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Results for “LUPUS ERYTHEMATOSUS, SYSTEMIC”

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PubMed2006

Cell-ELISA detection of antineuronal antibodies in central nervous system involvement in systemic lupus erythematosus.

OBJECTIVE: To develop a cell-ELISA method to detect antineuronal antibodies (anti-Ns) and evaluate the diagnostic value of anti-Ns in central nervous system involvement in systemic lupus erythematosus (CNS-SLE). METHOD: Anti-N was assessed in both serum and cerebrospinal fluid (CSF) samples from 38 patients with CNS-SLE, 29 with SLE without CNS involvement (non-CNS-SLE), 36 with other rheumatic diseases and 59 with non-rheumatic diseases with the CNS manifestations using a cell-ELISA method with 1% paraformaldehyde-fixed SK-N-MC neuroblastoma cells as substrate. Serum samples from 37 healthy donors were also included in this study. Patients with CNS-SLE who were anti-N positive in CSF were studied serially for CSF anti-N levels at times of treatment-associated improvement in CNS symptoms. RESULTS: Serum anti-N levels were significantly increased in patients with SLE compared with other groups, with a sensitivity of 61.2% (41/67) and a specificity of 91.8% (p<0.001). CSF anti-N levels were significantly increased in patients with CNS-SLE, with a sensitivity of 47.4% (18/38) and a specificity of 89.7%, whereas only 10.3% (3/29) of patients with non-CNS-SLE had increased anti-N in CSF (p<0.001). CSF anti-N levels decreased significantly after effective treatment of CNS-SLE (p<0.05). CONCLUSION: Serum anti-N is relatively specific to SLE. CSF anti-N is a sensitive and relatively specific antibody in diagnosing CNS-SLE and correlates with CNS-SLE activity.

Adolescent↗

PubMed1994

Cerebrospinal fluid interleukin-6, prostaglandin E2 and autoantibodies in patients with neuropsychiatric systemic lupus erythematosus and central nervous system infections.

Cerebrospinal fluid (CSF) from patients with a variety of central nervous system (CNS) disorders was assayed for cytokines, prostaglandins, and autoantibodies. CSF interleukin-6 (IL-6) in patients with CNS infection (374.24 +/- 92.61 pg/mL) and neuropsychiatric systemic lupus erythematosus (NP-SLE) (71.40 +/- 5.89 pg/mL) were significantly higher than in patients with CNS inflammation (33.92 +/- 29.36 pg/mL) or controls (non-inflammatory CNS diseases) (4.35 +/- 3.00 pg/mL). Interleukin-1 beta, interferon alpha, and tumor necrosis factor alpha were undetectable in these samples: CSF prostaglandin E2 (PGE2) also exhibited similar patterns as IL-6. CSF immunoglobulin G (IgG) in patients with NP-SLE (8.84 +/- 1.80 mg/dL) was much higher than in patients with CNS infection (4.65 +/- 3.09 mg/dL), CNS inflammation (2.54 +/- 1.24 mg/dL), or controls (2.11 +/- 1.03 mg/dL). CSF autoantibodies against calf thymus antigens were present in patients with NP-SLE but not in patients with CNS infection as demonstrated by immunoblot. These results suggest that high IL-6 and PGE2 in CSF favors the diagnosis of CNS infection, while modestly elevated IL-6, high IgG, and autoantibodies against calf thymus antigens in CSF are the features of NP-SLE.

Autoantibodies↗

PubMed1998

Differential roles of the anti-ribosomal P antibody and antineuronal antibody in the pathogenesis of central nervous system involvement in systemic lupus erythematosus.

