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PubMed1992

Systemic lupus erythematosus with central nervous system involvement.

Real or suspected brain involvement occurs in the majority of patients with systemic lupus erythematosus. The clinical manifestations are myriad and are accounted for by diverse pathogenic mechanisms. Purely psychological disturbances and psychiatric syndromes with organic components account for the majority of cases. Metabolic disturbances, drug effects, and infections may masquerade for immune-related brain dysfunction. In the absence of reliable and specific indicators of lupus brain activity, successful management requires the combined skills and clinical judgment of the rheumatologist, neurologist, and psychiatrist.

Brain Diseases↗
PubMed2026

Exploring shared biomarkers and their mechanisms in thyroid cancer and systemic lupus erythematosus via bioinformatics analysis.

BACKGROUND: Systemic lupus erythematosus (SLE), an autoimmune disorder, is linked to a heightened risk of multiple malignancies, including thyroid cancer. Thyroid cancer is the most prevalent malignancy of the endocrine system, and its autoimmune-related pathological features render it an optimal subject for investigating the mechanisms of their comorbidity. The molecular mechanisms underlying this comorbidity are still ambiguous. The accurate diagnosis and treatment of thyroid cancer urgently necessitate innovative molecular targets that extend beyond conventional pathological characteristics. This study seeks to employ integrated bioinformatics approaches to elucidate potential shared molecular mechanisms and immunological features between thyroid cancer and systemic lupus erythematosus (SLE), aiming to enhance understanding of their comorbidity and identify novel intervention targets. METHODS: This study initially acquired gene expression data for TC and SLE from the GEO database and subsequently screened and identified differentially expressed genes (DEGs) shared by both diseases. Subsequently, we conducted Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome functional enrichment analyses on these 46 shared differentially expressed genes (DEGs) and further assessed the activation status of pertinent pathways using Gene Set Enrichment Analysis (GSEA). Subsequently, we employed CIBERSORTx to examine immune infiltration patterns and developed protein-protein interaction networks utilising the STRING database. We identified hub genes utilising the MCODE and cytoHubba plugins and visualised the findings with Cytoscape software. We additionally assessed the diagnostic efficacy of these core hub genes in an independent dataset utilising ROC curves and investigated their prognostic relevance in thyroid cancer through Kaplan-Meier survival analysis and multivariate Cox proportional hazards regression. Ultimately, we employed the Network Analyst platform to forecast transcription factor-gene and miRNA-gene regulatory networks and identified potential targeted therapeutic compounds utilising the DSigDB database. RESULTS: This study identified 46 differentially expressed genes (DEGs) commonly linked to thyroid cancer and systemic lupus erythematosus (SLE), which were significantly enriched in signalling pathways associated with immune-inflammatory activation, type I interferon responses, and complement pathway activation. Moreover, GSEA findings validated that immune-inflammatory and autoimmune-related pathways are markedly activated in both conditions. Twelve hub genes were discerned through protein-protein interaction networks. Analysis of immune infiltration indicated that thyroid cancer and systemic lupus erythematosus exhibit a shared characteristic of innate immune dysregulation, marked by the infiltration of myeloid cells (neutrophils, M0/M2 macrophages). Receiver operating characteristic (ROC) curve analysis identified six significant core hub genes with substantial diagnostic value: C1QB, LCN2, C1QC, LTF, VSIG4, and C3AR1. Univariate survival analysis indicated that elevated expression of C1QC and C3AR1 significantly enhances overall survival in thyroid cancer patients; however, multivariate COX regression analysis revealed that their independent prognostic significance necessitates further validation. This study predicted the interaction networks of transcription factors and miRNAs regulating key genes, with LCN2 demonstrating the highest connectivity to miRNAs, and identified candidate therapeutic compounds linked to it. CONCLUSION: This study employed bioinformatics analysis to identify critical shared hub genes and molecular pathways connecting thyroid cancer and systemic lupus erythematosus, offering novel insights into their shared pathogenesis and the advancement of targeted biomarkers and therapeutic strategies.

