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)

Citrated samples from 100 patients on i.v. heparin and 20 normal patients were tested with three batches each of three activated partial thromboplastin time (APTT) reagents: Thrombosil I (Ortho); Automated APTT (Organon Teknika) and Actin FSL (Baxter). The ratio of APTT over the geometric mean normal APTT for each heparinized sample was calculated. One batch of reagent arbitrarily chosen as a reference gave the ratios APTRREF (y). The remaining reagents to be standardized against the reference system gave the ratios APTRTEST (x). The best correlation between systems was given by log vs log x. Standard curves were prepared from the APTT ratios of the 20 normal patients and 65 of the heparinized samples. On plotting log APTRTEST vs log APTRREF the y intercept was close to zero so x was expressed in terms of y using; log x = HSI. log y, where HSI (Heparin Sensitivity Index) = slope. The APTRTEST results of the remaining 35 heparinized samples were transformed using; APTRTRANS = (APTRTEST)HSI.APTRTRANS was then compared to APTRREF to determine whether the transformation brought the results closer to the reference. We conclude that although some improvement was found by using the transform, it was not possible to mathematically relate APTT results due to a high degree of variation between results using different reagents. A standard APTT reagent for the monitoring of heparin therapy is recommended. A separate APTT reagent may be required for the screening of factor deficiencies and lupus anticoagulants.
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PMID:An attempt to standardize APTT reagents used to monitor heparin therapy. 133 84

The Ortho activated partial thromboplastin time (APTT) reagent, Thrombosil 1 (TS), was compared to the General Diagnostics automated APTT reagent (GD). TS produced more precise results over a 38-day period of testing a normal control plasma, indicating that the upper limit of the normal range could be more precisely set with TS. This normal range was better represented if the normal values with both reagents were logarithmically transformed before calculating the mean +/- 2 SD. TS was more sensitive to plasma which had been heparinized in vitro. This was also demonstrated in vivo by the testing of 100 plasmas from heparinized patients. On testing of in-vitro dilutions of normal plasma with factor-deficient plasmas, TS was more sensitive to decreasing levels of factors VIII, IX and XI but less sensitive to decreasing factor XII. This was demonstrable in vivo in 71% of cases with plasmas from factor-deficient patients. GD was more sensitive to the lupus anticoagulant in most cases.
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PMID:A comparison of two APTT reagents which use silica activators. 255 32

An anti-C1q capture method kit (C1q-immunoglobulin G [IgG]) (Ortho Diagnostics, Inc., Raritan, N.J.) for measuring circulating immune complexes (CIC) was evaluated. The kit showed poor diagnostic sensitivity (P less than 0.005) for identifying CIC in patients with systemic lupus, rheumatoid arthritis, and bacterial endocarditis, as compared with polyethylene glycol-IgG and Raji cell tests (12, 24, and 24 positive, respectively, of 31 patients). Of the patients who were positive with the C1q-IgG test, 25% showed discrepancies when their results were compared with the polyethylene glycol-IgG and C1q-binding test results. Gel filtration chromatography of two of these discrepant sera showed the only peak of C1q-IgG activity to be associated with monomeric IgG (molecular weight, less than 200,000). We concluded that the kit method may be measuring substances other than CIC in some sera, because molecules of C1q attached to IgG should exhibit a molecular weight of greater than 500,000.
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PMID:Evaluation of anti-C1q capture assay for detecting circulating immune complexes and comparison with polyethylene glycol-immunoglobulin G, C1q-binding, and Raji cell methods. 295 87

ARACHnase (Hemostasis Diagnostics International Co., Denver, CO) is a normal plasma that contains a venom extract from the brown recluse spider, Loxosceles reclusa, which mimics the presence of a lupus anticoagulant (LA). Seven activated partial thromboplastin time (APTT) reagents were used for platelet neutralization procedure (PNP) testing with ARACHnase: Automated APTT (Organon-Teknika, Durham, NC); Thrombofax and Thrombosil (Ortho, Raritan, NJ); Actin and Actin FSL (Dade, Aguado, PR); and Thromboscreen-Kontact and Thromboscreen-APTT LS (Pacific-Hemostasis, Ventura, CA). ARACHnase consistently displayed a positive PNP result of greater than 5 seconds correction of the initial baseline APTT. Thus, ARACHnase may provide a positive control for LA testing, regardless of the choice of APTT reagent and activator/phospholipid combination.
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PMID:ARACHnase. An evaluation of a positive control for platelet neutralization procedure testing with seven commercial activated partial thromboplastin time reagents. 824 97

Tissue thromboplastin inhibition test (TTI) is a highly sensitive but poorly specific test used in the diagnosis of lupus anticoagulant (LA) which is usually requested for patient with inflammatory status. Therefore, we investigated the influence of fibrinogen level on TTI using Recombiplastin (Ortho), Neoplastine (Diagnostica Stago) and Thromborel S (Behring), in a group of 84 patients with fibrinogen levels ranging from 1.6 to 11.8 g/l. The highly significant (p < 0.0001) positive correlation observed between fibrinogen level and TTI with the 3 thromboplastins allowed the calculation of a new TTI value corrected for fibrinogen level named TTIfg. TTIfg was defined as TTI - ("S" x fibrinogen level) where "S" was the slope of the regression line defining TTI as a function of fibrinogen values. In the group studied, the low TTI specificity, respectively 64%, 67% and 75% with Recombiplastin, Neoplastine and Thromborel S, was greatly improved to respectively 95%, 93% and 95% when results were expressed as TTIfg. TTIfg remained as sensitive as TTI when evaluated in a group of 38 patients with previously diagnosed LA.
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PMID:The tissue thromboplastin inhibition test in the detection of lupus anticoagulants: importance of a correction factor eliminating the influence of fibrinogen level. 881 53

