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)

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

The immunological basis for the production of autoantibodies characteristic of systemic lupus erythematosus (SLE) against a wide range of antigens remains obscure. The specificity of (NZB x NZW)F1 (BWF1) or MRL/Mp-lpr/lpr (MRL/lpr) mouse monoclonal antibodies (mAb) was examined by immunofluorescence, immunoblotting and immunoprecipitation techniques. Using non-synchronized HEp-2 cells as substrate, the murine mAb were classified by indirect immunofluorescence into five groups on the basis of their staining patterns of subcellular components in interphase and mitotic stages of the cell cycle. The nature of the antigens recognized by the murine lupus was assessed by immunoblotting experiments in total, cytoplasmic and nuclear cell extracts from HEp-2 cells. The six antibodies used recognized in total cell extracts a range of polypeptides with apparent molecular weights from 25,000 to 210,000. Three polypeptides of 130,000, 110,000 and 45,000 MW were recognized by all six antibodies in both nuclear and cytoplasmic extracts. Immunoprecipitation of total cellular extracts labelled with [35S]methionine showed almost the same pattern as obtained in the immunoblotting assay. The labelling in vivo of HEp-2 cells with [32P], followed by the immunoprecipitation of the [32P]cell lysate showed that these mAb recognized phosphorylated proteins. The progressive decrease in reactivity of these mAb following treatment with higher concentrations of alkaline phosphatase in both [32P]cell lysate or nitrocellulose membranes indicates that these mAb recognize phosphorylated epitopes.
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PMID:Systemic lupus erythematosus murine monoclonal DNA-binding antibodies recognize cytoplasmic and nuclear phosphorylated antigens that display cell cycle redistribution in HEp-2 cells. 128

Anti-RNA polymerase I (RPI) antibodies in the sera of MRL/Mp-lpr/lpr and MRL/Mp(-)+/+ mice, which develop an autoimmune disease similar to human systemic lupus erythematosus, were screened for reactivity with purified RPI or RPI which had been dephosphorylated. In every case (n = 10), dephosphorylation of RPI resulted in a significant decrease (33-95%) in antibody binding. The anti-RPI antibodies in the sera of the same mice approximately 6 weeks later also reacted better with untreated as compared to dephosphorylated RPI but, in every case, the decrease in antibody (0-30%) caused by dephosphorylation was substantially diminished. That the proportion of anti-RPI antibodies in the sera of MRL mice decreased with progression of lupus-like disease was confirmed by closely monitoring the antibodies over the course of disease. Anti-RPI antibodies produced at the earliest stages appeared to be directed almost exclusively against phosphorylation-dependent determinants since dephosphorylation of RPI essentially abolished antibody binding. Subsequently, the percentage of the total anti-RPI antibodies in the sera of these mice directed towards phosphorylation-independent epitopes increased linearly with time. The importance of phosphorylation-dependent epitopes on RPI for the development of the anti-RPI autoimmune response was supported by the observation that treatment of mice with alkaline phosphatase partially attenuated anti-RPI antibody production.
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PMID:Anti-RNA polymerase I antibodies in the sera of MRL lupus mice at the initial stages of disease are directed primarily against phosphorylation-dependent epitopes. 137 12

A prospective study of systemic lupus erythematosus (SLE) patients under high doses of corticosteroid therapy (greater than 30 mg/day prednisolone) for a five-year period elucidated some risk factors of avascular necrosis of the femoral head (ANFH). A complete survey was performed on 62 patients, of whom nine patients developed ANFH during the period of study. The risk factors in the causation of ANFH were ascertained on the basis of characteristic clinical features of SLE, a typical pattern of laboratory data at the onset of ANFH, and the mode of glucocorticosteroid administration observed from a statistical point of view. The risk factors include stomatitis, drug-induced lupus, lupus erythematosus cell positive rheumatoid arthritis, interstitial pneumonitis, and thrombocytopenic purpura (characteristic clinical features); increased total cholesterol, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, alkaline phosphatase, red blood cell, hemoglobin, and albumin/globulin; advanced renal failure (pattern abnormality of laboratory data); and a rash introduction of high-dose corticosteroid therapy (greater than or equal to 30 mg/day prednisolone) without corticosteroid preloading (mode of administration).
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PMID:Risk factors of avascular necrosis of the femoral head in patients with systemic lupus erythematosus under high-dose corticosteroid therapy. 155 61