Bioinformatics analysis↗
PubMed1975

Systemic lupus erythematosus. Contrasts and comparisons.

Systemic lupus erythematosus, a disease capable of exhibiting virtually any clinical manifestation, is discussed in detail and the findings are compared to those in other, presumably systemic lupus erythematosus-related connective tissue diseases. More emphasis has been placed on the clinical features than on the numerous laboratory manifestations. The conference begins and ends with a brief consideration of current concepts of pathogenesis and suggests some future investigational directions.

Animals↗
PubMedDate not supplied

Association of the tumor necrosis factor alpha gene polymorphism with susceptibility and clinical-immunological findings of systemic lupus erythematosus.

The etiology of systemic lupus erythematosus (SLE) is unknown but genetic factors seem to play a role in the disease pathogenesis. The tumor necrosis factor alpha (TNFa) gene, encoded at the TNF locus in the MHC class III region, is now known to be an important candidate gene in SLE, due to the proinflammatory activities of the TNFa. The objectives of this study were to examine the role of the TNFa polymorphism for the susceptibility of Malaysian Chinese lupus patients to SLE and to determine its association with organ involvement. The allelic frequencies of the TNFa polymorphic variant (TNF2) of seventy lupus patients were determined during follow-up at the Medical Clinic of the National University Hospital Malaysia by PCR-RFLP technique. Sixty-four females and 6 males with a mean age of 33+/-12 years were included. Clinical data were obtained from case records. Autoantibody levels were measured by ELISA. Fifty-nine ethnically-matched blood donors were used as controls. The allelic frequency of the TNF2 variant was found to be significantly increased in the patients compared to the controls (52.8% vs 33.8%). SLE patients with the polymorphic TNF2 variant were found to be at increased risk of central nervous system involvement (p = 0.004, RR = 2.59) and to have an increased frequency of anti-La antibodies (p = 0.03). In view of these findings we suggest that TNF2 variant is playing a role in conferring susceptibility to SLE and in the disease pathogenesis.

Adult↗
PubMed1984

Systemic lupus erythematosus: the great masquerader.

Systemic lupus erythematosus is a chronic systemic autoimmune collagen vascular disease that can present itself in many forms throughout any system in the body. Classification, etiology, diagnosis, course of the illness with flares and remission, prognosis, treatment and emotional coping are covered. Five tables outline lab tests, classification of symptoms by tissues primarily affected, drugs used, dietary suggestions and symptoms which need the attention of a health care provider.

Adaptation, Psychological↗
PubMed2000

Cyclophosphamide versus methylprednisolone for the treatment of neuropsychiatric involvement in systemic lupus erythematosus.

BACKGROUND: Neuropsychiatric involvement in systemic lupus erythematosus is complex and several clinical presentations are related to this disease such as: convulsions, chronic headache, transverse myelitis, vascular brain disease, psychosis and neural cognitive dysfunction. OBJECTIVES: To assess the efficacy and safety of cyclophosphamide and methylprednisolone in the treatment of neuropsychiatric manifestations of systemic lupus erythematosus on mortality and side effects. SEARCH STRATEGY: We searched EMBASE, LILACS, Cochrane Controlled Trials Register and MEDLINE up to and including December 1999, additional articles were sought through handsearching in relevant journals, using the search strategy described in the Cochrane Handbook [Dickersin 1994]. There were no language restrictions. SELECTION CRITERIA: All randomized controlled trials which compared cyclophosphamide to methylprednisolone were to be included. Patients of any age and gender were included if they fulfilled the criterion of the American Rheumatology Association for the diagnosis of systemic lupus erythematosus and presented with any one of the following neuropsychiatric events; convulsions, organic brain syndrome; cranial neuropathy. Outcome measures included the following: a) Overall mortality (primary event); b) Motor and psychiatric deficit (primary event); c) Clinical improvement (secondary event). DATA COLLECTION AND ANALYSIS: The analysis planned was to do the following: Data would be independently extracted by the two reviewers and cross-checked. The methodological quality of each trial would be assessed by the same two reviewers. Details of the randomisation (generation and concealment), blinding, and the number of patients lost on follow-up would be recorded. The results of each RCT would be summarised on an intention-to-treat basis in 2 x 2 tables for each outcome. External validity would be defined by characteristics of the participants, the interventions and the outcomes. If appropriate, RCTs would be stratified based on control group and category of disease in accordance to the clinical homogeneity (external validity). The results obtained from these different methods are very similar, and therefore, only the results from the Risk Difference method, with the corresponding 95% confidence interval would be presented in this review. The fixed effects model would be used if there was no significant statistical heterogeneity. MAIN RESULTS: We found no randomised controlled trials comparing cyclophosphamide versus methylprednisolone for the treatment of neuropsychiatric involvement in the systemic lupus erythematosus. REVIEWER'S CONCLUSIONS: Cyclophosphamide regimen treatment is a form of care in neuropsychiatric involvement in systemic lupus erythematosus with no evidence to prove better effectiveness and safety when compared with methylprednisolone. This systematic review found no randomised controlled trials and its findings must be interpreted as 'no evidence of effect' and not as 'evidence of no effect'.

