photo sensitivity in lupus bjd

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British Journal of Dermatology 1 9 9 7 : 1 3 6 : 6 9 9 - 7 0 5 .

Photosensitivity in lupus erythematosus, UV photoprovocationresults compared with history of photosensitivityand clinical findingsT.HASAN. F .NYBERC* E.STEPHANSSON.* P .PUSKA. t M.HAKKINEN. S .SA RN A4A-M.ROS* AND A.RANKIDepartment of Dermatology. University of Tampere tiiid Tampere Umversity Hospital. PLIOOI). FIN-i3>21 Tampen '. I'iiilaud'Department of Dermatology. Karoliuskii Institute and Hospital. Stockholm. Sweden'\ Department of Dermatology, Helsinki University Central Hospital Helsinki. Finland^ Department of Public Health. University of Helsinki. Helsinki, FhilaiidAccepted for publication 28 November 1996

S u m m a r y Photosensitivity. o ne of the presenting sym ptoms in lupu s ery them atos us (LEI. is still poorly definedand varying prevalence figures have been reported. The possibility of a coexisting photodermatosis.especially polymorphous light eruption (PLE), has often not been taken into account. We report theresu lts of ultravio let A (UVA) and B (IIVB) pho topro voc ation tests in 67 c linically photo sens itivepa tien ts w ho h ad confirmed discoid LE (ULE). system ic LE (SLE) or su ba cu te cu tan eo us LE (SCLE).The results are co mpa red w ith a detailed history of photosensitivity and with clinical and serologicalfindings.

A pathological photoprovocation reaction, graded as weak, moderate or strong, was induced witheither UVA or UVB in 6 9% of pa tien ts w ith LE. in 100 % of those with SCLE, in 70% of those with SLEand in 64% of those with DLE. but in none of 14 controls. Only 16% of the pathological reactionswere strong and long-lasting, resembling LE lesions, while 48% were mo derate or weak andtransient, clinically like PLE. Fifty-three per cent of the provocation reactions which were biopsiedshowed a PLE-like histology or a non-specific inflammatory reaction, and most of them wereclinically moderate or weak reactions of short duration. In the remaining, mostly clinically strongor long-lasting reactions, the histology was consistent with LE. A history of sunlight sensitivity didnot predict a pathological photoprovocation result but a positive association between the presence ofSSA/Ro or SSB/La antibodies and a pathological photoprovocation reaction was found. We haveshown that PLE coexists with LE and that both PLE- and LE-like lesions can be induced with UVradiation in LE patients.

It is generally well established that sunlight canaggravate skin symptoms in patients with all subsetsof lupus er ythe ma tosu s (LE). Photose nsit ivity occu rsin l l % - 9 4 % of patients with systemic LE (SLE). '"^ in52%-100% of those wi th subacute cutaneous LE(SCLE)^"^ and in 6 9 % -9 0 % of discoid LE (DLE). '*^Such wide ranges may be due to the use of differentdiagn ostic c riteria for LE in older studies and due toracial differences.^ However, the lack of a uniformdefinition is the most l ikely explanation . Furth erm ore,the possibili ty of a coexisting ph otode rma tosis such aspolymorphous l ight eruption (PLE), is generally notconsidered . In our recent quest ionnai re s tudy '" weshowed tha t as man y as 49'Xt of Scan dinav ian patientswith LE also experience symptoms of PLE. This is more

than twice the overall prevalence of PLE, at 2 1 % , in aScandinavian populat ion .^ 'Photoprovocation is an objective way to evaluatepossible photosensitivity. The capacity of both ultravio-let A (UVA) and B (UVB) radiation to reproduce LE andPLE skin symptoms has been shown in several studies,the frequency of pathological photoprovocation resultsvarying between 20% and 10 0% .^^ ' '^ The cri ter ia for apathological reaction have also varied and the possibi-lity of inducing a PLE reaction in LE patien ts h as notbeen considered.

We wished to evaluate UVA and UVB photoprovoca-tion responses in correlation with a detailed history ofphotosensitivity. The type of symptoms previouslyexperienced were recorded in order to discriminate


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"00 T.HASAN etitl

between PLE and UV aggravation of LE. The kinetics ofthe provoked reactions were followed up and the resultscorrelated with clinical, histological and serologicalfindings.

