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  • A few days after UV exposure, erythema and itching developed, followed by characteristic morphologic skin lesions of LET with histological changes similar to those in primary lesions (Figure 5). Patients with LET had been found to be even more photosensitive than patients with SCLE and, in our study, experimental phototesting revealed characteristic skin lesions in 28 (70%) of the patients; 10 (56%) of the 18 tested patients reacted to UV-A and UV-B irradiation, 16 (40%) of the 40 patients to UV-A only, and 15 (38%) of the 40 patients to UV-B only. Twenty (50%) of the 40 patients were aware of an adverse effect of sunlight on their disease, and 15 (75%) of them showed pathologic test reactions. Pathologic test reactions were also induced in 12 (60%) of those patients who denied any effect of sun exposure on their disease. Figure 5. Positive results of provocative phototesting of lupus erythematosus tumidus. Development of characteristic skin lesions are seen 1 week after UV-A irradiation for 3 consecutive days. LABORATORY FEATURES Laboratory tests that were performed in all 40 patients with LET revealed ANAs with a titer of greater than 1:160 in 4 (10%) of the patients. The ANA fluorescence pattern was finely granular in all except 1 case, where it was homogeneous. AntiRo/SSA and La/SSB antibodies were detected in 2 (5%) of the patients with ANAs, and dsDNA antibodies were present at a low serum concentration in only 1 patient (3%). AntiU1RNP, Sm, Scl 70, or Jo 1 antibodies were not detected in any case. Anticardiolipin antibodies were temporarily positive at a low serum titer in 4 (10%) of the patients, but findings for KCT and ANCA were negative in all patients. Decreased C3 levels occurred temporarily in 11 (28%) of the patients and decreased C4 levels were detected in only 2 (5%). An elevated RF was present temporarily in 2 patients (5%), and findings for CRP were positive in 12 (30%). Levels of IgG and IgM were elevated in 3 patients (8%) and IgA in 4 (10%), whereas findings for CH50 were negative in all of the patients. Only 1 patient (3%) showed a transient leukopenia, and 3 (8%) disclosed a thrombopenia. A mildly elevated creatinine level from 97.3 to 141.5 mol/L (reference value, 88.4 mol/L) (1.1-1.6 mg/dL [reference value, 1.0 mg/dL]) was transiently found in 5 patients (12%), but a pathologic creatinine clearance was not detected. COURSE OF THE DISEASE AND THERAPY One of the patients had had LET for more than 30 years at presentation in our clinic; however, most patients had been affected for less than 6 years (Table 1). The youngest patient was aged 9 months at initial diagnosis and had already had recurrent skin lesions for 10 years. The clinical features observed during exacerbations of the disease activity in individual patients with LET occurred in most of the cases in summer due to sun exposure, and some patients reported that even after sitting behind glass windows, their skin disease had worsened, indicating that long-wavelength UV light is capable of activating LET. None of the 40 patients had a history of drug-induced LET in our study after up to 15 years of follow-up. Since the face is most often affected, LET obviously has a significant cosmetic implication. A complete resolution of the skin lesions was seen in 18 patients (45%) who had received only topical corticosteroids or sunscreens with a sun protection factor of 15 or greater. Twenty-two patients (55%) who had failed to respond to this regimen were treated with antimalarials. Chloroquine phosphate was successfully used in a daily dose of 3.5 to 4.0 mg/kg per day, and a complete resolution of the skin lesions was seen mostly after 4 to 6 weeks in the treated patients. In 3 patients (8%) who did not respond to this treatment, hydroxychloroquine sulfate was successfully used in a daily dose of 6.0 to 6.5 mg/kg per day. All patients receiving antimalarials for several months or years underwent laboratory studies, including complete blood cell counts and renal and liver function tests, before the onset of therapy and every 4 to 6 weeks thereafter, as well as ophthalmologic examinations (eg, fundoscopy, perimetry, color vision, and electro-oculography) every 6 months. Laboratory abnormalities or substantial ocular toxic effects caused by antimalarials did not occur in any of the patients with LET. Because of the rapid and effective improvement of the skin lesions after treatment with antimalarials, systemic corticosteroids or immunosuppressants were temporarily necessary in only 2 patients. COMMENT In this report, we have analyzed the clinical, histological, photobiological, and laboratory features of 40 patients with LET. Although the patients are clinically identified by a characteristic type of skin lesion, LET has been reported previously in the literature in only a few cases. This might be because other authors have not considered LET as an entity separate from other variants of CCLE and, therefore, it is quite likely that skin lesions described under different designations, such as "urticarial plaque lupus erythematosus," represent the same disease. Since some skin conditions share a number of similar features (Table 2), a correct diagnosis demands attention to rather subtle details and appreciation of the characteristic signs as well as the course of the disease (Table 3). Nearly all the case reports of LET in the literature are published by European countries, especially Germany and France, indicating that many more white patients are seen. However, in our opinion, there is no doubt about LET being a separate entity that has been neglected in the literature since first being described in 1930. Table 2. Differential Diagnosis of Lupus Erythematosus Tumidus* Disease (Source) Clinical Features Localization Histological Findings Direct IF of Lesional Skin Provocative Phototesting Results Presence of ANA, Ro/SSA, and La/SSB Antimalarial Treatment Systemic Involvement LET (6, 20, 28, 29, 31) Erythematous, succulent, nonscarring, urticarialike plaques with a smooth surface Sun-exposed areas (face, upper back, V area of the neck, extensor aspects of the arms, scalp, and shoulders) Perivascular and periadnexal lymphocytic infiltration with interstitial mucin deposition, scattered neutrophilis, no epidermal involvement Negative Positive in 70% of patients (development of skin lesions after several days) ANA in 10%, antiRo/SSA and antiLa/SSB antibodies in 5% of patients Effective in approximately 90% of patients None DLE (30, 32-34) Coin-shaped, erythematous, hyperkeratotic skin lesions with a scaly surface; central atrophic scarring; telangiectasia Face, scalp, ears, V area of the neck, extensor aspects of the arms Hyperkeratosis, follicular plugging, vacuolar degeneration, and thickening of the dermoepidermal junction Immunoglobulin and complement deposits at the dermoepidermal junction in approximately 90% of lesional skin Positive in approximately 50% of patients (development of skin lesions after several days) ANA in 30%-40% in low titers, less than 5% of patients with higher levels, antiRo/SSA and antiLa/SSB antibodies occasionally Effective in approximately 50% of patients 5%-10% of patients SCLE (30, 32, 33, 35) Nonscarring, erythematous, papulosqamous or annular/polycyclic skin lesions with a scaly surface; central hyperpigmentation; telangiectasia Sun-exposed areas (upper back, V area of the neck, shoulders, extensor aspects of the arms, less commonly on the face) Focally thinned epidermis with vacuolar degeneration at the dermoepidermal junction, superficial perivascular and interstitial lymphocyctic infiltration Immunoglobulin and complement deposits in a granular bandlike pattern in approximately 60% of lesional skin Positive in approximately 65% of patients (development of skin lesions after several days) ANA in 60%-81%, antiRo/SSA antibodies in 40%-100% antiLa/SSB antibodies in 12%-42% of patients Effective in approximately 80% of patients In approximately 50%; severe SLE in only 10% of patients PLE (36, 37) Papular or plaquelike skin lesions Sun-exposed areas Perivascular and periadnexal lymphocytic infiltration, dermal edema, no mucin deposition Negative Positive in approximately 75% of patients (development of skin lesions after several hours) ANA in low titers in 10%-14% of patients, no