SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Lupus erythematosus in childhood comprises the following distinctive lupus subsets: neonatal lupus erythematosus, systemic lupus erythematosus, discoid lupus erythematosus, subacute cutaneous lupus erythematosus, complement deficiency syndromes with subacute cutaneous lupus lesions, and lupus panniculitis. The clinical features and pathogeneses of each of these lupus syndromes is discussed in this review.
A kidney biopsy was performed in 7 hypocomplementemic discoid lupus erythematosus patients despite the absence of overt renal involvement. Five patients had glomerular immune deposits and 2 patients with disseminated discoid lupus erythematosus exhibited definite proliferative glomerulonephritis. Those findings show that silent lupus nephritis may be encountered in discoid as well as in systemic lupus erythematosus, providing additional evidence supporting the unity of the disease. We suggest that hypocomplementemic patients with discoid lupus erythematosus must be carefully screened for renal disease by periodic urinalysis examinations.
We describe a patient with discoid lupus erythematosus whose pattern of disease evolved into a systemic vasculitis polyarteritis nodosa.
We treated seven patients with discoid lupus erythematosus (DLE) with Vitamin E in an oral dose of 400 mg three times per day for 12 weeks. All other systemic and topical treatments were discontinued 1 month before initiation of the trial. The drug was then stopped and follow-up continued for at least another 4 weeks. No patient showed clearing of lesions. The trial was conducted during summer, when DLE is likely to be most active. There was no deterioration in any patient. No side effects were noted.
Regarding systemic (SLE) and chronic discoid lupus erythematosus (CDLE), the diagnostic value of the lupus band test ist generally accepted. In the literature, however, there are but few obligatory criteria concerning the definition of a positive lupus band. In order to illustrate the influence of sunlight on the evolution of junctional deposits of immunoglobulins, we examplarily studied actinic keratosis (AK) as a chronic light-dependent dermatosis. The junctional deposits in AK were qualitatively and quantitatively compared with the lupus band typical for CDLE. In CDLE we mostly found more distinct band-like junctional deposits of immunoglobulins and complements. Light-dependent, non-specific junctional patterns of immunofluorescence similar to LE, therefore, require clear morphological criteria of immunohistology.
Of twelve patients with discoid lupus erythematosus and dysgammaglobulinaemia, eight had a monoclonal gammopathy with a benign course to date, two had 'smouldering' myeloma, and two developed overt multiple myeloma. Six patients had generalized discoid lupus erythematosus, and six had skin lesions localized to the head and neck. Further screening of patients with discoid lupus erythematosus by serum protein electrophoresis is indicated to determine the significance of these findings.
The prevalence of antinuclar antibodies (ANA) in chronic cutaneous discoid lupus erythematosus (DLE) is influenced by both patient selection and test sensitivity. If one excludes serum samples from patients with DLE with a history suggesting extracutaneous disease and defines the significance of the ANA test by simultaneously testing serum samples from patients with well-characterized connective tissue diseases, then only a small percentage of the patients with DLE have ANA at significant titers. These patients with DLE do have a higher pervalence of positive ANA tests at low serum dilutions when compared with controls, but only a few have positive ANA tests at titers comparable to those seen in patients with active systemic connective tissue diseases.
Carpal tunnel syndrome developed concurrently with cutaneous connective tissue disease in five patients. The skin lesions varied from morphea, lichen sclerosus, fasciitis, and discoid lupus erythematosus to lupus panniculitis. Variable and transitory serologic and direct immunofluorescent findings were noted. In two cases, surgical specimens from carpal tunnel operations had lymphoid nodules. Treatment of the cutaneous connective tissue syndrome (antimalarials, four cases; corticosteroids, two cases) brought healing of the carpal tunnel syndrome as well as improvement of the skin lesions.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A 29-year-old woman with discoid lupus erythematosus had undetectable classic pathway complement activity. Hypocomplementemia was due to selective deficiency of C5. One of her children was also deficient. To our knowledge this is the first documented case of an association between discoid lupus erythematosus and C5 deficiency.
Discoid lupus erythematosus (DLE) is the most common form of chronic cutaneous lupus erythematosus. Classic DLE lesions begin as red-purple macules, papules, or small plaques and rapidly develop a hyperkeratotic surface. Most patients with untreated classic DLE lesions suffer indolent progression to large areas of cutaneous dystrophy and scarring alopecia that can be psychosocially devastating. A 44-year old male patient presented to the clinic with erythematous scaly patches that began on his nose 1 y before. His face was most affected, however, lesions were also noted on his scalp, ears, and limbs. Histopathologic examination verified a diagnosis of DLE. Laboratory examinations and consultations revealed no signs of systemic involvement. Imiquimod cream 5% was applied to the lesions once a day 3 times a week. After 20 applications, entire lesions regressed significantly. Imiquimod cream 5% may represent an alternative treatment method for patients with DLE.
A high incidence of discoid lupus erythematosus (DLE) and urticaria/angioedema was found among patients with selective low levels of the C4 component of complement. Although evidence for activation of C4 was present in patients' sera, studies to determine the presence of known activation mechanisms were negative. Genetic C4 typing in four pedigrees showed that all propositi carried the null allele B*QO. It is postulated that the low C4 levels in these patients are related to the skin lesions and this partial genetic deficiency.