Patients and methodsPatientsA photoprovocation test was performed in SO patien tswith DIM, \0 with SLK and seven with SCLE patients (1 (Imen and 57 women). All were clinically photosensitive.They were followed-up at three dermatological clinics inScandijitivia. namely at the Karoiinska Hospital. Stock-holm. Sweden, the Helsinki Universitj' Central Hospital,Helsinki. Finland, and the Tampere University Hospital.Tampere. Finland. Fourteen volunteer non-photosensitivecontrols, three men and 11 women were also studied. Allwere Caucasian, belonging to nationalities closely asso-ciated genetically.' ' Th e study was approved hy th e ethicscommittee of each hospital, and all patients gave writtenconsent before enrolment. The mean age of the patientswas 47 years (range 14-83) and the mean duration ofdisease was 12 years (range 1-37). The m ean age of thecontrols was 58 years (range lfi-6()).

The diagnosis of DLE was based on clinical and histo-logical findings: th e d iagno sis of SCLF, on the origina ldescription'' and skin histology. No patient with SCLH haddiscoid lesions. The diagnosis of SLE was based on the1982 revised criteria of the American College of Rheu-matology."" a combination of clinical, haematologicaiand serological features. All patients with SLE hadshown antinuclear antibodies (ANAs), and LE-specilicskin lesions;"' seven patients presented with acute skinlesions, e.g. a butterlly rash or widespread maculopapularrash, one had chronic discoid lesions, and two had bothacute and chronic skin lesions. The diagnostic criteria ofthe I,E subtypes were similar in the three clinics and basedon long-standing clinical collaboration.

Differentiation between UV aggravation or induction ofLE skin lesions and PLE-type photodermalosis'" wasemphasized with personal interviews. PLE was definedas a papular and/or vesicular pruritic eruption arising afew days after sun exposure on sun-exposed skin, some-times on a dilTerent skin area than LE lesions, and healingwithin a week. In the present study the term history ofphotosensitivity' refers either to a history of PLE or toaggravation or induction of LE skin lesions or both.Most patients were on no systemic medication fortheir skin disease at the time of photoprovocation. Two

patients were taking hy droxychloroq uine, 500 mg and

-)00 mg per day. respectively. Two patients received oracorticosteroid. co rrespon ding to 5 mg prednisolondaily, one also took cyclosporin. 125 mg daily.

PhotoU'stiiHj cqidimu'ut diid photopivvocatUvi protocolsLIVA ph oto tes tin g wa s perform ed with UVASUN 3{)()with an emiss ion spectrum of 540-400nm. ' ' I JVphototesting was performed with four different lighsources: ( i | Waldman 85 -lO OW /UV (S (main emissiospectru m of 2 9 0 - 5 7 0 nm: UVA. UVB and UVC irradance of l -5mW/cm" . 0 5mW/cm" and O( )mW/cmrespectively), (ii) Philips TL 2()W/12 (main emissiospectrum of 280-570nm: UVA. UVB and UVC irradance of 0-7m W /cm ". 1-3 mW/cm~ and 0-01 mW/cm respectively), (iii) Osram Xenon XBO 1 50 W Schott W29 5 filter (emission spectrum of 2 50-400 nm: UVAUVB and VV C irradiaiice of lfvOmW/cm". 2-()mWcm^an d 0 2 m W /cm ". respectively), and (iv) Osram HQTS 400 W/D (emission spectrum of 2 5 0- 40 0 nm: UVAUVB an d IW C irradiance of 5 2 mVV/cm", () 5 mW / cmand 0-2mW/cm". respectively).