antiRo/SSA or antiLa/SSB antibodies No improvement None Jessner's lymphocytic infiltration of the skin (38, 39) Asymptomatic papulonodular, erythematous, nonscarring skin lesions Face, back, chest, arms Perivascular and periadnexal lymphocytic infiltration, plasma cells, dermal edema, no mucin deposition Negative Negative Negative No improvement None REM (40,41) Ranging from erythematous, indurated plaques to reticulated macular erythema Central chest, upper back Copious mucin deposition with perivascular and periadnexal deep and superficial lymphocytic infiltration Negative Sun-inducible, but provocative phototesting results often negative Negative Usually effective None Pseudolymphoma (42, 43) Erythematous, infiltrated plaques Face, neck, chest, arms Top-heavy, wedge-shaped infiltrate composed mostly of small lymphocytes and plasma cells or eosinophils, no mucin deposition Negative Negative Negative No improvement None *LET indicates lupus erythematosus tumidus; DLE, discoid LE; SCLE, subacute cutaneous LE; PLE, polymorphous light eruption; REM, reticular erythematous mucinosis; IF, immunofluorescence; and ANA, antinuclear antibodies. Table 3. Diagnostic Criteria of Lupus Erythematosus Tumidus Criteria Findings in Study Patients Clinical Erythematous, succulent, urticarialike, nonscarring plaques with a smooth surface in sun-exposed areas Histological Perivascular and periadnexal lymphocytic infiltration, interstitial mucin deposition, and, in some cases, scattered neutrophils; no epidermal involvement or alteration of the dermoepidermal junction Phototesting Reproduction of skin lesions after UV-A and/or UV-B irradiation in 28 patients (70%) Treatment Rapid and effective systemic treatment with antimalarials in 20 (91%) of the 22 treated patients In contrast to different forms of CCLE or SCLE, a slight male predominance was detected in our study; however, this was not as prominent as previously reported for LET. The mean age at onset of the disease is nearly the same as described for DLE; therefore, compared with SCLE or SLE, patients with LET are older when the disease begins. Skin lesions of LET had already developed in a male patient when he was 9 months of age. Since several patients whom we had observed for up to 15 years had shown no recurrence after local or systemic treatment, the disease might spontaneously resolve; however, this would need to be confirmed by long-term investigations in a greater number of patients. In several aspects, the cutaneous manifestations of LET differ from other variants of CCLE. Scarring, the hallmark of DLE, does not occur in LET, even in patients with recurrent LET skin lesions at the same site for many years, and epidermal atrophy has not developed in any case. Follicular plugging and adherent hyperkeratotic scaling, which are also features of DLE, have not been seen in any of the patients. Hypopigmentation, frequently evident in patients with SCLE after the active phase with erythema and scaling, has never been detected in patients with LET. Since some of the patients had presented with annular skin lesions, there might be a possibility of development of annular erythema associated with Sjgren syndrome; however, this rare entity has mostly been reported for Asian patients. Histological evaluation of skin lesions is necessary to confirm the diagnosis of LET, and, therefore, it represents one of the major criteria of this disease (Table 3). In contrast to SCLE and DLE, follicular hyperkeratosis, epidermal atrophy, vacuolar degeneration, and thickening of the basement membrane zone usually are not found. The perivascular and periadnexal infiltrate is composed of lymphocytes and, in some cases, scattered neutrophils are seen. In all lesions of LET, a distinct subepidermal edema is present, and moderate to copious interstitial mucin deposition is detected with the use of colloidal iron staining. As previously described, results of direct immunfluorescence staining of lesional skin specimens of LET have mostly been negative for immunoglobulin or complement components. In contrast, early reports suggested that more than 90% of DLE lesions have granular, often thick, deposition of multiple