Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the UK, the Committee for Safety of Medicines (CSM) issued a warning in October 1995 about the possible increased risk of nonfatal deep venous thrombosis (DVT) among users of oral contraceptives (OCs) containing the third generation progestogens, desogestrel and gestodene. Subsequent media coverage increased the number of consultations and enquiries about these OCs. CSM had concluded that, overall, the third generation OCs are safe. CSM recommended their continued use. Nevertheless, many women stopped using them and induced abortions increased by 11%. In April 1996, the Committee for Proprietary Medicinal Products issued a more cautious statement about the OCs and called for further evaluation. Chance, confounding, and bias may account for the increased risk observed in the studies in question. Yet, it is possible that these OCs may increase the risk of DVT. The increased risk may be offset by a reduced risk of acute myocardial infarction. Physicians need to conduct careful and thorough counseling and to allow the patient to be involved and to take responsibility in making a decision about OC use. They should document all counseling with a note that the patient understands and accepts the increased risk of DVT. They should not prescribe the third generation OCs to women with any of the absolute contraindications to OC use (ischemic heart disease, hypertension, atherogenic lipid disorders, focal or crescendo migraine, cigarette smoking, transient ischemic attacks, past cerebral/subarachnoid hemorrhage, history of vascular thrombosis, prothrombotic abnormalities [e.g., Factor V Leiden], conditions predisposing to thrombosis [e.g., systemic lupus erythematosus], and obesity. Women who are intolerant of second generation OCs may prefer third generation OCs. Physicians should selectively screen women with a family history of a first-degree relative younger than 45 with thromboembolism for Factor V Leiden. They should also screen for protein C, protein S, and antithrombin III deficiency and for acquired antiphospholipid antibodies.
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PMID:Oral contraceptives and the risk of DVT. 898 64

We identified a group of 24 young (less than 50 years of age) women with isolated, premature atherosclerotic aortoiliac occlusive disease and attempted to identify distinguishing hemostatic characteristics. Most of these patients (62%) presented with acute thromboembolic events (blue toe syndrome, n = 6; macroemboli, n = 6; or aortoiliac thrombosis, n = 3). Aortoiliac reconstruction (aortoiliac endarterectomy, n = 10, aortobifurcation bypass grafts, n = 6; and percutaneous angioplasty, n = 4) was complicated by early thrombosis in 6 of 20 cases (30%), (1 of 10 endarterectomies, 4 of 6 bypass grafts, and 1 of 4 angioplasties). Fresh thrombus overlying an atherosclerotic plaque was a common finding at surgery. This observation and the relatively high incidence of thromboembolic events led us to hypothesize that a characteristic hemostatic profile might underlie the remarkably similar clinical presentations of these women. Levels of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant), plasminogen activator inhibitor-1, fibrinogen, antithrombin III, protein C, protein S, plasminogen, prothrombin fragment F1 + 2, and D-dimer were determined for these young women and for 21 age-matched white female control subjects without vascular disease and nine white male patients with aortoiliac occlusive disease (mean 61 years, range 43 to 74 years). The incidence of anticardiolipin antibodies was 42% (8 of 19) in the female patients, which was significantly elevated (p = 0.028). The female (62.5%) and male (100%) patients had significantly elevated D-dimer levels (p < 0.001). Deficiencies of antithrombin III, protein C, and protein S were rare. A unique pattern of premature aortoiliac atherosclerosis exists in some young women. Intra-arterial thromboembolic events are common at presentation and complicate surgical management. The role of antiphospholipid antibodies remains uncertain.
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PMID:Young women with advanced aortoiliac occlusive disease: new insights. 898 71

The advent of improved diagnostic tests for primary hypercoagulability has led to increased recognition of this entity as a problem in surgical patients. We treated 20 patients with documented evidence of increased coagulability from 1975 to 1995. Clinical presentations included venous (16) and arterial (4) thrombosis. Symptoms usually occurred early in life (mean age, 38 years) and developed spontaneously without a secondary inciting event or factor. Deficiencies in naturally occurring anticoagulant proteins including antithrombin III (n = 7), protein C (n = 3), and protein S (n = 1) were seen, as were problems with lupus anticoagulant (n = 2) and anticardiolipin antibody (n = 4) deficiencies. Treatment of these patients is difficult, and results are often suboptimal. A total of 12 vascular reconstructions were required in 5 of the 20 patients; 11 eventually failed. Patients with primary venous thrombosis were often successfully treated with anticoagulant therapy in the short term but fared less well in the long term. There were three deaths directly related to thrombotic complications. Surgeons may encounter patients with primary hypercoagulable syndromes. The diagnosis should be expected in patients with unusual patterns of vascular disease or arterial or venous thrombosis without cause or at an early age, or in patients with recurrent or migratory clotting. Evaluation of this population, although expensive, is indicated. Treatment with chronic anticoagulation is also generally indicated. Arterial reconstruction in this subset of patients usually leads to a poor outcome.
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PMID:Surgical implications of hypercoagulable syndromes. 901 31

