Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year-old man experienced chest pain, fever, bloody sputum and cough after diet therapy. Chest radiography and chest CT showed infiltration in the right lower lung field and right pleural effusion. Pulmonary embolism and infarction was diagnosed using 99mTc-MAA perfusion scans and chest enhanced CT. The patient did not have a thrombotic disposition and deep vein thrombosis in the lower extremities. This case did not have an acute onset or dyspnea, and was not typical of pulmonary embolism. The diet therapy may have caused dehydration and acted as a predisposing cause of pulmonary embolism.
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PMID:[A case of juvenile pulmonary infarction associated with diet therapy]. 1277 5

Chronic pulmonary thromboembolism is a rare but treatable cause of pulmonary hypertension. We are describing two patients with limited mobility and dyspnoea. Neither of the patients had clinical evidence of deep vein thrombosis. A high level of clinical suspicion is required for the diagnosis. Spiral CT scan establishes the diagnosis avoiding the need for pulmonary angiography. Surgical endarterectomy is the treatment of choice. Life-long anticoagulation therapy is recommended for patients in whom surgery cannot be performed. Untreated, the condition carries a high mortality.
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PMID:Chronic pulmonary thromboembolism. 1297 82

Venous thromboembolism (VTE) occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium. In the general population the incidence of pregnancy associated VTE is approximately 1 in 1500 deliveries The risk of VTE is five times higher in a pregnant than in a non-pregnant woman. Postpartum the VTE-risk is even higher. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose pregnancy-associated VTE clinically is generally poor, since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant of choice. In case of acute thrombosis during pregnancy, treatment is performed like in nonpregnant patients. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.
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PMID:Pregnancy-associated thrombosis. 1367 67

Venous thromboembolism occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium and remains a diagnostic and therapeutic challenge. In the general population the incidence of pregnancy associated VTE has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries. The risk of VTE is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum VTE is more common than antepartum VTE. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose deep-vein thrombosis clinically is generally poor and is further hampered during pregnancy since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury. Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant treatment of choice during pregnancy. In case of acute new onset of thrombosis during pregnancy, treatment is performed like in non-pregnant patients with acute deep vein thrombosis or pulmonary embolism. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.
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PMID:Thrombosis during pregnancy: risk factors, diagnosis and treatment. 1367 66

A 62-year-old man with a past medical history notable for hypertension, osteoarthritis, and calf deep vein thrombosis at age 55 following a total hip arthroplasty presents to the emergency department with acute-onset dyspnea and right-sided pleuritic chest pains. His medications consist of a calcium channel blocker and a COX-2 inhibitor. Pretest clinical suspicion for pulmonary embolism (PE) is high. Ventilation and perfusion lung scintigraphy are interpreted as being high-probability for PE. The nurse asks if a stat transthoracic echocardiogram should be ordered.
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PMID:Patients with acute pulmonary embolism should have an echocardiogram to guide treatment decisions. 1468 Mar 5

We describe a 30-year-old male who presented with acute onset of breathlessness, tachycardia, and palpitations associated with distension of jugular vein and clear lungs on physical examination. The chest X-ray was normal and ECG was showing S1Q3T3 and right ventricular strain pattern. His 2-D echocardiography was showing dilated right atrium, right ventricular dilatation and moderate pulmonary arterial hypertension. He was found to have thrombosis involving left side of deep venous system with normal superficial venous system (Doppler proved). All routine blood investigations for etiology of recurrent DVT were normal except serum homocyteine level, which was significantly raised. Megaloblastic anemia on peripheral smear and hyperhomocysteinemia prompted us to search for its cause, which was subsequently found to be vitamin B12 deficiency. Such an association of megaloblastic anemia due to vitamin B12 deficiency leading to hyperhomocysteinemia and subsequent thrombosis in left venous system presenting as acute pulmonary embolism has not been described earlier in the medical literature.
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PMID:Hyperhomocysteinemia masquerading as pulmonary embolism. 1471 Sep 83

Treatments effective against multiple myeloma may be useful in primary systemic amyloidosis (AL). Thalidomide is active in myeloma. Results of the first 12 patients enrolled on a phase II trial of thalidomide for AL are presented. Progressive edema, cognitive difficulties, and constipation occurred in approximately 75%; dyspnea, dizziness and rash in 50%. Five developed progressive renal insufficiency. Deep venous thrombosis and syncope each occurred in two. Median time on the study was 72 days, range was 25 to 333 days. All 12 have withdrawn from the study (side-effects, 6; progression, 4; and death, 2 patients). AL patients do not tolerate high dose thalidomide.
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PMID:Poor tolerance to high doses of thalidomide in patients with primary systemic amyloidosis. 1498 85

Overuse of the d-dimer to screen for possible pulmonary embolism (PE) can have negative consequences. This study derives and tests clinical criteria to justify not ordering a d-dimer. The test threshold was estimated at 1.8% using the method of Pauker and Kassirer. The PE rule-out criteria were derived from logistic regression analysis with stepwise backward elimination of 21 variables collected on 3148 emergency department patients evaluated for PE at 10 US hospitals. Eight variables were included in a block rule: Age < 50 years, pulse < 100 bpm, SaO(2) > 94%, no unilateral leg swelling, no hemoptysis, no recent trauma or surgery, no prior PE or DVT, no hormone use. The rule was then prospectively tested in a low-risk group (1427 patients from two hospitals initially tested for PE with a d-dimer) and a very low-risk group (convenience sample of 382 patients with chief complaint of dyspnea, PE not suspected). The prevalence of PE was 8% (95% confidence interval: 7-9%) in the low-risk group and 2% (1-4%) in the very low-risk group on longitudinal follow-up. Application of the rule in the low-risk and very low-risk populations yielded sensitivities of 96% and 100% and specificities of 27% and 15%, respectively. The prevalence of PE in those who met the rule criteria was 1.4% (0.5-3.0%) and 0% (0-6.2%), respectively. The derived eight-factor block rule reduced the pretest probability below the test threshold for d-dimer in two validation populations, but the rule's utility was limited by low specificity.
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PMID:Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. 1563 91

A 76-year-old woman underwent a left pneumonectomy for a primary adenocarcinoma. On the fourth postoperative day, when walking to the toilet, she suddenly developed syncope followed by dyspnea and cardiopulmonary arrest. Although we performed cardiopulmonary resusciation, she died 1 hour later. With her family's approval, we performed autopsy. We found massive pulmonary thromboembolism was identified in the right main artery. To prevent postoperative thromboembolic complications, we use postoperatively continuous intravenous heparin sodium infusion (5,000-6,000/24 h) for the patients underwent thoracotomy and examine the ultrasonography for deep vein thrombosis before they begin to walk.
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PMID:[Sudden death due to massive pulmonary thromboembolism after pneumonectomy; report of a case]. 1536 79

A 28-year-old man presented with mental retardation, peculiar facial features, radioulnar synostosis, hypogonadism, aplasia of the right kidney, a moderate degree of proteinuria, and peripheral cyanosis. The activated partial thromboplastin time was shortened, and the level of plasma factor VIII was high. A chromosomal analysis revealed a 49, XXXXY karyotype. From the 10th hospital day, he suffered from sudden dyspnea following swelling of the left leg. He was diagnosed as having deep vein thrombosis and pulmonary embolism, and was successfully treated with anticoagulant therapy. This is the first case of the 49, XXXXY syndrome complicated with unilateral renal aplasia, proteinuria, and venous thromboembolism.
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PMID:49, XXXXY syndrome with unilateral renal aplasia, proteinuria, and venous thromboembolism. 1564 56


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