The patients were tested in the autumn, winter oearly spring on intact skin of the upper back, upper armor forearm. Most patients were tested with both UVAand UVB. but 16 were on ly tested with UVB. First, thminimal erythema dose (MED) for both UVA and UVwas determined. The MED. defined as barely perceptiberythema with at least three visible sharp corners, waassessed after 24 h. In most pati ents , reacti on s witUVA up to 80 I/cm" were norm al a nd. thu s, the exacUVA MED could n ot be stated. Photop rovocation wathen performed, cither on 1 - i consecutive days (mostthree times: 40 patients) or every 2-5 days (mostly fivto six times: 27 patients). The patients in these twgroups did not differ statistically with regard to age osex, du rati on of LE skin sym ptom s, histo ry or type ophotose nsitivity, an d d istributio n or activity of LE skilesions. UVA doses varied between 20 and lOOJ/cm(ma xim um 2-7 MED) and UVB doses between 1 and MEIJ. so that moderate redness was achieved. Each UVdose was adjusted Individually according to the reactioof the previous provocation. The mean total UVA doswas 247 J/cm~ and the mean total UVB dose 5-7 MED the patient group provoked on consecutive days. Threspective values were 18 2 J/cm " and 7-9 MED in thpatient group provoked every 2-5 days. The test arevaried from 5 x 8 cm to 2 x 2 cm. Provocation reactionwere evaluated a bou t 24 h after each irradiation , anthereafter every 4 - 7 days up to 5 weeks. Fou rteecontrols were provoked according to either protocol.


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P H OT O SE N SI TI VI TY IN L UPU S E RY TH EM A TO SU S 7(31

Biopsy specimens were obtained from the pathologicalprovocation reaction sites for routine histology. Sectionswere stained with haematoxylin and eosin and most alsow ith periodif-acid-SchiiT (Py\SI reage nt. Biopsy specimenswere examined by experienced pathologisls. The histolo-gical diagnosis of LE and PLE were based o n generallyaccepted criteria.^ *~" The main histological criteria forLE were hydropic degeneration of the epidermal basalcells, and a perivascular and periappendageal lymphoidcell intiltrate. The features of PLH were a perivascuiarlymphoid cell inliitrate. with parakeratosis, focal spon-giosis and slight vaeuolization of basal keratinocytes.

Table 1. I'liotnprDvocation resul tservtheniiitosiis lLE| and in controlsin piitieiils with [iipiis

DiagnosisDLESLESCLETotalControls

H

5010

7ft714

18*4*h

28 *0

UVA

(55%)

Paihological reactionsUVB

31ft7

4 4 ( 6 6 % )0

UVA or UVBU 164%)7 |7U%)7 ( 1 0 0 % )

4ft (69%)0

" Five SIJE and 11 DL E patients were not pholoprovoked with U\'ADLE, Discoid LE; SLE, svsteinic LE: SCLE, subacute cutaneous 1.1].

Sewiogkal evahmtkmANA assay W H S performed with routine indirect immu-nofluorcscence using rat fixed liver tissue or Hep-2 cellsas the antigens. In sera from 51 patients, antibodies toSSA/Ro and SSB/La extraclable nuclear antigens (ribo-nucleoproteins) were assayed by a standard immuno-dilfusion technique with the mixture of soluble proteinsof rabbit thymus and pig spleen as antigen. In 16 cases.a commercial enzyme immnnoassay lEIA) methodIENA4 ELISA. Quanta Lite. Inova Diagnostics, SanDiego. CA. U.S.A.) was used for screening Sm. RNP.SSA/Ro and SSB/La IgG antibodies. In case of a positivescreening result |2() units), the specificity of the anti-bodies was determined with a specilic EIA assay (SSAHLISA, SSB ELISA: Quanta Lite. Inova Diagnostics).

were considered pathological either with UVA. UVB orboth. All seven patients with SCLE, seven of 10 (70%)wi th SLE an d 32 of SO (fS4'X,) with DLE gave p ath ol o-gical provocation reactions. UVB induced a pathologicalprovocation reaction slightly more often than UVA(Table 1).

Seventy per cent of ail pathological reactions wereweak or moderate, the rest being strong. Eighty-four percent of pathological reactions ap peared within 1 week ofthe last provocation and the remaining 16% more than Sdays after the last provocation. In one patient with SIJi.the reaction first appeared 3 weeks after the pr ovo cation.Eifty-nine reactions were followed up for at least 21 daysor un til they sub sided. Most reactions (6 3%) disappearedwithin 14 days after the last provocation (transient

Stiilistiai} auaUjsisfor testing associations with clinical and serologicaldata, Fisher's exact and Maiilel-Haenszel two-sidedtests were used, respectively. The statistical analysiswas performed with StatXact (Statistical Software forExact Nonparametric Inference),^"' Statistical signifi-cance was considered as y'ui3Z

302 5

201 510

50

n long-lasting reactionsn transient reactions

strong moderate/weakClinical appearance of photoprovocated reaction

Figure 1, Reitctioii kinetics ol 59 pliotiiprnviikwi skin reatlions. Siroiigand long-ltistiiig rea ctions had a statistifally sii^niticant association( P < 0 - 0 0 1 ) .

