Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to determine the prevalence of lupus anticoagulant (LA) antibody and several antibodies for antiphospholipid syndrome (APS) in patients with deep vein thrombosis (DVT)/pulmonary embolism (PE) (n = 48), cerebral thrombosis (CT, n = 30), systemic lupus erythematosus (SLE, n = 22), and idiopathic thrombocytopenic purpura (ITP, n = 30). The presence of antibodies was examined by using the respective ELISA kits. LA was positive in 38.6% of patients with DVT/PE, suggesting that LA is one of the most important risk factors in DVT/PE. The highest prevalence of anti-beta(2) glycoprotein I (beta(2)GPI) IgG was in CT and SLE, followed by DVT, and none in ITP and healthy volunteers (control, n = 40), suggesting that it is related to thrombosis, particularly arterial thrombosis. The highest prevalence of anti-prothrombin (aPT) IgG antibody was in DVT, followed by CT and SLE, and none in ITP and the control, suggesting that it is related to thrombosis, especially venous thrombosis. The highest prevalence of antiphospholipid (aPL) IgG was in DVT, CT, and SLE, but 0% in ITP and control. On the other hand, aPL IgM, anti-annexin V IgG, and anti-annexin V IgM were positive in patients both with and without thrombosis, suggesting that they are not related to thrombosis. Our results indicated that among the anti-phospholipid antibodies, LA is the most sensitive marker for APS while anti-beta(2)GPI IgG, aPT IgG, and aPL IgG are risk factors for thrombosis. In particular, aPT IgG is a significant marker for DVT/PE.
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PMID:High prevalence of anti-prothrombin antibody in patients with deep vein thrombosis. 1528 65

In patients undergoing arthroscopic knee surgery, deep venous thrombosis and pulmonary embolism are rare and there is not clear indication as to the necessity of thromboprophylactic treatment in these patients. However, the role of coagulation disorders in thrombotic events following arthroscopy is unknown. We report 2 cases of massive deep venous thrombosis and pulmonary embolism after knee arthroscopy in athletes carrying the thrombophilic factor lupus anticoagulant, but with no personal or familial history of thrombotic diseases. A few days after the arthroscopic intervention, both patients presented with deep venous thrombosis and 1 developed a severe pulmonary embolism. Blood examination showed that both athletes were lupus anticoagulant-positive. This is the first description of an association between venous thromboembolism, knee arthroscopy, and a prothrombotic condition. This report suggests that screening for hypercoagulability might be useful in athletes undergoing even minimally invasive orthopaedic surgery and that in cases of venous thromboembolism after knee arthroscopy, a prothrombotic disorder should be suspected.
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PMID:Deep venous thrombosis and pulmonary embolism after knee arthroscopy in athletes carrying the thrombophilic factor lupus anticoagulant. 1565 Jun 75

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

We retrospectively studied a large cohort of patients with primary antiphospholipid syndrome (APS) from 4 different referral centers to analyze the clinical and serologic features and, specifically, to determine the number of patients going on to develop systemic lupus erythematosus (SLE) or other autoimmune disease after long-term follow-up. The study included 128 unselected patients with primary APS who fulfilled the Sapporo International Criteria from 4 different tertiary hospitals in the United Kingdom, Mexico, and Spain. The patients had attended the referral centers between January 1987 and July 2001. We reviewed clinical and serologic characteristics according to a pre-established protocol. We used univariate analysis with the chi-squared or Fisher exact test and logistic regression to analyze possible factors related to the coexistence of SLE and APS. Ninety-seven female and 31 male patients fulfilled the criteria, with a median age of 42 +/- 12 years (range, 16-79 yr), and with a mean follow-up of 9 +/- 3 years (range, 2-15 yr). The main manifestations included deep vein thrombosis in 62 patients (48%), arterial thrombosis in 63 (49%) patients, pregnancy loss in 177/320 (55%) cases, and pulmonary embolism in 37 (30%) patients. Other clinical manifestations were migraine in 51 (40%) patients, thrombocytopenia in 48 (38%), livedo reticularis in 47 (37%), and valvular disease in 27 (21%). Serologic findings were anticardiolipin antibodies (aCL) IgG positive in 110 (86%) patients, aCL IgM in 36 (39%), lupus anticoagulant in 71 (65%), antinuclear antibodies in 47 (37%), and positive Coombs test in 5 (4%) patients. During the follow-up and after a median disease duration of 8.2 years (range, 1-14 yr), 11 (8%) patients developed SLE, 6 (5%) developed lupus-like disease, and 1 (1%) developed myasthenia gravis. The remaining 110 patients (86%) continued to have primary APS. After the univariate analysis, a family history of lupus, the presence of Raynaud phenomenon, migraine, psychiatric features, multiple sclerosis-like features, hemolytic anemia, low C3 and C4, and Coombs positivity conferred a statistically significant risk for the subsequent development of SLE (p < 0.05). Only the presence of Coombs positivity had statistical significance (odds ratio, 66.4; 95% confidence interval, 1.6-2714; p = 0.027) after the logistic regression evaluation. The current study confirms that progression from primary APS to SLE or lupus-like disease is unusual, even after a long follow-up. Only 3 patients developed anti-dsDNA antibodies. The presence of a positive Coombs test might be a marker for the development of SLE in patients with primary APS.
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PMID:Long-term follow-up in 128 patients with primary antiphospholipid syndrome: do they develop lupus? 1601 Feb 7