Antirheumatic Agents↗
PubMed1995

[The long-term parenteral use of cyclophosphane in treating patients with systemic lupus erythematosus and central nervous system involvement].

In the treatment of systemic lupus erythematosus (SLE) with acute CNS affections good results may be obtained with intravenous cyclophosphamide (CP) + methylprednisolone followed with long-term parenteral CP administration. CNS abnormalities in SLE patients can be effectively managed by parenteral CP in combination with minimal-dose glucocorticoids given for 5-7 years.

Administration, Oral↗
PubMed2000

Comparable heavy and light chain pairings in normal and systemic lupus erythematosus IgG(+) B cells.

Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the presence of high immunoglobulin serum titers, but the mechanism by which these arise remains unclear. It has been suggested that the disease is associated with specific antibody features, including variable gene use, the presence of charged complementarity-determining region residues and/or an aberrant process of secondary light chain rearrangement. To study this in more detail, we compared variable, diversity and joining gene segment use, somatic mutation, and heavy and light chain pairings in single peripheral IgG(+) B cells between one normal (209 B cells) and two SLE (156 B cells) donors. In contrast to others, we found no systematic differences, indicating that the memory B cell repertoires in normal and SLE donors are shaped in a similar way.

Adult↗
PubMed2000

Interleukin-10 blockade corrects impaired in vitro cellular immune responses of systemic lupus erythematosus patients.

OBJECTIVE: Many systemic lupus erythematosus (SLE) patients display impaired cellular immune responses against allo- or recall antigens. Given the down-regulating properties of interleukin-10 (IL-10) on antigen-presenting cell functions, this study was undertaken to investigate whether the well-known overproduction of IL-10 by SLE peripheral blood mononuclear cells (PBMC) was involved in this process. METHODS: We measured the proliferation of SLE or control PBMC against irradiated allogeneic dendritic cells in the absence or presence of antibodies blocking IL-10 activity, or in the absence or presence of IL-12. RESULTS: As a group, SLE PBMC proliferated against allogeneic targets less than control PBMC. However, SLE patients could be categorized as good responders or poor responders according to the amplitude of their allogeneic response. Interestingly, serum IL-10 concentrations were significantly higher in the poor responders than in the good responders or in the controls, and addition of antibodies blocking IL-10 activity significantly increased the proliferative responses of the group. We confirmed the role of IL-10 in the impaired allogeneic responses displayed by SLE PBMC by demonstrating that addition of IL-10-containing SLE PBMC supernatants inhibited a normal allogeneic response between unrelated healthy controls, and by showing that this inhibitory effect was commensurate with the concentrations of IL-10 measured in the supernatants. In this experimental setting, we also demonstrated that IL-10-containing SLE PBMC supernatants inhibited IL-12 p35 and IL-12 p40 gene expression. Consistent with the last observation, we found that addition of exogenous IL-12 restored the proliferation of poor-responder SLE patients' PBMC. CONCLUSION: Taken together, these results indicate that dysregulation of the IL-10/IL-12 balance plays a critical role in the impaired cellular immune responses observed in SLE patients.

