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)

Two groups of 22 patients suffering from either systemic lupus erythematosus (SLE) or infectious mononucleosis (IM) were checked for Epstein-Barr virus capsid antigen antibody (EB-VCA) production. The average significant antibody levels as well as the frequency of their occurrence were clearly higher in SLE than in IM patients.
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PMID:Enhancement of Epstein-Barr virus antibody production in systemic lupus erythematosus patients. 3 42

The anti-complement immunofluorescence (ACIF) method was used to demonstrate EBNA in B lymphocytes separated from the peripheral blood of patients with infectious mononucleosis (IM) or other diseases. In the acute phase of IM of Epstein-Barr virus (EBV) origin, 0.5--1% of the B lymphocytes proved to be positive in 6 of the 8 patients tested. In two of the positive cases the test was repeated 20 and 26 days, respectively, after clinical symptoms had appeared; the result was negative in both cases. No EBNA-positive cells were found in the peripheral blood of 17 patients with Hodgkin disease, 3 with systemic lupus erythematosus and 2 with lymphosarcoma. It is supposed that EBNA-positive cells appear in detectable amount exclusively in the acute phase of EBV infection.
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PMID:Cells containing Epstein--Barr nuclear antigen (EBNA) in peripheral blood. 22 32

Immune complexes were detected in 51 sera from patients with a variety of immunological diseases; 14 systemic lupus erythematosus (SLE); 14 infectious mononucleosis (IM); 12 rheumatoid arthritis (RA) and 11 subacute bacterial endocarditis (SBE). Three methods were used to detect complexes: the fluid--phase Clq binding assay (Clq.BA); the solid--phaseClq binding assay (Clq.SP) and the Raji cell radio-immunoassay (RIA). Modification of the Clq.SP and the Raji cell RIA by use of monospecific antisera to immunoglobulins G, A and M enabled the class of antibody in the immune complexes to be determined. Antibodies of all three classes were found in each disease, the predominant ones being IgG and IgM in SLE and SBE, IgM and IgA in RA and IgM in IM.
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PMID:The detection of immune complexes of different immunoglobulin class. 29 21

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2

A 41-year--old woman with thrombotic thrombocytopenic purpura (TTP) was treated with prednisone and splenectomy with complete recovery from her illness. Analysis of the patient's platelets for immunoglobulins showed abnormally elevated levels in the range of those seen in thrombocytopenic patients with systemic lupus erythematosus, immune vasculitis, and infectious mononucleosis. This finding is consistent with the concept that the immune system may play a role in the pathogenesis of TTP.
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PMID:Elevated platelet-associated IgG in thrombotic thrombocytopenic purpura. 57 56

Pleural tissues from a group of 36 consecutive patients comprised of 15 malignancies, 3 tuberculous, 2 rheumatoid arthritis, 3 procainamide-induced systemic lupus erythematosus (SLE) syndromes, 1 infectious mononucleosis, and 12 nonspecific pleural effusions undergoing needle biopsy were studied by immunofluorescent techniques for antibody deposition. Specific nuclear fluorescence was detected only in procainamide-induced SLE and was characterized by in vivo staining with either IgG, IgM, and in one case, also C3. C1q could not be detected. Two other patients who had antinuclear antibodies (ANA) in their peripheral blood did not have detectable in vivo antinuclear staining in their pleural tissue. The presence of in vivo fixation of ANA in the pleura may be of etiologic and diagnostic significance in procainamide-induced SLE syndrome.
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PMID:Antibody deposition in the pleura: a finding in drug-induced lupus. 65 31

