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

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

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

We have evaluated the technical performance of the MDA-180 automated coagulation analyser in a working diagnostic hemostasis laboratory environment. The analyser has been on site now for over 18 months, and has undergone considerable testing. More than 22,000 samples have been processed, with over 90% of these via the MDA-180's cap-piercing facility. The instrument has been primarily assessed for its technical ease of use and continued reliability, as well as its analytical performance. The instrument has also been successfully interfaced to, and used with, our Laboratory information (CERNER PATHNET) system. A major feature of our evaluation has been an assessment of the MDA-180's ability to perform assays currently performed using alternative methodology or instrumentation (eg; ELISA methodology or the Coagamate-X2 and ACL-300R instruments), as well as its potential to streamline the technical performance of some of these assays. We have co-evaluated the following assays: PT/INR, APTT, TT, Fibrinogen, Protein C, ATIII, Factors II, V, VII, VIII, IX, X, XI, and XII, Lupus anticoagulant (dRVVT), and heparin (alpha Xa). In addition, a number of different reagents (particularly for PT and APTT assays) have been tested on the instrument. Intra-assay and inter-assay variation appears to be remarkably low (five different plasmas tested: PT: 0.6 to 1.3% and 0.5 to 1.3% respectively; APTT: 0.7 to 3.2% and 0.6 to 3.6% respectively; single day analysis). Other comparative assessment data typically showed good correlation to existing test assay systems. A review of other features which may enhance or detract from the instrument's worth in a given hemostasis laboratory is also presented. In summary however, we conclude that the instrument is reliable, easy to use and capable of fast sample through-put.
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PMID:The MDA-180 coagulation analyser: a laboratory evaluation. 921 38

We examined thrombophilic mechanisms and outcome in 54 patients with deep-vein thrombosis (DVT), who were otherwise apparently healthy and aged < or = 50 years. Patients were followed up 6 years (median) after a confirmed first DVT between 1987-1992 with no known predisposing illnesses. Patients were traced through the hospital registry and compared with 25 matched controls. Tested thrombophilic mechanisms were either genetic (activated protein C [APC] resistance; anti-thrombin III deficiency [ATIII]; protein C or protein S deficiency [PC, PS]) or acquired (lupus anti-coagulant [LAC]/anti-cardiolipin antibodies [ACA]; subsequent diagnosis of cancer). Twenty-nine DVT patients attended for full studies. The remaining 25 were interviewed by phone and none had a reported neoplastic disease, confirmed by their hospital records and the National Cancer Registry. These patients' demographics, risk factors and subsequent course were similar in all respects to the studied group. In the control group, APC resistance was the only coagulopathy found (1/25, 4%), and it was also the most common abnormality among DVT patients (8/29, 28%) (p = 0.009). Three DVT patients had LAC/ACA (10%) and one each, ATIII, PC and PS deficiencies (3.3% each). No malignancy was encountered during a follow-up of 7.9 +/- 5.7 years. Circumstantial risk factors were found in 52% of the patients, 21% had a family history of DVT, and 41% had recurrent DVT. These characteristics were not significantly different when DVT patients with and without coagulopathy were compared.
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PMID:Causes and outcome of deep-vein thrombosis in otherwise-healthy patients under 50 years. 930 63

We have established a system for etiological analysis of thrombophilia which includes assays of antithrombin III, protein C, protein S, plasminogen, fibrinogen, heparin cofactor II and lupus anticoagulants as well as gene analysis. The analysis conducted on 115 patients with venous thrombosis, arterial thrombosis and small vessel thrombosis revealed that forty-one patients(36% of the examined patients) were accompanied with decreased activities of protein S, protein C, antithrombin III and plasminogen. Eleven candidate causal mutations were found by gene analysis. These studies indicate that a comprehensive examination is instrumental in identifying and confirming the etiology in patients with thrombophilia.
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PMID:[Etiological analysis of thrombophilia]. 939 41

Sixteen patients with Moyamoya disease and four with quasi-Moyamoya disease were investigated in order to elucidate the presence of thrombophilia. The assay system for diagnosing thrombophilia consisted of assessing both the activity and antigen levels of antithrombin III, protein C, protein S, fibrinogen and plasminogen as well as detecting lupus anticoagulants. The analysis revealed that one third (four definite cases and three quasi-cases) of the examined patients demonstrated either congenital or acquired thrombotic tendency. Protein C deficiency was found in two definite cases and in two quasi-cases among whom one quasi-case was identified to have a hereditary type I Protein C deficiency. Protein S deficiency was found in one definite case and in one quasi-case. Type II plasminogen deficiency was found in one quasi-case, and lupus anticoagulant was present in one quasi-case. Based on these findings, an evaluation of thrombophilia should thus be performed when both diagnosing and treating suspected cases of Moyamoya disease.
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PMID:Thrombophilia found in patients with moyamoya disease. 940 44

The pathophysiological basis of blood coagulation includes hemostatic causes and thrombophilia (protein C deficiency, protein S deficiency, APC resistance, plasminogen deficiency, antithrombin III deficiency, hyperhomocystinemia, lupus anticoagulans and anticardiolipin antibodies). The effect of female sexual steroids on coagulation has been observed: ethinyl estradiol produced an increased risk of thromboembolism. Also, there was a pronounced increase of fibrin division products among users of higher EE doses. The effect of gestagens on coagulation was found to be contradictory. The risk of thrombosis as related to oral contraceptives (OCs) was investigated in several studies. Desogestrel and gestoden-containing OCs produced a higher incidence of thrombosis than levonorgestrel-containing pills. A WHO multinational case-control study was carried out in 21 centers and 17 countries during 1989-93, including a total of 1143 cases and 2998 controls. The risk of thrombosis was 2-3 times higher among women using gestoden or desogestrel-containing OCs than those using LNG-containing OCs. Similarly, there was a 1.58 increased risk according to a case-control study using data from England and Germany. A 1995 study of 700 medical practices in Great Britain involving 238,130 women showed increased risk for gestoden (1.8) and desogestrel (1.9). Another 1995 study used the data of 697,000 women from 398 practices in England and registered 116 cases of thromboembolism. There was a risk three times higher for all ovulation inhibitors among cases compared to controls, as well as a pregnancy risk 5.9 times higher. Nonetheless, no definitive conclusion can be drawn from all of these epidemiological studies, which could challenge the prevailing view on contraceptive behavior.
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PMID:[Contraceptive agents and risk of thrombosis]. 941 70


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