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PubMed2000

Interstitial lung disease in systemic lupus erythematosus.

Systemic lupus erythematosis (SLE) is a heterogenous disease of unknown etiology. It is not uncommon to see pleuropulmonary involvement in isolation or along with the involvement of other organ systems in SLE. Pulmonary manifestations of SLE can involve the pleura, lung parenchyma, airways, pulmonary vasculature, and the respiratory muscles. In this review we discuss two important pulmonary manifestations of SLE: acute lupus pneumonitis and diffuse interstitial lung disease. These two conditions have a major impact on the mortality and morbidity of patients with SLE and it is essential to recognize and treat them appropriately. High-resolution computed tomographic scans of the chest and pulmonary function tests help to establish a diagnosis and aid long-term follow-up of these patients. High-dose corticosteroids are the mainstay of treatment for the two conditions, although other agents such as cyclophosphamide, azathioprine, intravenous gamma globulin, and plasmapheresis have been used with varying degrees of success.

Acute Disease↗
PubMed1986

Lupus anticoagulant and anticardiolipin antibodies in systemic lupus erythematosus.

The lupus anticoagulant (LA) is an acquired autoantibody of the IgG or IgM type that acts on platelet factor III, inhibiting the generation of the prothrombin activator complex. It is prevalent in 5-10% of SLE cases and, in contradistinction to the name anticoagulant, it may be associated with thrombotic events, recurrent abortion or intrauterine death. Anti-cardiolipin antibody like LA, is an anti-phospholipid antibody and also causes recurrent thrombotic events. Mention has been made of a possible cross-reactivity between anti-phospholipid antibodies and anti-DNA antibodies. The optimal treatment for this problem is at present unknown.

Antibody Specificity↗
PubMed2003

Possible role of Hsp70 in autoantigen shuttling to the dermo-epidermal junction in systemic lupus erythematosus.

The lupus band is the result of immune complex deposition along the dermo-epidermal junction; such complexes are formed in situ by the interaction of antinuclear antibodies with their respective autoantigens. Dermal autoantigens are released after sun exposure, concurrently a heat shock protein production take place and would participate in autoantigen transfer to the dermo-epidermal junction. In this work the presence of Hsp70 along with the lupus band was investigated by immunofluorescence in twenty SLE skin biopsies. Immune deposits were mainly composed by IgM, IgG and C3 and were found in all lupus biopsies at the dermo-epidermal junction. Immunoreagents were also present into papillary vessels and, with less extent, into epidermal keratinocytes. Hsp70 was present in 60% of lupus biopsies, and was mainly distributed along dermo-epidermal junction and around papillary vessels. Furthermore, by double fluorescence labelling assays, we found that immuno-reactants are co-localized with Hsp70. Our results suggest that Hsp70 would shuttle autoantigens to the dermo-epidermal junction.

Adolescent↗
PubMed1992

[Lupus anticoagulant and antiphospholipid antibody values in a family with systemic lupus erythematosus].

The Lupus Anticoagulant (LA) is an immunoglobulin directed towards the phospholipid portion of the prothrombin activator complex. This immunoglobulin because first identified in the plasma of patients with Systemic Lupus Erythematodes, was named as Lupus Anticoagulant. Although initially described in patients with SLE, it was subsequently observed in other diseases and also in patients without any manifest disease. SLE or similar diseases are present in 35% of LA (+) patients. The LA prevalence in SLE patients has been found as 34% whereas ACA prevalence was found as 44%. While searching for the presence of LA and the levels of APA in cases having unexplained recurrent fetal losses, a family (a mother and 3 daughters) was discovered, whose each member has been diagnosed as SLE at different times and with different symptoms. Data suggesting the presence of LA and high APA levels were determined in all the members of the family and also it was realised that cause who had recurrent fetal losses had the highest APA levels. In addition to immunoassay methods to detect APA, examination of coagulation tests in patients with unexplained thrombosis and/or fetal losses, would be of great help.

