SEARCH · PubMed Health

Results for “LUPUS ERYTHEMATOSUS, SYSTEMIC”

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.

At least 1,117 records · Page 62Linked to original sources

PubMed1996

Genetic basis of systemic lupus erythematosus.

Recent studies have emphasized that systemic lupus erythematosus is a complex genetic trait with contributions from the MHC and multiple non-MHC genes. Genome-wide linkage studies in murine models of lupus have mapped the positions of a number of non-MHC loci, but the contributing genes have not yet been identified. Recent studies in human systemic lupus erythematosus have found an association with a particular FCGR2A allele. Although susceptibility genes in lupus are unlikely to involve mutations with severe functional consequences, murine knockout models that develop lupus-like features may provide insight into the pathogenetic mechanisms and contributing genes in the human disease.

Animals↗

PubMed1989

The lupus anticoagulant in systemic lupus erythematosus.

The lupus anticoagulant was found in six of 41 unselected patients with systemic lupus erythematosus (14%). Three of these six patients had episodes of thrombosis. Thrombosis occurred in only one patient in the remainder of the series without the lupus anticoagulant. The lupus anticoagulant should be considered as one of the criteria for the diagnosis of systemic lupus erythematosus, and it may be a useful marker for those patients at risk from thromboembolism. It should be looked for in young adults with thrombotic episodes.

Adolescent↗

PubMed2002

Endogenous retroviruses in systemic lupus erythematosus: candidate lupus viruses.

Although the etiology of systemic lupus erythematosus (SLE) remains unclear, there is substantial circumstantial evidence that the development of SLE is dependent on environmental, genetic, and retroviral factors. SLE patients produce high titer antibodies to various retroviral proteins, including Gag, Env, and Nef of HIV and HTLV, in the absence of overt retroviral infection. We review the factors linking HERVs to SLE and consider the various processes utilized by endogenous retroviruses in the etiopathogenesis of SLE. In particular, we consider the role of HTLV-1-related endogenous sequence (HRES-1) in SLE. We propose that molecular mimicry between HRES-1 and the small ribonucleoprotein complex initiates the production of autoantibodies, leading to immune complex formation, complement fixation, and pathological tissue deposition.

Antibodies, Viral↗

PubMed1986

Budd-Chiari syndrome as the major thrombotic complication of systemic lupus erythematosus with the lupus anticoagulant.

A patient with systemic lupus erythematosus was first diagnosed after she had developed the Budd-Chiari syndrome. We believe that the Budd-Chiari syndrome was part of her tendency for thrombosis, induced by the presence of a lupus anticoagulant. The association between enhanced thrombosis and the lupus anticoagulant is discussed, and the need for prompt recognition and administration of anticoagulant therapy is emphasised.

Adult↗

PubMed2000

Features of systemic lupus erythematosus in Dnase1-deficient mice.

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease that affects over one million people in the United States. SLE is characterized by the presence of anti-nuclear antibodies (ANA) directed against naked DNA and entire nucleosomes. It is thought that the resulting immune complexes accumulate in vessel walls, glomeruli and joints and cause a hypersensitivity reaction type III, which manifests as glomerulonephritis, arthritis and general vasculitis. The aetiology of SLE is unknown, but several studies suggest that increased liberation or disturbed clearance of nuclear DNA-protein complexes after cell death may initiate and propagate the disease. Consequently, Dnase1, which is the major nuclease present in serum, urine and secreta, may be responsible for the removal of DNA from nuclear antigens at sites of high cell turnover and thus for the prevention of SLE (refs 7-11). To test this hypothesis, we have generated Dnase1-deficient mice by gene targeting. We report here that these animals show the classical symptoms of SLE, namely the presence of ANA, the deposition of immune complexes in glomeruli and full-blown glomerulonephritis in a Dnase1-dose-dependent manner. Moreover, in agreement with earlier reports, we found Dnase1 activities in serum to be lower in SLE patients than in normal subjects. Our findings suggest that lack or reduction of Dnase1 is a critical factor in the initiation of human SLE.

3T3 Cells↗

PubMed2003

Rapid clinical progression to diagnosis among African-American men with systemic lupus erythematosus.