immunoreactants at the dermoepidermal junction, and that approximately 60% of SCLE lesions show immune deposits in a bandlike pattern at the dermoepidermal junction or in a dustlike pattern scattered through the epidermis and the cellular infiltrates. However, the diagnostic significance of immunohistological examination has been the subject of much controversy during recent years. Since immune deposits are not specific for LE (similar deposits can be found in nonlesional and sun-damaged skin or in other skin diseases), considerable caution must be taken when interpreting the results of immunopathologic findings in lesional and nonlesional skin specimens. Photosensitivity, one of the 11 ARA criteria for the diagnosis of SLE, was investigated in all of the 40 patients with LET by means of experimental reproduction of skin lesions after UV radiation. Because of the latency period in development of positive phototest reactions, it may be difficult for patients to link sun exposure with their skin lesions. Interestingly, in our study, there was a positive history for UV sensitivity in 20 patients (50%) and positive phototest reactions in 15 (75%) of these patients. As previously described, patients with LET were even more photosensitive than those with SCLE or DLE. In contrast to the studies by Kind et al in 1993, our data showed a positive result of provocative phototesting in all 4 patients (10%) with ANAs, and all 6 patients (15%) with moderate ANA titers also had development of skin lesions after UV radiation. Antibodies to the nucleoprotein antigens Ro/SSA, and sometimes also La/SSB, have been described to be highly associated with photosensitivity in SCLE, SLE, and neonatal LE (NLE). In NLE, the percentage of patients with antibodies specific for antiRo/SSA antibodies approaches 100%, and in SCLE, the association varies from a minority of patients to 90% or more because of differences between the diagnostic criteria used at various institutions and because of varying methods for detecting antiRo/SSA antibodies. In our study, none of the 40 patients with LET fulfilled 4 or more ARA or European Academy of Dermatology and Venerology (EADV) criteria. Although joint symptoms occurred temporarily in some of the patients, no signs of inflammatory joint disease or rheumatoid arthritis were detected in any patients. Further systemic manifestations, such as renal, central nervous system, or lung involvement, have not yet manifested in any of the 40 patients during our study after up to 15 years. In contrast, Kind and Goerz have reported a rare but possible systemic involvement in patients with LET, but no specific manifestations have been documented. Lupus erythematosus tumidus bears striking similarities to PLE, Jessner's lymphocytic infiltration of the skin, REM, and pseudolymphoma (Table 2). Polymorphous light eruption is a frequent UV-induced dermatitis of papular, papulovesicular, or plaquelike appearance. The skin manifestations are monomorphous in the individual patient, and the disease is most common from March through June in geographic areas with a temperate climate, but can appear at any time of the year in tourists traveling to sunny areas. Young women are most often affected, and there is no restriction to race or age. The clinical distinction between PLE and LET can be difficult; however, LET shows a much more delayed reaction after sun exposure, and healing of skin lesions takes much longer, even when sun exposure is avoided and a sun block is applied daily. Histological and immunological investigations provide further criteria to differentiate PLE from LET, showing a sparse to moderately dense superficial or superficial and deep perivascular lymphocytic infiltration. In contrast to LET, a marked edema is seen in the papillary dermis and interstitial mucin deposition in the reticular dermis is not detectable. In 2 studies determining ANAs in patients with PLE, 10% to 14% showed titers of 1:80 or higher, correlating positively in a study with a longer duration of skin lesions. In particular, desensitization phototherapy or photochemotherapy are the most effective forms of preventive treatment in PLE; nevertheless, the