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A 36-years-old female presented with hypertrophic, depigmented plaques on both forearms and a fungating cauliflower-like growth on the left forearm. Histologically, the plaque lesions were discoid lupus erythematosus, and the fungating growth was a well-differentiated squamous cell carcinoma.
The expression of lymphocyte activation markers (IL2 receptors, transferrin receptors and HLA-DR) was examined in cutaneous lymphoid infiltrates of 12 patients with lichen ruber planus (LP) and 10 individuals with discoid lupus erythematosus (DLE). The cell infiltrates in both conditions were generally of considerable size. The vast majority of the infiltrating cells were T cells. The reactivity of the anti-IL2 receptor antibody used was confined to lymphocytes. In patients with LP 26 +/- 17% of the infiltrating cells were IL2 receptor positive, 20 +/- 8% carried transferrin receptors and greater than 90% HLA-DR. In patients with DLE less than 1% were IL2 receptor positive, less than 5% carried transferrin receptors and greater than 90% were HLA-DR positive. These data indicate that IL2 receptor expression distinguishes the infiltrating T-lymphocytes in LP and DLE, although in both conditions the vast majority of the infiltrating cells were activated as revealed by their expression of HLA-DR.
Necrotizing fasciitis (NF) is an uncommon, but devastating, disease with a significant morbidity and mortality, unchanged in the last several decades. This case report is the first successful management of a patient with NF secondary to discoid lupus erythematosus. A review of the literature describes current concepts of etiology, pathophysiology, diagnosis, and treatment of NF. This case report represents a growing class of patients at increased risk of NF due to iatrogenic immune compromise.
The author notes that psoriasis is a common condition and primary care physicians should be aware of drugs that can worsen this disease. He describes the case of a patient with coexistent discoid lupus erythematosus (LE) and psoriasis. He discusses therapeutic problems encountered in this case and reviews drugs reported to exacerbate psoriasis.
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Squamous cell carcinoma (SCC) is the most common skin cancer in black patients. In half of the cases, it is associated with predisposing factors. We present a patient who has been evaluated for thirty-nine years with a diagnosis of discoid lupus erythematosus (DLE) and has multiple SCCs. The lesions occurred in chronic hyperkeratotic lesions of DLE.
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A family with hereditary deficiency of the second component of complement was studied. Three siblings were homozygous for C2 deficiency and two of them had associated skin diseases. One sister presented with idiopathic atrophoderma and the other had clinical and pathological manifestations of discoid lupus erythematosus. This is the first description of an association between idiopathic atrophoderma and C2 deficient state.
BACKGROUND: Secondary localized cutaneous amyloidosis is a clinically unapparent phenomenon associated with various cutaneous pathologies, usually tumours of epidermal origin. The amyloid is thought to be derived from keratinocytes. OBJECTIVES: To characterize the amyloid deposition observed incidentally within lesional biopsies from three patients with discoid lupus erythematosus (DLE), and retrospectively to study the phenomenon within DLE skin samples. METHODS: Localized amyloid deposition was observed in three cases of DLE by immunofluorescence studies, and these cases were further studied by histology and immunohistochemistry using a monoclonal anticytokeratin antibody. Retrospective histological review of DLE tissue specimens archived over 12 months was performed to look for evidence of previously undetected amyloid. RESULTS: Amyloid deposition was confirmed histologically in the three index cases by staining with Congo red and thioflavin T. Positive staining with an anticytokeratin antibody demonstrated the epidermal origin of the amyloid protein. Of the 18 archived cases reviewed amyloid was retrospectively detected in one sample. CONCLUSIONS: Secondary cutaneous amyloidosis of keratinocyte origin can be seen in DLE lesions. It may be a not infrequent occurrence and may remain under-reported. We discuss the possible role of disease chronicity and colloid body degradation in the pathogenesis of amyloidosis.
A 65-year-old woman with facial erythema and hypergammaglobulinemia developed excessive fatigability. A diagnosis of Lambert-Eaton myasthenic syndrome (LEMS) was made from electrophysiological studies. She had symptoms and laboratory data compatible with probable Sjögren's syndrome. Skin biopsy revealed the histological findings of discoid lupus erythematosus. Treatment with 3,4-diaminopyridine resulted in the improvement of fatigability. LEMS should be recognized as a treatable complication of systemic autoimmune diseases.
