Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the prevalence of anti-HCV in 585 sera from various individuals, using enzyme immunoassay (EIA, Abbott Lab.). Anti-HCV was detected in 16 (10.7%) out of the 150 patients with HBsAg positive liver diseases diagnosed by liver biopsy and they consisted of none out of 10 acute viral hepatitis, 3 out of 15 chronic persistent hepatitis, 4 out of 50 chronic active hepatitis, 2 out of 32 liver cirrhosis, and 7 out of 43 hepatocellular carcinoma. Anti-HCV was detected in 43 (45.3%) out of 95 patients with HBsAg negative liver diseases diagnosed by liver biopsy and they consisted of 5 out of 8 acute viral hepatitis, 2 out of 10 chronic persistent hepatitis, 17 out of 30 chronic active hepatitis, 4 out of 15 liver cirrhosis, and 15 out of 32 hepatocellular carcinoma. Anti-HCV was detected in 22 (38.6%) out of 57 hemodialysis patients, in 3 (6.7%) out of 45 kidney transplants, in 2 (11.1%) out of 18 fatty liver diagnosed by liver biopsy, in 2 (1.3%) out of 150 healthy blood donors, in none out of 40 healthy volunteers, in 6 (31.6%) out of 19 rheumatoid arthritis and in 6 (54.5%) out of 11 systemic lupus erythematosis cases. There were familial clusters of chronic liver diseases in 4.7% of patients with HBsAg negative/anti-HCV positive chronic liver diseases, while in 19.4% of patients with HBsAg positive/anti-HCV negative liver diseases. Incidence of anti-HCV within patients with HBsAg positive liver diseases was higher in HBsAg negative patients than in HBsAg positive patients (17.6% and 10.3%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seroprevalence of antibody against hepatitis C virus (anti-HCV) in various groups of individuals in Korea. 190 58

A new microparticle enzyme immunoassay (MEIA), the Cytomegalovirus (CMV) Immunoglobulin M (IgM) test, was developed on the Abbott AxSYM analyzer. This test uses recombinant CMV antigens derived from portions of four structural and nonstructural proteins of CMV: pUL32 (pp150), pUL44 (pp52), pUL83 (pp65), and pUL80a (pp38). A total of 1, 608 specimens from random volunteer blood donors (n = 300), pregnant women (n = 1,118), transplant recipients (n = 6), and patients with various clinical conditions and disease states (n = 184) were tested during development and evaluation of this new assay. In a preliminary clinical evaluation we tested specimens collected prospectively from pregnant women (n = 799) and selected CMV IgM-positive archived specimens from pregnant women (n = 39). The results from the new CMV IgM immunoassay were compared to the results of a consensus interpretation of the results obtained with three commercial CMV IgM immunoassays. The results for specimens with discordant results were resolved by a CMV IgM immunoblot assay. The relative sensitivity, specificity, and agreement for the AxSYM CMV IgM assay were 94.29, 96.28, and 96.19%, respectively, and the resolved sensitivity, specificity, and agreement were 95.83, 97.47, and 97.37%, respectively. We also tested serial specimens from women who experienced seroconversion or a recent CMV infection during gestation (n = 17) and potentially cross-reactive specimens negative for CMV IgM antibody by the consensus tests (n = 184). The AxSYM CMV IgM assay was very sensitive for the detection of CMV IgM during primary CMV infection, as shown by the detection of CMV IgM at the same time as or just prior to the detection of CMV IgG. Specimens from individuals with lupus (n = 16) or parvovirus B19 infection (n = 6) or specimens containing hyper IgM (n = 9), hyper IgG (n = 8), or rheumatoid factor (n = 55) did not cross-react with the AxSYM assay. One specimen each from individuals infected with Epstein-Barr virus (n = 26), measles virus (n = 10), herpes simplex virus (n = 12), or varicella-zoster virus (n = 13) infection, one specimen from an influenza vaccinee (n = 14), and one specimen containing antinuclear antibody cross-reacted with the assay. The overall rate of cross-reactivity of the specimens with the assay was 3.3% (6 of 184). The AxSYM CMV IgM assay is a sensitive and specific assay for the detection of CMV-specific IgM.
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PMID:Development and clinical evaluation of a recombinant-antigen-based cytomegalovirus immunoglobulin M automated immunoassay using the Abbott AxSYM analyzer. 1074 29