A 37 year old woman with extravascular hemolytic anemia had a positive Monospot test associated with positive antiglobulin and anticomplement Coombs' tests, cold agglutinins and warm autoantibodies. IgG-kappa (k) antibodies, which reacted with all panel red cells at 37 degrees C, were eluted from her circulating red cells. However, neither immunoglobulins nor C3 was detected after her serum was adsorbed with heterologous red cell stroma at 37 degrees C and eluted at the same temperature in glycine buffer. In contrast, IgM-kappa and IgM-lambda (lambda), IgG-3-kappa, IgG4-lambda, IgA-lambda and C3 were eluted at 37 degrees C from heterologous red cell stroma after adsorption with her serum at 0 degrees C. Thus, antibodies of several types, which were present in the patient's serum, reacted optimally with red cell antigens at low temperature. Cold-reactive IgG3-kappa antibodies, which also capable of interacting with red cells at 37 degrees C, probably accounted for the IgG-kappa antibodies eluted from the patient's circulating red cells. The patient's serum C4 titers were decreased, with low normal to moderately depressed C3 and low normal C5, indicating that the anti-red cell IgM and/or IgG3-kappa antibodies probably fixed complement. A localized cold stress test resulted in a transient increase in plasma hemoglobin and a decrease in serum C3 titer. These findings, and the beneficial clinical response obtained with small doses of prednisone, suggest that both the cold-reactive antibodies and the IgG-kappa on circulating red cells were pathophysiologically significant. This is the first report of a patient with multiple red cell autoantibodies in whom serum complement component titers were determined in conjunction with characterization of the anti-red cell immunoglobulins. Subclinical infectious mononucleosis may have preceded the prolonged hemolytic episode. Clinical evidence of systemic lupus erythematosus has not appeared.
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PMID:Hemolytic anemia associated with multiple autoantibodies and low serum complement. 107 54

The DNA bentonite flocculation test was used to investigate the presence of antibody to DNA. In most sera a prozone-like phenomenon was found, caused by a non-specific inhibition of serum. Anti-DNA was found with extreme frequency in patients with SLE, chronic liver disease, acute hepatitis, infectious mononucleosis, and blood donors over the age of 60, but was found rarely or not at all in patients with some other disease or blood donors under 60 years of age.
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PMID:Anti-DNA Investigated the DNA bentonite flocculation technique. 107 89

1. Antimitochondrial antibody titers of 1:160 are practically diagnostic of primary biliary cirrhosis [71]. Serum antimitochondrial antibody titers of less than 1:16 are seen in 10% of cases of primary biliary cirrhosis. The antimitochondrial antibodies are usually absent in jaundiced patients with extrahepatic obstruction, drug sensitivity, and viral hepatitis. 2. Anti-smooth-muscle antibodies are noted in the various autoimmune liver disorders, viral hepatitis, infectious mononucleosis, malignancy, and intrinsic bronchial asthma. The smooth muscle antibody test helps in the differential diagnosis of lupoid hepatitis vs. systemic lupus erythematosus. The anti-smooth-muscle antibodies are usually absent in systemic lupus erythematosus. 3. The antinuclear antibody is frequently positive in the autoimmune liver diseases. In cases of chronic aggressive hepatitis associated with a high titer of antinuclear antibody the prognosis is usually grave. 4. The presence of antimicrosomal liver and kidney antibody is indicative of chronic aggressive liver disease, which is different from the classic lupoid hepatitis [95, 97]. 5. Hepatitis-B-antigen assay should be performed routinely to exclude viral hepatitis, type B. Heterophile antibody tests should done when the possibility of infectious mononucleosis must be considered. 6. Serum immunoglobulin determinations are of secondary importance in the laboratory diagnosis of autoimmune liver disorders. There is usually a polyclonal elevation of the major immunoglobulin in most chronic parenchymal liver diseases[48].
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PMID:Laboratory tests for diagnosis of autoimmune diseases. 110 71

Anticardiolipin antibodies (aCL) purified from patients with autoimmune disease have recently been shown to interact with a phospholipid-binding plasma protein, beta 2-glycoprotein I (beta 2-GPI). The aim of this study was to determine whether aCL purified from patients with infection also interact with beta 2-GPI. aCL purified from 23 patients with malaria, infectious mononucleosis, tuberculosis, hepatitis A or syphilis did not require the presence of beta 2-GPI to bind cardiolipin (CL). In contrast, aCL were purified from 11 out of 12 patients with autoimmune disease that bound CL only in the presence of beta 2-GPI. Thrombotic complications appear to be associated with aCL occurring in autoimmune disease but not with aCL associated with infections. We postulate that this increased risk of thrombosis in the autoimmune group may be due to the presence of aCL that bind CL in association with beta 2-GPI, a plasma protein with anticoagulant activity.
Lupus 1992 Feb
PMID:A phospholipid-beta 2-glycoprotein I complex is an antigen for anticardiolipin antibodies occurring in autoimmune disease but not with infection. 130 67


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