uncertain long-term risks have to be weighed against the benign and self-limited disease. In Jessner's lymphocytic infiltration of the skin, the development of asymptomatic, papulonodular, nonscarring lesions classically involving the face is unrelated to UV exposure in most of the patients. Male patients are predominantly affected, and there is no sign of systemic involvement. In contrast to LET, histological features of Jessner's lymphocytic infiltration of the skin show no interstitial mucin deposition, but varying numbers of plasma cells may be present. However, Jessner's lymphocytic infiltration of the skin is not always considered as a specific disease entity, and some of the cases described in the literature might, in our opinion, represent LET. There is only one study to date comparing Jessner's lymphocytic infiltration of the skin with LET. Reticular erythematous mucinosis is also considered to be a variant of DLE or LET by some authors, especially because REM can be induced by sun exposure and antimalarials have been reported as the most effective therapy. In contrast to LET, young to middle-aged women are mostly affected, and the skin lesions, ranging from erythematous, indurated papules to reticulated, macular erythema, are mainly localized on the central chest or upper back. Histological features of REM show a mild to dense perivascular infiltrate of lymphocytes with abundant mucin deposition in the dermis. Furthermore, pseudolymphoma also can simulate LET clinically; however, in most of the cases, histological evaluation shows a top-heavy, usually wedge-shaped infiltrate of small lymphocytes as well as plasma cells and eosinophils. In summary, LET presents a rare, but distinct, subset of CCLE with characteristic clinical features requiring correlation with histological, photobiological, and laboratory findings, since, taken in isolation, other diagnoses can be indicated. Our data emphasize the importance of defining LET as a separate entity and demonstrate that this disease has been neglected in the literature since first described in 1930. TT Provost The relationship between discoid and systemic lupus erythematosus. Arch Dermatol. 1994;130:1308-1310. KC Kalunian Definition, classification, activity, and damage indices. In: Wallace DJ, Hahn BD, eds. Dubois' Lupus Erythematosus. 5th ed. Baltimore, Md: Williams Wilkins; 1997:19-29. JN Gilliam The cutaneous signs of lupus erythematosus. Contin Educ Fam Physician. 1977;6:34-70. JN Gilliam RD Sontheimer Distinctive cutaneous subsets in the spectrum of lupus erythematosus. J Am Acad Dermatol. 1981;4:471-475. RD Sontheimer The lexicon of cutaneous lupus erythematosus: a review and personal perspective on the nomenclature and classification of cutaneous manifestations of lupus erythematosus. Lupus. 1997;6:84-95. H Gougerot R Burnier Lupus rythmateux "tumidus". Bull Soc Fr Dermatol Syphiligr. 1930;37:1291-1292. H Gougerot R Burnier Lupus rythmateux tumidus. Bull Soc Fr Dermatol Syphiligr. 1931;38:195. H Gougerot R Burnier Lupus rythmateux tumidus. Bull Soc Fr Dermatol Syphiligr. 1931;38:195-196. H Gougerot R Burnier Lupus rythmateux tumidus. Bull Soc Fr Dermatol Syphiligr. 1932;39:21. A Bazex R Salvador A Dupr M Parant B Christol Ist es berechtigt, die lymphozytre Infiltration der Haut von Jessner und Kanof als nosologische Entitt anzusehen? Hautarzt. 1965;16:250-254. P De Graciansky C Grupper L Sirkis Dermato-mycose Trichophyton rubrum simulant un lupus rythmateux tumidus. Bull Soc Fr Dermatol Syphiligr. 1965;72:809-810. AM Casala C Bianchi O Bianchi SG Stringa Lupus rythmateux tumidus (lymphocytic infiltration of the skin) et lupus rythmateux chronique associs chez le mme malade. Bull Soc Fr Dermatol Syphiligr. 1971;78:256-258. JC Mosquera-Vieitez C de la Torre Fraga MJ Cruces Prado Gougerot's lupus erythematosus tumidus. Med Cutan Ibero Lat Am. 1984;12:425-429. P Kind G Goerz Klinik und Differentialdiagnose des kutanen Lupus erythematodes. Z Hautkr. 1987;62:1337-1347. P Kind G Goerz Der kutane Lupus erythematodes (LE). In: Macher E, Knop J, Brcker EB, eds. Jahrbuch der Dermatologie. Mnster, Germany: Biermann Verlag; 1988:85-103. G Goerz P Lehmann HC Schuppe HJ Lakomek P Kind Lupus erythematodes (LE). Z Hautkr. 