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Genital involvement is a rare manifestation in discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE), and there are few reports on vulvar clinical features. We describe a 41-year old Caucasian woman with bilateral vulvar DLE. Although vulvar lesions in lupus are probably more common than is realized, the present report is the first case of genital DLE documented in a female.
Lichen planus (LP) and discoid lupus erythematosus (DLE) are separate disease entities. Nevertheless, patients with a so-called "overlap syndrome" have been described occasionally. The aim of the present study was to establish whether the LE/LP overlap syndrome, based on clinical and routine histological features, could be delineated from DLE or LP using immunohistochemical techniques. Formalin-fixated, paraffin-embedded skin biopsies of patients with DLE, LP and the overlap syndrome were compared regarding immunohistochemical markers for epidermal growth and differentiation and extracellular matrix components. With the markers for extracellular matrix proteins, it was possible to delineate the overlap syndrome from LP. This was not possible for the overlap syndrome and DLE. These findings might indicate that the LE/LP overlap syndrome could be considered as LP-like DLE rather than as a distinct disease entity.
Chronic inflammatory discoid lupus erythematosus (DLE) and Jessner's lymphocytic infiltration of the skin (LIS) are both characterized by dermal infiltrates of activated T lymphocytes. However, an inflammatory involvement of the epidermis is only found in DLE. We therefore compared the phenotypic properties of the keratinocytes using immunohistochemical stainings of biopsies from typical DLE and LIS. Keratinocytes failed to express HLA-DR in LIS and surprisingly also in DLE. The adhesion molecule ICAM-1 was only expressed in DLE, with focal staining of the basal keratinocytes in close association with intraepidermal lymphocytes. The monoclonal antibody 27E10, a distinct marker for macrophage activation and differentiation, revealed a strong band-like labelling of the suprabasal and upper keratinocytes in DLE. In contrast, no epidermal expression of this biologically active heterodimer of the calcium-binding proteins MRP-8 and MRP-14 was found in LIS. The staining patterns provide a new method to differentiate DLE and LIS by immunohistochemistry and suggest a distinct type of keratinocyte activation and differentiation in DLE which would in turn mediate epidermal T cell infiltration.
Squamous cell carcinoma developing in lesions of discoid lupus erythematosus is rare. This article describes two patients, one with a carcinoma of the scalp and one with carcinoma of the upper lip. A review of the literature on squamous cell carcionoma in black persons as well as squamous cell carcinoma of the upper lip is presented.
A case of discoid lupus erythematosus with oral manifestations only is presented. The patient complained of painful palatal ulcers that limited her dietary intake. A topical therapeutic regimen using plastic carriers containing clobetasol propionate was beneficial in significantly relieving the oral discomfort. The clinical and microscopic differential diagnoses for this mucocutaneous disease are also discussed.
In the present study, keratin and involucrin expression were studied in cutaneous lesions of discoid lupus erythematosus and lichen planus in order to gain a better understanding of the abnormal differentiation or maturation of the epidermal cells in these dermatoses. Ten specimens each from discoid lupus erythematosus and lichen planus were analyzed by immunohistochemical techniques, using a panel of monoclonal antikeratin antibodies and polyclonal anti-involucrin antibody, and five specimens each were analyzed by one- and two-dimensional gel electrophoresis and immunoblot analysis using three antikeratin antibodies. No significant difference was found between the dermatoses. The expression of differentiation-specific keratins showed a similar pattern to that in normal epidermis, and involucrin was expressed even in the lower part of the stratum spinosum. Keratins 6 and 16, which are characteristic markers of hyperproliferative states, and keratin 17 were detected in nonhyperproliferative and atrophic epidermis with hydropic degeneration and inflammatory infiltrates in the dermis. These results suggest that expression of keratins 6, 16 and 17 in discoid lupus erythematosus and lichen planus may reflect a wound healing response to the damage to the basal cell layer, or may be under the control of cytokines produced by infiltrating inflammatory cells in the dermis.
Serologic and clinical data were obtained from forty patients with discoid lupus erythematosus in 1982. Clinical disease was characterized by quality, extent, severity, activity, photosensitivity, and systemic manifestations. The patient's sera were examined for the presence of antinuclear, anti-Ro and anti-La, anti-ribonucleoprotein and anti-Sm, anti-single-stranded deoxyribonucleic acid (ssDNA), and antinative DNA antibodies. In late 1984, thirty-three patients had follow-up clinical examinations. On the initial evaluation the patients with positive antinuclear antibody (ANA) findings were clinically characterized by a significantly higher incidence of photosensitivity and arthritis, an elevated erythrocyte sedimentation rate, and cutaneous lesions of subacute cutaneous lupus erythematosus. The activity and extent of disease in 1982 did not correlate with the presence of ANA. Elevated levels of ssDNA antibodies were present in seven of the forty patients (significantly greater than control subjects; (p less than 0.005) and correlated with widespread, active discoid lupus erythematosus, an elevated erythrocyte sedimentation rate, and a slightly greater risk of systemic lupus erythematosus in 1982. At the 2-year follow-up examination, thirteen of the seventeen patients with a positive ANA had active clinical cutaneous disease, and ten of the sixteen patients with negative ANA findings had continued activity (not statistically significant). However, all seven patients with elevated ssDNA antibody levels had continued activity, and disease progression had occurred in three. Thus the presence of ssDNA seems to correlate strongly with active, progressive lupus erythematosus. The presence of antibody abnormalities in patients with discoid lupus erythematosus correlates with clinical disease and provides more support for the theory linking discoid lupus erythematosus to systemic lupus erythematosus as part of a continuum.