C' 149 7 British Association of Dermalologi.sls. Brilisli Jinininl ofDcniuiloloqij. 1 ?6 ,


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70 2 T.HASAN etal.

Figure 2. (al A normal UVA and a pathological UVB provocationreaction 10 days after the last provocation in a 34-year old man withdiscoid lupus erythematosus. The large rectangular ligures are provo-cation areas and the small squares are graded exposures of UV fordetermining the minimal erythem a dose, (bl The same UVB provocationreaction as in (a | shown in close-up S months later. The reactionresembles a spontaneous lesion of discoid lupus erythematosus.

reactions), while 3 7% were visible for more than 21 da(long-lasting reactions). There was a strong statisticallsignificant association between strong and long-lastinreactions (Fig. 1). Forty-eight per cent of the pathologicreactions were both moderate/weak and transient, clincally resembling PIJi more than LE. Sixteen per cent oreactions were both strong and long-lasting, clinicalllike LE lesions. A classic lesion of D\. was provoked only 14 of 50 (28%) pathological reactions in patienwith DLE (Fig. 2). Controls developed pigmentatioerythema or slight oedema, the latter two subsidinwithin 3 days.The irradiation protocol used did not particularaffect th e final provocation results as 73 % of patienprovoked with UVB every day and 63% of patienprovoked w ith UVB every oth er to every third da

gave a pathological reaction. Comparison of the resulbetween protocols using UVB devices with e ithnarrow or wide UV spectrum did not differ statisticallneither did the strength and persistence of the reactionbetween the three clinics.

Histology uf the pathological photoprovocation resultsThirty-six of 73 reactions (49%) were evaluated histlogically. 10 of them in serial biopsies so th at 51 biopsiewere examined altogether. Fifty-three per cent of threactions biopsied showed histological features of PLEa dermal perivascular lymphocytic infiltrate (Table 2In the remaining 47 % of the reactions, the histologicdiagno sis was co nsisten t w ith LE. LE histology corelated significantly with the strong as well as lonlasting clinical reaction types. In some cases, thhistological picture changed from PLE to LE in seribiopsies during follow-up (Table 2). The detailed timpoints of the biopsies are shown in Fig. 3. UVA- anUVB-provoked skin lesions showed the histology of LE38 % and 52% . respectively (statistically not significantMost of the pathological reactions not examined histlogically were weak or moderate and transient, manlasting only a few days.

Association of pbotoprovocation results with demographdata, clinical findings and autoantib odiesIn 84% (9 5% Cl 73% -92 % ) of patien ts. LE skin symtoms were exacerbated on exposure to sunlight. Sixtseven per cent (95% CI 55%-78%) of the patienreported a history of typical PLE. Most patients (68%with moderate or weak and transient provocation reations had had a PLE-like rash.


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PHOTOSENSITIVITY IN LUPUS ERYTHEMATOSUS 703

Table 2. The histology of 36 pathological provocation reactions compared with the appearance and duration of the reaction

LE-like histology * PLE-like or non-specific h istology Statistical significance tClinical appearance of the reactionstrong J

weak/moderate The duration of the reaction

more than 21 days (long-lasting)lesK than 14 days (tran sientinot followed-upAll pathological reactions examined

8 (80%)9 ( 3 5 % )1 2 ( 7 5 % )2{137n)

31 7 ( 4 7 % !

2 (20%)1 7 ( 6 5 % )4 ( 2 5 % )13 (87%)2

19 (53%)

P = 0-001

' In six reactions the histologicai picture changed from PLE-Iike/non-specific to LE-like in the repeated biopsies. These are included in the group 'LE-like histology', t Fisher's exact, two-tailed. $ strong = either erythema, papules/plaques and DLE-like scaling or erythema with papules and markedoedem a, weak = just erythe ma lasting for at least t week, moderate erythem a with papules lasting longer tha n 3 days.LE, lupus erythematosus: PLE, polymorphous light eruption: DLK. discoid lupus erythematosus.