OBJECTIVE: To compare the role of antibodies against the ribosomal P protein (anti-P) with that of antibodies against neuronal cells (anti-N) in the pathogenesis of central nervous system (CNS) involvement in systemic lupus erythematosus (SLE). METHODS: Sera from 87 SLE patients (27 with non-CNS SLE, 34 with lupus psychosis, and 26 with nonpsychotic CNS lupus) and from 20 control patients with neurologic manifestations without SLE and cerebrospinal fluid (CSF) from 41 patients with CNS lupus and from the 20 control patients were assayed for IgG anti-P and anti-N by an enzyme-linked immunosorbent assay (ELISA) using ribosomal P synthetic peptides and by a cell ELISA using paraformaldehyde-fixed SK-N-MC neuroblastoma cell lines, respectively. RESULTS: Serum anti-P levels were significantly elevated in patients with lupus psychosis compared with those with non-CNS SLE or those with nonpsychotic CNS lupus, whereas there were no significant differences in serum anti-N levels among these 3 groups. In contrast, CSF anti-N levels were significantly elevated in patients with lupus psychosis compared with those with nonpsychotic CNS lupus and compared with non-SLE controls, whereas CSF anti-P were not detected in most of the patients. CONCLUSION: The results indicate that anti-P in the systemic circulation and anti-N in the CSF are involved in the development of lupus psychosis.

Antibody Specificity↗

PubMed1995

Pulmonary thromboembolic hypertension in systemic lupus erythematosus with lupus anticoagulant: histopathological analysis of localization and distribution of thromboemboli in pulmonary vasculature.

We report a systemic lupus erythematosus patient with lupus anticoagulant accompanied by pulmonary thromboembolic hypertension possibly due to large vegetation of the tricuspid valve of the heart. Histopathological analysis of localization and distribution of thromboemboli in pulmonary vasculature revealed that the organized thromboembolic occlusion of multiple blood vessels (99 out of 222 arteries), might be responsible for the pulmonary hypertension both in quality and quantity. The contribution of lupus anticoagulant to the pathogenesis of Libman-Sacks endocarditis in systemic lupus erythematosus, and its possible relationship to pulmonary thromboembolic hypertension are discussed.

Adult↗

PubMed2006

Urinary neutrophil gelatinase-associated lipocalin as a biomarker of nephritis in childhood-onset systemic lupus erythematosus.

OBJECTIVE: Renal involvement in systemic lupus erythematosus (SLE) is associated with poor prognosis. Currently available renal biomarkers are relatively insensitive and nonspecific for diagnosing SLE nephritis. Previous research suggests that neutrophil gelatinase-associated lipocalin (NGAL) is a high-quality renal biomarker of acute kidney injury, while its usefulness in SLE is unclear. We undertook this study to determine the relationship between urinary NGAL excretion and SLE disease activity or damage, with a focus on nephritis. METHODS: A cohort of 35 patients diagnosed as having SLE prior to age 16 years (childhood-onset SLE) was assessed for disease activity (using the Systemic Lupus Erythematosus Disease Activity Index 2000 update) and damage (using the Systemic Lupus International Collaborating Clinics/American College of Rheumatology SLE Damage Index) in a double-blind, cross-sectional study. Information on current markers of renal function and disease was obtained and compared with NGAL levels (ng/mg of urinary creatinine) measured by enzyme-linked immunosorbent assay. Eight children with juvenile idiopathic arthritis (JIA) served as controls. RESULTS: NGAL levels did not differ with the age, weight, height, sex, or race of the patients. Patients with childhood-onset SLE had significantly higher NGAL levels than did those with JIA (P < 0.0001). NGAL levels were strongly to moderately correlated with renal disease activity and renal damage (Spearman's r >/= 0.47, P < 0.0001 for both comparisons), but not with extrarenal disease activity or extrarenal damage. NGAL levels of >0.6 ng/mg urinary creatinine were 90% sensitive and 100% specific for identifying childhood-onset SLE patients with biopsy-proven nephritis. CONCLUSION: Urinary NGAL is a promising potential biomarker of childhood-onset SLE nephritis. The results of the current study require validation in a larger cohort to more accurately delineate urinary NGAL excretion in relation to the diverse SLE phenotypes.

Acute-Phase Proteins↗

PubMed1991

Quantitative nailfold capillary microscopy in cutaneous and systemic lupus erythematosus and localized and systemic scleroderma.