By electron microscopy colloid bodies have been shown to be derived from epithelial cells. It has been suggested, however, that connective tissue cells or components from the basement membrane zone contributed to the formation of colloid bodies. In order to examine these possibilities we stained oral lesions of discoid lupus erythematosus (DLE) with antibodies against intermediate filaments (keratin, vimentin), basement membrane components (laminin, collagen type IV) and fibronectin. IgM was used as a marker for colloid bodies. Colloid bodies were stained positive for keratin, whereas vimentin was never found in colloid bodies. Laminin and collagen type IV were occasionally seen in their periphery probably owing to adherence of basement membrane fragments during apoptosis. Fibronectin was frequently seen at the entire periphery of colloid bodies which may facilitate their elimination by macrophages. In conclusion, connective tissue cells or basement membrane components do not seem to contribute to the formation of colloid bodies in oral DLE.
AIM: To investigate whether p53 expression and apoptosis play a role in the pathogenesis of discoid lupus erythematosus (DLE) and whether they are associated with a hyperproliferative state in the epidermis of DLE lesions and epidermal atrophy. METHODS: A total of 70 skin biopsy specimens, 35 DLE and 35 normal, were used. Expression of protein p53 and Ki-67 was examined immunohistochemically. Apoptotic cells were identified by terminal deoxynucleotidyl transferase (TdT)-mediated nick end labeling (TUNEL). Histopathological examination of hematoxylin-eosin-stained sections of DLE included analysis and scoring of epidermal atrophy and other histopathological parameters. RESULTS: p53 expression was greater in DLE than in normal skin (14.5 vs 0.6%, P<0.001). Ki-67 expression was also greater in DLE than in normal skin (8.0 vs 3.1%, P<0.001). A significant positive correlation between p53 and Ki-67 expression was found in both groups (normal skin, r=0.46, P<0.009; DLE, r=0.72, P<0.001). A significant negative correlation (r=-0.75, P<0.001) between Ki-67 expression and the intensity of epidermal atrophy was found. The degree of apoptosis in the epidermis of DLE lesions with higher Ki-67 and p-53 expression was higher than when the expression of these molecules was low (3.0+/-1.8 vs 1.6+/-1.5 on a scale from 0-5; P=0.048). CONCLUSION: Aberrant p53 expression occurs in the keratinocytes of DLE and is associated with keratinocyte hyperproliferation and epidermal atrophy. Accumulation of p53 protein, together with an extensive apoptosis, suggests that the activation of a p53-induced apoptotic pathway may play a role in the pathogenesis of skin lesions in DLE.
Verruciform xanthoma (VX) is an uncommon lesion occurring primarily in the oral cavity. Cutaneous lesions are much less common and they preferentially arise on anogenital skin. They are not necessarily associated with a pre-existing inflammatory process. We report a VX in association with a long-standing lesion of discoid lupus erythematosus (DLE) on the scalp of a 34-year-old black woman. This association, which to our knowledge has not been previously reported, is consistent with the proposed pathogenetic mechanism of entrapment and subsequent degeneration of epithelial cells in the papillary dermis of VX. Histological distinction of VX from squamous cell carcinoma, with which this lesion may be clinically confused, is straightforward.
A combined indirect immunofluorescence technique with a murine monoclonal antibody against human Ia-like antigens (OKIal) and an IgG F(ab')2 preparation of a rabbit anti-T lymphocyte serum was used to study Ia-like antigens on T lymphocytes in skin lesions of psoriasis, lichen planus and discoid lupus erythematosus. The majority of the T lymphocytes in the various skin lesions expressed Ia-like antigens. T lymphocytes expressing Ia-like antigens were also demonstrated in the dermis and the epidermis in sections of unaffected skin, although of a markedly lower proportion than in affected skin. The results may indicate that the T lymphocytes in these skin lesions are activated cells involved in cell-mediated immune reactions.
Thalidomide, an oral drug introduced in Germany in 1953 as a mild sedative, was withdrawn from the world market when its teratogenic effect was discovered some years later. It has since been selectively reintroduced to treat a variety of autoimmune or inflammatory diseases such as erythema nodosum leprosum, prurigo nodularis, graft-versus-host disease, and discoid lupus erythematosus (DLE). We report on three patients with long-standing, severe DLE showing no response to systemic first-, second- and third-line treatments. After four weeks of therapy with thalidomide the skin lesions had improved dramatically and after three to six months all three patients responded with an almost complete remission. The side effects of thalidomide, especially somnolence and paresthesias, were minor and well tolerated by the patients. Our data confirm that thalidomide provides one of the most useful therapeutic alternatives for chronic refractory DLE, despite the risks of teratogenicity and polyneuropathy.