Pulmonary capillaritis and alveolar hemorrhage are rare yet serious and life threatening complications of systemic lupus erythematosus (SLE). Pulmonary manifestations of antiphospholipid syndrome (APS) are similar and include, apart from pulmonary embolism and pulmonary hypertension, pulmonary capillaritis, diffuse alveolar hemorrhage and respiratory insufficiency in patients with catastrophic APS. Herein, we described the radiological features of three patients with pulmonary and SLE-associated APS, manifested with pulmonary edema, capillaritis and alveolar hemorrhage. We observed that the radiological features of pulmonary APS shared close resemblance to those of pulmonary SLE. Based on these findings, we conclude that both entities are not only histologically, but also radiologically indistinguishable from each other, suggesting a mutual pathogenetic mechanism. This raises the question of whether some of the reported lupus pneumonitis cases in the past might be manifestations of APS rather than of SLE.
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PMID:Acute pulmonary edema, capillaritis and alveolar hemorrhage: pulmonary manifestations coexistent in antiphospholipid syndrome and systemic lupus erythematosus? 1613 May 14

It has been widely accepted that the antiphospholipid syndrome (APS) is an autoimmune hypercoagulability syndrome in which a variety of venous and arterial thrombotic events may occur. Peripheral obliterating arterial disease characterized by aortoiliac steno-occlusion occurring in young women, is reported in the literature under the name of Small Aorta Syndrome (SAS). Although it remains unclear whether SAS represents a separate entity, the small size of the distal aorta increases the risk for aortoiliac occlusive disease. A 41-year old white woman was admitted with acute digital ischemia of the left foot. She had positive lupus anticoagulant and IgG anti-cardiolipin antibodies (61 UI/mL), but antinuclear antibodies and anti-ds-DNA antibodies were negative. She previously had two deep venous thromboses of the legs and, despite the oral anticoagulant therapy, pulmonary embolism occurred. Shortly thereafter, abdominal angio-magnetic resonance imaging suggested that the infra-renal aorta was narrowed more than 50%, without thrombotic occlusion of the terminal aorta and common iliac arteries. These findings were compatible with the features of SAS. There were no atherosclerotic changes in the artery wall and no other prediposing risk factors such as smoking, oral contraceptive or hyperlipidemia. After adequate anticoagulation and intravenous prostacyclin treatment the patient's symptoms and the ischemic lesions improved markedly. To our knowledge this is the first report of the association of SAS and primary APS. The occurrence of SAS in patients with APS may dramatically increase the risk of trombothic events.
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PMID:Primary antiphospholipid syndrome associated with small aorta syndrome: a case report. 1668 64

Although there is increasing awareness of the important disease burden associated with chronic thromboembolic pulmonary hypertension (CTEPH), the pathogenesis of the disease has not been fully elucidated, and factors contributing to its development remain poorly defined. Although current data suggest that CTEPH does not result from traditional, known thrombophilia or defective plasma fibrinolysis, it has been suggested that levels of Factor VIII and antiphospholipid antibodies (alongside increased lupus anticoagulant), two thrombophilic factors associated with recurrent thrombosis, are elevated in association with CTEPH. Differences in the expression of type-1 plasminogen activator-inhibitor in CTEPH thrombi (compared with thrombi seen in acute pulmonary embolism) suggest that in situ thrombosis within vascularized fibromuscular obstructions may favor the persistence of thrombi, contributing to disease progression. Additional risk factors have been evaluated in patients with CTEPH, including blood groups (which reflect genetically determined erythrocyte-bound oligosaccharide structures) and lipoprotein (a). Certain medical conditions (splenectomy, ventriculo-atrial shunt/(infected) intravenous lines, acute pulmonary embolism, and chronic inflammatory states) have been established as independent risk factors for CTEPH. In particular, the link between splenectomy and CTEPH has gained considerable attention, with speculation that abnormal post-splenectomy erythrocyte activities or abnormal platelet activation may be involved. Although some patients may be genetically susceptible to pulmonary arterial hypertension, genetic variants linked with CTEPH have yet to be determined. Improved understanding of risk factors for CTEPH is an important goal, allowing better targeting of at-risk groups, facilitation of appropriate intervention, and potential limitation of disease progression.
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PMID:Risk factors for chronic thromboembolic pulmonary hypertension. 1696 35

