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 compared the performance characteristics of a commercial dilute Russell's viper venom (DRVV)-based APC resistance assay (Gradipore PC Impedance Test) to a routinely utilized commercial APTT based assay (Coatest APC Resistance Assay). The DRVV based assay offers improved sensitivity and specificity for the factor V Leiden mutation. However, the routine use of both assays provides optimum reliability for diagnosis of genetic APC resistance. Our results suggest that when both tests are either positive or negative, DNA analysis is unnecessary. Interference by lupus anticoagulants is dramatically minimized by the phospholipid rich DRVV reagent used in the assay and it is insensitive to high factor VIII activity. Additionally, discrepant functional assay results allow identification of patients who may have an acquired APC resistant phenotype.
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PMID:The use of two different APC resistance assay systems provides optimal sensitivity and specificity for diagnosing genetic APC resistance. 928 90

We describe prevalences of prolonged activated partial thromboplastin time(APTT) and lupus anticoagulant(LAC) in autoimmune thyroid disease(AITD). Prolonged APTTs were observed in 33(6.2%) blood samples out of 532 AITD cases(327 Graves' diseases and 205 Hashimoto's thyroiditis), but in only 8(2.0%) samples out of 396 non AITD cases(213 thyroid tumors, 14 subacute thyroiditis and 169 normal thyroids). The samples with prolonged APTT showed no abnormality in coagulation factors(factor VIII, IX, XI, XII, von Willebrand factor(vWF), prekallikrein, or high molecular weight kininogen) or factor VIII, IX inhibitor. Among samples with prolonged APTT, LAC evaluated by platelet neutralization procedure(PNP) was positive in 17(51.5%) samples of AITD, and in 2(25.0%) samples of non AITD. In prolonged APTT cases, the frequency of fetal loss in patients with AITD was higher than non AITD patients. But no significant difference was obtained between thyroid autoimmune antibody and the frequency of fatal loss. These indicate unknown biological association of between AITD and LAC.
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PMID:[Prevalence of prolonged APTT and lupus anticoagulant in autoimmune thyroid disease]. 931 Dec 65

Lupus anticoagulants (LA) are immunoglobulins which inhibit one or more of the in-vitro phospholipid (PL) dependent tests of coagulation. Virtually any physician may encounter LA-positive patients. Such patients present with a variety of diagnostic challenges including arterial and venous thromboembolic events, recurrent fetal loss, TIAs, livedo reticularis, etc. LA and anticardiolipin antibodies (ACA) are the most common cause of acquired thrombophilia. Consequently, it is imperative for clinicians and laboratorians to work together in establishing the diagnosis of LA/ACA. The laboratory diagnosis of LA requires careful adherence to the SSC Subcommittee on Lupus Anticoagulants/Phospholipid-dependent Antibodies guidelines. Four sequential steps are required, including: screening tests, mixing studies (to establish the presence of an inhibitor), confirmatory tests based on increased or altered PL concentrations, and ruling out other coagulopathies (for example, factor VIII inhibitor).
Lupus 1998
PMID:Many faces of lupus anticoagulants. 981 66

Activated protein C (APC) resistance has been identified in many studies as a major cause of venous thromboembolism. The most common genetic polymorphism of clinical relevance causing APC resistance is the factor V Leiden mutation (FVL). Besides the FVL mutation, several acquired risk factors like lupus anticoagulant or elevated levels of acute phase proteins are known to induce APC resistance in plasma. Oral contraceptive (OC) users are known to be at higher risk for deep vein thrombosis than nonusers. Therefore, this BATER-cohort study (Bavarian Thromboembolic Risk Study) was conducted in Bavaria, Germany, during 1996-97. A total of 821 women were randomly selected and enrolled in the study to examine the effects of OCs on hemostasis variables known to be risk factors for venous thromboembolism, especially looking for acquired APC resistance and the plasmatic factors of the protein C system. Findings revealed that APC resistance was significantly lower in OC users in comparison with nonusers and was not attributable to the increased factor VIII:C levels. APC methods applied in this study revealed no significant difference between OC users of any type. Therefore, an increase of the risk related to OC use and/or FVL mutation was statistically insignificant.
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PMID:Resistance to activated protein C in women using oral contraceptives. 983 8