The age of the patient, the duration of LE. and theoverall activity of skin lesions at the time of testing didnot correlate w ith the photoprov ocation results. UVprovocation was pathological in 76% (95% CI 6 0 % -89'X)) of pat ient s w ith a dissem inated distrih ution of skinlesions compared with 5y% (95% CI 4O%-77%) ofpatients with lesions localized to the face or scalp(statistically not significant).

Patients with SSA/Ro and/or SSB/La antibodies gavea pathological provocation reaction significantlymore often (8 3% . 95 % CI 63% -95 % ) tha n thoselacking these antibodies (60%. 95% CI 44%-75%)

2 01 81 6

a>0}a.0n"o1 .

E2

14121 0

86420

DLE-likehistologyD PLE-like ornon-specifichistology

< 4 days 4-7 days 8-14 days > 21daysTime-point of the biopsy after the lastprovocation

Figure 3. Histological diagnosis in relation to the timing of the biopsy.Fifty-one biopsies from 36 reactions were evalu ated, 1 5 of these wereadditional serial samples from 10 pathological reactions.

( P = 0 -04 8. com mon odds ratio (OR) 3-50). The ser-ological method was not found as a confounding factor( O R E U S A = 3 - 0 0 . ORi,,,munudinuMon= 3-85 ). The fewpatients belonging to different LE subgroups did notallow us to study further associations, ANA results didnot correspond to photoprovocation results.DiscussionPhotoprovocation with both UVA and UVB radiationwas performed in 67 patients with either discoid, sub-acute or systemic LE to confirm the type of photosensi-t ivity and to evaluate reaction pattern s a nd kinetics. In69% of the patients provocation yielded a pathologicalreaction. Only about 16'Ki of reactions were strong andlong-lasting, resemb ling LE lesions. The clinical p atte rnand kinetics in 48% of the reactions were of doubtful LElesions that more resembled PLE.

Our observation that ail patients with SCLE. 70% ofthose with SLE and 64'X. of those with DLE give apathological respo nse to photoprov ocation. UVB beingslightly more effective than UVA. is in agreement withrecent provocation st ud ies .' ' '" UVB-provoked skinlesions slightly m ore often gave histology typical of LEthan did lesions provoked by UVA.

Early LE may be difficult to distinguish from PLE. asthere are cases with strikingly similar clinical, histologi-cal, photobiological and serological lindings.'''*"*"''""'We recently conducted a questionnaire-based study, inwhich we showed tha t 49 % of LE patients also have ahistory suggestive of PLE.'" This is more than twice thereported prevalence of PLE in a corresponding Scandina-vian population.'' Coexistence of PLE and LE seemscommon, although PLE has not been identified as apredisposing factor for LE in previous studies. * ' ' " This

1997 British Association of Dermatologists, British journal ofDermatoIoiiii. 1 3 6 , 6 9 9 - 7 0 5


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704 T.HASAN I'tal.

coexistence may have led to diiliculties in the interpreta-tion of photoprovocation reactions and may be onereason for diiTering results.'""'"

As about half of the pro\'ocation reactions in thepresent study were clinically non-specitic. histologicalexamination was performed. In only 47% of the reac-tions biopsied was the histology consistent with LE(Table 2). fn some long-lasting reatUons. only repeatedbiopsies revealed the true nature of the skin lesion.because the bistological picture changed from non-specitic or PI.K-like lo that resembling LE. Most reactionswhich showed a histological picture of PLE disappearedin few days, excluding the possibility of later developingthe changes of LE. In these cases the histology of thesingle biopsy was considered reliable.

The pathomechanism of LlV-induced LE lesions is notknown, UVB radiation has been shown to induceexpression of the nuclear autoantigen Ro/SSA at thecell surface iu vitro.^"^ but contradictory results havebeen reported about possible associations betweenphotosensitivity and the occurrence of circulatingSSA/Ro antibodies in LE patients."''" '"^""^ Our obser-vation about a statistically significant associationbetween occurrence of SSA/Ro and/or SSB/La antibo-dies and a positive photoprovocation test resultstrengthens the role of these autoantigens in the patho-mechanism of UV-induced LE skin lesions.

