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)

We report on a man with a long history of systemic lupus erythematosus, who had signs and symptoms of a dissecting aortic aneurysm 25 days after receiving a living related donor transplant. The aneurysm was repaired successfully while the patient was on immunosuppression. However, the patient died 3 weeks later of cytomegalovirus pneumonia.
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PMID:Acute dissecting aneurysm of the aorta after renal transplantation. 634 24

A 58 year old woman developed systemic symptoms, interstitial lung disease, splenomegaly, leukopenia and anti-histone and anti-nuclear antibodies (ANA), while treated with hydralazine for hypertension. Five months after presentation she was admitted with high fever, skin rash and atypical lymphocytosis due to acute cytomegalovirus (CMV) infection. Worsening leukopenia and increased ANA were found, and high titres of anti-DNA antibodies, anti-cardiolipin antibodies and rheumatoid factors appeared. Hydralazine was stopped and the patient gradually became asymptomatic. All autoantibodies spontaneously disappeared (over 16 weeks), and the white cell count and spleen size became normal. The patient was found to be a slow acetylator and to have both HLA-DR4 and selective IgA deficiency. Thus, a multifactorial genetic susceptibility to develop drug-induced lupus was brought out in stages first by hydralazine and then by CMV, yet all manifestations and autoantibodies resolved spontaneously, demonstrating the complex interplay of varied environmental factors with a genetic predisposition in the pathogenesis of autoimmunity.
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PMID:Effect of acute cytomegalovirus infection on drug-induced SLE. 783 Nov 73

The role of infectious agents in the pathogenesis of autoimmune diseases has long been a matter of debate. This study investigated the possible role of Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) infections in the pathogenesis of autoimmune diseases by an attempt to demonstrate the presence of the viral genome in the leukocyte of 21 juvenile rheumatoid arthritis (JRA) patients, 20 childhood-onset systemic lupus erythematosus (SLE) patients, and 20 age-matched normals, using polymerase chain reaction (PCR) and DNA probes. The results showed: (1) there was no difference in serum IgG anti-EBV antibody titers among three groups; (2) the EBV PCR-positive rates for JRA and SLE patients and normal controls were 5% (1/21), 10 (2/20), and 0% (0/20), respectively; (3) the HCMV PCR-positive rates for JRA and SLE patients and normal controls were 33% (7/21), 25 (5/20), and 10% (2/20), respectively, and (4) the HCMV-positive rate was 25% for JRA patients with steroid treatment and 33% for those without steroid treatment. It is, therefore, concluded that: (1) the data do not support the participation of EBV and HCMV in the pathogenesis of childhood-onset SLE and JRA; (2) steroid therapy does not increase the frequency of HCMV infection in JRA patients, and (3) immunoincompetence might be one of the major factors contributing to increased susceptibility to HCMV infection in JRA and SLE patients.
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PMID:Detection of Epstein-Barr virus and cytomegalovirus genome in white blood cells from patients with juvenile rheumatoid arthritis and childhood systemic lupus erythematosus. 788 86