1990;65:226-234. DA Norris LA Lee Antibody-dependant cellular cytotoxicity and skin disease. J Invest Dermatol. 1985;85(suppl):165S-175S. F Furukawa M Kashihara-Sawami MB Lyons DA Norris Binding of antibodies to the extractable nuclear antigens SS-A/Ro and SS-B/La is induced on the surface of human keratinocytes by ultraviolet light (UVL): implications for the pathogenesis of photosensitive cutaneous lupus. J Invest Dermatol. 1990;94:77-85. P Kind P Lehmann G Plewig Phototesting in lupus erythematosus. J Invest Dermatol. 1993;100(suppl):53S-57S. P Kind HC Schuppe G Goerz Kutaner Lupus erythematodes. Dtsch rztebl. 1992;49:2121-2130. P Lehmann E Hlzle R von Kries G Plewig Lichtdiagnostische Verfahren bei Patienten mit Verdacht auf Photodermatosen. Z Haut Geschlechtskr. 1986;152:667-682. E Hlzle G Plewig P Lehmann Photodermatoses: diagnostic procedures and their interpretation. Photodermatol. 1987;4:109-114. P Lehmann E Hlzle P Kind G Goerz G Plewig Experimental reproduction of skin lesions in lupus erythematosus. J Am Acad Dermatol. 1990;22:181-187. EM Tan AS Cohen JF Fries The revised criteria for the classification of systemic lupus erythematosus: 1982. Arthritis Rheum. 1982;25:1271-1277. P Lehmann Photosensitivitt des Lupus erythematodes. Akt Dermatol. 1996;22:47-51. M Walchner G Messer P Kind Phototesting and photoprotection in LE. Lupus. 1997;6:167-174. A Kuhn HC Schuppe M Megahed G Goerz P Lehmann Kutaner Lupus erythematodes im Kindesalter (Tumidus-Typ). Z Hautkr. 1997;72:299-300. A Kuhn HC Schuppe P Lehmann G Goerz T Ruzicka Cutaneous manifestations of lupus erythematosus: what is important for rheumatologists? Rheumatol Eur. 1998;27:95-101. S Ruhdorfer R Hein J Ring Differentialdiagnostische und pathogenetische Aspekte des Lupus erythematodes tumidus. Z Hautkr. 1998;9:602-606. RD Sontheimer TT Provost Lupus erythematosus. In: Sontheimer RD, Provost TT, eds. Cutaneous Manifestations of Rheumatic Diseases. Baltimore, Md: Williams Wilkins; 1996:1-71. CL Dekle KD Mannes LS Davis OP Sangueza Lupus tumidus. J Am Acad Dermatol. 1999;41:250-253. JL Bangert RG Freemann RD Sontheimer JN Gilliam Subacute cutaneous lupus erythematosus and discoid lupus erythematosus: comparative histological findings. Arch Dermatol. 1984;120:332-337. KM David-Bajar BM Davis Pathology, immunopathology, and immunohistochemistry in cutaneous lupus erythematosus. Lupus. 1997;6:145-157. EL Pohle DL Tuffanelli Study of cutaneous lupus erythematosus by immunohistochemical methods. Arch Dermatol. 1968;97:520-526. RD Sontheimer Subacute cutaneous lupus erythematosus: a decade's perspective. Med Clin North Am. 1989;73:1073-1090. P Lehmann E Hlzle Polymorphous light eruption. In: Demis DJ, ed. Clinical Dermatology. 26th rev. Philadelphia, Pa: Lippincott-Raven Publishers; 1999;4:1-8. P Petzelbauer B Binder P Nikolakis B Ortel H Hnigsmann Severe sun sensitivity and the presence of antinuclear antibodies in patients with polymorphous light eruption. J Am Acad Dermatol. 1992;26:68-74. J Toonstra A Wildschut J Boer Jessner's lymphocytic infiltration of the skin. Arch Dermatol. 1989;125:1525-1530. J Ashworth WN Morley Jessner's and Kanof's lymphocytic infiltration of the skin: a familial variant. Dermatologica. 1988;177:120-122. PR Cohen AD Rabinowitz AM Ruszkowski VA DeLeo Reticular erythematous mucinosis syndrome: review of the world literature and report of the syndrome in a prepubertal child. Pediatr Dermatol. 1990;7:1-10. SW Braddock HD Kay D Maennle Clinical and immunologic studies in reticular erythematous mucinosis and Jessner's lymphocytic infiltration of the skin. J Am Acad Dermatol. 1993;28:691-695. H Kerl AB Ackerman Inflammatory diseases that simulate lymphomas: cutaneous pseudolymphomas. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Dermatology in General Medicine. 4th ed. New York, NY: McGraw-Hill Co; 1993:1315-1327. T Ploysangam DL Breneman DF Mutasim Cutaneous pseudolymphomas. J Am Acad Dermatol. 1998;38:877-895. JP Callen Chronic cutaneous lupus erythematosus: clinical laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. T Ruzicka J Faes T Bergner RU Peter O Braun-Falco Annular erythema associated with Sjogren's syndrome: a variant of systemic lupus erythematosus. J Am Acad Dermatol. 