Abortion, Habitual↗
PubMedDate not supplied

[Neuropsychiatric and vascular manifestations of disseminated lupus erythematosus].

Disseminated lupus erythematous is an auto-immune disease with systemic manifestations that develops by outbreaks. It's pathogenesis is unknown. The physiopathology jeopardizes auto-immune phenomenon whose most important biological effect is the polyclonal activation of B Lymphocytes. The tissue's lesions are due to several mechanisms, being, perhaps, the deposition of immune complexes of a great value. On account of a young woman with recurrent deep venous thrombosis and neuropsychiatric manifestations the bibliographic data are reviewed, especially those that concern with the etiopathogenesis, treatment and prognosis.

Adolescent↗
PubMed2001

Estrogen and progesterone receptors in murine models of systemic lupus erythematosus.

Estrogens are believed to play a role in the etiology of both human and murine systemic lupus erythematosus (lupus; SLE), presumably through the agency of their cellular receptor proteins. There is now considerable interest in the molecular mechanism of action of estrogens in immune tissues, particularly with regard to autoimmune disorders, which are generally more prevalent in women. In this laboratory, an attempt is being made to characterize estrogen receptors in murine models of SLE and to try and relate this to estrogen receptor function in vivo. The initial aim was to compare binding properties of estrogen receptors in brain, reproductive and immune tissues of BALB/c and MRL/MP-lpr/lpr mice. The latter strain spontaneously develops an autoimmune disease resembling human systemic lupus erythematosus (lupus; SLE). It is hypothesized that estradiol, through its receptors, mediates the progression of murine SLE, and that in autoimmune disease, the estrogen receptor is functionally and/or structurally changed. Initial studies suggest that there are differences in estrogen receptors between BALB/c mice, which do not get autoimmune disease, and two strains that do, MRL/MP-lpr/lpr and NZB/W mice. In MRL mice, these differences may be reflected in impaired priming of the progesterone receptor.

Animals↗
PubMed1996

Systemic lupus erythematosus with ischemic peripheral neuropathy and lupus anticoagulant: response to intravenous prostaglandin E1.

We report a case of systemic lupus erythematosus with cutaneous vasculitis and peripheral neuropathy. Results of laboratory examinations revealed lupus anticoagulant in the patient's serum. His lower limbs showed asymmetry. A sural nerve biopsy specimen showed modest degeneration of nerve fibers and incomplete obstruction of nutrient vessels. His cutaneous vasculitis responded to treatment with high-dose corticosteroid, but the lower limb neuropathy responded incompletely. Daily intravenous prostaglandin E1 treatment improved his neurologic and cutaneous symptoms markedly. Our case implied that nutritional vascular ischemia caused by lupus anticoagulant is involved in the pathogenesis of lupus neuropathy in addition to well-known peripheral nerve vasculitis. It also documented the effectiveness of intravenous prostaglandin E1 in the treatment of systemic lupus erythematosus.

Adult↗
PubMed2005

[Neuropsychiatric lupus and lupus nephritis as a clinical manifestations of systemic lupus erythematosus].

Neuropsychiatric (NP) lupus and lupus nephritis are one of the most profound manifestations of the Systemic lupus erythematosus (SLE), with wide variety of clinical manifestations. Especially NP lupus is the most poorly understood subset of the disease, and the most difficult therapeutic problem. We present case report of female SLE patient with the associated difficult and different clinical manifestations of central and peripheral nervous system disease end renal involvement. Agressive treatment option with intermittent pulsed intravenous cyclophosphamide and corticosteroids after the second month of treatment brought to complete remission of nephrotic syndrome. Improving of life-threating clinical manifestations of NP lupus was obtained after six months treatment by this immunosupressive therapy and included intravenous immunoglobulin 400 mg/kg body weight during five days monthly.

Adult↗
PubMedDate not supplied

[Cerebral infarct in systemic lupus erythematosus].