We report a case of primary biliary cirrhosis with negative anti-mitochondrial antibody which were anteceded by rheumatoid arthritis. The patient was a 46-year-old female who was admitted due to low grade fever and elevated serum alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (gamma-GTP) levels. She had been diagnosed as having erythema nodosum and rheumatoid arthritis 6 years before. Her family history disclosed that her mother had rheumatoid arthritis and her sister systemic lupus erythematosus. On admission, she had moderately elevated erythrocyte sedimentation rate, and elevated serum ALP, gamma-GTP and IgM levels. Anti-mitochondrial antibody and anti-pyruvate dehydrogenase complex antibody were negative but anti-nuclear antibody was positive. However, the histology of liver showed chronic non-suppurative destructive cholangitis. AMA was always negative and serum ALP and bilirubin levels remained constant during the following two years. The pathogenesis of primary biliary cirrhosis with negative anti-mitochondrial antibody is discussed.
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PMID:[A case of primary biliary cirrhosis with negative anti-mitochondrial antibody anteceded by rheumatoid arthritis]. 155 53

Fifty-four patients with cutaneous tuberculosis, consisting of 23 with lupus vulgaris, 22 with scrofuloderma, and nine with verrucosa cutis, were investigated for cell-mediated immunity, through estimation of peripheral total T lymphocytes (CD3+), CD4+ (helper/inducer), and CD8+ (cytotoxic/suppressor) lymphocytes, by immunohistochemical staining of peripheral blood smears, using specific monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase (APAAP) method. Absolute values of total T lymphocytes (CD3+), and CD4+ and CD8+ subsets, were found to be significantly raised in scrofuloderma, but the percentage values and the CD4+/CD8+ ratio remained unaltered. In tuberculosis verrucosa cutis, only the percentage of the CD8+ subset of T lymphocytes was found to be significantly lowered, and this altered the CD4+/CD8+ ratio. No significant change was observed in the peripheral blood T cells and their subpopulations in patients suffering from lupus vulgaris.
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PMID:Peripheral T lymphocytes and their subsets in cutaneous tuberculosis. 155 33

Among 30 consecutive patients diagnosed with primary biliary cirrhosis (PBC) in Taiwan, 27 were females and the median age of symptom onset was 54.5 years. Most had similar clinical manifestations to those reported in the Western countries, but ascites and oesophageal varices as commonly found at the late stages of cirrhosis of liver were noted in nine patients (30%) and 13 patients (43%) respectively. Only one patient was asymptomatic. Hyperbilirubinaemia was noted in 21 patients (70%) and hypoalbuminaemia in 8 patients (27%). All patients had elevated serum alkaline phosphatase and alanine aminotransferase and 28 (93%) had antimitochondrial antibodies. Ten out of 21 patients (48%) were positive in antinuclear antibodies, of which most were of speckled type. Sixteen out of 18 patients (89%) had elevated serum IgM levels. Interestingly, only one of 26 patients (3.8%) was positive for hepatitis B surface antigen, in contrast to its high prevalence (15%) in the Taiwan population. Special associated diseases, including systemic lupus erythematosus, scleroderma, malignant lymphoma and hepatocellular carcinoma, were each noted in one patient respectively. Eight patients had a history of gallstones before the diagnosis of PBC. The mean follow-up period was 23.6 +/- 19.8 months, and nine patients died during that period. In conclusion, the clinical manifestations of PBC in Taiwan are similar to those in Western countries, but most of our cases were at later stages.
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PMID:Primary biliary cirrhosis in Taiwan. 212 28

