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Figure 1.
Polymorphic light eruption (PLE)is provoked with solar-simulated radiation. A, Typical papular PLE lesionsare seen on buttock skin after 3 exposures of 0.75, 1.0, 1.25, and 1.5 minimal erythemal doses (MEDs). As shown here, reactions were generally stronger withhigher doses. B, Papulovesicular PLE lesions are visible on the arm after 3 exposures of 1.25 and 1.5 MED.

Polymorphic light eruption (PLE)is provoked with solar-simulated radiation. A, Typical papular PLE lesionsare seen on buttock skin after 3 exposures of 0.75, 1.0, 1.25, and 1.5 minimal erythemal doses (MEDs). As shown here, reactions were generally stronger withhigher doses. B, Papulovesicular PLE lesions are visible on the arm after 3 exposures of 1.25 and 1.5 MED.

Figure 2.
Erythemal polymorphic light eruption(PLE) responses are greater on previously unexposed sites . The slopes of erythemadose-response curves were significantly steeper on previously unexposed sitesin all patients (P= .02 in nonresponders [PLE−]and P= .002 in responders [PLE+]). There was no differencein the erythema responses, on either site, between patients who respondedand those who did not.

Erythemal polymorphic light eruption(PLE) responses are greater on previously unexposed sites . The slopes of erythemadose-response curves were significantly steeper on previously unexposed sitesin all patients (P= .02 in nonresponders [PLE−]and P= .002 in responders [PLE+]). There was no differencein the erythema responses, on either site, between patients who respondedand those who did not.

Figure 3.
Patients respond to a wide range of solar-simulated radiation (SSR) doses. Seventeen (68%) of 25 patients showeda polymorphic light eruption (PLE) reaction on any SSR-exposed site. The data show the number of sites with a PLE response at a given SSR dose, regardlessof the number of exposures. The theoretical maximum for each site is the number of patients (N = 25). This means that 1 (4%) of 25 buttock sites respondedwith 0.25–minimal erythemal dose (MED) exposures and that 12 (48%) of 25 arm and/or back sites responded with 1.5-MED exposures. Arm and/or backskin was more responsive than buttock skin despite having lower inflammatory doses.

Patients respond to a wide range of solar-simulated radiation (SSR) doses. Seventeen (68%) of 25 patients showeda polymorphic light eruption (PLE) reaction on any SSR-exposed site. The data show the number of sites with a PLE response at a given SSR dose, regardlessof the number of exposures. The theoretical maximum for each site is the number of patients (N = 25). This means that 1 (4%) of 25 buttock sites respondedwith 0.25–minimal erythemal dose (MED) exposures and that 12 (48%) of 25 arm and/or back sites responded with 1.5-MED exposures. Arm and/or backskin was more responsive than buttock skin despite having lower inflammatory doses.

Figure 4.
Three exposures are generally necessary to provoke polymorphic light eruption (PLE). The results show thecumulative percentage of patients with positive reactions on buttock and arm and/or back skin with the minimum solar-simulated radiation (SSR) dose used.At least 3 exposures were necessary to provoke PLE in at least 50% of patients. There is no difference between previously exposed and previously unexposedskin. Not all patients reacted on both sites. Two important caveats: (1) 1 patient was included who showed PLE on the buttock minimal erythemal dosetest site after a single exposure; (2) the cumulative value does not reach 68% because patients required different numbers of exposures on differentsites and some patients reacted on one site but not on the other.

Three exposures are generally necessary to provoke polymorphic light eruption (PLE). The results show thecumulative percentage of patients with positive reactions on buttock and arm and/or back skin with the minimum solar-simulated radiation (SSR) dose used.At least 3 exposures were necessary to provoke PLE in at least 50% of patients. There is no difference between previously exposed and previously unexposedskin. Not all patients reacted on both sites. Two important caveats: (1) 1 patient was included who showed PLE on the buttock minimal erythemal dosetest site after a single exposure; (2) the cumulative value does not reach 68% because patients required different numbers of exposures on differentsites and some patients reacted on one site but not on the other.