INTRODUCTION AND OBJECTIVE: Systemic lupus erythematosus is a syndrome of variable clinical and immunological expression, which may affect any organ. Stroke is an uncommon complication of systemic lupus erythematosus, attributed to many different etiopathogenic mechanisms such as early atherosclerosis, coagulopathy, vasculitis, cardiogenic embolism, etc. Our objectives were to analyze the incidence, clinical and immunological characteristics of this condition and to evaluate the therapeutic approach and evolution. CLINICAL CASES: We present the cases of six patients with cerebral infarcts who also had systemic lupus erythematosus. The frequency of cerebral infarct in our series of systemic lupus erythematosus was 6%. The average age was 45 years (range 13-67). All the cerebral infarcts occurred whilst the systemic lupus erythematosus was active. There were positive antiphospholipid antibodies in three of the patients and two patients had potentially embologenic cardiopathy (33%). Fifty percent of the patients required treatment with cyclophosphamide for their severe systemic disease and 66% received anticoagulants for an antiphospholipid syndrome and/or suspected thromboembolism. The clinical course was satisfactory in all cases but the one who died. CONCLUSIONS: The incidence of cerebral infarct in relation to systemic lupus erythematosus is low, and generally appears during advanced, active phases of the disease. The many etiopathogenic mechanisms involved generally act together so that it is difficult to say which is the main cause, especially in elderly patients. Amongst these mechanisms is the presence of antiphospholipid antibodies, detection of which is essential in this condition, and cardiogenic embolism. The evolution depends mainly on the multi-organ involvement and how early immunosuppressive and/or anticoagulant treatment is started.

Adolescent↗
PubMed1983

Thrombosis in systemic lupus erythematosus: striking association with the presence of circulating lupus anticoagulant.

The lupus anticoagulant was found in the plasma of 31 of 60 patients with systemic lupus erythematosus and other connective tissue disorders (mixed connective tissue disease, systemic vasculitis, polyarteritis nodosa, primary sicca syndrome, discoid lupus, Behcet's syndrome, and systemic sclerosis). Strong associations were found with biological false positive seroreaction for syphilis and thrombocytopenia. The most striking association, however, was with the high prevalence of thrombosis. This tendency to thrombosis was independent of disease activity of systemic lupus erythematosus. The lupus anticoagulant appears to be a useful marker for a subset of patients with systemic lupus erythematosus at risk for the development of thromboembolic complications.

Adolescent↗
PubMed1992

Immunofluorescence microscopy of healthy skin from patients with systemic lupus erythematosus: more than just the lupus band.

Many papers have been published on the lupus band in systemic lupus erythematosus (SLE), but little information exists on the possible diagnostic value of the lupus band and other microscopic immunofluorescence phenomena found in clinically normal skin of patients with SLE. In a study of 297 subjects (66 patients with SLE, 81 patients with other forms of LE, and 150 patients with other systemic connective tissue disorders) it was found that: (a) granular deposits of IgA, IgG, and IgM in the basal membrane zone and in the deeper blood vessels were more common in patients with SLE than in the other two groups; (b) depending on the clinical differential diagnosis, IgA and IgG deposits at the epidermal basal membrane can be specific for SLE; (c) using logistic regression analysis sets of variables can be selected with a high potential to discriminate between SLE and the other groups; and (d) immunofluorescence variables do not duplicate the information for the diagnosis of SLE given by the American Rheumatism Association (ARA) criteria or other laboratory methods. From these results, it is concluded that immunofluorescence microscopy of clinically normal skin is a valuable diagnostic method which should be reconsidered as a potential criterion for the diagnosis of SLE in the next evaluation of the ARA criteria.

Adolescent↗
PubMed2003

The pathogenetic role of immunoglobulin G from patients with systemic lupus erythematosus in the development of lupus pleuritis.

