Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calreticulin is an abundant intracellular protein which is involved in a number of cellular functions. During cytomegalovirus infection, as well as inflammatory episodes in autoimmune disease, calreticulin can be released from cells and detected in the circulation, where it may act as an immunodominant autoantigen in diseases such as systemic lupus erythematosus. Calreticulin is known to bind to the molecules of innate immunity, such as C1q, the first subcomponent of complement. However, the functional implications of C1q-calreticulin interactions are unknown. In the present study we sought to investigate, in greater detail, the interaction between these two proteins following the release of calreticulin from neutrophils upon stimulation. In order to pinpoint the regions of interaction, recombinant calreticulin and its discrete domains (N-, P- and C-domains) were produced in Escherichia coli. Both the N- and P-domains of calreticulin were shown to bind to the globular head regions of C1q. Calreticulin also appeared to alter C1q-mediated immune functions. Binding of calreticulin to C1q inhibited haemolysis of IgM-sensitized erythrocytes. Both the N- and P-domains of calreticulin were found to contain sites involved in the inhibition of C1q-induced haemolysis. Full-length calreticulin, and its N- and P-domains, were also able to reduce the C1q-dependent binding of immune complexes to neutrophils. We conclude that calreticulin, once released from neutrophils during inflammation, may not only induce an antigenic reaction, but, under defined conditions, may also interfere with C1q-mediated inflammatory processes.
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PMID:Release of calreticulin from neutrophils may alter C1q-mediated immune functions. 906 75

A 30-year-old woman with systemic lupus erythematosus was admitted to our hospital because of a slight fever and diffuse interstitial shadows on a chest X-ray film. She had taken prednisolone (60 mg per day) at another hospital for six weeks. At the time of admission to our hospital, she had been treated with antituberculosis drugs (streptomycin, isoniazid, and rifampicin) for two weeks because of suspected miliary tuberculosis. Chest radiography on admission revealed diffuse nodular and micronodular shadows in the middle and lower lung fields on both sides. Examination of transbronchial lung biopsy specimens revealed intranuclear viral inclusion bodies in infected alveolar epithelial cells, which suggested the diagnosis of cytomegalovirus infection. The elevation of serum IgM antibody to cytomegalovirus and positive results of in situ hybridization for cytomegalovirus DNA supported this diagnosis. The symptoms and radiographic abnormalities resolved completely without ganciclovir. Although we cannot exclude the possibility that the antituberculosis drugs caused the resolution of the cytomegalovirus pneumonia, it appears most probable that the cytomegalovirus pneumonia resolved spontaneously.
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PMID:[Spontaneous recovery from cytomegalovirus pneumonia]. 907 Nov 59

We report a rare case of cytomegalovirus (CMV) retinitis in association with systemic lupus erythematosus (SLE). A 36-year-old female was admitted to our hospital because of nephrotic syndrome and renal insufficiency due to lupus nephritis. After steroid and immunosuppressant treatment for lupus nephritis, she began to complain of floaters and visual disturbance. She was diagnosed as having CMV retinitis based upon the depressed immune status and the clinical appearance of fundus. As soon as CMV retinitis was diagnosed, antiviral treatment with intravenous ganciclovir was instituted and maintained for 7 months. She was treated successfully and almost no progression or relapse of CMV retinitis was documented without ganciclovir maintenance treatment during a 2 year follow-up period. It is suggested that CMV retinitis can occur in patients with SLE treated with steroid and immunosuppressant, indicating the importance of early diagnosis and treatment for CMV retinitis.
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PMID:[Cytomegalovirus retinitis in a patient with systemic lupus erythematosus]. 916 90

A patient with systemic lupus erythematosus (SLE) developed bilateral cytomegalovirus (CMV) retinitis and was treated with a total of 9 intravitreal ganciclovir injections at a dose of 400 micrograms/50 microliters in each eye under topical anesthesia. She was unable to receive systemic antiviral therapy because of bone marrow suppression and renal failure. The condition of both eyes improved after the intravitreal injections. Recurrence of CMV retinitis was not seen until death. Intravitreal injections of ganciclovir are useful even for the non-acquired immunodeficiency syndrome (AIDS) immunocompromised patients with CMV retinitis when the patients can not receive intravenous medications because of systemic complications.
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PMID:[Use of intravitreal ganciclovir for cytomegalovirus retinitis in a patient with systemic lupus erythematosus]. 920 42