Patients with antiphospholipid antibody syndrome (APS) experience a higher rate of recurrence of thrombosis than the general population of patients with thrombotic disease. Based on a retrospective analysis, it has been suggested that patients with APS should be kept on prolonged anticoagulation aiming at international normalised ratio (INR) values > 3.0. To evaluate whether the requirement for more intense anticoagulation depends on the variable sensitivity of thromboplastin reagents to the influence of aPLA, we monitored oral anticoagulant treatment in 10 patients with persistent lupus anticoagulants (LA) and venous thromboembolic disease using two thromboplastin reagents: Pro-IL-Complex (Instrumentation Laboratory, combined) and Recombiplastin (Ortho, recombinant). Acenocoumarol dosage was always assigned based on INR values obtained with the combined thromboplastin using diluted (1:20) test plasma, aiming at an INR interval of 2.0 to 3.0. Single INR determinations with both reagents were obtained throughout the study period for 110 aPLA-free patients on stable oral anticoagulation. Using the manufacturer's instrument-certified international sensitivity index (ISI) values, INR obtained with the recombinant reagent were significantly higher than those obtained with the combined reagent in LA-positive patients, but they were lower in LA-negative patients. After correction for local ISI calibration in LA-negative patients, INR values of 3.1 and 4.6 with Recombiplastin corresponded, respectively, to INR values of 2.0 and 3.0 with Pro-IL-Complex. These results indicate the thromboplastin-dependency of INR values in patients with LA, thereby questioning the validity of the INR system for the monitoring of oral anticoagulant treatment in these patients.
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PMID:Potential failure of the International Normalized Ratio (INR) System in the monitoring of oral anticoagulation in patients with lupus anticoagulants. 895 52

Nasal septal ulceration can have multiple etiologies. Determining the exact cause depends on who the consulting specialist is, who could either be the ENT surgeon or the dermatologist. The common causes are infections (tuberculosis, leprosy, leishmaniasis), vasculitis (Wegener's granulomatosis and Churg-Strauss syndrome), and lupus erythematosus. Traumatic causes and malignancy can also be seen in tertiary referral centers. The diagnosis often requires thorough investigations and multiple tissue specimens from various sites, and in chronic cases, a suspicion of lymphoma should be considered. Apart from disease-specific therapy, a multidisciplinary approach is required in most cases to tackle the cosmetic disfigurement.
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PMID:Nasal septal ulceration. 2544 76

Suicidal NETosis differs from other mechanisms of cell death by the release of a lattice, composed of DNA associated with proteins citrullinated by protein-arginine deiminase 4, from neutrophils. These 'NETs' are composed of granule-derived proteins with microbicidal activity. A similar type of release occurs during vital NETosis, in which anuclear neutrophils maintain their chemotactic ability and imprison live bacteria, even after NET extrusion. Mitochondrial NETosis is limited to the expulsion of oxidised mitochondrial DNA and cytoplasmic enzymes. NETs include the targets of most autoantibodies found in rheumatoid arthritis, lupus, and vasculitis. The clinical and biological overlaps sometimes observed between bronchectiasis and RA, RA and SLE, or SLE and vasculitis, implicate NETosis as a major triggering event common to these disorders. NETosis increases the possibility of association between autoantigens and infectious antigens in mucosal biofilms, impairing the clearance of pathogens and possibly triggering autoimmune reactions. NETosis aggravates these three conditions and increases endothelial damage and the risk of thrombosis. However, the pathogenesis of RA, SLE, and vasculitis is not confined to autoantibodies against NET components, and other mechanisms have been suggested to explain the breakdown of tolerance to NET autoantigens, such as hypercitrullination. The question of whether continuous presentation of autoantigens mixed with antigens from dormant intracellular pathogens (released following suicidal, vital, or mitochondrial NETosis) is required to induce and sustain autoimmunity must be addressed. Inhibiting NETois may not be sufficient to improve autoimmune disorders whereas such latent infections remain uncontrolled.
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PMID:NETosis: At the crossroads of rheumatoid arthritis, lupus, and vasculitis. 2742 44

Acute chemotherapy-induced lupus erythematosus (ALE) is rare. A few cases have been reported in the literature criminalizing capecitabine, paclitaxel and docetaxel. We report the case of a 64-year old female patient without a history of autoimmune diseases or of drug allergy followed up for invasive ductal carcinoma in the right breast immediately metastatized to the liver and to the lymph nodes. After AC60 first line chemotherapy regimen (a total of 6 cycles), she was treated with docetaxel at a dose of 100 mg/m2. After 5 cycles, she had diffuse erythematous lesions on both hands, forearms, cheeks and on the peribuccal area. She underwent corticosteroid therapy with sun protection and could continue the same chemotherapy until the eighth cycle. Patient's evolution was marked by the progression of the disease. She was treated with capecitabine at a dose of 1250 mg/m2 twice a day. After six cycles she had erythematosquamous and itchy patches on the face resembling the wings of a butterfly (Panel A, Panel B) with oral ulceration and digital pulpitis (Panel C). This initially suggested acute chemotherapy-induced cutaneous lupus erythematosus. Biopsy suggested lichenoid toxidermia. Immunological assessment was performed to exclude chemotherapy-induced cutaneous lupus erythematosus, which showed anti-native DNA antibodies and negative anti-histone antibodies. Anti-nuclear antibody test is positive at 320; this test may be positive in 50-70% of patients with breast cancer, ENT or lymphoma. In the light of these results the diagnosis of toxidermia was the more likely.
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PMID:[Toxidermy mimicking acute chemotherapy-induced lupus erythematosus]. 2987 47