The clinicopathologic features of 23 patients with hematophagic histiocytosis (HH) are described. All of them exhibited increased histiocytes associated with hemophagocytosis in the marrow. The patients usually presented with fever, hepatosplenomegaly, lymphadenopathy, and cytopenia. The underlying illnesses were heterogeneous, including non-Hodgkin's lymphoma in 17, systemic lupus erythematosus in one, diabetes mellitus in one, acute myelomonocytic leukemia in one, myelodysplastic syndrome in one, and unknown cause in two. Among 17 non-Hodgkin's lymphoma, 14 were peripheral T-cell lymphoma, two were B-cell lymphoma, and one was an undefined phenotype. Among 14 patients with peripheral T-cell lymphoma, six of the patients had nasal T-cell lymphoma. Five of these 14 patients initially diagnosed as malignant histiocytosis turned out to be T-lineage lymphoma after immunophenotypic studies. Active infections, most of viral origin, were documented in eight patients, including Epstein-Barr virus in three, cytomegalovirus in three, herpes simplex virus in three, Pseudomonas aeruginosa in one, Bacteroides vulgatus in one, and mycoplasma in one. Some of them had mixed virus and bacteria infection. Sixteen (70%) of our patients died of their acute illness within 10 weeks of the diagnosis of HH. In the past, the clinical and histologic differentiation between hematophagic histiocytosis and true histiocytic neoplasm (histiocytic medullary reticulosis/malignant histiocytosis) has proved difficult, but now these can be distinguished with immunohistologic, immunogenetic, and cytogenetic studies, especially in the cases of peripheral T-cell lymphoma with hemophagocytic syndrome.
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PMID:Hematophagic histiocytosis: a clinicopathologic analysis of 23 cases with special reference to the association with peripheral T-cell lymphoma. 792 83

Specific but ubiquitous cytoplasmic proteins are the targets of autoantibodies such as anti-Ro/SS-A, anti-La/SS-B, and anti-calreticulin. These antibodies may be pathogenic in systemic lupus erythematosus (SLE) and Sjogren's syndrome (SS). Tissue localization of the pathogenic process could be best explained by an abnormal expression of these cytoplasmic proteins. Several factors could likely displace the host proteins to the cell surface. This study was designed to use cytomegalovirus (CMV) infected human fibroblasts (MRC-5) as a model, to test whether a viral infection would induce the expression of the human autoantigen(s). Expression of Ro/SS-A, calreticulin, and MHC class I antigens, both in the cytoplasm and on the cell surface, was examined by a fixed cell ELISA, immunofluorescence, and immunoblotting. Infection of fibroblasts with CMV was found to increase the cell surface expression of calreticulin (p = 0.0314), but not the 60KD Ro/SS-A. Cytoplasmic expression of both the autoantigens tested increased following CMV infection. Enhanced expression of class I MHC was detected on the cell surface in response to the virus infection. The expression of the autoantigens and MHC class I polypeptides, as well as the virally induced elevated mitotic rate, diminished after 24 h of infection. Viral infection was found to alter the distribution of host cell proteins, including autoantigens. Cell surface expression of calreticulin could provide a target for circulating autoantibody and contribute to the autoimmune process.
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PMID:Viral induction of the human autoantigen calreticulin. 792 96

The purpose of our pilot study was to evaluate the short-and long-term efficacy of T-lymphocyte depletion in the management of patients with refractory, systemic autoimmune diseases. Nine patients with severe, therapy-resistant autoimmune diseases were subjected to T-cell depletion procedure using polyclonal anti-T-cell antibodies combined with peroral administration of azathioprine and/or cyclosporine. The proband group consisted of 4 patients with systemic lupus erythematosus, 3 with progressive systemic sclerosis, and 2 with rheumatoid arthritis. Administration of polyclonal anti-T-cell antibodies was performed at a single occasion via a central venous catheter during 9-10 days. Immunological analyses of T-cell phenotypes and function and assessment of organ function (kidneys, lungs, bone-marrow) has been performed prospectively in all the patients studied. This treatment resulted in prompt and long-lasting (mean follow-up time: 25.6 months) improvement of autoimmune hemolytic anemia, glomerulonephritis, lung fibrosis, skin and joint involvements in the majority of cases. Adverse effects of this treatment included two episodes of infection (E. coli and Cytomegalovirus) and three cases of serum sickness, and were all easily managed. We suggest that this treatment modality adopted from transplant rejection therapy could be employed in cases of severe autoimmune diseases unresponsive to regular immunosuppressive treatment.
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PMID:Use of anti-thymocyte globulin in the management of refractory systemic autoimmune diseases. 826 27