Quantitative television microscopy of nailfold capillaries of the fingers was performed in 12 patients with cutaneous lupus erythematosus (six with discoid type and six with disseminated type), in six patients with localized scleroderma (two with circumscribed type, two with linear types, and two with atrophic type), in 10 patients with systemic lupus erythematosus, and in eight patients with systemic scleroderma. The following features were analyzed and compared with a control group (n = 15) of similar age: venous plexus visibility; density of capillaries; avascular fields; hemorrhages; giant capillaries; diameters of the transitional segment, the arterial, and the venous limbs; loop width; and flow stop caused by local cooling test. The patient groups with cutaneous lesions only showed no essential differences as compared with the controls. Patients with systemic scleroderma differed in almost every finding from the controls and from patients with localized scleroderma. Patients with systemic lupus erythematosus exhibited significant differences in several findings as compared with the controls and the cutaneous lupus erythematosus group, but there was overlap.

Adolescent↗

PubMed1984

The coexistence of systemic lupus erythematosus and psoriasis.

Systemic and discoid lupus erythematosus (LE) have both been reported in association with psoriasis. Four additional patients who had systemic LE are reported. All of them had a high titer of antinuclear antibodies (ANAs) and were SS-A(Ro)-negative. Only one patient exhibited photosensitivity. SS-A(Ro) antibodies do not appear to be specific markers for the coexistence of LE and psoriasis, and screening for them in all psoriatics prior to ultraviolet B phototherapy is not recommended. Pitfalls in the management of patients with systemic LE and psoriasis are discussed.

Adult↗

PubMed1990

Systemic manifestations of systemic lupus erythematosus.

Twenty five cases with systemic lupus erythematosus admitted to a referral service hospital over a period of 6 years have been studied to analyse the pattern of multisystem involvement. Febrile polyarthritis, renal involvement and skin changes dominated the clinical picture. Important serological abnormalities included the presence of antinuclear antibody and anti ds DNA. Renal biopsy carried out in all cases helped to reveal lupus nephritis in subclinical cases. The pattern of renal involvement varied, with diffuse proliferative glomerulonephritis being the commonest. Oral steroids was given to all cases and cyclophosphamide was given to severe and resistant cases. The severity of system involvement, especially renal, influenced the response to treatment. Changes in presentation between Indian and Western patients are highlighted.

Adult↗

PubMed2003

Beneficial effects of the anti-oestrogen tamoxifen on systemic lupus erythematosus of (NZBxNZW)F1 female mice are associated with specific reduction of IgG3 autoantibodies.

BACKGROUND: Sex hormones have been shown to influence the immune system and to modify the course of autoimmune disorders. OBJECTIVE: To examine the effects of the oestrogen antagonist tamoxifen on the course of systemic lupus erythematosus (SLE) in (NZBxNZW)F1 mice. METHODS: Groups of 8 week old (NZBxNZW)F1 female mice were treated with tamoxifen (800 micro g/mouse; twice a week) or with double distilled water for four months. Mice were evaluated monthly for the presence of autoantibodies directed against DNA and nuclear extract (NE) by enzyme linked immunosorbent assay (ELISA). White blood cells and thrombocytes were quantified by a cell counter and proteinuria by combistix kit. At 6 months of age, all mice that did not die spontaneously were killed and evaluated for the presence of glomerular immune deposits by indirect immunofluorescence assay. IgG isotypes of autoantibodies in the mouse sera and glomeruli were determined by gamma chain specific antibodies. RESULTS: Tamoxifen treatment significantly reduced autoantibody production directed against either NE or DNA. The latter reduction was mainly in autoantibodies of the IgG3 isotype. Furthermore, tamoxifen had significant beneficial effects on the course of SLE in (NZBxNZW)F1 mice. At 6 months of age, 40% of the untreated mice died spontaneously, whereas all the tamoxifen treated mice were still alive. All untreated mice showed severe thrombocytopenia and persistent proteinuria, with diffuse glomerular immune deposits of IgG2a and IgG3 isotypes in their kidneys. In contrast, the tamoxifen treated mice had a normal number of thrombocytes and only minimal proteinuria. Moreover, glomerular immune deposits were detected in <40% of the tamoxifen treated mice. The latter were mainly of the IgG2a but not of the IgG3 isotype. CONCLUSION: The results clearly show the remarkable therapeutic effects of tamoxifen on SLE of (NZBxNZW)F1 female mice and suggest that these beneficial effects are related to the specific reduction of IgG3 autoantibodies.