Adolescent↗
PubMed1991

Aplastic anemia associated with systemic lupus erythematosus.

Hematologic complications of systemic lupus erythematosus (SLE) usually involve peripheral destruction of blood cells. We report a case of aplastic anemia associated with SLE observed during the remission phase of SLE 3 months after the beginning of treatment. CD8+ T cells in the patient's bone marrow may have suppressed maturation of hematopoietic progenitor cells, which may have induced the aplastic anemia associated with SLE. Repeated therapy with high-dose methylprednisolone resulted in lasting remission.

Anemia, Aplastic↗
PubMedDate not supplied

Migrainous phenomena in systemic lupus erythematosus.

Eleven patients with systemic lupus erythematosus (SLE) also had headaches and/or visual hallucinations typical of those found in migraine. These migrainous symptoms were commonly associated with exacerbations of SLE and abated as disease activity subsided. In some cases corticosteroids were more effective than conventional antimigraine therapy in controlling headaches and scotomas. The data suggest that migraine-like phenomena may arise as a result of vascular dysfunction in SLE.

Adult↗
PubMed1979

Deposition of antibodies to a soluble cytoplasmic antigen in the kidneys of patients with systemic lupus erythematosus.

Two patients with systemic lupus erythematosus were studied whose sera contained precipitating antibodies to a soluble cytoplasmic antigen, termed Ro. A reduction in the amount of these antibodies in each case was accompanied by a deterioration in the clinical status with the development of nephritis leading to death. Acid elution of gamma globulin was performed from homogenates of the renal cortex, and in both instances antibodies to Ro were demonstrated in the eluates by double immunodiffusion. The titer of these antibodies was measured in both sera and eluates, and specific enrichment of anti-Ro in the eluates was demonstrated in both patients. This strongly suggests the direct participation of Ro-anti-Ro immune complexes in the progressive renal disease and may underlie the association seen here between the decreasing serum titers of antibodies to Ro and the clinical deterioration in these two cases.

Antibody Specificity↗
PubMed1991

Strategies for reducing excess morbidity and mortality in blacks with systemic lupus erythematosus.

The epidemiology of systemic lupus erythematosus suggests that the excess morbidity and mortality in blacks with the disease is related to lower socioeconomic status. Poverty and factors associated with poverty are powerful predictors of poor outcome in a variety of chronic diseases, and lupus appears to be no exception. A body of studies in other illnesses suggests ways to neutralize, at least partially, the disadvantages of lower socioeconomic status, even though the root causes of poverty may be insurmountable. These include improving access to quality health care; targeting educational programs to promote recognition and understanding of the disease and the comorbid conditions that affect outcome; implementing programs to improve self-monitoring and adherence to medical regimens; developing opportunities to facilitate homemaking, childrearing, and working outside the home; and applying psychosocial interventions to enhance self-confidence and social support. Improved access to quality health care may actually lead to a decrease in health care costs.

Black or African American↗
PubMed1993

Concomitant development of chronic active hepatitis and antibodies to ribosomal P proteins in a patient with systemic lupus erythematosus.

We describe a systemic lupus erythematosus (SLE) patient who for several years had typical SLE features and positive antinuclear antibodies (ANA), including anti-native DNA. Over the course of a year, 4 years after the SLE was diagnosed, the ANA disappeared and antibodies to cytoplasmic component ribosomal P protein (anti-P) appeared. Associated with the appearance of anti-P antibodies was the development of biochemical evidence of liver disease, later shown histologically to be chronic active hepatitis. The temporal relationship between the occurrence of anti-P antibodies and the development of liver disease raises the possibility of a role for anti-P antibodies in liver disease.

Adult↗
PubMed1996

Defective antigen-presenting cell function in patients with systemic lupus erythematosus.