BACKGROUND: Hypertrophic discoid lupus erythematosus (HDLE) may resemble cutaneous squamous cell carcinoma (SCC) histologically. OBJECTIVE: The histologic features that help to differentiate HDLE from SCC are reviewed. METHODS: Two patients are described with HDLE. RESULTS: Both patients were treated initially with Mohs surgery for "biopsy-proven" SCC. Subsequent biopsies confirmed the diagnosis of HDLE and the patients responded well to appropriate therapy. No significant complications occurred in either patient. CONCLUSION: Lesions of HDLE may imitate SCC. Strategies are suggested to avoid surgical procedures based on an incorrect biopsy report.
21 lesions from 16 patients with discoid lupus erythematosus (DLE) were examined immunohistologically using monoclonal antibodies to keratins (K). Markers of basal epithelial cells (the keratin conformation specific basal markers LH6 and LH8), differentiating keratinocytes (K1 and K10), hyperproliferating keratinocytes (K16) and panepidermal keratin (K14), were used. A monoclonal antibody to type VII collagen was used as a guide to the state of the basement membrane zone (BMZ). Keratin distribution in DLE differed from controls. Suprabasal cells were labelled by LH6 in 95% of specimens (19/20) and LH8 in 79% (15/19) in contrast to the basal distribution in normal skin. Reduction of suprabasal LL017 (K1) expression was seen in 59% (10/17) of lesions. An increase of LL025 (K16) expression was seen in 33% (5/15) of specimens. Where LL025 (K16) expression was increased, LL017 (K1) expression was reduced in 80% (4/5). Dermal colloid bodies expressed both basal and suprabasal keratins and were present at sites of maximal basement membrane disruption. These findings are consistent with a model of DLE in which there is an increase in the proliferative basal compartment. This compartment and the associated BMZ suffer fragmentation and loss of colloid bodies to the dermis which express a range of keratins not uniformly associated with basal keratinocytes.
Ten cases of localized and generalized discoid lupus erythematosus are reported in which previously untreated patients were given hydroxychloroquine sulphate 600 mg daily for 10 days followed by 400 mg for 20 days. The purpose of the study was to evaluate the effect of this drug on the 'lupus band' before and after treatment, in diseased, unaffected sun-exposed, and unaffected non sun-exposed skin. A good response from both the clinical and immunopathologic (i.e. reduction or disappearance of the immune reactants) standpoint was evident in 6/10 patients; in another 3 patients a good clinical but not immunopathologic response was recorded, while in 1 case a clinical worsening corresponded to an immunofluorescence improvement. In 5/10 cases (4 females, 1 male) one or more immunoglobulin classes which were present in the 'lupus band' before therapy remained at the dermoepidermal junction after treatment.
Results of a detailed clinical and laboratory study of 37 Nigerian patients with chronic discoid lupus erythematosus are presented. Patients with chronic discoid lupus erythematosus constituted 0.46% of all out-patients seen in the skin clinic between May 1974 and December 1977. A preponderance of females was noticed (female/male ratio of 5:1), while the age distribution of African patients corresponded to values characteristic for the condition seen in other geographical regions. Several morphological types of the condition have been seen. The vitiligoid variant of chronic discoid lupus erythematosus seems to be common in West Africans. Sixteen out of 37 patients presented laboratory abnormalities considered as markers of the association between chronic and systemic lupus erythematosus. Their significance, however is, uncertain as it has been demonstrated on several occasions that in a tropical milieu heavy parasitic infections produce marked immunological disturbances. The problem of the relationship between chronic and systemic lupus erythematosus is discussed and the literature on the incidence of chronic discoid lupus erythematosus in various African countries is reviewed.
BACKGROUND: Although multiple studies suggest a dysregulated T-cell cytokine production in systemic lupus erythematosus, the cytokine profile in discoid lupus erythematosus (DLE) lesions is unknown. OBJECTIVES: To characterize the cytokine profile in DLE by immunohistochemical and molecular methods, and to investigate the role of cytokines in the pathogenesis of DLE. DESIGN: Patients were evaluated clinically, and biopsy specimens of lesional skin were examined by light microscopy. Reverse transcriptase-polymerase chain reaction and immunohistochemical analysis were performed on 11 biopsy specimens. We investigated the presence of interleukin (IL) 2, interferon gamma (IFN-gamma), IL-4, tumor necrosis factor alpha, (TNF-alpha), and IL-1beta messenger RNA (mRNA) in 8 biopsy specimens of DLE and compared it with 3 biopsy specimens of normal skin. SETTING: Academic referral research hospital. PATIENTS: Eight consecutive patients with a clinical and histologic diagnosis of DLE. RESULTS: Localized DLE was found in 7 patients and widespread in 1. During the 4 years of the investigation, none of the patients developed systemic lupus erythematosus. We found significantly elevated levels of IL-2 and IFN-gamma mRNA in all 8 biopsy specimens of DLE; in contrast, no transcripts of IL-2 or IFN-gamma were detected in 3 biopsy specimens of normal skin (P<.01). Similarly, elevated levels of TNF-alpha mRNA were detected in 8 DLE biopsy specimens, while no TNF-alpha mRNA was detected in 3 biopsy specimens of normal skin (P<.01). No IL-4 or IL-1 beta mRNA was detected in 8 biopsy specimens of DLE lesional skin and 3 biopsy specimens of normal patient skin. Immunohistochemical analysis showed increased staining for IL-2 and IFN-gamma receptors, while no detectable IL-4 receptor was found. No cytokine mRNA or cytokine receptor protein was detected in biopsy specimens of normal skin. CONCLUSIONS: These findings suggest that DLE is associated with type 1 cytokines characterized by the expression of IL-2 and IFN-gamma. Type 1 cytokines may be critical for induction, development, and maintenance of DLE.