The initial clinical course of systemic lupus erythematosus (SLE) is variable, ranging from relatively minor manifestations progressing over years to rapid onset of fulminate disease. We sought to identify factors associated with the rapid manifestation of SLE. Chart review of military medical records was used to identify 130 patients who met the American College of Rheumatology classification criteria for SLE. Demographics, clinical criteria date of occurrence, and the date of SLE classification (at least four clinical criteria) met were documented. Prospectively stored serum samples prior to the diagnosis were evaluated for SLE autoantibodies. Median time from the first recorded criteria to diagnosis was significantly shorter in African-American (AA) males compared with AA females and European American (EA) females and males combined. AA males were more likely to have nephritis as their first clinical symptom. Also, less time transpired between the first clinical criterion and SLE diagnosis in AA males with nephritis than in other groups presenting with nephritis. Even when cases presenting with nephritis were excluded, a diagnosis of SLE was made more rapidly in AA males. African-American men progress from initial clinical manifestations to SLE diagnosis more rapidly than other ethnic or gender groups.

Black People↗

PubMedDate not supplied

Plasma exchange and immunosuppressive therapy in a paediatric patient with systemic lupus erythematosus.

A case is reported of systemic lupus erythematosus (SLE) associated with steroid-resistant nephrotic syndrome. Serial plasma exchanges (PE) combined with prednisolone treatment induced complete normalization of the immunological findings: the anti-DNA antibody, antinuclear antibody, LE cell phenomenon and circulatory immune complexes became negative. The prostacyclin (PGI2) production-supporting activity in the plasma increased to the control range; inhibitors of PGI2 production were eliminated. The creatinine clearance normalized, the urinary protein excretion decreased significantly, and the facial erythema disappeared. Continued treatment with chlorambucil + low-dose prednisolone led to a complete and stable remission of the nephrotic syndrome, and the C3 complement normalized. The low level of PGI2 production-supporting activity in the plasma may be explained by the inhibitor of PGI2 production. PE + immunosuppressive therapy might have beneficial effects on the immunological changes and PGI2 metabolism, and also on the remission of SLE-nephrotic syndrome.

Autoantibodies↗

PubMed1988

Myocardial involvement in systemic lupus erythematosus detected by magnetic resonance imaging.

Myocardial involvement in systemic lupus erythematosus is commonly found at autopsy but seldom recognized clinically or by routine cardiological investigations. As the magnetic resonance relaxation parameter, T1, is altered by changes in tissue cellularity, we carried out magnetic resonance imaging in 10 patients with systemic lupus erythematosus. Five had active systemic lupus erythematosus when assessed using the lupus activity criteria count. The mean (+/- SD) T1 was 319 +/- 12 in normal volunteers and 321 +/- 10 in a second control group with hypertrophic cardiomyopathy. In the group with systemic lupus erythematosus, there was a higher mean value of 336 ms with a wider scatter of individual results (SD +/- 22 ms). In the subgroup of patients with active disease, T1 was significantly higher (349 +/- 24) than in either of the two control groups. In addition, there was an inverse correlation between serum complement and myocardial T1 in patients with systemic lupus erythematosus. Myocardial abnormalities in systemic lupus erythematosus were demonstrated by magnetic resonance imaging even where other non-invasive cardiac investigations were negative. We conclude that T1 calculated from magnetic resonance imaging is often abnormal in systemic lupus erythematosus and probably indicates myocardial involvement.

Adult↗

PubMed1991

NIH conference. Systemic lupus erythematosus.

Although the cause of systemic lupus erythematosus remains unknown, pathogenic mechanisms are becoming clearer. Both genetic and environmental factors have been implicated in the induction and in the perpetuation of lupus. Implicated environmental triggers include ultraviolet light, chemicals (hydrazines, hair dyes, drugs), some foods, and possibly infectious agents. Lupus is mediated by the immune system. Patients have excess numbers of antibody-forming cells, including those that produce antibodies reactive with self-antigens. Patients also have an increased number of activated T cells, some of which help B cells to produce autoantibodies. A loss of tolerance is a critical immune abnormality in lupus; many of the activated helper T cells may result from a failure in normal tolerance mechanisms. A hematopoietic stem-cell defect could give rise to both B- and T-cell abnormalities. Such a stem-cell abnormality might lead to both a loss of self-tolerance and polyclonal B-cell activation. Antigen-driven, T-cell-dependent expansion of B-cell clones would then give rise to pathogenic autoantibodies, including anti-DNA. We believe that lupus is a syndrome: Patients differ regarding specific inciting factors and immune defects. Some patients have genetically conditioned abnormalities, similar to those found in mice with lupus; others have a combination of genetic and acquired defects. We hope that insights into pathogenesis lead to improved and more individualized therapy.

Animals↗

PubMed1991

Treatment of systemic lupus erythematosus.

