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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some studies have suggested that thrombotic and fibrinolytic disorders may be etiologic causes of osteonecrosis of the femoral head. A case-control study was done to determine whether these disorders are associated with osteonecrosis of the femoral head in East Asian patients with nontraumatic osteonecrosis of the femoral head. Twenty-four consecutive patients who had been diagnosed as having nontraumatic osteonecrosis of the femoral head were matched with 24 control subjects for gender, age (1-year range), and the time of presentation (1-year range). Thrombotic factors including protein C activity, protein S activity, antithrombin III, anticardiolipin antibody immunoglobulins G and M, and lupus antibody were investigated. Fibrinolytic factors including tissue-plasminogen activator, plasminogen activator inhibitor-1, tissue-plasminogen activator and plasminogen activator inhibitor-1 ratio, lipoprotein (a), and plasminogen also were investigated. There were no significant differences in the levels of thrombotic and fibrinolytic factors. In eight patients with idiopathic osteonecrosis, anticardiolipin antibody immunoglobulin G, an antiphospholipid antibody which is associated with thrombotic phenomena, was lower than that in respective control subjects. These data do not confirm an etiologic role for thrombotic and fibrinolytic disorders in East Asian patients with nontraumatic osteonecrosis of the femoral head.
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PMID:Role of thrombotic and fibrinolytic disorders in osteonecrosis of the femoral head. 1464 26

Management of central nervous system (CNS) involvement still remains one of the most challenging problems in systemic lupus erythematosus (SLE). The best available evidence for the treatment of CNS lupus is largely based on retrospective series, case reports and expert opinion. Current therapy is empirical and tailored to the individual patient. Symptomatic, immunosuppressive and anticoagulant therapies are the main strategies for the management of CNS lupus. The choice depends on the most probable underlying pathogenic mechanism and the severity of the presenting neuropsychiatric symptoms. Thrombotic and nonthrombotic CNS disease needs to be differentiated and requires different management strategies. However, this is often challenging since many, if not most CNS manifestations, may be due to a combination of different pathogenic mechanisms and multiple CNS events may occur in the individual patient. Patients with mild manifestations may need symptomatic treatment only, whereas more severe acute nonthrombotic CNS manifestations may require pulse intravenous cyclophosphamide. Plasmapheresis may also be added in patients with more severe illness refractory to conventional treatment. Recently, the use of intrathecal methotrexate and dexamethasone has been reported in a small series of patients, with a good outcome in patients with severe CNS manifestations. Anticoagulation is warranted in patients with thrombotic disease, particularly in those with the antiphospholipid syndrome (APS). This article reviews the clinical approach to therapy in patients with CNS lupus.
Lupus 2003
PMID:Central nervous system lupus: a clinical approach to therapy. 1471 14

Thromboembolism in pregnancy and the puerperium and inherited or acquired thrombophilia are associated. Thrombophilia can be revealed by pregnancy. Thrombotic risk during pregnancy and the puerperium is higher in asymptomatic women with than without thrombophilia. Antithrombin deficiency, combined deficiencies and homozygous or double-heterozygotes factor V Leiden and factor II G 20210 A mutations are associated with a higher thrombotic risk than heterozygote mutations or protein S and C deficiencies, whereas hyperhomocysteinemia does not appear as a risk factor for maternal thromboembolic disease. Antiphospholipid syndrome with lupus anticoagulant is strongly associated with thrombotic risk in pregnancy and the puerperium. Further studies are required to assess the thrombotic risk in women with preeclampsia as well as early or late recurrent pregnancy loss.
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PMID:[Risk factors of thromboembolism associated with pregnancy and the puerperium. Role of inherited and acquired thrombophilia]. 1502 82