Provocation Tests Since 1980
Provocation Tests Since 1980
1.
Pao  CNorris  PGCorbett  MHawk  JL Polymorphic light eruption: prevalence in Australia and England Br J Dermatol. 1994;13062- 64
PubMedArticle
2.
McGregor  JMGrabczynska  SVaughan  RHawk  JLLewis  CM Genetic modelling of abnormal photosensitivity in families with polymorphic light eruption and actinic prurigo J Invest Dermatol. 2000;115471- 476
PubMedArticle
3.
Millard  TPBataille  VSnieder  HSpector  TDMcGregor  JM The heritability of polymorphic light eruption J Invest Dermatol. 2000;115467- 470
PubMedArticle
4.
Kolgen  WVan Weelden  HDen Hengst  S  et al.  CD11b+ cells and ultraviolet-B-resistant CD1a+ cells in skin of patients with polymorphous light eruption J Invest Dermatol. 1999;1134- 10
PubMedArticle
5.
Van de Pas  CBKelly  DASeed  PTYoung  ARHawk  LMWalker  SL UVR-induced erythema and suppression of contact hypersensitivity responses in patients with polymorphic light eruption J Invest Dermatol. In press.
6.
Stevanovic  DV Polymorphic light eruption Br J Dermatol. 1960;72261- 270Article
7.
Levy  EJCahn  MMShaffer  B Polymorphous light eruption: some unusual reactions in ultraviolet test sites J Invest Dermatol. 1957;28147- 153
8.
Cahn  MMLevy  EJShaffer  BBeerman  H Lupus erythematosus and polymorphous light eruptions J Invest Dermatol. 1953;21375- 396Article
9.
Harber  LCHolloway  RMMoragne  ME Polymorphous light eruptions;office diagnosis and management N Y State J Med. 1964;64619- 623
10.
Frain-Bell  WDickson  AHerd  JSturrock  I The action spectrum in polymorphic light eruption Br J Dermatol. 1973;89243- 249
PubMedArticle
11.
Epstein  JH Polymorphous light eruptions: phototest technique studies Arch Dermatol. 1962;85502- 504Article
12.
Ortel  BTanew  AWolff  KHonigsmann  H Polymorphous light eruption: action spectrum and photoprotection J Am Acad Dermatol. 1986;14748- 753
PubMedArticle
13.
Miyamoto  C Polymorphous light eruption: successful reproduction of skin lesions , including papulovesicular light eruption, with ultraviolet B Photodermatol. 1989;669- 79
PubMed
14.
Holzle  EPlewig  GHoffman  CRoser-Maass  E Polymorphous light eruption J Am Acad Dermatol. 1982;7111- 125
PubMedArticle
15.
McFadden  NLarsen  T Polymorphous light eruption: the properties of a UVA-induced PLME patient group Photodermatol. 1986;336- 40
PubMed
16.
Neumann  RAPohl-Markl  HKnobler  RM Polymorphous light eruption: experimental reproduction of skin lesionsby whole-body UVA irradiation Photodermatol. 1987;4252- 256
PubMed
17.
Pryzbilla  BGalosi  AHeppeler  MRuzicka  TRing  J Polymorphous light eruption: eliciting and inhibiting wavelengths Acta Derm Venereol (Stockh). 1988;68173- 176
PubMed
18.
Barnadas  MAMoreno  APujol  R  et al.  Repeated exposure to ultraviolet A in polymorphous light eruption patients and normal subjects: a clinical and histopathological study Photodermatol Photoimmunol Photomed. 1990;7207- 212
PubMed
19.
Verheyen  AMLambert  JRVan Marck  EADockx  PF Polymorphic light eruption: an immunopathological study of provoked lesions Clin Exp Dermatol. 1995;20297- 303
PubMedArticle
20.
Lambert  JVerheyen  ADockx  P Experimental reproduction of polymorphous light eruption and benign summer light eruption by whole-body UVA irradiation Dermatology. 1997;194388- 391
PubMedArticle
21.
Mastalier  UKerl  HWolf  P Clinical, laboratory, phototest and phototherapy findings in polymorphic light eruption: a retrospective study of 133 patients Eur J Dermatol. 1998;8554- 559
PubMed
22.
Cahn  MMLevy  EJShaffer  B Experimentally induced reaction to ultraviolet light, I: polymorphous light eruption and phototoxicity to drugs J Invest Dermatol. 1959;32355- 361Article
23.
Epstein  JH Polymorphous light eruptions: wavelength dependency and energy studies Arch Dermatol. 1962;8582- 88Article
24.
Magnus  IA Studies with a monochromator in the common idiopathic photodermatoses Br J Dermatol. 1964;76245- 264Article
25.
Norris  PGMorris  JMcGibbon  DMChu  ACHawk  JL Polymorphic light eruption: an immunopathological study of evolving lesions Br J Dermatol. 1989;120173- 183
PubMedArticle
26.
Tannenbaum  LMark  GJMihm  MCParrish  JA The role of histopathology in polymorphic light eruption light testing Clin Exp Dermatol. 1981;6123- 132
PubMedArticle
27.
Jansen  C The polymorphic phototest reaction Arch Dermatol. 1982;118638- 642
PubMedArticle
28.
Moncada  BGonzalez-Amaro  RBaranda  MLLoredo  CUrbina  R Immunopathology of polymorphous light eruption J Am Acad Dermatol. 1984;10970- 973
PubMedArticle
29.
Boonstra  HEvan Weelden  HToonstra  Jvan Vloten  WA Polymorphous light eruption: a clinical, photobiologic, and follow-up study of 110 patients J Am Acad Dermatol. 2000;42199- 207
PubMedArticle
30.
McFadden  JPNorris  PGCerio  ROrchard  GHawk  JL Heat shock protein 65 immunoreactivity in experimentally induced polymorphic light eruption Acta Derm Venereol. 1994;74283- 285
PubMed
31.
Norris  PBacon  KBird  CHawk  JCamp  R The role of interleukins 1, 6 and 8 as lymphocyte attractants in the photodermatoses polymorphic light eruption and chronic actinic dermatitis Clin Exp Dermatol. 1999;24321- 326
PubMedArticle
32.
Harrison  GIYoung  AR Ultraviolet radiation-induced erythema in human skin Methods. 2002;2814- 19
PubMedArticle
33.
Young  ARChadwick  CAHarrison  GINikaido  ORamsden  JPotten  CS The similarity of action spectra for thymine dimers in human epidermis and erythema suggests that DNA is the chromophore for erythema J Invest Dermatol. 1998;111982- 988
PubMedArticle
Study
March 2004