OBJECTIVE: To evaluate the effect of long-term treatment with tetracycline and niacinamide on antibody production in dogs by measuring postvaccinal serum concentrations of antibodies against canine parvovirus and canine distemper virus. ANIMALS: 10 dogs receiving long-term treatment with tetracycline and niacinamide (treatment group) and 10 healthy dogs (control group). PROCEDURE: The treatment group included 9 dogs with discoid lupus erythematosus and 1 dog with pemphigus foliaceus on long-term treatment (> 12 months) with tetracycline and niacinamide. The control group included 10 healthy dogs with no clinical signs of disease and no administered medications for the past 3 months. Blood samples were obtained from all dogs by jugular venipuncture. Serum antibody titers against canine parvovirus and canine distemper virus antigens were measured, using hemaglutination inhibition and serum neutralization, respectively, and compared between groups. RESULTS: A significant difference in antibody titers between treatment- and control-group dogs was not found. All dogs had protective antibody titers against canine distemper virus, and 8 of 10 dogs from each group had protective titers against canine parvovirus infection. CONCLUSION AND CLINICAL RELEVANCE: These results provide evidence that long-term treatment with tetracycline and niacinamide does not interfere with routine vaccinations and thus does not seem to influence antibody production in dogs.
BACKGROUND: Infiltrating T lymphocytes are considered to play a major pathological role in skin lesions of cutaneous lupus erythematosus (CLE), a cutaneous autoimmune disease of unknown aetiology. Earlier histological studies revealed that the inflammatory infiltrate in CLE skin lesions is predominantly composed of T lymphocytes, with a slight predominance of CD4+ over CD8+ T cells, but failed to explain the development of scarring skin lesions, characteristic for chronic discoid lupus erythematosus (CDLE). Because recent investigations have highlighted the relevance of cytotoxic lymphocytes in autoimmune tissue destruction, we hypothesized that the scarring CDLE lesions might be caused by cytotoxic T lymphocytes. OBJECTIVES: To analyse skin biopsies of 15 patients with CLE [10 female, five male; localized CDLE (lCDLE), n = 5; disseminated CDLE (dCDLE), n = 5, subacute CLE (SCLE), n = 5] and five control biopsies taken from healthy controls and to characterize the inflammatory infiltrate. Methods We used immunohistochemistry, including staining for the cytotoxic molecule granzyme B, the skin-homing molecule cutaneous lymphocyte antigen (CLA) and the protein MxA, which is specifically induced by type I interferons (IFNs). RESULTS: We found a strong coexpression of granzyme B and CLA on lesional lymphocytes of patients with scarring lCDLE and dCDLE, which was significantly enhanced when compared with nonscarring SCLE and healthy controls. The increased expression of granzyme B was closely associated with the lesional expression of the type I IFN-induced protein MxA. CONCLUSIONS: Our results provide evidence that type I IFNs and potentially autoreactive cytotoxic lymphocytes targeting adnexal structures are highly associated with scarring lupus erythematosus lesions and might be responsible for their scarring character.
Mononuclear cells in skin lesions were characterized using an indirect immunofluorescence test with monoclonal antibodies. Most cells in the dermal infiltrates were stained with OKT3 (pan T cell) antibodies and with OKT4 (helper/inducer T cell) antibodies. Fewer cells were stained with OKT8 (suppressor/cytotoxic T cell) antibodies. Results obtained using a double marking technique with monoclonal antibodies and a hetero-anti-T lymphocyte serum showed that suppressor/cytotoxic cells comprised 15-25% of the T lymphocytes in lesions of psoriasis and discoid lupus erythematosus (DLE), and 25-35% in lesions of lichen planus. OKM1 (monocyte) antibodies stained few of the infiltrating cells in sections of the various skin lesions. The highest numbers of OKM1+ cells were found in sections of lesional skin from patients with erythrodermic and pustular psoriasis. Some T lymphocytes were also demonstrated in the epidermis in the various skin lesions. The highest numbers were found in the psoriatic lesions. The epidermal T lymphocytes were mainly suppressor/cytotoxic cells, and may be involved in a cell-mediated immune reaction of importance in the pathogenesis of these dermatoses.