1991;25:557-560. A Kuhn D Richter-Hintz HC Schuppe T Ruzicka P Lehmann Anulres Erythem bei Sjgren-Syndrom: eine Variante des kutanen Lupus erythematodes? Hautarzt. 2000;51:270-275. AB Ackerman Lupus erythematosus. In: Histologic Diagnosis of Inflammatory Skin Diseases. 2nd ed. Baltimore, Md: Williams Wilkins; 1997:525-546. D Lipsker MP di Cesare B Criber E Grosshans E Heid The significance of the "dust-like particles" pattern of immunofluorescence: a study of 66 patients. Br J Dermatol. 1998;138:1039-1042. MV Dahl Usefulness of direct immunofluorescence in patients with lupus erythematosus. Arch Dermatol. 1983;119:1010-1017. VC Fabre S Lear M Reichlin SJ Hodge JP Callen Twenty percent of biopsy specimens from sun-exposed skin of normal young adults demonstrates positive immunofluorescence. Arch Dermatol. 1991;127:1006-1011. AR Ahmed TT Provost Incidence of a positive lupus band test using sun exposed and unexposed skin. Arch Dermatol. 1979;115:228-232. CB Mond MG Peterson NF Rothfield Correlation of anti-Ro antibody with photosensitivity rash in systemic lupus erythematosus patients. Arthritis Rheum. 1989;32:202-204. LA Lee MB Frank VR McCubbin M Reichlein Autoantibodies of neonatal lupus erythematosus. J Invest Dermatol. 1994;102:963-969. RD Sontheimer Questions pertaining to the true frequencies with which anti-Ro/SSA autoantiboby and the HLA-DR3 phenotype occur in subacute cutaneous lupus erythematosus patients. J Am Acad Dermatol. 1987;16:130-134. A Parodi A Rebora ARA and EADV criteria for classification of systemic lupus erythematosus in patients with cutaneous lupus erythematosus. Dermatology. 1997;194:217-220. T Hasan A Ranki CT Jansen J Karvonen Disease associations in polymorphous light eruption. Arch Dermatol. 1998;134:1081-1085. GM Murphy JLM Hawk The prevalence of antinuclear antibodies in patients with apparent polymorphous light eruption. Br J Dermatol. 1991;125:448-451. B Ortel A Tanew K Wolff H Hnigsmann Polymorphous light eruption: action spectrum and photoprotection. J Am Acad Dermatol. 1986;14:748-753. D Bilsband SA George NK Gibbs T Aitchinson BE Johnson J Ferguson A comparison of narrow band phototherapy (TL-01) and photochemotherapy (PUVA) in the management of polymorphous light eruption. Br J Dermatol. 1993;129:708-712. R Willemze BJ Vermeer CJLM Meijer Immunohistochemical studies in lymphocytic infiltration of the skin (Jessner) and discoid lupus erythematosus. J Am Acad Dermatol. 1984;11:832-840. M Bonczkowitz W Weyers Differenzierung von Lupus erythematodes und lymphocytic infiltration. Verh Dtsch Ges Pathol. 1996;80:235-240. R Akasu HJ Kahn L From Lymphocyte markers on formalin-fixed tissue in Jessner's lymphocytic infiltrate and lupus erythematosus. J Cutan Pathol. 1992;19:59-65. W Weyers M Bonczkowitz I Weyers LE or not LEthat is the question: an unsuccessful attempt to separate lymphocytic infiltration from the spectrum of discoid lupus erythematosus. Am J Dermatopathol. 1998;20:225-232. JM Weinberg AH Rook SR Lessin Molecular diagnosis of lymphocytic infiltrates of the skin. Arch Dermatol. 1993;129:1491-1500. Accepted for publication October 19, 1999. This work was supported by a Lise-Meitner scholarship and a research grant from the Heinrich-Heine-University Dsseldorf, Dsseldorf, Germany (Dr Kuhn). We thank Richard Weller, MD, Department of Dermatology, Edinburgh University, Edinburgh, Scotland, for critical reading of the manuscript. Reprints: Annegret Kuhn, MD, Institute of Cell Biology, ZMBE, Westflische Wilhelms-University, Von-Esmarch-Strasse 56, 48149 Mnster, Germany (e-mail: kuhnan@uni-muenster.de).
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  • Kuhn, A., Richter-Hintz, D., Oslislo, C., Ruzicka, T., Megahed, M., & Lehmann, P. (2000). Lupus Erythematosus Tumidus. Arch Dermatol, 136(8), 1033-1041. https://doi.org/10.1001/archderm.136.8.1033.
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  • Annegret Kuhn MD, Dagmar Richter-Hintz MD, Claudia Oslislo MD, Thomas Ruzicka MD, Mosaad Megahed MD, Percy Lehmann MD
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