An Optimal Method for Experimental Provocation of Polymorphic Light Eruption

Author Affiliations

From the St John's Institute of Dermatology, Guy's, King's, and St Thomas' School of Medicine, King's College London, England. The authors haveno relevant financial interest in this article.

Arch Dermatol. 2004;140(3):286-292. doi:10.1001/archderm.140.3.286
Abstract

Background  There is controversy about the best method to induce polymorphic light eruption (PLE) experimentally.

Objectives  To review articles on PLE induction and design a UV radiation protocol that improves success rates with clinically relevant doses of environmentallyrelevant solar-simulated radiation (SSR).

Design and Setting  All articles on the experimental provocation of PLE published since 1980 were reviewed. Photoprovocation of lesions was studied in 25 PLE patients.The 24-hour minimal erythemal dose (MED) of SSR was determined. Thereafter, six 4 × 4-cm adjacent sites on previously affected and previously unaffectedskin were exposed to 0.25, 0.5, 0.75, 1.0, 1.25, 1.5 MED of SSR for 3 to 4 consecutive days. The study periodwas autumn to spring in London, England(51° north latitude).

Main Outcome Measures  Relationship between PLE induction and biological and physical exposure parameters.

Conclusions  The review shows that fractionated erythemally effective UV-A exposures were more successful than single-sunburning UV-B doses. Photoprovocation ofPLE was successful in 68% of patients after 2 to 3 SSR exposures that were not necessarily erythemal. There was no difference in success rate betweenpreviously affected and previously unaffected skin. Our data indicate that PLE is more likely to be induced when the natural causes of the disease aresimulated.

Polymorphic light eruption (PLE) is the most common of the so-called idiopathic photodermatoses. In a recent population survey1 inthe United Kingdom, PLE was found to affect 15% of healthy people, with a female-male ratio of approximately 2:1. Genetic modeling using twin studiesand families with PLE provides unequivocal evidence for a genetic basis for PLE and predicts that susceptibility to PLE is a polygenic trait with multiplesusceptibility loci.2,3 Polymorphic light eruption is characterized by a delayed abnormal reaction to the UV radiation(UVR) component of sunlight consisting of transient, nonscarring, pruritic papules and vesicles, typically developing hours or days after sun exposureand resolving over several days without sequelae. The pathogenesis of PLE is unclear, but histologic and immunologic studies suggest that the normalUVR-induced suppression of cell-mediated immunity is impaired and, as a result, these patients develop a T-cell mediated response to a UVR-activated antigen(photoantigen).4,5