OBJECTIVE: To investigate the pathophysiological effect of immunoglobulin G (IgG) from systemic lupus erythematosus (SLE) patients on pleural mesothelial cells and related mechanisms. METHODS: Serum IgG from 28 lupus patients and 13 healthy controls was purified by protein-G affinity chromatography. The concentrations of anti-dsDNA-, anti-histone- and/or anti-nucleohistone-containing IgGs were determined by enzyme-linked immunosorbent assay (ELISA). Lupus patients were divided into an active (n = 12) and an inactive group (n = 16) on the basis of the SLE Disease Activity Index (SLEDAI). The binding of IgG to a human pleural mesothelial cell line (MeT-5A) under different conditions, including pretreatment with DNase and preincubation with exogenous histone, DNA or nucleohistone, was examined using flow cytometry and cellular ELISA. The effect of IgG on MeT-5A cell proliferation was studied using an MTT assay. Gene expression and protein synthesis for interleukin 1beta (IL-1beta), monocyte chemoattractant protein 1 (MCP-1) and transforming growth factor beta1 (TGF-beta1) in MeT-5A cells were determined using reverse transcription-polymerase chain reaction and ELISA. RESULTS: The binding of IgG to MeT-5A cells was higher in the active lupus group than the inactive lupus group (P = 0.047) and controls (P = 0.003). The binding decreased in both lupus groups following pretreatment of MeT-5A cells with DNase. The binding of IgG to MeT-5A cells was greater by 112% in the active lupus group after preincubation with histone (P < 0.001), but not with DNA or nucleohistone. Exposure of MeT-5A cells to IgG from either lupus group induced cell proliferation when compared with IgG from healthy controls (P = 0.04). Gene expression and protein synthesis of MCP-1, TGF-beta1 and IL-1beta in MeT-5A cells were significantly increased after incubation with IgG from patients with active lupus when compared with IgG from the inactive lupus and control groups (P < 0.01). The concentration of anti-dsDNA antibodies correlated with the binding of IgG to MeT-5A cells and the synthesis of cytokines by MeT-5A cells. The serum level of anti-histone antibodies in the active lupus group was higher than that in the inactive group (P = 0.015) and the serum concentration correlated with cell binding and MCP-1 production. CONCLUSIONS: IgG from lupus patients can bind to MeT-5A cells and the binding is modulated by DNA or histone. Binding of anti-dsDNA-containing IgG to MeT-5A cells induces the synthesis of proinflammatory cytokines. Our findings suggest that the binding of anti-dsDNA antibodies, particularly the IgG isotype, to pleural mesothelium plays a direct pathogenetic role in inducing inflammatory injury in the serositis of SLE.

Acute Disease↗
PubMed2026

The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease closely associated with enzyme dysfunction, yet its underlying molecular mechanisms remain incompletely understood. This study aims to characterize enzyme-network alterations associated with SLE status and disease activity and to identify candidate molecules with potential clinical relevance. METHODS: We integrated proteomic and phosphoproteomic data from peripheral blood mononuclear cells (PBMCs) of 130 SLE patients and 90 healthy controls (HC), along with transcriptomic data from 1461 SLE patients. Through systematic analysis of key enzyme phosphorylation sites, upstream transcription factors (TFs), and computationally prioritized candidate compounds, we sought to characterize enzyme-centered regulatory associations. RESULTS: Integrated proteomic and phosphoproteomic analyses revealed significant metabolic and signaling pathway disturbances, along with distinct phosphorylation patterns in SLE immune cells. Multiple SLE-associated and disease-activity-associated candidate molecules were identified. Regulatory network analysis uncovered an upstream transcription factor cluster centered around STAT1. Computational drug screening identified computationally prioritized candidate compounds with multi-gene DSigDB associations, which require further clinical safety evaluation and experimental validation. CONCLUSIONS: This study constructs a molecular map of SLE, highlighting associations between enzyme-network alterations, catalytic dysregulation, and SLE-related immune molecular signatures, and identifies candidate molecules for future clinical and functional evaluation.