The aim of this study was to evaluate critically the recently modified activated-partial-thromboplastin-time (APTT)-based activated protein C (APC)-resistance tests, which are more specific for the factor V Leiden mutation than the first generation APC-resistance tests. The only modification to these tests is the predilution of the plasma sample in factor-V-deficient plasma. The intended effect of this predilution is to bring the concentrations of all clotting factors, except factor V, to the same normal levels. This, in principle, makes the tests also suitable for assaying the plasma of patients treated with oral anticoagulants and heparin, or of patients with a lupus anticoagulant. However, not every factor-V-deficient plasma is suitable for this application. Because the factor V:factor VIII ratio is important in establishing the APC ratio, the factor-V-deficient plasma should contain a sufficiently high factor VIII concentration. We also found that the optimal dilution to obtain the same APC ratios for patients, whether or not treated with coumarins or heparin, is not the same for each test or factor-V-deficient plasma. We compared two modified APTT-based APC-resistance tests (one developed in our laboratory and one commercial) with respect to their ability to discriminate between carriers and non-carriers of the factor V Leiden mutation. Both modified tests gave complete separation of carriers and non-carriers of the factor V Leiden mutation whether or not they are treated with anticoagulants. This makes these tests very suitable for routine screening.
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PMID:Careful selection of sample dilution and factor-V-deficient plasma makes the modified activated protein C resistance test highly specific for the factor V Leiden mutation. 1007 Aug 30

Activated partial thromboplastin time may be prolonged as the result of either of two different autoimmune complications of chronic lymphocytic leukemia: the development of antiphospholipid antibodies, such as lupus anticoagulant or anticardiolipin antibodies, or anti-factor VIII inhibitors, such as acquired hemophilia A. In the rare simultaneous occurrence of both inhibitors, differential diagnosis of a prolonged activated partial thromboplastin time poses a number of problems during laboratory work-up, due to mutual interference of the commonly performed tests. Only careful clinical follow-up can disclose the significance of the laboratory findings. We report the case of concurrent antiphospholipid antibodies (lupus anticoagulant positivity, anticardiolipin antibodies; IgM 3880 MPL/mL and IgG 265 GPL/mL) and anti-factor VIII antibodies (46.8 Bethesda Units) in a patient with chronic B-cell lymphocytic leukemia who had prolonged activated partial thromboplastin time (78.8 s). The relationship between lymphoproliferative and antiphospholipid syndrome, laboratory work-up in the case of the association of antiphospholipid and anti-factor VIII antibodies, and related problems that occur during clinical management of the patient are also discussed.
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PMID:[The antiphospholipid syndrome during chronic lymphatic leukemia. An association with anti-factor VIII antibodies]. 1052 24

Acquired deficiency of clotting factor VIII (FVIII) is a rare bleeding diathesis seldom encountered in systemic lupus erythematosus (SLE). Reduction of FVIII activity by autoantibodies can cause potentially life-threatening situations. Herein, an SLE patient with a positive lupus anticoagulant (LAC) test who abruptly developed metrorrhagia 4 yr after diagnosis is reported. Coagulation tests revealed FVIII activity reduced to 3% and a prolonged aPTT. FVIII inhibitor(s) were found to be as high as 3.0 Bethesda Units. Plasmapheresis, immunoglobulins, prednisolone and FVIII plasma concentrates induced the cessation of metrorrhagia, but the clotting tests were barely improved. One month later, extensive ecchymosis appeared and worsened, despite re-administration of the previous therapy. Pulse cyclophosphamide followed by oral administration was then started with normalization of coagulation parameters and long-lasting disease remission.
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PMID:Long-lasting remission and successful treatment of acquired factor VIII inhibitors using cyclophosphamide in a patient with systemic lupus erythematosus. 1095 57