Reports on a variety of therapies for systemic lupus erythematosus have been published over the past year. Most of these are single case reports or open studies. As reported last year in this journal, the potential uses of intravenous gamma globulin and plasmapheresis continue to be explored. The use of cyclophosphamide for nonrenal manifestations follows studies last year of its use for lupus nephritis. No major double-blind studies of therapy for lupus nephritis were published; however, the course of lupus patients receiving dialysis or grafts was the subject of three interesting studies. An interesting study on the ability of hydroxychloroquine to prevent disease exacerbations was also published. In summary, the reports of therapy over the past year represent variations on themes. The use of new agents will most likely be based on improvements in our understanding of the pathogenesis of systemic lupus erythematosus.

Hematologic Diseases↗

PubMed2000

Novel approaches to therapy for systemic lupus erythematosus.

Current therapies for systemic lupus erythematosus (SLE) are targeted at immunosuppression and at reducing inflammation. The current therapies are broad-spectrum and include steroids and cytotoxic agents that are counterbalanced by toxicity and side effects of the medications. Methotrexate can be utilized to reduce steroid requirements in mild to moderate SLE. Manipulation of the hormonal axis includes DHEA and bromocriptine. Mycophenolate mofetil is an immunosuppressive agent that is being investigated for SLE renal disease. Autologous stem cell transplantation or high-dose cyclophosphamide may be an option for severe refractory SLE. The aim of the future is to target therapies by altering specific known mechanisms of inflammation and autoimmunity. Although the inciting antigen is still unknown in SLE, it may be possible to alter the regulation of the immune response by targeted molecular therapy. Methods to do so would include manipulation of idiotypes, manipulation of second signal stimulation of the immune response, manipulation of cytokines, and the induction of tolerance by administration of blocking peptides. IVIg is an immunomodulator that has been successful in the treatment of SLE. Targeted molecular therapy is undergoing phase I trials with monoclonal anti-CD40L, a signaling inhibitor. Anti-CTLA4Ig, another signaling blocker, is presently being investigated for psoriasis, but may be a potential therapy for SLE. Finally, therapies may include the administration of peptides to induce tolerance.

Journal Article↗

PubMed1994

[Cortisone-induced delusional depression in systemic lupus erythematosus].

A case of systemic lupus erythematodes (SLE) with development of a delusional depression is presented. Psychiatric symptoms in patients with SLE and in patients treated with glucocorticoids are discussed. The main psychiatric side effects of a therapy with steroids are a dose-dependent, reversible dementia like syndrome and a probably not dose-dependent provocation of psychosis. Furthermore the role of the dysregulation of the limbic-hypothalamic-pituitary-adrenocortical axis in major depression is stressed and consequences for psychopharmacological treatment are emphasized.

Adult↗

PubMed1996

Photosensitivity and antinuclear antibodies in black patients with systemic lupus erythematosus.

Black patients with systemic lupus erythematosus (SLE) have a lower prevalence of photosensitivity rashes than white patients. The reasons for this are unknown, but some studies suggest a correlation between the presence of antinuclear antibodies and protection from photosensitivity. In our study, we determined serum antinuclear-antibody profiles, including anti-dsDNA, anti-Sm, anti-RNP, anti-Ro/SS-A, and anti-La/SS-B antibodies, in 91 black Jamaican patients with SLE. All 91 serum samples from SLE patients (100%) were positive in the fluorescent antinuclear-antibody test. Using the crithidia luciliae immunofluorescence test, anti-dsDNA was found in 27.5% of the samples. By a double immunodiffusion method, anti-Sm antibodies were found in 15.4%, anti-RNP in 18.7%, anti-Ro/SS-A in 9.9%, and anti-La/SS-B in 11.0%. However, no statistically significant differences were observed in the seroprevalence of these antinuclear antibodies when sera from patients of the following groups were compared: only photosensitivity rashes (n = 17), photosensitivity and other rashes (n = 23), other rashes without photosensitivity (n = 27), and patients with no skin rash of any type (n = 24). These results suggest that photosensitivity in black Jamaican patients with SLE is not associated with antinuclear-antibody specificity.

Adolescent↗

PubMedDate not supplied

Complement system studies in systemic lupus erythematosus (SLE)

Complement system involvement has been studied in 16 patients with systemic lupus erythematosus (SLE). Circulating conversion products of C3 were observed in 4 cases. Low mean values of C4 and C3 were found, while C3 proactivator (properdin factor B) levels were low in only a few of the patients. The levels of C4, C3 and C3 proactivator were not lower in the 4 patients in whom C3 conversion products could be demonstrated than in the others. It is concluded that the low complement values found in SLE may be caused mainly by deficient synthesis. Signs of complement activation are in this patient material demonstrated early in the disease, and chiefly in patients not receiving immunosuppressive therapy.

Adolescent↗

PubMed2002

The association between systemic lupus erythematosus and deficiencies of the complement system.