We present the case of two patients with an unusual form of discoid lupus erythematosus that was confined almost exclusively to the palms and soles. In both patients this form of discoid lupus erythematosus did not respond to conventional therapies, which included topical steroids, intralesional steroids, prednisone, quinacrine hydrochloride, hydroxychloroquine sulfate, colchicine, and dapsone. Both patients were then treated with azathioprine. One patient dramatically improved with azathioprine, worsened each time the azathioprine was stopped or reduced, and responded again to the reinstitution of therapy. The other patient began taking azathioprine 8 months ago and has also experienced relief of her symptoms. These cases suggest that discoid lupus erythematosus principally involving the palms and soles is difficult to treat with conventional medication and that azathioprine, which appears to be useful, should be tried after the failure of other therapies.
Immune response to ultraviolet radiation-modified skin antigens has been suggested as a pathomechanism of skin lesions in discoid lupus erythematosus and polymorphous light eruption. In order to elucidate the role of T-lymphocyte subsets in this response, we studied the distribution of CD45RO+, CD45RA+ and CD31+ cells and the endothelial expression of adhesion molecules E-selectin/P-selectin, intercellular adhesion molecule-1 and CD31 antigen in photoprovoked and spontaneous skin lesions. Typically, CD45RA+ cells were the prevailing inflammatory cell population of discoid lupus erythematosus, whereas CD45RO+ cells prevailed in both diseases and in healthy controls. Epidermotrophism of any T-cell subsets was more typical of discoid lupus erythematosus, whereas no major differences in endothelial adhesion molecule expression was found between the 2 diseases. Strong keratinocyte ICAM-1 expression was associated with adjacent CD45RO+ cell infiltrates, not with CD45RA+ or CD31+ cell infiltrates. We conclude that the cellular immune response to UV radiation is dissimilar in discoid lupus erythematosus and polymorphous light eruption.
We studied the expression of the C3b receptor, CR1, on erythrocytes (E-CR1) of patients who, in spite of having mild systemic symptoms, were diagnosed as having discoid lupus erythematosus and followed accordingly. We found that E-CR1 was markedly reduced in these patients, similar to that seen in patients with systemic disease. In contrast, those patients with completely asymptomatic discoid lupus erythematosus had the same expression of E-CR1 as the normal population.
We report on a patient with chronic discoid lupus erythematosus who was treated with argon-laser. The patient suffered from long-standing lesions and had been pretreated with various drugs; with no or slight improvement. After a few argon-laser applications, the treated skin lesions improved dramatically while the untreated lesional skin showed continuous disease activity. Histological and immunohistological investigations of biopsies from treated and untreated lesional skin suggest that endothelial mechanisms play a role in the generation and maintenance of discoid lesions in lupus erythematosus. This is the first reported case of successful treatment of chronic discoid skin lesions of a lupus erythematosus patient with argon-laser.
We report the case of a patient suffering from vitiligo and discoid lupus erythematosus. The nails of the left hand were involved with subungual hyperkeratosis. He was treated by local and systemic corticosteroid and chloroquine but hyperkeratotic lesions progressed on the affected sites and were found to be caused by Trichophyton violaceum.
A female is presented with multiple longstanding hypertrophic discoid lupus erythematosus lesions resistant to topical and systemic therapy for years. She suffered severe itching and pain localized to the lesions. Treatment with cryosurgery resulted in complete healing of the lesions, leaving slightly hypopigmented soft scars. There was no tendency of relapse during a follow-up period of ten years.
We report a patient with discoid lupus erythematosus (DLE) and associated allergic contact dermatitis (ACD) in the eyelids. In women, ACD caused by nail varnish is frequent and often seen in the eyelids. ACD caused by drugs (e.g. neomycin) is also frequent in this region. However, DLE with periorbital presentation without evidence of systemic or other cutaneous involvement is rare.
Skin cancer is relatively uncommon among black individuals. Squamous cell carcinoma occurred in a scar of chronic discoid lupus erythematosus in a black patient. A review of 7 previously reported cases of squamous cell carcinoma in blacks with chronic discoid lupus erythematosus indicates a tendency of the cancer to metastasize. Sun exposure of the hypopigmented lesions of chronic discoid lupus and possibly other factors predispose to cancer of the skin. Poorly healing skin lesions in chronic discoid lupus should arouse suspicion of malignant change.
Although HIV infection is often associated with several rheumatic diseases, the coexistence of this retroviral infection and systemic lupus erythematosus (SLE) is extremely uncommon. Generally, HIV-related immunosuppression improves SLE symptoms, and antiretroviral therapy may lead to an autoimmune disease flare subsequent to the increase of circulating CD4+ cell number. Two HIV-infected female patients with SLE and discoid lupus erythematosus (DLE) diagnosed a few months after the highly active antiretroviral therapy initiation, are described. To our knowledge, this is the second case of DLE and the twenty-seventh case of SLE reported to date in association with HIV infection.
Two cases of squamous cell carcinoma developing in lesions of chronic cutaneous discoid lupus erythematosus are presented. One of the patients was white and the other was black. The squamous cell carcinoma in the black patient proved to be rapidly metastatic and eventually fatal. The white patient developed seven squamous cell carcinomas over 8 years with no evidence of metastatic spread. The role of ultraviolet light in inducing skin cancer in these patients is discussed.
Biopsies of oral lesions from 21 patients with diagnostic skin lesions of discoid lupus erythematosus and from 21 patients with oral lichen planus and leukoplakia were examined blindly by light microscopy. The correct histologic diagnosis (DLE) was established in less than half of the cases. In one-third of the cases differentiation between DLE and lichen planus could not be made. In the rest of the cases histologic diagnoses other than DLE were stated. The study shows the need for better diagnostic methods for oral lesions.