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)

We report a 14-year-old boy with systemic lupus erythematosus and anticardiolipin antibodies. He developed asymptomatic superior vena cava thrombosis and silent pulmonary embolism. Computed tomographic scan of his chest and abdomen showed features of long standing obstruction secondary to superior vena cava thrombosis. Asymptomatic thrombosis of the major vessels and silent pulmonary emboli are part of the disease spectrum of pediatric antiphospholipid syndrome.
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PMID:Asymptomatic superior vena cava thrombosis and pulmonary embolism in an adolescent with SLE and antiphospholipid antibodies. 803 93

Recurrent pulmonary emboli or microthromboses are hypothesized as possible causes of pulmonary hypertension in the antiphospholipid syndrome (APS), but thrombosis of the pulmonary vessels has been rarely documented. We describe the case of a 45-year-old Caucasian man affected by thrombocytopenia, recurrent deep venous thrombosis, recurrent pulmonary embolism and fatal chronic pulmonary hypertension (systolic pressure: 85 mm Hg). Anticardiolipin antibodies were highly positive, and the lupus anticoagulant was present. At autopsy, recent thromboses of small vessels were observed in the lung, with organized clots and recanalized channels. Furthermore, friable and firm vegetations and nodules were observed on the cusps of the mitral and tricuspid valves, intermingled with recent surface fibrinous thrombi. In the adrenals we found vascular thrombotic lesions similar to those in the lungs. The pathological lesions suggest pulmonary hypertension secondary to pulmonary arterial microthromboses. Moreover, this is the first documentation of tricuspid valve pathology in a patient with APS.
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PMID:Pulmonary hypertension secondary to thrombosis of the pulmonary vessels in a patient with the primary antiphospholipid syndrome. 806 40

The association of deep vein thrombosis with systemic necrotizing vasculitis is infrequent. Herein are referred two patients with microscopic polyarteritis and one patient with overlap syndrome who developed deep vein thrombosis which complicated in two cases with pulmonary embolism. The clinical features and the pathogenic mechanisms involved in this infrequent association are analyzed. In two patients the thrombosis was simultaneous with the diagnosis of vasculitis. In one patient deep vein thrombosis was the cause of hospital admission. Advanced age and thrombocytosis are factors associated to vasculitis, which may favor the development of thromboembolic disease. The presence of antiphospholipid syndrome was discarded. Although infrequent, this association should be considered because of the potential severe complications.
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PMID:[Deep venous thrombosis associated with necrotizing vasculitis]. 811 40

Clinical manifestations of the antiphospholipid syndrome result from thromboembolic phenomena that occur in all vascular territories. Cardiac manifestations frequently associated with this syndrome include valvular and myocardial lesions. We present a case report of primary antiphospholipid syndrome in a pregnant young woman with a right atrial mass detected by echocardiography. Its morphological characteristics presented problems in establishing differential diagnosis within atrial thrombus and atrial myxoma. This case was complicated by pulmonary embolism and recurrence of the mass within four months. Cardiac surgery was performed and two masses excised. Histopathological studies showed them to be thrombotic in nature.
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PMID:[A recurrent intracardiac mass in a pregnant woman with the antiphospholipid antibody syndrome]. 814 Sep 22

Pulmonary manifestations of the antiphospholipid syndrome (APS) include pulmonary hypertension, pulmonary embolism, and in patients with the catastrophic APS, respiratory insufficiency associated with diffuse pulmonary infiltrates. There are few descriptions of pathological findings associated with these pulmonary complications. We document pulmonary capillaritis, recurrent microvascular thrombosis and alveolar hemorrhage in patients with APS. These patients have a wide spectrum of clinical presentations, ranging from recurrent episodes of fever, minimal hemoptysis, and mild dyspnea, to respiratory insufficiency requiring mechanical ventilation. Pulmonary involvement can occur alone or simultaneously with other manifestations of APS and may range from mild to severe. Pulmonary capillaritis and alveolar hemorrhage are complications of APS, and whether they are causally related to recurrent thromboembolism and pulmonary hypertension remains undetermined.
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PMID:Pulmonary capillaritis, alveolar hemorrhage, and recurrent microvascular thrombosis in primary antiphospholipid syndrome. 837 Dec 25

Systemic lupus erythematosus (SLE) is the most common of the connective tissue disorders and can involve virtually any organ in the body. It is associated with pleuropulmonary manifestations in well over 50% of cases. Pleuritis with or without pleural effusion is the most common manifestation and can be particularly troublesome to manage but is rarely life-threatening. More serious manifestations in the lung include acute lupus pneumonitis with or without alveolar haemorrhage, chronic lupus pneumonitis and pulmonary hypertension. These all contribute significantly to overall mortality in SLE. The association between SLE and the antiphospholipid syndrome, leading to venous thrombosis and pulmonary embolism, is well recognized. Up to 20% of all cases of SLE present in childhood and many of these have pulmonary features at presentation or during the course of their illness. Sepsis is one of the main causes of death in SLE and pulmonary sepsis in these often immunocompromised patients contributes a significant proportion. Several drugs can produce a clinical syndrome that has many of the clinical and immunological features of SLE. Pleuritis may be seen in up to half of these cases of drug induced SLE. The development of SLE and conditions such as sarcoidosis or asbestosis in the same patient may represent a simple coincidence but there is some evidence for a closer association between these disorders.
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PMID:Systemic lupus erythematosus. 851 77