Patients with severe gastrointestinal motility disorders are often found to have intravenous access clots or deep venous thrombosis. It has previously been reported that many patients who have intravenous access thrombosis have concomitant thrombotic risk factors. In this study, the goal was to determine the underlying prevalence of hypercoagulable risk in a series of patients with documented gastroparesis. Investigators studied 62 consecutive patients (52 female; mean age, 42 y) who had symptoms of gastroparesis. All patients were evaluated for placement of a gastric neural stimulation device, or they had had one placed previously. Patients underwent a hematologic interview and standardized coagulation measures of thrombotic risk. Laboratory studies measured acquired elevations of Factor VII, Factor VIII, fibrinogen, lupus anticoagulant panel, antiphospholipid antibody panel, homocysteine (in the setting of kidney disease), and activated protein resistance. Investigators also measured congenital factors: Factor VIII (with C-reactive protein levels), antithrombin III, protein C, protein S (total and free), Factor II mutation, Factor V Leiden, methylenetetrahydrofolate reductase, and homocysteine. Fifty-five patients (89%) were found to have detectable hypercoagulable risk factors. Twenty-five of the 62 patients (40%) had a documented history of abnormal clotting, including deep venous thrombosis, intravenous access thrombosis, and pulmonary embolism. All patients with a previous history of thrombosis had detectable clotting abnormalities. Of 56 patients, 40 (71%) had hypercoagulability and did not have diabetes (P=.036), and 20 (36%) had hypercoagulability and no known history of infection. However, this value was not statistically significant when infection and hypercoagulability were compared (P=.408). A high prevalence of acquired and congenital hypercoagulable defects has been observed in patients with gastroparesis, which may predispose them to arterial and venous clots. This unique finding warrants consideration of coagulation evaluation in patients with severe gastroparesis, especially when these patients are placed in high-risk thrombophilic situations, such as hospitalization, prolonged intravenous access, and surgery.
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PMID:Assessing thrombosis risk in patients with idiopathic, diabetic, and postsurgical gastroparesis. 1714 10

Mixed connective tissue disease (MCTD) is a systemic disease seen in a group of patients with overlapping clinical features of lupus, scleroderma, polymyositis, and rheumatoid arthritis. A defining feature of MCTD is the presence of antibodies against the U1-ribonucleoprotein (U1-RNP) complex. Pulmonary hypertension is the major cause of death in MCTD. We report an autopsy case of MCTD with pulmonary hypertension. The U1-RNP antibody of this patient was 171.9 U (normal < 25.0 U). The immediate cause of death was attributed to acute pulmonary embolism at left lower lobe. A severe vasculopathy characterized by fibrotic occlusion of small veins and venules, associated with prominent capillary congestion, was consistent with pulmonary veno-occlusive disease (PVOD). This is the first case reported in which PVOD is the primary cause of pulmonary hypertension in MCTD.
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PMID:Pulmonary veno-occlusive disease as a primary cause of pulmonary hypertension in a patient with mixed connective tissue disease. 1752 Feb 58

A 36-year old woman with recurrent thrombosis manifested in the form of venous thrombosis of the leg, thrombus in the right atrium and ventricle of the heart, pulmonary embolism and recurrent foetal loss, is described. Laboratory results showed prolonged APTT and normal coagulation factors. All this suggested to lupus anticoagulant (LA), which was confirmed by prolonged KCT, DRVVT, false positive VDRL test, and high level of anticardiolipin antibodies (ELISA). The diagnosis of primary antiphospholipid syndrome was established by clinical findings of recurrent thrombosis, foetal loss, presence of LA and anticardiolipin antibodies.
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PMID:[Antiphospholipid sydrome--recurrent thrombosis and foetal loss due to antiphospholipid antibodies]. 1797 23


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