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 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

A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cis-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both 'soluble' and high-molecular-weight membrane particles (vacuolar blebs, greater than 10(6) dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular 'histuria' which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.
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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76

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

In the population of peripheral blood lymphocytes from systemic lupus erythematosus (SLE) patients activity of gamma-glutamyl transpeptidase (GGTP) was lower than in healthy individuals. However, when erythrocyte-rosette forming cells (E-RFC) and non erythrocyte-rosette forming cells (non E-RFC) were separated by E-RFC method it was found that in SLE patients the activity of GGTP was increased in E-RFC and decreased in the population of non E-RFC. The altered activity of GGTP may be due to impaired surface membranes and changes in activation of these cells in SLE patients.
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PMID:Activity of gamma-glutamyl transpeptidase in peripheral blood lymphocytes in systemic lupus erythematosus. 612 65

The aim of this work is to evaluate the concentration of serum bile acids (SBA) as an index of impaired liver function in systemic lupus erythematosus (SLE) patients versus usual laboratory tests of hepato-biliary system diseases. In patients with SLE the mean fasting SBA concentration was 9.6 +/- 1.4 mumol/L; in normal subjects the concentration was 2.9 +/- 0.6 mumol/L (P less than 0.01). In patients with SLE, mean gamma-glutamyl transpeptidase (GGTP) concentration was 31.5 +/- 5.9 mU/ml versus 10.05 +/- 1.1 mU/ml in controls (P less than 0.01). The bromsulphalein (BSP) excretion test, 45 minutes after injection, was 6.8 +/- 1% in SLE patients versus 2.8 +/- 0.4% in controls (P less than 0.02). No significant difference was found between these two groups of subjects with respect to leucine aminopeptidase (LAP), alkaline phosphatase (AlPh), glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), bilirubin serum rates. SBA rate was abnormal in 50% of the SLE patients; GGTP rate and the BSP excretion test were abnormal in 38% and 27% respectively. Our findings show the presence of an actual liver impairment in SLE patients, significantly demonstrated by fasting SBA concentration, GGTP rate and BSP excretion test. Other liver function tests are less useful in evaluating hepatic damage in SLE.
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PMID:Concentration of serum bile acids as an index of hepatic damage in systemic lupus erythematosus. 646 63

A 69-year-old Japanese female was admitted because of general fatigue. Laboratory data showed elevation of serum total bilirubin, transaminase, gamma-glutamyl transpeptidase, and creatinine levels. An immunological study revealed hypergammaglobulinemia, low titer of complement, and high titers of antinuclear antibody, anti-DNA antibody, and circulating immune complexes. Antibodies to parainfluenza virus 3 were positive. Histology of the liver disclosed numerous giant cell hepatocyte transformations with the lobular architecture being slightly distorted by portal inflammation and fibrosis. These findings led us to make a diagnosis of giant cell hepatitis associated with systemic lupus erythematosus. Prednisolone was effective in improving the anemia and the serum immunoglobulin, immune complex, and antinuclear antibody levels. The addition of cyclosporine to the initial corticosteroid therapy was also beneficial in decreasing the transaminase level and in improving liver histology. The patient died of acute pneumonitis and renal failure on the 166th day after admission. Parainfluenza virus 3 and autoimmune mechanisms were thus considered to be the causes of the giant cell hepatitis.
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PMID:Post-infantile giant cell hepatitis in an elderly female patient with systemic lupus erythematosus. 806 7

The authors present a case of Kikuchi's disease associated with systemic lupus erythematosus (SLE) and autoimmune-like hepatitis. Kikuchi's disease, or histiocytic necrotizing lymphadenitis is occasionally associated with SLE and mildly elevated aminotransferases. A 17-year old woman presented with fever, arthritis and bilateral cervical adenopathy. Histopathological and immunohistochemical examinations of an excised lymph node showed evidence of Kikuchi disease. An elevation of hepatocytic enzymes (aminotransferases and gamma-glutamyl transpeptidase) associated with smooth muscle antibodies in a titer of 1/320 was present. Clinical symptoms and laboratory tests improved after "pulse" corticotherapy. The association described has not been described in the literature, but is considered possible due to the immune pathogenicity of the 3 simultaneous diseases. Kikuchi-Fujimoto's disease, or histiocytic necrotizing lymphadenitis (HNL), is a rare condition first described in 1972 independently by Kikuchi and Fujimoto. HNL is rarely associated with systemic lupus erythematosus (SLE). It is a benign illness characterized by fever and cervical adenopathy and has a self-limiting course.
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PMID:Kikuchi's disease associated with systemic lupus erythematosus and autoimmune-like hepatitis. 1552 14