Investigations into the pathogenesis of PLE have been frustrated by the lack of reliable laboratory methods for the induction of clinical lesions.The results of such studies have varied considerably. The early PLE induction studies reported success rates from as low as 10% to 30%68 toas high as 60% to 95%.911 These studies were based on one or more exposures of a single test site to between1 and 10 times the minimal erythemal dose (MED) of nominal UV-B radiation (ie, 290-320 nm), although these sources almost certainly contained otherUVR wavelengths. Initially, induction was achieved with UV-B,613 but several authors also succeeded in reproducing PLE lesions with UV-A irradiation(320-400 nm).12,1421

There are somewhat contradictory results about the wavelength dependence of PLE. In general, UV-A appears to be more effectivethan UV-B in eliciting lesions.14 In a comprehensive study of 142 patients in which induction was attempted with increasing exposuresof buttock skin to UV-A and/or UV-B daily for 4 to 8 days, the most effective waveband was UV-A (56%), followed by UV-A/UV-B combination (27%), then UV-B>(17%).12 However, Miyamoto13 has confirmed earlier reports2224 that UV-B can also be successful in a high proportion (57%) of selected patients.In a retrospective study of 30 patients by Mastalier et al,21 the action spectrum fell within the UV-A range in 59% of patients, the UV-B range in 23%, and both ranges in 18%. The diversity in the wavelength-dependence studies remains unexplained. It would be puzzling if a single chromophoreand a uniform mechanism could be activated by different parts of the UVR spectrum and result in such a morphologic diversity of lesions. This would indicatedifferent pathogenic mechanisms or that there is a range of UVR-induced antigens.

According to Norris et al,25 studies of laboratory-induced lesions have generally used UVR doses considerably inexcess of the MED.2628 This makes histologic interpretation difficult because of coexistent sunburn, whichresults in mononuclear cell infiltration. Even recent studies have used high doses to provoke a PLE reaction (3.3 MED of UV-B19;6 MED of UV-B20; and 2-4 MED of UV-B or UV-A29).

Different locations have been used to provoke PLE with varying degrees of success. Barnadas et al,18 McFadden et al,30 Mastalier et al,21 andNorris et al31 used previously affected skin with success rates of 30%, 100%, 57%, and 100% respectively. Boonstra et al29 provoked PLE in previously affected skin to UV-B/UV-Acombination exposure in 88% of men and 52% of women. Within this group, PLE was also induced by UV-B alone in 9% of the men and 24% of the women. Reactionsto UV-A alone occurred in 3% of men and 24% of women and to visible light in 43% of men and 11% of women. Verheyen et al19 andLambert et al20 used whole body and upper arm exposure and had UV-A success rates on previously affected sites of 100% and87%, respectively, and 0% and 6.7% with UV-B. Holzle et al14 tried to provoke PLE on previously exposed and previously unexposed skin. The successrates ranged from 0% to 90% on previously exposed skin, but it was 0% on previously unexposed skin.

A synopsis of findings from our literature review is provided in Table 1. The aim of our investigation was to evaluate provocation test methods introduced since 1980 and to developa reliable test using physiologically relevant doses of SSR to study the pathogenesis of PLE.

METHODS
VOLUNTEERS

Twenty-five patients diagnosed with PLE at the Photobiology Clinic of St John's Institute of Dermatology, London, England, were randomly recruitedinto the study (21 women, 4 men; age range, 18-55 years; mean age, 38 years; skin types I-V). Diagnosis was made on the basis of clinical history and examination.All patients had PLE for at least 6 years, and the condition was defined as a fully resolving macular, papular, or papulovesicular photoeruption occurring30 minutes to 48 hours after sun exposure and lasting for hours to at least a day.

Patients were screened by blood analysis to exclude those with porphyria and by estimation of antinuclear and extractable nuclear antigen autoantibodiesto exclude those with lupus. Skin type was assessed by interview. Exclusion criteria for all volunteers included ingestion of any medication during or2 weeks prior to the study (oral contraceptives excepted), phototherapy during or in the 6 months prior to the study, previous exposure of buttock skin tosunlamps or sunlight, and/or a recent sunburn. Pregnant or lactating women were also excluded. The local ethics committee approved the study, and eachvolunteer was fully informed of the procedures and gave written informed consent to participate.