Antiphospholipid antibody syndrome (APS) is one of the most important causes of thrombophilia, presenting most often as venous or arterial thrombosis, recurrent pregnancy loss, or thrombocytopenia. Both the lupus anticoagulant and anticardiolipin antibody are associated with APS. The mechanism of the prothrombotic state is not understood, but may involve beta-2 glycoprotein 1 (a naturally occurring anticoagulant), platelet aggregation, the protein C pathway, or endothelial cell function. The current treatment recommendation, after a venous or arterial thrombosis, is high-intensity, long-term warfarin therapy.
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PMID:Pathogenesis and treatment of the antiphospholipid antibody syndrome. 901 59

Plasma activated factor VIIa (FVIIa) levels were measured in various diseases using mutant tissue factor (TF). FVIIa levels in thrombotic patients and patients with idiopathic thrombocytopenic purpura were significantly higher than those in healthy control subjects. The plasma FVIIa levels in thrombotic patients treated with warfarin were similar to those of control subjects. The plasma FVIIa levels in pregnant women and patients with systemic lupus erythematosus, infection or malignancies were high. However, the levels in patients with disseminated intravascular coagulation (DIC) were not significantly increased. DIC patients are in a severe hypercoagulable state, and exhibit severe consumption of coagulation factors. The slightly increased FVIIa level in the DIC patients observed is probably considered to be caused by consumption of coagulation factors. The plasma FVIIa level was poorly correlated with other hemostatic parameters except for protein C in our analysis of all cases. In the analysis of DIC and thrombotic patients treated without warfarin, the plasma FVIIa level was negatively correlated with TF antigen. Plasma FVIIa levels might reflect hypercoagulability in thrombotic diseases, and a normalized FVIIa level in patients with thrombotic diseases should be considered to be associated with DIC.
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PMID:Plasma levels of activated FVII in various diseases. 903 61

Primary hypercoagulable states are hereditary disorders that result in arterial and venous thromboses. The purpose of this report is to present three patients with hypercoagulable states, and offer current guidelines for diagnosis and treatment. Primary hypercoagulable disorders such as antithrombin III, protein C and protein S deficiencies, fibrinolytic disorders such as decreased plasminogen levels and plasminogen activator deficiency, and antiphospholipid syndromes such as anticariolipin antibody and lupus anticoagulants will be reviewed. We will emphasize clinical characteristics that should prompt evaluation for hypercoagulation, appropriate laboratory tests for hypercoagulable disorders, and treatment. Other secondary and recently investigated hypercoagulable disorders, including heparin-associated thrombocytopenia, homocystinemia, lipoprotein (a), plasminogen activator inhibitor, and factor V Leiden, will also be reviewed.
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PMID:The surgical implications of primary hypercoagulable states. 904 71

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the synthesis of antinuclear antibodies. Nucleosomes-the disc-like-structural unit of chromatin being composed of histones and DNA-are the primary antigenic structure that induces the formation of complement-activating antigen-antibody complexes in basement membranes. The autoreactivity in SLE has been elucidated in drug-induced SLE: Hypomethylation of DNA leads to overexpression of integrin CD 11a/CD 18, increased binding of T-cells to macrophages and B-cells, a higher rate of apoptosis of macrophages and elevated B-cell activity with consecutive production of autoantibodies. Disturbances of apoptosis (e.g. mutation of Fas gene) are relevant also in non drug-induced SLE. The morphologic diagnosis-by light microscopy, immunohistology and electron microscopy-of skin and renal biopsies can confirm the diagnosis and help in prognostic assessment as well as therapeutic decisions in SLE. The value of the morphologic diagnosis in SLE is enhanced by reporting semiquantitative scores of disease activity and chronicity. The antiphospholipid syndrome (APS) is characterized by thrombosis, thrombocytopenia, recurrent fetal loss and antiphospholipid antibodies. APS associated with SLE or other systemic autoimmune diseases has been termed secondary APS. Antibodies in APS are directed against phospholipids and phospholipid-protein complexes. One of these proteins is beta 2-glycoprotein 1. An important mechanism of the increased rate of thrombosis in APS is probably the inhibition of the protein C catalyzed inactivation of clotting factors V and VIII. Venous thrombosis with recurrent pulmonary emboli and arterial thrombi in brain, heart and kidney (thrombotic microangiopathy) can lead to divergent clinical manifestations in APS.
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PMID:[Systemic lupus erythematosus and antiphospholipid syndrome]. 906 4