Abetimus [Abetimus sodium, LJP 394, Rentol, Riquent] is a synthetic Toleragen molecule consisting of four double-stranded oligodeoxyribonucleotides attached to nonimmunogenic polyethylene glycol, a proprietary carrier platform. It was originated by La Jolla Pharmaceuticals. Abetimus is an immunomodulating agent that induces tolerance in B cells directed against double-stranded DNA (dsDNA). It does this by cross-linking surface antibodies. These antibodies are thought to be responsible for lupus nephritis, a chronic kidney disease that develops in patients with systemic lupus erythematosus. A phase III trial of abetimus was completed in December 2002. La Jolla Pharmaceuticals previously established two licensing agreements for abetimus, which have since been terminated. One of the agreements was with Leo Pharmaceutical Products of Denmark. The company was licensed rights to abetimus covering Europe and the Middle East. The other agreement was with Abbott Laboratories. Abbott returned all rights to abetimus to La Jolla Pharmaceuticals in September 1999 based on the results of an analysis of the phase II/III trial of abetimus in lupus patients with a history of renal disease. A phase III trial, named "PEARL" (Program Enabling Antibody Reduction in Lupus), has been conducted in the US in patients with lupus nephritis. It enrolled 317 patients with a history of lupus who were treated with a weekly dose of abetimus 100mg or placebo. The trial was completed in December 2002 and preliminary results were reported in February 2003. PEARL was designed to determine whether abetimus can significantly delay renal flares and delay the need for treatment with high-dose corticosteroids and/or cyclophosphamide in patients with high affinity IgG antibodies to the double-stranded oligonucleotide epitope in abetimus. Patients with high-affinity antibodies, were selected using a surface plasmon resonance (SPR)-based pharmacoproteonomics assay provided by Biacor International. Following the completion of PEARL in December 2002, La Jolla Pharmaceuticals initiated an on-going, open-label, follow-on trial. All patients who had completed PEARL were eligible to enroll and receive weekly treatment with abetimus. However, in April 2003, La Jolla Pharmaceuticals announced that it was closing this trial, which was designed to collect additional long-term safety data, to conserve resources for the continued development of the drug. Previously, La Jolla Pharmaceuticals and Abbott initiated a phase II/III trial of abetimus in more than 200 patients with lupus nephritis. However, this trial was discontinued in May 1999 because the primary end-point (time to renal flare) was much shorter than expected. After the trial was halted, further analysis of trial data using a new blood test to measure the strength of the binding between abetimus and a patient's antibodies to dsDNA was conducted. The additional analysis showed that the number of renal flares in the high-affinity patients (responders) treated with abetimus was less than half of the number of renal flares in high-affinity patients treated with placebo. Responders also showed a significant reduction in the use of high-dose corticosteroids and cyclophosphamide. Being able to screen patients to identify those likely to respond to therapy lead La Jolla Pharmaceuticals to initiate PEARL after Abbott's withdrawal from the drug. It is believed that screening patients will help increase the cost-effectiveness of clinical development. In September 2000, the US FDA granted orphan drug status for abetimus in the treatment of lupus nephritis. The European Commission followed suit in November 2001, granting orphan drug status for abetimus in the EU.
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PMID:Abetimus: Abetimus sodium, LJP 394. 1274 59

