2007 Jan. 56(1):255-64. [Medline].
Schornagel IJ, Guikers KL, Van Weelden H, Brijnzeel-Koomen CA, Sigurdsson V. The polymorphous light eruption-severity assessment score does not reliably predict the results of phototesting. J Eur Acad Dermatol Venereol. 2008 Jun. 22(6):675-80. [Medline].
Leroy D, Dompmartin A, Verneuil L, Michel M, Faguer K. [Polychromatic phototest sensibility is superior to UVA phototest in polymorphic light eruptions]. Ann Dermatol Venereol. 2002 Jun-Jul. 129(6-7):860-4. [Medline].
Vincent JG, Chan MP. Specificity of dermal mucin in the diagnosis of lupus erythematosus: comparison with other dermatitides and normal skin. J Cutan Pathol. 2015 Oct. 42 (10):722-9. [Medline].
Aljasser MI, Lui H, Ball NJ, Kalia S. Persistent polymorphous light eruption after ultraviolet A1 phototherapy. Photodermatol Photoimmunol Photomed. 2013 Feb. 29:52-54. [Medline].
Hadshiew IM, Treder-Conrad C, v Bülow R, et al. Polymorphous light eruption (PLE) and a new potent antioxidant and UVA-protective formulation as prophylaxis. Photodermatol Photoimmunol Photomed. 2004 Aug. 20(4):200-4. [Medline].
Gruber-Wackernagel A, Bambach I, Legat FJ, et al. Randomized double-blinded placebo-controlled intra-individual trial on topical treatment with a 1,25-dihydroxyvitamin D(3) analogue in polymorphic light eruption. Br J Dermatol. 2011 Jul. 165(1):152-63. [Medline].
Jeanmougin M, Peyron JL, Thomas P, Beani JC, Guez E, Bachot N. [Polymorphic light eruption: prophylaxis using a topical combination of antioxidants and UVA protection formulations]. Ann Dermatol Venereol. 2006 May. 133(5 Pt 1):425-8. [Medline].
DeLeo VA, Clark S, Fowler J, Poncet M, Loesche C, Soto P. A new ecamsule-containing SPF 40 sunscreen cream for the prevention of polymorphous light eruption: a double-blind, randomized, controlled study in maximized outdoor conditions. Cutis. 2009 Feb. 83(2):95-103. [Medline].
Fourtanier A, Moyal D, Seite S. Sunscreens containing the broad-spectrum UVA absorber, Mexoryl SX, prevent the cutaneous detrimental effects of UV exposure: a review of clinical study results. Photodermatol Photoimmunol Photomed. 2008 Aug. 24(4):164-74. [Medline].
Bissonnette R, Nigen S, Bolduc C. Influence of the quantity of sunscreen applied on the ability to protect against ultraviolet-induced polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2012 Oct. 28(5):240-3. [Medline].
Murphy GM, Logan RA, Lovell CR, Morris RW, Hawk JL, Magnus IA. Prophylactic PUVA and UVB therapy in polymorphic light eruption--a controlled trial. Br J Dermatol. 1987 Apr. 116(4):531-8. [Medline].
Bilsland D, George SA, Gibbs NK, Aitchison T, Johnson BE, Ferguson J. A comparison of narrow band phototherapy (TL-01) and photochemotherapy (PUVA) in the management of polymorphic light eruption. Br J Dermatol. 1993 Dec. 129(6):708-12. [Medline].
Barolet D, Boucher A. LED photoprevention: reduced MED response following multiple LED exposures. Lasers Surg Med. 2008 Feb. 40(2):106-12. [Medline].
Jansen CT. Oral carotenoid treatment in polymorphous light eruption: a cross-over comparison with oxychloroquine and placebo. Photodermatol. 1985 Jun. 2(3):166-9. [Medline].
Neumann R, Rappold E, Pohl-Markl H. Treatment of polymorphous light eruption with nicotinamide: a pilot study. Br J Dermatol. 1986 Jul. 115(1):77-80. [Medline].
Ahmed RS, Suke SG, Seth V, Jain A, Bhattacharya SN, Banerjee BD. Impact of oral vitamin E supplementation on oxidative stress & lipid peroxidation in patients with polymorphous light eruption. Indian J Med Res. 2006 Jun. 123(6):781-7. [Medline].
Norris PG, Hawk JL. Successful treatment of severe polymorphous light eruption with azathioprine. Arch Dermatol. 1989 Oct. 125(10):1377-9. [Medline].