Antiphospholipid antibodies (APLA) present very heterogeneous groups of antibodies which can significantly and in various ways influence processes on different levels of coagulation cascade. Their presence can be accompanied with repetitive venous and arterial thromboses, recurrent loses of foetus, and thrombocytopenia. Incidence of these thrombotic disorders was monitored in a group of 46 patients with systemic lupus erythematodes (SLE). Positive lupus anticoagulant (LA), antiphospholipid antibodies complex, and thrombocyte counts were assessed. Thrombotic disorders were assessed in a retrospective analysis. In the LA+ group 62% of patients had history of venous thromboses, 31% had history of arterial thromboses, and 18% had history of spontaneous abortions. In a group without positive LA 18% of venous thromboses (p = 0.0006) and 6% of arterial thromboses (p = 0.03) were indicated. In the assessment of spontaneous abortions no statistically significant difference was found. An average value of thrombocytes in LA+ group was 152 +/- 66 x 10(5)/l, in LA- group 223 +/- 86 x 10(5)/l, which is statistically significant difference (p < 0.05). In the assessment of thrombotic disorders in a group with combination LA+ and APA+ statistical significance was indicated only in venous thromboses (p = 0.004). We can state from the results that in thrombotic disorders which can be seen in the framework of systemic tissue disorders positive LA and APA and a range of other factors such as activity of a basic disease, associated diseases, and treatment which can aggravate thrombotic disorders of individual patients can participate.
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PMID:[Incidence of selected antiphospholipid antibodies in a group of patients with systemic lupus erythematosus]. 1521 92

Background: Splenectomy has been performed to treat refractory autoimmune thrombocytopenia. However, some reports have suggested that an increased risk of thrombosis could be present in splenectomized patients. This study aims to evaluate the possibility of an increased risk of thrombosis after splenectomy in patients with systemic lupus and antiphospholipid syndrome. Methods: Thrombotic-related events in patients with systemic lupus erythematosus (SLE) and/or primary antiphospholipid syndrome (PAPS), before and after splenectomy for severe thrombocytopenia, were compared. Clinical data, laboratory investigations, and anticoagulation or antiaggregation treatment data were collected from the notes of outpatients attending three European centers. Results: Twenty patients who had had a splenectomy were identified: eight with SLE, five with PAPS, and seven with SLE and APS. The mean time between diagnosis and splenectomy was 3.1 years and mean follow-up was 6.5 years. There were no differences in anticardiolipin antibody titers, lupus anticoagulant, anti-DNA or anti-nuclear antibodies before and after surgery. The incidence of venous events before and after splenectomy was not significantly different. There was a trend towards an increase in the total number of arterial events post-splenectomy. In aCL-positive patients, and in the pre-splenectomy period, the total number of miscarriages was higher (p=0.017), as was the number of patients who had had a miscarriage (p=0.025). Conclusions: The total risk of thrombosis in patients with PAPS and SLE was not increased after splenectomy, but there was a trend towards an increase in the number of arterial events. Splenectomy induced long-term remission of thrombocytopenia (partial or complete) in all patients.
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PMID:Thrombotic risk in patients submitted to splenectomy for systemic lupus erythematosus and antiphospholipid antibody syndrome-related thrombocytopenia. 1524 18

Antiphospholipid antibodies detected by lupus anticoagulant, anticardiolipin or anti-beta2 glycoprotein I assays were associated with fetal loss. Rather than being diagnostic tools only, antiphospholipid antibodies are thought to be pathogenic. The strongest demonstration of their pathogenic role lies in the ability to induce fetal resorptions--the experimental equivalents of the human fetal losses--when passively infused in pregnant naive animals. However, still debated is how the antibodies might induce the obstetrical manifestations. Thrombotic events at the placental levels might be related to endothelial cell activation, inhibition of protein C/S system and fibrinolysis as well as to Annexin V displacement. However, the thrombophilic state apparently cannot explain all the miscarriages and a direct antibody-mediated damage on the trophoblast has been suggested. During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2 glycoprotein I, the main cationic phospholipid binding protein recognized by the antiphospholipid antibodies. Adhered beta2-glycoprotein I might be recognized by the antibodies that, once bound, strongly interfere with in vitro trophoblast cell maturation so resulting in a defective placentation. These mechanisms have been suggested to play a role in early fetal loss, while thrombotic events would be responsible for miscarriages late in the pregnancy.
Lupus 2004
PMID:Antiphospholipid antibodies as cause of pregnancy loss. 1548 95