Previous studies on the prevalence of biological abnormalities causing venous thrombosis and the clinical characteristics of thrombotic patients are conflicting. We conducted a prospective study on 2.132 consecutive evaluable patients with venous thromboembolism to determine the prevalence of biological causes. Antithrombin, protein C, protein S, plasminogen and heparin cofactor-II deficiencies, dysfibrinogenemia, lupus anticoagulant and antiphospholipid antibodies were investigated. The risk of any of these alterations in patients with familial, recurrent, spontaneous or juvenile venous thrombosis was assessed. The overall prevalence of protein deficiencies was 12.85% (274/2,132) and antiphospholipid antibodies were found in 4.08% (87/2,132). Ten patients (0.47%) had antithrombin deficiency, 68 (3.19%) protein C deficiency, 155 (7.27%) protein S deficiency, 16 (0.75%) plasminogen deficiency, 8 (0.38%) heparin cofactor-II deficiency and 1 had dysfibrinogenemia. Combined deficiencies were found in 16 cases (0.75%). A protein deficiency was found in 69 of 303 (22.8%) patients with a family history of thrombosis and in 205/1,829 (11.2%) without a history (crude odds ratio 2.34, 95% CI 1.72-3.17); in 119/665 (17.9%) patients with thrombosis before the age of 45 and 153/1,425 (10.7%) after the age of 45 (crude odds ratio 1.81, 95% CI 1.40-2.35); in 103/616 (16.7%) with spontaneous thrombosis and in 171/1,516 (11.3%) with secondary thrombosis (crude odds ratio 1.58, 95% CI 1.21-2.06); in 68/358 (19.0%) with recurrent thrombosis and in 206/1,774 (11.6%) with a single episode (crude odds ratio 1.78, 95% CI 1.32-2.41). Patients with combined clinical factors had a higher risk of carrying some deficiency. Biological causes of venous thrombosis can be identified in 16.93% of unselected patients. Family history of thrombosis, juvenile, spontaneous and recurrent thrombosis are the main clinical factors which enhance the risk of a deficiency. Laboratory evaluation of thrombotic patients is advisable, especially if some of these clinical factors are present.
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PMID:Laboratory evaluation and clinical characteristics of 2,132 consecutive unselected patients with venous thromboembolism--results of the Spanish Multicentric Study on Thrombophilia (EMET-Study). 906 91

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the synthesis of antinuclear antibodies. Nucleosomes- the disc-like structural units of chromatin, composed of histones and DNA-are the primary antigenic structure that induces the formation of complement-activating antigen-antibody complexes in basement membranes. The autoreactivity in SLE has been elucidated in drug-induced SLE: hypomethylation of DNA leads to overexpression of integrin CD11a/ CD18, increased binding of T-cells to macrophages and B-cells, a higher rate of apoptosis of macrophages, and elevated B-cell activity with consecutive production of autoantibodies. Disturbances of apoptosis (e.g. mutation of Fas gene) are relevant also in non-drug-induced SLE. The morphologic diagnosis-by light microscopy, immunohistology and electron microscopy-of skin and renal biopsies can confirm the diagnosis and help in prognostic assessment as well as therapeutic decisions in SLE. The value of the morphologic diagnosis in SLE is enhanced by reporting semiquantitative scores of disease activity and chronicity. The antiphospholipid syndrome (APS) is characterized by thrombosis, thrombocytopenia, recurrent fetal loss and antiphospholipid antibodies. APS associated with SLE or other systemic autoimmune diseases has been termed secondary APS. Antibodies in APS are directed against phospholipids and phospholipid-protein complexes. One of these proteins is beta 2-glycoprotein 1. An important mechanism of the increased rate of thrombosis in APS is probably the inhibition of the protein C-catalyzed inactivation of clotting factors V and VIII. Venous thrombosis with recurrent pulmonary emboli and arterial thrombi in brain, heart and kidney (thrombotic microangiopathy) can lead to divergent clinical manifestations in APS.
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PMID:[Systemic lupus erythematosus and antiphospholipid syndrome]. 908 61

We examined the incidence of thrombophilia in deep vein thrombosis (DVT). Of 38 cases, we found 4 cases of protein C abnormality, 2 cases each of protein S abnormality and lupus anticoagulant, 1 case of antithrombin III abnormality. The total incidence was 23.7%, whereas only 2 cases (6.2%) of plasminogen abnormality were found among 32 healthy individuals. The incidence of thrombophilia was apparently higher among patients with DVT than that of healthy subjects, although the incidence of Japanese DVT was lower than that of Caucasian DVT, as previously reported. By SSCP analysis in one case of protein C abnormality, we demonstrated an abnormality of exon 9-3. To establish laboratory diagnosis of thrombophilia, it is recommended that (1) severe liver diseases, DIC, and oral anticoagulant be ruled out, (2) abnormality be confirmed by repeated examination, (3) family study determine inheritance mode, if possible. It was strongly suggested that laboratory examination of thrombophilia should be routinely applied to cases of venous thrombosis including DVT, not only for diagnostic interest but also for appropriate treatment of these cases.
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PMID:[Laboratory diagnosis of congenital thrombophilia]. 913 96


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