When antigens are isolated from staphylococcal protein A immunoprecipitation pellets for analysis by SDS polyacrylamide gel electrophoresis and immunoblotting, severe background problems, due to the presence of antisera and bacterial proteins, can result. We describe a procedure for the analysis of immunoprecipitated systemic lupus erythematosus antigens (e.g., La, Ro, and Sm) which significantly reduces this background while retaining sensitivity with respect to antigen detection. We have adapted a method previously described (MacSween, J.M. and Eastwood, S.L. Methods Enzymol. 1981; 73:459-471) in which lithium diiodosalicylate is used to separate the immunoprecipitated antigen from a covalent antibody-staphylococcal protein A complex. In addition, a modified series of immunoblot incubations was employed, in which antigenic proteins were identified by incubating blots with the antiserum used for the original immunoprecipitation (e.g., La) followed by protein A-biotin and avidin-alkaline phosphatase. Overall, the procedure is straight-forward and may be applicable to other immunoblot systems.
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PMID:Detection of immunoprecipitated systemic lupus erythematosus antigens by immunoblot analysis. 228 92

Ninety-nine sera from patients with different rheumatic diseases (systemic lupus erythematosus, rheumatoid arthritis, progressive systemic sclerosis, and mixed and unidifferentiated connective tissue disease) were applied to a newly developed isoelectric focusing (IEF) immunoblot system for the demonstration of antinuclear antibodies. Nucleoproteins were separated according to their isoelectric points (pI) and immobilized onto nitrocellulose, and binding of serum antibodies was determined by an alkaline phosphatase labelled second antibody. 89.8% of all sera positive in indirect immunofluorescence assays with Hep 2 as substrate showed positive reactivity in IEF immunoblot. Furthermore, 88% of patients' sera negative on Hep 2 cells gave a positive reaction in IEF immunoblot. The predominant antibody banding pattern observed showed parallel bands in the acidic as well as the neutral pH ranges. Antibody specificities found in the IEF immunoblot system turned out to be patient-specific, but no marker antibody for a discrete disease entity was obtained. Even when monoclonal antibodies or WHO standard sera were applied to nuclear antigen they exhibited heterogeneity in their binding pattern. Bands with the same pI were observed using sera from patients with different rheumatic disease entities. Immunodeletion experiments suggest the recognition of identical antigenic proteins by the different patients' sera.
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PMID:Patient-specific heterogeneity of antinuclear antibodies as revealed by an isoelectric focusing immunoblot system. 244 56

Excretion patterns of kidney related urinary proteins such as lysosomal beta-N-acetylglucosaminidase (beta NAG), brush-border Ala-(Leu-Gly)-aminopeptidase (AAP), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (AP) as well as of IgG, albumin, and alpha-1-microglobulin, were assessed in patients with chronic glomerulonephritis (n = 53), pyelonephritis (n = 27), systemic lupus erythematodes (n = 5), and patients with essential arterial hypertension (n = 18). Excretion of tubular marker enzymes and serumproteins (related to urine creatinine concentration = protein creatinine index) in spontaneously voided second morning urine was significantly higher as compared to the controls (n = 2). Alpha-1-microglobulin was markedly elevated in both pyelonephritis and glomerulonephritis indicating disturbance in tubulointerstitial handling of microglobulins also in cases with primary glomerulopathy. Rise of albumin, IgG, and alpha-1-microglobulin as well as of tubular kidney markers AAP, AP, GGT, and beta NAG in cases with arterial hypertension without preexisting nephropathy support the hypothesis of a defect in charge and size permselectivity in these patients which is probably due to an increase in glomerular capillary perfusion pressure and hyperfiltration.
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PMID:Kidney- and serum derived proteins in urine of patients suffering from renal diseases or arterial hypertension. 247 9


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