UVR SOURCE AND DOSIMETRY

Solar-simulated radiation (SSR) was generated by a 1-kW xenon arc solar simulator (Oriel, Stratford, Conn) fitted with a WG320/1-mm-thick glass filter,giving an even field of irradiance (approximately 290-400 nm) of about 15 mW/cm2 on the skin surface at 11 cm from the source. Irradiancewas routinely determined with a wideband thermopile radiometer (Medical Physics, Dryburn Hospital, Durham, England) calibrated against a DM150 double monochromatorBentham spectroradiometer (Bentham Instruments, Reading, England). See filter 2 of the first figure in Harrison and Young32 foremission spectrum details. Eighty-eight percent of the erythemally effective energy of the source was in the UV-B range, and the remaining 12% was UV-A.

INDUCTION OF LESIONS

In each patient, the just visibly perceptible 24-hour MED was determined on previously unexposed buttock skin using eight 25% doseincrements. Photoprovocation was attempted on 2 body sites: (1) previously affected skin (either the arm or upper back) and (2) previously unaffectedskin (buttock). Six adjacent sites (4 × 4 cm each), were exposed to0.25, 0.5, 0.75, 1.0, 1.25, 1.5 buttock MED in an attempt to induce PLE lesions.The exposures were repeated daily until a positive PLE response was obtained. If no lesions appeared after 3 or 4 days of exposure, the test was considerednegative. (Twenty-three of 25 patients had a maximum of 3 exposures; only 2 of 25 patients had a maximum of 4 exposures.) Photoprovocation in 18patients was performed from October 2001 to May 2002 and in a further 7 patients from November 2002 to March 2003.

UVR-INDUCED ERYTHEMA

Using a reflectance meter (Diastron, Andover, England), we took 3 quantitative measurements of erythema 24 hours after the second SSR exposure and calculatedthe mean per site. For each site, the increase in erythema index was calculated by subtracting the mean background reading of adjacent nonirradiated skin.

STATISTICAL METHODS

Microsoft (Redmond, Wash) Excel 2000 was used for statistical analysis. Linear regression was performed for increase in erythema index vs SSR dose(MED fraction) for each volunteer on previously exposed and previously unexposedtest sites to generate erythema dose-response slopes (83% of the regressionshad R2 values ≥0.7), the slope being indicative of the overall erythema response. The distribution of the slopeswas shown to be normal (Kolmogorov-Smirnov test), and so unpaired t tests were used to compare the slopes between patients who showed a PLE response and those who did not on both treatment sites. Significancewas assumed at P<.05.

RESULTS
CLINICAL PRESENTATION

The morphologic features of PLE lesions induced by photoprovocation were consistent with the response reported by each patient after previoussun exposure. Thus, with SSR we were able to produce lesions comparable to those seen in the genuine disease. The PLE lesions developed 1 to 24 hoursafter the last irradiation and consisted of macular, small papular (Figure 1A), or papulovesicular (Figure 1B) lesions scattered over the irradiated site. The papular or papulovesicular lesions were sometimes sparsely scatteredover the irradiated area, although almost confluent lesions developed as well.

In all patients, the recurrence of the rash was associated with pruritus. Shortly thereafter, patchy or confluent erythema developed in which the characteristicskin lesions emerged. Lesions persisted for at least 12 hours and up to 2weeks after the last exposure. Figure 1Ashows a papular reactions of increasing severity after 3 consecutive exposures to 0.75, 1.0, 1.25, and 1.5 MED. Figure 1B shows a papulovesicular PLE reaction after 3 consecutive exposureson 1.25 and 1.5 MED sites. Experimentally induced skin lesions usually resolved over the next 1 to 3 days, but it generally took 1 to 3 weeks before theycompletely disappeared.

ERYTHEMA

Erythema was shown to be SSR dose dependent, and the slopes were significantly steeper on the buttock site than on the previously exposed site (Figure 2). There was no difference in theerythema response on either test site between patients in whom PLE was successfully induced and those in whom it was not (Figure2).