Systemic lupus erythematosus (SLE), an autoimmune disease characterized by chronic nephritis, arthritis or dermatitis and the presence of antinuclear autoantibodies is associated with deficiencies of complement factors of the classical activation pathway. Results accumulated over the past few years with the use of complement gene deficient mice made it possible to update the conventional hypothesis for this association in regard to the etiology of the disease, whereby the early events leading to induction of autoimmunity can be explained by various functions of complement. As a conclusion, a new model for the etiology of the SLE based on the reduced elimination of apoptotic cells, the increased uptake of IgM containing immune complexes into the spleen and the CD21/CD35 dependent B cell toleration in the periphery demonstrates the importance of complement in the prevention of autoimmunity whereas the inflammatory reactions occurring in later stages of the disease are relatively independent from complement. The results obtained with complement deficient mice contribute to a better understanding of tolerance-inducing mechanisms and offers the option to develop new therapeutic procedures for autoimmune diseases.

Animals↗

PubMed1998

Alterations of cerebral blood flow and antiphospholipid antibodies in patients with systemic lupus erythematosus.

Twenty-two patients with systemic lupus erythematosus and 13 healthy controls were included in a cerebral blood flow study and underwent brain-dedicated single-photon emission computed tomography using 99m technetium-d, l-hexamethylpropylene amine oxime together with a brain computed tomography scan. Plasma levels of antiphospholipid antibodies (lupus anticoagulant and anticardiolipin IgM and IgG antibodies) were also determined. Brain computed tomography showed signs of focal cerebral ischemia in 4 patients (18%), whereas cerebral blood flow by single-photon emission computed tomography was abnormal in 13 of 22 patients (59%), who showed bilateral or monolateral hypoperfusion in the temporo-parietal regions. Patients with abnormal cerebral blood flow had a longer duration of disease than those with normal blood flow (8.9 +/- 1.9 years vs. 5.3 +/- 1.5 years, P < 0.05). Plasma antiphospholipid antibodies were present in 15 patients (68%), but the prevalence was similar in those with normal (6/9, 66%), or abnormal (9/13, 69%) cerebral blood flow. No statistically significant difference in lupus anticoagulant or anticardiolipin antibodies was observed between patients with and without cerebral blood flow abnormalities. Our study shows that patients with systemic lupus erythematosus frequently have cerebral blood flow abnormalities, which could precede those observed by computed tomography. Plasma lupus anticoagulant and anticardiolipin titers were not correlated with normal cerebral blood flow.

Adolescent↗

PubMed1995

Neurologic manifestations of pediatric systemic lupus erythematosus.

Central nervous system involvement is a common but rarely reviewed feature of pediatric systemic lupus erythematosus (SLE). We retrospectively reviewed the charts of 91 patients with pediatric SLE and using a standardized data abstraction form documented 40 patients with central nervous system (CNS-SLE) involvement. The mean age of onset of SLE was 13.3 years. In 19 patients the CNS manifestation was a presenting symptom, in 12 patients CNS involvement was present within the first year of diagnosis, and in 9 patients it took up to 7 years for CNS disease to become evident. Nineteen children (48%) manifested neuropsychiatric SLE, which included depression, concentration or memory problems, and frank psychosis. Seizures were present in 8 patients (20%), 6 had cerebral ischemic events (15%), 1 had chorea (3%), 2 had papilledema (5%), and 2 patients had a peripheral neuropathy (5%). Nine patients (22%) had severe headache consistent with lupus headache. Seven children had more than one CNS manifestation. In the investigation of CNS-SLE, computed tomography and/or magnetic resonance imaging scans were helpful in patients with focal ischemic lesions and venous sinus thrombosis. Electroencephalography was abnormal only in 33% of patients with seizure disorders and rarely helpful in patients with diffuse neuropsychiatric symptoms. Single-photon emission computed tomography scans were abnormal in most patients with neuropsychiatric SLE, especially in those with frank psychosis. The lupus anticoagulant was present in the patient with chorea and was frequently present in patients with cerebral vascular events. Long-term outcome was good: only 1 child died of cerebral hemorrhagic infarction and 3 others had significant persistent CNS deficits. The majority of patients (90%) had excellent recovery from CNS-SLE.

Adolescent↗

PubMed1989

[Circulating immune complexes and clinico-immunologic subtypes of systemic lupus erythematosus. II].

Characterization of clinicoimmunological subtypes of systemic lupus erythematosus was based on a detailed serological investigation of 90 SLE patients. Association between excessive formation of circulating immune complexes and the development of some clinical and serological manifestations of systemic lupus erythematosus including active lupus nephritis without the nephrotic syndrome, systemic vasculitis and Sjogren's syndrome was established.

Adult↗