A patient receiving long-term immunosuppressive treatment of systemic lupus erythematosus developed multiple large painful ulcers on her upper body. Histologic analysis showed cytopathic changes typical of cytomegalovirus infection that was confirmed by immunoperoxidase staining and polymerase chain reaction analyses. Treatment with ganciclovir and foscarnet resulted in clinical resolution. No recurrence was evident 6 months later.
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PMID:Diagnosis and treatment of a case of cutaneous cytomegalovirus infection with a dramatic clinical presentation. 948 14

We assessed the value of the cytomegalovirus (CMV) antigenemia assay for diagnosing primary CMV infection in adults. The CMV antigenemia assay was performed for 40 patients admitted to our unit over a 2-year period with unexplained fever and suspected primary CMV infection. Nine of the 10 patients with primary CMV infection had positive CMV antigenemia assays, and the results were available within 5 hours. All 10 patients had a mononucleosis-like syndrome. All but one of the 30 other patients had negative CMV antigenemia assays. A false-positive result was obtained for a patient with systemic lupus erythematosus. Overall, the CMV antigenemia assay was 90% sensitive and 96% specific for the diagnosis of primary CMV infection. Therefore, the CMV antigenemia assay appears to be a simple, rapid, inexpensive test for the diagnosis of primary CMV infection in hospitalized adults.
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PMID:Use of the cytomegalovirus (CMV) antigenemia assay for the rapid diagnosis of primary CMV infection in hospitalized adults. 952 38

We describe here the broad spectrum of acute renal insufficiency occurring in the course of human immunoinsufficiency virus infection. In our renal unit in Tenon hospital, 90 human immunoinsufficiency virus-infected adult patients were admitted for acute renal insufficiency between June 1988 and December 1996. Sixty out of them had a pathological diagnosis. The remaining patients did not have renal biopsy because of obstructive renal failure (n = 2), bleeding risk (n = 11), or clinically evident hypovolemic and/or sepsis-related acute tubular necrosis (n = 17). Nine different causes of acute renal insufficiency were listed. Human immunoinsufficiency virus-associated nephropathy, the most specific human immunoinsufficiency virus-related renal disease, which was diagnosed in 14 patients, is characterized by focal and segmental glomerulosclerosis with an important hyperplasia and/or proliferation of podocytes and huge tubular distension. The rapid progression to end-stage renal failure was not a constant feature since 10/14 patients had a partial renal recovery. Hemolytic-uremic syndrome was the other major cause of acute renal failure in these patients (32 cases) and was found to be associated with active cytomegalovirus infection. Cytomegalovirus-infected cells were present in half of the renal biopsies performed in this group of patients. Furthermore, these patients had an increased plasma tissue-type plasminogen activator activity whereas its type 1 inhibitor was not significantly increased, as opposed to non human immunoinsufficiency virus-associated hemolytic-uremic syndrome. Half of the patients had a complete renal recovery. The other causes of acute renal insufficiency were 1) intratubular deposition of either drugs (Adiazine, Foscavir, Indinavir) in 13 patients, or monoclonal light chain in one patient with B cell-lymphoma; 2) lupus-like glomerulonephritis characterized in one case by a complete clinical remission after 6 month-treatment by antiproteases; 3) acute tubular necrosis. In this setting, rhabdomyolysis could reveal HIV infection. The heterogeneity of renal diseases could be explained by the variation of human immunoinsufficiency virus-associated infections along time and by the different drugs which permit a better survival. We can hypothesize that new HIV-associated diseases will occur with the long term use of antiproteases.
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PMID:[Human immunodeficiency virus and acute renal insufficiency]. 961 98

We report two patients with systemic lupus erythematosus (SLE) in whom cytomegalovirus (CMV) infection may have played a significant role in the exacerbation or onset of symptoms. The first patient had thrombocytopenia and the second had proteinuria. CMV infection was observed in both patients when their symptoms developed.
Lupus 1998
PMID:Exacerbation of systemic lupus erythematosus related to cytomegalovirus infection. 986 1