Pulmonary hypertension may occur in the antiphospholipid syndrome as a result of recurrent pulmonary embolism or microthrombosis of pulmonary vessels. We describe 3 cases of primary antiphospholipid syndrome (APS) and cor pulmonale that fulfilled the criteria for chronic major vessel thromboembolic pulmonary hypertension. Pulmonary thromboendarterectomy was performed in all 3 patients and it was successful in 2. One patient died in the immediate postoperative period from hemorrhagic pulmonary edema. Chronic thromboembolic pulmonary hypertension should be added to the list of pulmonary vascular complications of primary APS. Despite its risk, pulmonary thromboendarterectomy represents a treatment option for this otherwise lethal condition.
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PMID:Primary antiphospholipid syndrome presenting as chronic thromboembolic pulmonary hypertension. Treatment with thromboendarterectomy. 873 Jan 45

Chronic pulmonary embolism may occur in the antiphospholipid syndrome. Antiphospholipid antibodies including the lupus anticoagulant and anticardiolipin should therefore be searched for systematically in these patients. Blood clotting (lupus anticoagulant) and immunological (anticardiolipin) investigations are complementary; their positivity may be dissociated. If the thrombus is located in the proximal pulmonary artery, surgical thrombectomy is possible. Operative mortality ranges from 12.6% to 20%. The association of oral anticoagulants with low dose aspirin is indicated for the long term treatment of these patients. The role of steroid therapy is discussed. The authors report the case of a patient with antiphospholipid antibodies who successfully underwent surgical removal of a chronic pulmonary embolism.
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PMID:[Pulmonary thrombectomy in a patient with antiphospholipid syndrome]. 874 22

Pregnancy is a risk factor for deep and superficial venous thrombosis because of hemodynamic changes and modifications of the coagulation and fibrinolitic systems. In case of a patient suffering from a congenital or acquired thrombophilia, risk of severe and recurrent thrombosis becomes much higher, with the possibility of a life threatening complication as pulmonary embolism. Recently a number of congenital thombophilic syndromes have been described, in particular congenital hereditary deficit of coagulation inhibitors. Among the acquired pathologies, the antiphospholipid syndrome has been recently object of studies. Diagnostic and therapeutic options are still controversial. The authors present a case of recurrent deep vein thrombosis in pregnancy treated with positioning of a caval filter for the prophylaxis of pulmonary embolism. Diagnostic difficulties are discussed, as the patient presented with low levels of the coagulation inhibitor protein S, and also circulating antibodies anticardiolipin.
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PMID:[Deep venous thrombosis in pregnancy: diagnostic difficulties and therapeutic indications. Discussion of a clinical case]. 892 85

Thromboprophylaxis with oral anticoagulants up to six months is established in patients after a first venous thromboembolic event (VTE). The risk of recurrent VTE is still considerable thereafter, and it is uncertain whether some patients might benefit from extended anti-coagulation. We performed a prospective, multicenter trial (4 thrombosis centers) and evaluated in 380 patients with a first or recurrent VTE (patients with a deficiency of antithrombin, protein C, protein S or plasminogen; cancer; or an antiphospholipid antibody syndrome were excluded) the risk of recurrence after discontinuation of secondary thromboprophylaxis with oral anticoagulants. It was the aim of the study to evaluate whether patients, with factor V Leiden are at an increased risk of recurrent VTE. 112 (29.5%) patients were carriers of factor V Leiden (26.9% heterozygous, 2.6% homozygous). After a median observation time of 19.3 months the overall recurrence rate of VTE was 9.9%. Recurrent deep vein thrombosis and/or pulmonary embolism occurred in 26 of 268 patients without factor V Leiden (9.7%) and in 10 of 112 patients with factor V Leiden (8.9%). The probability of recurrent VTE two years after discontinuation of oral anticoagulants was 12.4% (95% CI 7.8-17) in patients without factor V Leiden and was 10.6% (95% CI 3.8-17.4) in carriers of the mutation. This difference was statistically not significant. Patients with factor V Leiden are not at a higher risk of recurrent VTE within two years after discontinuation of oral anticoagulants than patients without factor V Leiden. Balancing the risk of recurrent VTE and bleeding from oral anticoagulants, patients with factor V Leiden are not likely to benefit from oral anticoagulant therapy extended beyond six months.
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PMID:The risk of recurrent venous thromboembolism in patients with and without factor V Leiden. 913 32


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