Humans↗
PubMed2003

Prevalence and correlates of accelerated atherosclerosis in systemic lupus erythematosus.

BACKGROUND: Although systemic lupus erythematosus is associated with premature myocardial infarction, the prevalence of underlying atherosclerosis and its relation to traditional risk factors for cardiovascular disease and lupus-related factors have not been examined in a case-control study. METHODS: In 197 patients with lupus and 197 matched controls, we performed carotid ultrasonography, echocardiography, and an assessment for risk factors for cardiovascular disease. The patients were also evaluated with respect to their clinical and serologic features, inflammatory mediators, and disease treatment. RESULTS: The risk factors for cardiovascular disease were similar among patients and controls. Atherosclerosis (carotid plaque) was more prevalent among patients than the controls (37.1 percent vs. 15.2 percent, P<0.001). In multivariate analysis, only older age, the presence of systemic lupus erythematosus (odds ratio, 4.8; 95 percent confidence interval, 2.6 to 8.7), and a higher serum cholesterol level were independently related to the presence of plaque. As compared with patients without plaque, patients with plaque were older, had a longer duration of disease and more disease-related damage, and were less likely to have multiple autoantibodies or to have been treated with prednisone, cyclophosphamide, or hydroxychloroquine. In multivariate analyses including patients with lupus, independent predictors of plaque were a longer duration of disease, a higher damage-index score, a lower incidence of the use of cyclophosphamide, and the absence of anti-Smith antibodies. CONCLUSIONS: Atherosclerosis occurs prematurely in patients with systemic lupus erythematosus and is independent of traditional risk factors for cardiovascular disease. The clinical profile of patients with lupus and atherosclerosis suggests a role for disease-related factors in atherogenesis and underscores the need for trials of more focused and effective antiinflammatory therapy.

Adrenal Cortex Hormones↗
PubMed2006

Aggressive periodontitis in a patient with chronic cutaneous lupus erythematosus: a case report.

Lupus erythematosus is considered to be a high risk factor for periodontitis. As an autoimmune disease of unknown origin, cutaneous lupus erythematosus (CLE) is subdivided into 3 categories: chronic (CCLE), subacute (SCLE), and acute (ACLE). While the ACLE has a high prevalence of conjunctive periodontal lesions, aggressive periodontitis in patients with CCLE has been rarely reported. This article describes the case of a patient diagnosed with aggressive periodontitis. Three months after the diagnosis of periodontitis, the patient experienced advancing hair loss (alopecia), pale fingers and toes, as well as edema in the legs and around the eyes. Skin biopsy showed follicular hyperkeratosis with perivascular mononuclear cell infiltrate. Colliquation of the basal cells, thickening of the basal lamina, and vacuolar degeneration of basal keratinocytes were also found. A lupus band test was positive, and diagnosis of CCLE was established. Three months following the treatment of lupus with antimalarial agents, the periodontal condition became stable with no further exacerbation or progression of the existing periodontitis. An 11-month postsurgical follow-up revealed stable periodontal and general medical conditions. A patient's medical history should be re-evaluated in the event of recurrence of periodontal lesions refractory to periodontal treatment. The control of systemic conditions like lupus erythematosus is essential for a good prognosis in the treatment of periodontitis as well as for the general health of the patient.

Adult↗
PubMed1988

Development and assessment of a computerized index of clinical disease activity in systemic lupus erythematosus. Members of the British Isles Lupus Assessment Group (BILAG).

Five centres in Great Britain and the Republic of Ireland have collaborated to produce a computerized index of clinical disease activity in systemic lupus erythematosus, based on the principle of the physician's intention to treat. The index assesses separately eight organ-based systems. The index has proved quick and easy to use despite a comprehensive database and compares favourably with two other indices of disease activity. It has great potential for use in multicentre studies of disease outcome and new therapies in systemic lupus erythematosus.

Humans↗