Osteopontin (OPN) is an Arg-Gly-Asp-containing phosphoprotein that is secreted by activated T cells. The concentration of serum OPN protein is elevated in autoimmune-prone MRL-lpr mice as well as in patients with systemic lupus erythematosus. Previously, it was shown that OPN induces the polyclonal activation of B cells, resulting in the augmented production of immunoglobulin, indicating that OPN plays some role in the development of autoimmune disease. However, the link between OPN and development of autoimmune disease remains unclear. To analyze the role of OPN in immune system and autoimmune diseases, we have generated two kinds of transgenic mice: one carries the immunoglobulin (Ig) enhancer/SV40 promoter and the other carries the cytomegalovirus enhancer/chicken beta-actin (CAG) promoter. In both groups of transgenic mice, the B1 cell population in peritoneal cavity was markedly increased and titer of IgM and IgG3 antibodies in the serum was considerably higher than that in wild-type mice. Most important, the titer of the IgM class of anti-double-stranded DNA antibody was significantly elevated in transgenic mice. These results strongly suggest that OPN may have an important role in the propagation and differentiation of B1 cells and production of autoantibodies.
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PMID:Introduction of an osteopontin gene confers the increase in B1 cell population and the production of anti-DNA autoantibodies. 988 52

Relationships between viruses and autoimmune diseases such as systemic lupus erythematosus (SLE) are still elusive. Recent reports demonstrated the association of some viral infections with peculiar clinical events in the general population, such as cytomegalovirus (CMV) with arterial damage and Parvovirus B19 (PV-B19) with hematologic abnormalities. We planned to look for this kind of viral imprinting in SLE, hypothesizing that traces of specific features of some viral infections might be found in some subsets of seropositive SLE patients. In 60 SLE patients recruited at our nephrologic center, serology for CMV, PV-B19, Epstein-Barr virus viral capsid antigen (EBV-VCA), Epstein-Barr nuclear antigen (EBNA) and Epstein-Barr virus early antigen (EBV-EA) was performed. chi2 and ANOVA were employed to compare the frequency and titers of antiviral antibodies in SLE patients with groups of transplant, hemodialysis and blood donor subjects. chi2, Fisher's test, Bonferroni and Scheffe's test were employed to compare the different biochemical/clinical features between seropositive and seronegative SLE patients. Univariate and multivariate analysis (logistic regression models) were employed to evaluate the odds ratio (OR) of different risk factors for vascular events (including Raynaud's phenomenon, deep venous thrombosis) and hematologic abnormalities (including severe anemia, leukopenia and thrombocytopenia). Anti-CMV (82%), anti-PV-B19 (60%), anti-EBV-VCA (92%) and EBV-EA (45%) IgG antibodies were frequent in SLE, with higher prevalence in comparison with the blood donor group and higher titers in comparison with transplant and hemodialysis groups. CMV seropositivity was a highly significant risk factor for Raynaud's phenomenon (OR +alpha in univariate and multivariate analysis = 13.51 using a correction of 0.5 in case of a zero event), but not for venous vascular events (OR = 1.31). An increased though not significant risk factor was found for antiphospholipid antibodies (OR = 2.71, p = 0.19), while the presence of nephrotic syndrome during the follow-up was a significant protective factor (OR = 0.15, p = 0.035). There was no significantly increased OR for PV-B19 seropositivity in cases with severe anemia (OR = 2.09, p = 0. 29). No significant associations were found with the status of EBV reactivation. In conclusion, our results support the hypothesis that viral infection may imprint the course of SLE leading to specific clinical subsets (i.e. CMV and 'vascular' SLE, with more frequent Raynaud's phenomenon and a less frequent typical histological renal picture responsible for nephrotic syndrome). Further prospective studies are justified to validate these correlations, mainly dealing with associations between acute viral infections and vascular events, thus eventually leading to a better understanding of mutual relationships between viruses and SLE.
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PMID:Correlation between cytomegalovirus infection and Raynaud's phenomenon in lupus nephritis. 1036 7


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