Cytomegalovirus (CMV) infection is serious complication after clinical renal transplantation. A case of CMV hepatitis and nephropathy after living related renal transplantation was reported. A 32-year-old women with chronic renal failure due to systemic lupus erythematosis received a renal transplant from her mother. On day 35 after operation, she developed high fever with hepatic and renal damage and was diagnosed as CMV infection from clinical course and virological examination. Although the use of anti-CMV high titer gamma globulin with reduction of immunosuppressant therapy could not cure the infection, the administration of Ganciclovir improved hepatic and renal damage without deterioration of renal graft function.
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PMID:[A case report of CMV hepatitis and nephropathy after living related renal transplantation]. 827 70

To investigate the effect of human cytomegalovirus (CMV) infection on the expression of Ro autoantigen in human keratinocytes, the binding of anti-Ro peptide antibodies (anti-60 KD/Ro, anti-52 KD/Ro and anti-calreticulin) to cultured human keratinocytes was detected by fixed cell enzyme-linked immunoassay (ELISA), immunofluorescence, flow cytometry (FACS) analysis and immunoblotting. There was a significant increase in the binding of anti-60 KD/Ro antibody but not anti-52 KD/Ro or anti-calreticulin antibody to the surface of cultured keratinocytes at 24 h after CMV infection compared with uninfected cells, by ELISA and immunofluorescence. Surface binding of anti-60 KD/Ro was found in 71.2% (+/- 5.5%) of CMV-infected cells compared with 26.2% (+/- 4.1%) of untreated cells (P < 0.05) by FACS analysis. Similar observations were made with a human serum which contained anti-60 KD/Ro antibodies. Immunoblotting was used to analyse total cellular 60 KD/Ro antigen expression in keratinocytes infected with CMV or without infection. No increase in the intensity of the 60 KD band was found in extracts of the CMV-infected cells, suggesting that the 60 KD/Ro antigen is redistributed from the cytoplasm to the cell surface after viral infection. The effects of CMV infection on cell cultures were compared with those of ultraviolet B (UVB) irradiation. The 60 KD/Ro, 52 KD/Ro and calreticulin were all induced on the UVB-irradiated cell surface but not significant synergistic effect of UVB and CMV was found. This study provides evidence that CMV infection induced 60 KD/Ro antigen expression on the surface of human keratinocytes, suggesting that CMV may play a role in development of skin lesions in systemic lupus erythematosus (SLE).
Lupus 1995 Oct
PMID:Cytomegalovirus infection induces expression of 60 KD/Ro antigen on human keratinocytes. 856 35

We report an unusual case of cytomegalovirus (CMV) interstitial pneumonitis (IP) occurring in a 51-year-old Japanese woman with systemic lupus erythematosus (SLE). She developed hypoxemia after intensive immunosuppressive therapy with prednisolone and cyclophosphamide. Fine crackles were audible in the lower lungs bilaterally. Chest X-ray and computed tomography confirmed the presence of IP. CMV-antigenemia was confirmed by immunological staining of leukocytes using the peroxidase-labeled monoclonal antibody, HRP-C7. Hypoxemia improved gradually on methylprednisolone pulse therapy and gancyclovir, and CMV-antigen positive leukocytes disappeared from the peripheral blood. Data suggest the importance of CMV as a cause of IP in SLE, and the usefulness of the assay for CMV-antigenemia with C7-HRP for rapid diagnosis.
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PMID:Cytomegalovirus-induced interstitial pneumonitis in a patient with systemic lupus erythematosus. 883 9

The authors describe three cases of systemic lupus erythematosus (SLE) associated with Kikuchi's histiocitic necrotizing lymphadenitis (HNL). Two patients presented a cytomegalovirus infection concomitantly with Kikuchi's lymphadenitis; in one of them the onsets of SLE and HNL were simultaneous. In the third case an inguinal HNL was concomitant with vaginitis of unknown aetiology.
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PMID:Three clinical reports of Kikuchi's lymphadenitis combined with systemic lupus erythematosus. 892 83


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