Both PLE- and LE-!ike lesions can be induced with UVradiation in LE patients. This is important to considerwhen further investigations into the pathomechanismof LE are planned.AcknowledgmentsWe thank Ms Kirsti Leszczynski. Ph.L and Mr ReijoVisuri. M.Sc. Finnish Centre for Radiation and NuclearSafety. Helsinki, for spectral measurement results andMs Laura Huurto. Ph.L., Turku University CentralHospital. Turku, for dosimetric calculations of photo-testing equipment In Helsinki and Tampere UniversityHospitals. Finland. We also thank Ms Liisa Kannas.Helsinki University Central Hospital lor skilful practicalassistance. This study was supported by grants from theMedical Research Fund of Tampere University Hospital,Tampere. Finland, the Finnish Rheumatism Associa-tion. Finland, the Edvartl Welaiider Foundation, Swedenand the Finsen Foundation, Sweden.References

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2 Harvey AM, Shulmini LK. Tumulty AP t'( ill. Systemic lupuerythemiitosuK. Keview of ihe literature iinci clinical analysis o15S cases. Medinm- t954; 3J: 291-457.

3 Wysenbeek AJ, Block DA. Eries IJi. Pre\'alence and expression ophotoscnsitivity in systemic lupus erythematosus. Ann Rheum D1989: 48: 4(nl-5.

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PHOTOSENSITIVITY IN LUPUS ERYTHEMATOSUS 70S

2 } Lever W F, Sch aum bur g-l^v cr G. Histopcitlmhijii of thf Skin, / i hcdn. I'hiiaddphid: l.B.I.Ippincoli. 19')1).24 va n Bra ag MCCl, Boom BW. Vernieer B). Diagnosis and trca tme iilof polymorphous lighl eruption. Int I Dermato! 1994 : 33 : 233-9 .2 S Slatistical Software for Exact Nonparametric Inference. Cytel Soft-ware Corporation 1992. Cambridge, MA. U.S.A.2f) Gardner \ 1 | , Gardner SB. Winter I'D. Coiifidfticf liili'rvn! Aiuiliisis.version T-II: London: British Medical Associalion, I99fi.27 Murphy G, Hawk J. The prevaleiKe uf antinuclear antibodies Inpatients with apparent polymorphic liglit eruption. Br / DITIIKIIOI1991; 1 2 5 : 4 4 8 - 5 1 .28 Ortel B. Tanew A. Woll'f K, Hoiiigsmanii H. Polymorplious li(^hteruption: action spectrum and photoprotectlon. / Am Attid Dcniui-

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SSA/Ko and anti-SSB/La antibodies in patienis with polymor-phous light eruption. Aciti Derm Venerfo! 1991: 71; J4] - 5.51 Cahn M. Ixvy li\. Shalfer B, Polymorphous light eruption. A ten-year lollow-up and evaluation. Arih Dcrmalol ]9l i5; 88: 75(1-8.il Jansen CT, Karvonen |. Polymorphous light eruption. A seven-year-lbllow-up evaluation of 114 patients. Arcli Oenmitol 1984 :

120: Sf>2-S.5 3 Furukawa K Kashihara-Sa waini M. Lyons MB. Norris DA. Hiruiin;;of antibodies to the extractable nuclear antigens SS-A/Ko and SS-B/La is induced on the surface of human keratinocytes by ultra-violet light (UVL): implication.s for the pathogenesis of photosen-sitive cutaneous lupus. / Invest Dcrwalol 1990 : 94 : 77 -8S .34 Mond CB. Peterson MGE, Rothfield NF. Correlation of anti-Koantihody with photosensitivity rasli in systemic lujnis erythema-losus patieiits. Arthrilis Rheum 1489 : J2 : 202-4 .3 5 Kind P, Lehmann 1'. i'lewig C. Photolesting in lupuserythematosus. / Invest Dmmito! 1995 : 100: 5 5 - 7 S .56 Lee LA. Roberts CM. Frank MB ci al. The autoantibody response toRo/SSA in cutaneous lupus erythcmatosus. Arch Uermaiol 1994 ;

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photo sensitivity in lupus bjd

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