Animals↗

PubMed1980

Evidence of an immediate hypersensitivity mechanism in systemic lupus erythematosus.

In 30 patients with systemic lupus erythematosus the number of a circulating basophils was countered in different stages of activity. An inverse correlation was found between the absolute basophils count and anti-DNA antibodies and presumptive circulating immune complexes (as judged by polyethylene glycol precipitation of serum). A positive correlation was found between the absolute basophil count and C3 or C4 levels. IgE on the basophil surface was determined by radioimmunoassay in 7 patients. All of them showed a significantly higher surface IgE number. When the count of circulating basophils was roughly normal, 5 out of the 6 patients showed a positive basophil degranulation test with native DNA. These results suggest the existence of an anti-DNA specific IgE in lupus patients. Depression of the circulating basophil count may be a useful index of lupus activity.

Antibodies, Antinuclear↗

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↗

PubMed2003

Update on vascular disease in systemic lupus erythematosus.

PURPOSE OF REVIEW: Young women with systemic lupus erythematosus have strikingly high rates of coronary heart disease. Current knowledge indicates that atherosclerosis is an active inflammatory and immune-mediated process. Therefore, the chronic inflammation and immune dysregulation characteristic of systemic lupus erythematosus undoubtedly contribute to the accelerated vascular disease seen in these patients. Carefully considering what is known about atherogenesis in the general population will provide clues to unraveling the complexity of why systemic lupus erythematosus and atherosclerosis are linked so frequently. RECENT FINDINGS: Inflammation is involved in all aspects of atherogenesis from the initial endothelial "response to injury," to foam cell formation leading to the atherosclerotic lesion, to the rupture of the "vulnerable" fibrous cap, resulting in the acute coronary syndrome and potentially in death. The authors review how factors commonly seen in systemic lupus erythematosus or inherent to the underlying disease mechanism may contribute to each of the stages of atherogenesis. SUMMARY: Our focus on the causes of vascular disease in systemic lupus erythematosus must now include nontraditional risk factors such as immune and inflammatory mediators. With the advent of noninvasive screening tools for atherosclerosis, we are better equipped to measure subclinical vascular disease and associated risk factors, including immune and inflammatory mediators. When considering strategies for preventing premature cardiovascular disease in systemic lupus erythematosus, modifying immune and inflammatory risk factors will likely become a major component of the program in addition to modifying the current traditional risk factors.

Adult↗

PubMed1993

Co-twin control study on cerebral manifestations of systemic lupus erythematosus.

All available twin pairs systemic lupus erythematosus (SLE) derived from the Finnish Twin Cohort were studied by clinical evaluation, magnetic resonance imaging (MRI), anticardiolipin (aCL), and antineurofilament (ANFA) antibodies. One of the five monozygotic and one of the eight dizygotic pairs were concordant for SLE. 10 of the 15 patients showed clinical neurological abnormalities, and 11 had abnormal MRI of the brain. Altogether, 12 patients were considered to have neuropsychiatric lupus (NPSLE). Seven of the 11 patients with long-term corticosteroid treatment had either central or cortical atrophy. High or moderate aCL level was found in eight patients and two co-twins. Of them, six patients had at least two manifestations of the antiphospholipid syndrome. ANFAs were found in five patients and four co-twins. Five co-twins fulfilled some of the SLE criteria. Of them, three MZ twins and one additional DZ co-twin with no ARA criteria had findings suggesting central nervous system (CNS) involvement. The results indicate that the majority of SLE patients has cerebral abnormalities either as a result of SLE, or concomitant risk factors. The co-twins without clinical SLE often have minor signs of SLE, and even they may have neurological and MRI abnormalities. However, their aCL and ANFA levels seem not to correlate with MRI abnormalities.

Adolescent↗

PubMed1994

Brain reactive autoantibodies and cognitive impairment in systemic lupus erythematosus.