Acquired and inherited thrombophilic factors increase the risk for (recurrent) venous thrombotic disease. However, little is known about the pathophysiological mechanisms causing these recurrences, or the persistence of thrombosis despite adequate treatment. Because residual thrombosis has been associated with a worse prognostic outcome, we performed an explorative study in order to investigate the prevalence of residual thrombotic lesions after anticoagulant treatment in patients with deep venous thrombosis. Thrombotic parameters as assessed by ultrasonography after a 12-week course of anticoagulants were used. Both thrombophilia in general and acquired thrombophilia in particular were found to be associated with the extent of residual thrombosis. Of the individual thrombophilic factors, protein C deficiency, prothrombin 20210A mutation, active malignant disease and lupus anticoagulant were associated with an increased risk of residual thrombotic mass. Patients with inherited thrombophilia did not differ from patients without any thrombophilic abnormality with regard to residual thrombotic mass [relative risk (RR) 1.3, 95% confidence interval (CI) 0.9-1.8], while acquired thrombophilic disorders increased the risk for residual thrombotic mass as compared to patients without any defect (RR 1.7, 95% CI 1.2-2.2). Although these results should be confirmed in a larger study, they might help us form hypotheses concerning why patients with thrombophilia are more prone to recurrent venous thromboembolic disease.
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PMID:Acquired and inherited thrombophilic factors and the risk for residual venous thrombosis. 1558 48

Deep vein thrombosis and its sequelae pulmonary embolism and post-thrombotic syndrome are some of the most common disorders. A thrombus either arises spontaneously or is caused by clinical conditions including surgery, trauma, or prolonged bed rest. In these instances, prophylaxis with low-dose anticoagulation is effective. Diagnosis of deep vein thrombosis relies on imaging techniques such as ultrasonography or venography. Only about 25% of symptomatic patients have a thrombus. Thus, clinical risk assessment and D-dimer measurement are used to rule out deep vein thrombosis. Thrombus progression and embolisation can be prevented by low-molecular-weight heparin followed by vitamin K antagonists. Use of these antagonists for 3-6 months is sufficient for many patients. Those with antithrombin deficiency, the lupus anticoagulant, homozygous or combined defects, or with previous deep vein thrombosis can benefit from indefinite anticoagulation. In cancer patients, low-molecular-weight heparin is more effective than and is at least as safe as vitamin K antagonists. Women seem to have a lower thrombosis risk than men, but pregnancy or use of oral contraceptives or hormone replacement therapy represent important risk factors.
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PMID:Deep vein thrombosis. 1600 25

Unfractionated heparin has been a near universal anticoagulant for cardiac surgery; however it is contraindicated in heparin-induced thrombocytopenia type II. Alternative anticoagulants such as bivalirudin (a direct thrombin inhibitor) are being utilized. Bivalirudin was successfully used in an immunologically complex patient (diagnoses of heparin-induced thrombocytopenia type II, systemic lupus erythematosus, antiphospholipid syndrome, and dialysis-dependent renal failure) requiring cardiopulmonary bypass. Thrombotic events are common in antiphospholipid syndrome patients undergoing cardiac surgery utilizing high-dose heparin. This may represent unrecognized heparin-induced thrombocytopenia type II. Our patient did not experience perioperative thrombotic or bleeding complications. The possible cross-reactivity between heparin induced thrombocytopenia type II and antiphospholipid syndrome has not been investigated.
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PMID:Bivalirudin anticoagulation for a patient with hypercoagulable immune syndromes undergoing mitral valve surgery. 1673 Nov 83

Thrombotic events account for significant morbidity and mortality among patients with antiphospholipid syndrome. The cornerstone of management includes long-term anticoagulation. However, the benefit of long-term anticoagulation must be weighed against the risk of bleeding complications. This article presents the case of a patient with systemic lupus erythematosus and antiphospholipid syndrome who experienced severe intramuscular hemorrhage as a complication of warfarin anticoagulation. This case emphasizes the importance of careful monitoring of anticoagulation treatment, and of recognizing a new differential diagnosis when dealing with a painful, swollen calf in the setting of lupus and antiphospholipid syndrome.
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PMID:Intramuscular bleeding as a complication of anticoagulation treatment in a patient with systemic lupus erythematosus and antiphospholipid syndrome. 1704 6


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