In a whole year from July 1997 to June 1998, a total of 50 patients with sonogram-proved venous thrombosis who called on our hematology clinic consecutively entered into the study. Their mean age was 59.1 +/- 17.5 years, range 18-83 years, and 29 were male. A series of examinations were performed in order to find out the cause of venous thrombosis. These examinations included antithrombin, protein C, protein S, plasminogen, heparin cofactor II, activated protein C ratio, factor V Leiden mutation, fibrinogen, factors VIII and XII, euglobulin lysis time, 677 C-->T mutation of methylenetetrahydrofolate reductase (MTHFR), prothrombin 20210 (PT 20210) A allele mutation, lupus anticoagulant, anticardiolipin antibody, and complete blood count. Five patients (10%) were found to have malignancy; an inferior vena cava thrombosis in one patient was due to venous compression by hydronephrosis; two patients had lupus anticoagulant; two had varicose veins of legs; two had protein C deficiency; four had protein S deficiency; two had plasminogen deficiency; two had antithrombin deficiency. No activated protein C resistance, elevated factor VIII level, factor V Leiden, PT 20210 A allele or heparin cofactor II deficiency was found in the present study. Homozygous MTHFR 677 C-->T gene mutation was found in 7 patients (14%); one of them also had a plasminogen deficiency. No possible risk factor of venous thrombosis could be found in 24 patients (48%). In conclusion, malignancy and protein S deficiency were the most frequent acquired and congenital causes of venous thrombosis in the Chinese, respectively.
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PMID:Causes of venous thrombosis in fifty Chinese patients. 1062 72

Markers of thrombotic risk--fibrinogen, factor VIII and immunoglobulin G (IgG) anticardiolipin titres--were measured, and the presence of lupus anticoagulant and factor V Leiden were assessed in 84 patients with a solid or haematological malignancy. These patients were monitored, following the insertion of an indwelling venous catheter, for thrombosis. Fifty-five were given prophylactic low-dose warfarin. Over a mean of 15 weeks there were 10 (12%) thrombotic events in 10 patients. Seven were on warfarin. Haemorrhagic problems occurred in three (5%), all on warfarin. Of the 84 patients, 86% had raised fibrinogen levels, 37% elevated factor VIII and 44% raised anticardiolipin levels. Lupus anticoagulant was present in five and three were heterozygous for factor V Leiden. A high prevalence of a range of prothrombotic changes was confirmed and the frequent presence of low-titre anticardiolipin antibody in subjects with malignancy demonstrated. However, none of these parameters predicted the development of thrombosis (P > 0.05).
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PMID:Thrombosis, markers of thrombotic risk, indwelling central venous catheters and antithrombotic prophylaxis using low-dose warfarin in subjects with malignant disease. 1064 78

Spontaneous inhibitors to coagulation factors are autoantibodies that usually appear in the elderly, but may also occur in patients with immunological disorders such as lupus, lymphoma, asthma or drug reactions. Most antibodies are directed against factor VIII, but any coagulation protein may be affected. They should be suspected in individuals who previously had normal haemostasis, but who now begin to experience bleeding into the skin and muscles, or suffer haemorrhages after routine procedures such as insertion of vascular catheters, intramuscular injections, or minor surgery. The haemostasis laboratory is critical in identifying the particular inhibitor and quantitating its potency. Factor VIII inhibitors prolong the partial thromboplastin time (PTT) but not the prothrombin time (PT), and incubating mixtures of patient plasma and normal plasma enhances the prolongation of the clotting time. The Bethesda assay provides a rough assessment of inhibitor potency. Inhibitors of von Willebrand factor prolong the bleeding time and impair ristocetin-induced platelet aggregation. Factor V inhibitors are associated with a prolonged PTT and PT, not correctable with normal plasma. Patients will often have a history of exposure to bovine thrombin in fibrin glue. The antibodies most difficult to recognize are those that alter fibrin polymerization or stabilization. Abnormal clot retraction or clot solubility in urea solutions are an important clue. The management of these disorders depends on characterization of the inhibitor, and using appropriate clotting factor concentrates to control acute bleeding. For example, recombinant human factor VIII or desmopressin may be effective for patients with low titre factor VIII inhibitors, whereas porcine factor VIII, recombinant factor Vlla, or prothrombin complex concentrates stem bleeding in those with high titres. Inhibitors of von Willebrand factor may be amenable to desmopressin, cryoprecipitate, or von Willebrand factor concentrates. Some patients with factor V inhibitors have responded to platelet transfusions, as the platelet factor V may be shielded from the autoantibody. Bleeding due to factor XIII inhibitors may be managed with fibrogammin, a factor XIII concentrate. All patients should be treated for underlying disorders and given drugs such as corticosteroids and cytotoxic agents to suppress inhibitor formation. Major advances in new immunosuppressive technologies, such as monoclonal B-cell antibodies, offer hope of more effective therapies for spontaneous inhibitors to coagulation factors.
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PMID:Spontaneous inhibitors to coagulation factors. 1125 55


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