Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
22,386 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

Selected adverse reactions of penicillamine encountered in our clinic since 1975 are described. They include: proteinuria (26 cases), lupus erythematosus (six cases), myasthenia gravis (two cases), pemphigus (three cases), obliterative bronchiolitis (two cases) and obstructive jaundice (one case).
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PMID:Selected adverse reactions of D-penicillamine. 672 28

Patients with systemic lupus erythematosus (SLE) have a 25-50% chance of developing abnormal liver tests in their lifetime. This percentage does not include unconjugated hyperbilirubinaemia due to haemolysis associated with SLE, or elevated aspartate-aminotransferase caused by SLE-associated myositis. The most common cause is drug-induced hepatitis, while mild, predominantly lobular-but sometimes also portal and periportal-hepatitis reflecting SLE activity is another possibility. Other liver disease in SLE can be related to thrombotic events, whether or not associated with the lupus anticoagulant, including Budd-Chiari syndrome and veno-occlusive disease. Other liver abnormalities have been more or less frequently associated with SLE, such as nodular regenerative hyperplasia, perihepatitis, and hepatic or splenic rupture. Also viral hepatitis, obstructive jaundice, autoimmune hepatitis, primary biliary cirrhosis, granulomatous hepatitis, cryptococcus infection of the liver, chronic hepatitis with IgA or IgD deficiency, porphyria or idiopathic portal hypertension co-existing with SLE have been described.
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PMID:The spectrum of liver disease in systemic lupus erythematosus. 871 47