LEVEL OF RESPONSE

Seventeen (68%) of 25 patients developed PLE on at least 1 test site. Figure 3 showsthe number of sites with a positive response at a given dose level, regardless of the number of exposures. Six patients developed PLE only on previously affected sites (upper back or arm); 4 patients developed PLE only on previouslyunaffected sites (buttock); and 7 patients showed responses on both sites.Polymorphic light eruption was readily provoked on both previously exposed and previously unexposed skin. Eleven (65%) of 17 patients responded on buttockskin and 13 (77%) of 17 responded on arm and/or back.

NUMBER OF EXPOSURES

Successful provocation of PLE was dependent on the number of exposures.In both skin sites, success increased with increasing number of daily exposures. Figure 4 shows the cumulative success ratefor both sites, regardless of the dose used. The data show that 3 exposures are necessary to obtain a success rate of more than 50%. However, Figure 3 also shows that it is possible toprovoke PLE with a single SSR exposure on buttock skin (1 patient with macular lesions) and on arm and/or back skin (2 patients with papular lesions).

COMMENT

A summary of articles published since 1980 on the experimental provocationof PLE is provided in Table 1.This shows a very diverse range of UVR spectra, doses, and induction protocols, and sometimes it is difficult to determine the exact radiation protocol. Ingeneral, the doses given, whether single or repeated, have been greater than 1 MED. Only our group25 has previously usedSSR in a suberythemal protocol. Furthermore, in some cases the doses would have been phototoxic, causing a severe erythemal reaction.

In general, studies with UV-A have been more successful than those with UV-B. Solar UVR is mostly UV-A (approximately 95%), yet the approximate 5%UV-B causes more than 80% of the sunburn. Patients often report PLE without sunburn, which has led clinicians to believe that the disease may be triggeredwith suberythemal UV-A exposure. Yet, success with UV-A dose-response studies has been with doses that were certainly erythemal (eg, 60-100 J/cm2 in Holzle et al14 and >50 J/cm2 in 20 of 22 patients in McFadden and Larsen15).In this context, such studies do not reproduce the natural situation.

We have successfully reproduced PLE in a small group of PLE patients using environmentally and physiologically relevant UVR exposures. This wasdone with comparable rates of success on previously exposed and unexposed skin. The erythemal response after 2 exposures on the buttock was much greaterthan that on the arm and/or back, as shown in Figure 2, almost certainly because buttock MED was lower than the MED of sites that had a history of exposure. In other words, our protocolwas less inflammatory on the arm and back than on the buttock.

Polymorphic light eruption can be induced by suberythemal exposures, as shown in Figure 3. Figure 2 shows PLE in association with very shallow erythema dose-responsecurves, especially on the arm and back. These observations are consistent with patient reports that PLE may evolve without concomitant sunburn. Overall, our data show that erythema and PLE are independent clinicaloutcomes, suggesting that they have different chromophores. DNA is thought to be the major chromophore for erythema,33 butas yet we have no candidate chromophores for PLE.

The most frequent outcome was pruritus and erythema in combination with papular or papulovesicular lesions, which accounted for 88% of the positivereactions. The remaining 12% involved pruritis, erythema, and macules that persisted for at least 12 hours after the last exposure. The lesions weresometimes sparsely scattered over the irradiated area, which means that test areas should not be too small. Thus, we believe that our 4 × 4-cm testarea for each dose is appropriate. Larger areas are not necessary: Neumann et al16 have shown that whole body UV-A exposurewas no more effective than the exposure of smaller previously involved skin sites.

Our success rate was 68% (17/25), which is good compared with most of the reports in Table 1. Therewas little difference between the success rates on previously affected sites(13/17; 76%) and previously unaffected sites (12/17; 71%). Most studies haveattempted to induce PLE on previously sun-exposed sites.12,14,15,18,31 Only 2 other studies14,18 attempted,without clear success, to induce PLE on previously unaffected (ie, non–sun-exposed) sites. Our results clearly show that successful provocation of PLE is notdependent on skin site.

Polymorphic light eruption usually requires several consecutive exposures to sunlight. We thus tried to simulate the natural conditions with repeateddaily exposures of 0.25, 0.5, 0.75, 1.0, 1.25, and 1.5 just perceptible MEDs. Unfortunately, the total number of exposures was limited because most patientswere not willing to cooperate for more than 4 consecutive exposures. The influence of number of exposures is shown in Figure4. This shows that at least 3 exposures are necessary to obtaina success rate of at least 50% on previously exposed and previously unexposedskin.