The treatment of rheumatoid arthritis (RA) has changed dramatically over the past 15 years with the realisation that earlier, aggressive therapy limits progression. There is evidence that biological response modifiers (BRMs), which target specific cytokines such as TNF-alpha and IL-1, are more effective than traditional disease-modifying antirheumatic drugs (DMARDs), especially in combination with methotrexate. Four therapies are approved for use in RA; three target TNF-alpha (etanercept [Enbrel, Amgen Inc.], infliximab [Remicade, Centocor Inc.], and adalimumab [Humira, Abbott]), and one targets IL-1 (anakinra [Kineret, Amgen Inc.]). It is clear from both the clinical trials and postmarketing reports that all four agents have a different safety profile compared with traditional DMARDs. There are several areas of concern with the use of the BRMs, which include serious and opportunistic infections, malignancy/lymphoma, congestive heart failure, demyelination, injection/infusion reactions, development of autoantibodies and lupus-like disease. It is important to be fully aware of the safety profile and differences between BRMs in order to use them appropriately.
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PMID:Considerations with the use of biological therapy in the treatment of rheumatoid arthritis. 1533 95

Homocysteine (Hcy), a sulfur-containing amino acid, is eliminated through B vitamins-dependent pathways. Hyperhomocysteinemia has been found to be an independent risk factor for atherosclerotic cardiovascular, cerebrovascular, and peripheral vascular diseases. Recently, psoriasis, lupus, and rheumatoid arthritis were reported to be associated with hyperhomocysteinemia. This study was aimed to evaluate the changes of plasma Hcy level before and after sulfasalazine and MTX therapy in patients with ankylosing spondylitis (AS). One hundred and two patients with AS and ten normal controls were enrolled in the cross-sectional case-control study. Fasting plasma Hcy levels were determined by ELISA kits (IMX, Abbott). Hcy levels were compared to their Bath AS disease activity index (BASDAI) and the usage of sulfasalazine and/or MTX. Active disease was defined by BASDAI as more than 3 in a 10-cm scale with ESR >20 mm/h. For those patients with plasma Hcy >or=15 micromol/l, a perspective trial of daily supplement of vitamin B-12 0.5 mg, B-6 50 mg, and folic acid 5 mg for 2 weeks were also tested for the efficacy. Plasma Hcy level increased significantly in AS patients under sulfasalazine (10.4+/-3.8 micromol/l, p<0.05), MTX (11.9+/-4.7, p<0.05) and sulfasalazine/MTX combination treatment (11.2+/-2.6, p<0.05) compared with normal controls (8.6+/-1.2 micromol/l) and AS patients without DMARD(9.4+/- 2.6 micromol/l). No correlation between disease activity and plasma Hcy level was found. Daily supplement of vitamin B-12 0.5 mg, B-6 50 mg, and folic acid 5 mg can lower Hcy level in 2 weeks (32.3+/-24.0 vs 15.6+/-11.1 micromol/l, p=0.007). Plasma homocysteine level did significantly increase in AS patients under sulfasalazine or MTX treatment. B-vitamins should be considered as a routine supplementation for patients who underwent sulfasalazine and/or MTX treatment. Further longitudinal studies are required to confirm the conclusions.
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PMID:Plasma homocysteine status in patients with ankylosing spondylitis. 1702 18

We describe a patient at high surgical risk who was successfully treated with a MitraClip (Abbott Vascular, Menlo Park, CA) without transmitral gradient. She received corticosteroid therapy for systemic lupus erythematosus, and progressive mitral stenosis developed late after MitraClip implantation. It gradually increased and reached 23 mm Hg at 28 months after the procedure; during the same period, her dose of prednisone had to be increased owing to lupus flare. Systemic inflammatory disease has the potential to result in mitral valve inflammation and fibrosis, ultimately causing thickening of the tissue bridge and worsening of the mitral valve obstruction. Preprocedural counseling regarding durability may help in this population.
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PMID:Progressive Mitral Stenosis After MitraClip Implantation in a Patient With Systemic Inflammatory Disease. 2744 66