OBJECTIVE: Patients with systemic lupus erythematosus (SLE) who exhibit defective in vitro responses to recall antigens and normal responses to alloantigens have been shown to have an abnormality in antigen-presenting cell (APC) function. This study was undertaken to further characterize this defect in APC function in lupus patients. METHODS: Mononuclear cells (MNC) from the peripheral blood of patients with SLE and from normal individuals were cultured in the presence of either recall antigen tetanus toxoid (TT), anti-CD3 (OKT3) monoclonal antibody, or alloantigens, and proliferative or interleukin-2 responses were assessed. Cell surface expression of B7-1 was assessed by flow cytometry. RESULTS: MNC from all normal individuals and from 7 patients with SLE responded to both TT and alloantigen and were designated +/+. Twelve SLE patients did not respond to TT but did respond to alloantigen stimulation and were designated -/+. In both normal subjects and SLE patients, the ability to respond to OKT3 correlated strongly with the ability to respond to recall antigen. A defect in APC costimulatory function was suggested by data demonstrating that interferon-gamma-induced expression of B7-1 was significantly reduced in SLE patients compared with controls. Neither controls nor SLE patients expressed detectable amounts of surface B7-1 molecule on resting APC. Defective recall and anti-CD3-stimulated responses could be enhanced in SLE patients in the presence of B7/BBl-transfected P815 murine mastocytoma cells underscoring an SLE-associated defect in costimulatory activity. However, nontransfected P815 cells were also able to enhance responses to OKT3 in -/+ patients; blocking experiments showed that this was mediated through an IgG Fc receptor-dependent mechanism. CONCLUSION: These data indicate that SLE-associated defects in APC function in vitro can be accounted for by abnormalities in APC surface membrane molecules such as B7, IgG Fc receptors, and possibly others.

Adolescent↗
PubMed2004

Outcomes of hospitalizations for myocardial infarctions and cerebrovascular accidents in patients with systemic lupus erythematosus.

OBJECTIVE: Patients with systemic lupus erythematosus (SLE) have increased risks of acute myocardial infarction (AMI) and cerebrovascular accident (CVA), but it is not known whether they have worse outcomes after AMI or CVA compared with patients without SLE. This study compared in-hospital mortality, length of stay, and other measures of severity (congestive heart failure or need for coronary artery bypass grafting after AMI; discharge to a skilled nursing facility after CVA) between patients with SLE and patients without SLE who were hospitalized for AMI or CVA. METHODS: Data on all patients hospitalized in California with either AMI or CVA from 1996 to 2000 were abstracted from a state hospitalization database. Outcomes after AMI were compared between 519 patients with SLE and 214,771 patients without SLE, and outcomes after CVA were compared between 905 patients with SLE and 293,326 patients without SLE. Analyses were performed separately for men and women. RESULTS: Among women with AMI, there were no differences in the risk of in-hospital mortality, long length of stay, or congestive heart failure between patients with SLE and those without SLE, but women with SLE were less likely to undergo coronary artery bypass grafting. Outcomes after AMI did not differ between men with SLE and men without SLE. Among women with CVA, there were no differences in outcomes between patients with SLE and patients without SLE. Men with SLE were almost twice as likely to have a long length of stay after CVA than were men without SLE. CONCLUSION: Outcomes after AMI and CVA are generally similar between patients with SLE and those without SLE.

Aged↗
PubMed1990

Laminar periostitis and multiple osteonecrosis in systemic lupus erythematosus.

Bone affectation in systemic lupus erythematosus (SLE) is caused both by the disease itself and by the treatment used. We report the case of a woman diagnosed of SLE, who, in the course of her illness, develops multiple aseptic osteonecrosis (AON) and laminar periostitis, radiologically compatible with the diagnosis of hypertrophic osteoarthropathy (HOA), with no evidence of acropaquia. In this case, the patient shows all the risk factors involved in the pathogenesis of the development of ischemia in bone microcirculation.

Adult↗