The SSR dose (cumulative physical dose) required to induce PLE ranged from 1.7 to 25 J/cm2 (mean MED, 4.9 J/cm2 ; range, 2.6-10.1J/cm2), and there was no evident correlation between outcome and cumulative physical dose. In a recent study,5 membersof our group used single exposure doses of 0.6, 1, or 2 MED to induce immunosuppression in PLE patients and in age- and skin type–matched controls. Exposureto 1 MED suppressed contact hypersensitivity response by 78% in controls but induced significantly less suppression (44%) in PLE patients (P<.01). Suppression was also less in PLE patients than in controlsafter 0.6 MED (31% vs 43%), but this did not reach significance (P = .50). In contrast, suppression was almost complete (93%) in both PLE patients and controls after exposure to 2 MED, suggesting that PLE patientshave a resistance to immunosuppression after low to moderate doses of UVR, but resistance to immunosuppression can be overcome if higher UVR doses aregiven.

It is possible that more exposures would have increased our success rate. On the other hand, the clinical symptoms of PLE are likely to representa balance between the induction of the putative photoantigen and the UVR-induced suppression of the immunologic response to the antigen. Such a balance islikely to be highly dependent on individual immunologic and UVR exposure parameters. Polymorphic light eruption was provoked after a single exposure in 3 (18%)of 17 patients, and in 1 of these cases the PLE was evident after the MED series. This contrasts with the findings of other authors,15,25,27,28,30,31 whoreported good results from a single exposure with a wide range of sources and doses.

In conclusion, we have shown that PLE can be readily induced when thenatural causes of the disease are simulated. The lack of consistent resultsfrom studies of the PLE action spectrum further supports the use of SSR. We have also shown, for the first time, that the condition can be just as readilyprovoked on previously unexposed sites. This indicates that the putative photoantigencan be induced de novo. Finally, we believe that a standard protocol for theinduction and assessment of PLE would benefit research and clinical practice, and we advocate that researchers in this field work toward this end.

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Article Information

Corresponding author and reprints: Antony R. Young, PhD, St John'sInstitute of Dermatology, Photobiology Unit, King's College London, SecondFloor South, Wing Block 7, St Thomas' Hospital, London SE1 7EH, England (e-mail: antony.r.young@kcl.ac.uk).

Accepted for publication June 25, 2003.

This study was supported by a personal training award from the Guy's & St Thomas' Charitable Foundation, London, England (Dr van de Pas), anda project grant from the Claneil Foundation Inc, Plymouth Meeting, Pa.

References
1.
Pao  CNorris  PGCorbett  MHawk  JL Polymorphic light eruption: prevalence in Australia and England Br J Dermatol. 1994;13062- 64
PubMedArticle
2.
McGregor  JMGrabczynska  SVaughan  RHawk  JLLewis  CM Genetic modelling of abnormal photosensitivity in families with polymorphic light eruption and actinic prurigo J Invest Dermatol. 2000;115471- 476
PubMedArticle
3.
Millard  TPBataille  VSnieder  HSpector  TDMcGregor  JM The heritability of polymorphic light eruption J Invest Dermatol. 2000;115467- 470
PubMedArticle
4.
Kolgen  WVan Weelden  HDen Hengst  S  et al.  CD11b+ cells and ultraviolet-B-resistant CD1a+ cells in skin of patients with polymorphous light eruption J Invest Dermatol. 1999;1134- 10
PubMedArticle
5.
Van de Pas  CBKelly  DASeed  PTYoung  ARHawk  LMWalker  SL UVR-induced erythema and suppression of contact hypersensitivity responses in patients with polymorphic light eruption J Invest Dermatol. In press.
6.
Stevanovic  DV Polymorphic light eruption Br J Dermatol. 1960;72261- 270Article
7.
Levy  EJCahn  MMShaffer  B Polymorphous light eruption: some unusual reactions in ultraviolet test sites J Invest Dermatol. 1957;28147- 153
8.
Cahn  MMLevy  EJShaffer  BBeerman  H Lupus erythematosus and polymorphous light eruptions J Invest Dermatol. 1953;21375- 396Article
9.
Harber  LCHolloway  RMMoragne  ME Polymorphous light eruptions;office diagnosis and management N Y State J Med. 1964;64619- 623
10.
Frain-Bell  WDickson  AHerd  JSturrock  I The action spectrum in polymorphic light eruption Br J Dermatol. 1973;89243- 249
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