Nervous system involvement in SLE encompasses a wide array of clinical manifestations which may reflect multiple etiologic factors including autoantibodies to nervous tissue antigens. The aim of the present study was to examine the association between autoantibodies to a wide range of brain antigens and cognitive abnormalities in an unselected population of 70 SLE patients. Using a battery of standardized neuropsychological tests, cognitive impairment was identified in 15/70 (21%) SLE patients compared with 1/25 (4%) patients with rheumatoid arthritis and 1/23 (4%) healthy subjects (P = 0.04). Integral membrane proteins were isolated from dissociated brain cells by temperature-induced phase separation with Triton X-114. Synaptosomes were isolated by differential centrifugation and membrane enriched fractions were prepared by lectin affinity chromatography. Western blotting identified IgG reactivity to a wide range of proteins (MW 22-52 K) in SLE patients. The proteins identified were distinct from well-characterized intracellular antigens including ribosomal P proteins. There was no significant difference in the prevalence of anti-brain antibodies between SLE patients who were cognitively impaired and those who were not impaired. Furthermore, there was no association between the presence of autoantibodies and subsets of cognitive dysfunction. These results suggest that circulating autoantibodies to brain antigens are not responsible for the abnormalities in cognitive function in SLE patients.

Adolescent↗

PubMed1986

Neonatal lupus erythematosus with congenital heart block associated with maternal systemic lupus erythematosus.

We report the presence of complete heart block in a girl whose mother has anti-Ro antibodies and is suffering from systemic lupus erythematosus with Sjögren's syndrome. HLA antigens studies in the two patients support the hypothesis described recently that HLA DR3 is responsible for the production of anti-Ro antibodies and not for the phenotypic expression of the tissue injury.

Adolescent↗

PubMed2005

[Association of systemic lupus erythematosus and Sjögren's syndrome].

INTRODUCTION: Systemic lupus erythematosus and Sjögren's syndrome are multisystemic autoimmune diseases which can be associated to each other. OBJECTIVE: To investigate if there are any distinct clinical, laboratory or serologic features due to the association of the two diseases that can influence the follow up of these patients. PATIENTS AND METHODS: The authors proved the association of these two autoimmune diseases in 56 patients, and these patients' clinical, laboratory and immunoserologic alterations. 50 patients with Sjögren's syndrome and 50 patients with systemic lupus erythematosus were used as control groups. RESULTS: Compared with Sjögren's syndrome alone, in the cases of the association of the diseases, rheumatoid factor was present less frequently, Ro/SS-A, La/SS-B and DNA antibodies were present more frequently, such as antiphospholipid autoantibodies and antiphospholipid syndrome. Anaemia, leukopenia and lymphopenia were detected more often and the patients were younger than in Sjögren's syndrome. Also, affection of the lung, kidney, skin, central nervous system and serous membranes are more common. The group with systemic lupus erythematosus differs in being older, having thyroiditis, Ro/SS-A, La/SS-B and DNA more frequently. CONCLUSION: Definitive clinical, laboratory and serological features make the difference between the association of the two diseases and the diseases observed alone.

Adult↗

PubMed1978

Cardiopulmonary manifestations of systemic lupus erythematosus.

Nine of 17 patients (52%) with systemic lupus erythematosus participating in a controlled prospective study were found to have maximal mid-expiratory flow rates suggestive of obstructive or obstructive and restrictive pulmonary disease. Cigarette smokers with systemic lupus erythematosus had significantly lower (P less than .05) maximal mid-expiratory flow rates than either non-smokers with systemic lupus erythematosus or smokers with degenerative joint disease. By echocardiography, pericardial thickening was seen in six of 17 patients (41%) and mitral valvular abnormalities were noted in four of 17 (24%) patients with systemic lupus erythematosus. Echocardiography was found to be an effective means of detecting pericardial disease in patients with systemic lupus erythematosus.

Adolescent↗

PubMed1997

Systemic lupus erythematosus: demographics, prognosis, and outcome.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder with an annual incidence of 50 to 70/million and a prevalence of 500/million population. The highest incidence is observed in women aged 20 to 40 years. The clinical manifestations of SLE are remarkably heterogeneous. Major organ system involvement may occur in the heart, lungs, kidneys, and central nervous system and is responsible for most of the mortality and morbidity caused by the disease. Complications of drug treatment, in particular corticosteroid side effects, contribute to longterm morbidity. The major causes of death are directly related to the disease and include acute vascular neurologic events, renal failure, cardiovascular or pulmonary involvement, infection, and coronary artery disease.

Adolescent↗