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 78-year-old male underwent coronary angiography because of angina pectoris. He was revealed to have essential thrombocythemia with a platelet count of over 1,000,000/mm3. Essential thrombocythemia belongs to the group of chronic myeloproliferative disorders. It displays both thrombogenic and bleeding tendency due to the increased platelet count, as well as to dysfunction. CABG was performed using the left internal thoracic artery and the right gastroepiploic artery. Hydroxycarbamide was taken to regulate the platelet count before surgery. There was no difficulty with hemostasis during surgery. Warfarin and hydroxycarbamide were used as anticoagulant therapies after surgery. Postoperative CAG demonstrated both grafts to be patients. The patient remained in good condition until he died suddenly on the 159th postoperative day. The cause of death was not clear because no autopsy was carried out. The death may have been associated with a thromboembolism, acute graft thrombosis or cerebral infarction, or pulmonary embolism. This patient did not take antiplatelet drugs because the platelet count and prothrombin time was well controlled. Nonetheless, an antiplatelet agent might reduce the risk of thromboembolism in such patients. It is suggested that meticulous anticoagulation therapy must be important for a patient with essential thrombocythemia, especially in the postoperative period.
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PMID:[A case of coronary artery bypass surgery using left internal thoracic artery and right gastroepiploic artery for a patient with essential thrombocythemia]. 978 79

Thrombogenicity of factor IX complex or prothrombin complex concentrates (PCC) is a well-acknowledged problem. The exact incidence is unknown but has decreased with the improvement of the quality of coagulation factor concentrates and a more judicious use of these products. The clinical spectrum of thrombogenicity ranges from superficial thrombophlebitis, deep-vein thrombosis and pulmonary embolism, and arterial thrombosis to disseminated intravascular coagulation. Several risk factors have been identified: (a) predisposing clinical factors (underlying disease and clinical condition), (b) therapy factors (dosing, concomitant therapy and drug interactions), and (c) quality of the PCC used. It is generally assumed that the risk of thromboembolic adverse effects is greater in patients with acquired disorders of hemostasis than in patients with inherited coagulation factor deficiencies. In hemophilia B, clinical conditions with an increased risk include large muscle hematomas, immobilization, surgery (especially orthopedic surgery), and liver disease. In acquired disorders of hemostasis, a prethrombotic state can be assumed in all patients where an indication for PCC concentrates is considered. Liver disease and/ or antithrombin deficiency are considered as major risk factors. Therapy factors with an increased risk include large, repetitive doses of PCC. It is assumed that heparin and, in the case of antithrombin deficiency, antithrombin substitution decrease the incidence of thromboembolic adverse effects. Heparin neutralisation with protamine and aprotinin therapy may be additional risk factors. The declining incidence and the recent cluster of fatal thromboembolic adverse events in Germany with one brand of PCC is strong evidence for the crucial role of the quality of PCC in the occurrence of thromboembolic adverse effects.
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PMID:Thrombogenicity of prothrombin complex concentrates. 1049 4

A 46-year old nurse complaining of multiple hematomas including bleeding into the tongue was referred for hemostasis evaluation. A very low Quick percentage value, i.e. a severely prolonged prothrombin time with severely depressed vitamin K-dependent coagulation factors (FII:C, FVII:C, FX:C) and normal FV:C and fibrinogen level was found. In the absence of cholestasis, malabsorption and broad-spectrum antibiotic therapy, ingestion of vitamin K antagonists was suspected. Three years previously, she had been on oral anticoagulant treatment with phenprocoumon (Marcoumar) for postoperative pulmonary embolism. She denied having voluntarily ingested anticoagulant drugs. A high plasma level of coumarins was found. To exclude accidental ingestion, the patient's son living in the same household was tested as well. Surprisingly, a low level of coumarin was found also in his plasma. We suspect that the patient voluntarily intoxicated herself and gave a low dose of coumarin anticoagulant to her son as well.
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PMID:[46-year-old woman with multiple hematomas and bleeding of the base of the tongue: phenprocoumon poisoning]. 1051 30

With the aim of establishing whether the HR2 haplotype in factor V affects the risk of venous thromboembolism, a retrospective multicenter cohort study was performed in 810 family members identified through 174 probands who suffered from at least 1 episode of deep vein thrombosis and/or pulmonary embolism and had an inherited defect associated with thrombophilia (antithrombin, protein C, or protein S deficiency; factor V R506Q or prothrombin G20210A). Fifty-eight percent (468/810) of the family members had an inherited defect and 10% (47/468) were symptomatic. The HR2 haplotype was found in association with factor V R506Q more frequently in family members with venous thromboembolism (18%) than in those without (8%). Double heterozygosity for factor V R506Q and HR2 conferred a 3- to 4-fold increase in the relative risk of venous thromboembolism compared with factor V R506Q alone. The median age at first event was lower when the 2 defects were associated (46 v 52 years). No increase in risk of venous thromboembolism could be demonstrated when the HR2 haplotype was associated with inherited thrombophilic defects other than factor V R506Q. Because both factor V R506Q and the HR2 haplotype are very frequent, the effect of their coinheritance on the risk of venous thromboembolism might represent a clinically relevant issue, and screening for HR2 in carriers of factor V R506Q should be considered.
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PMID:Coinheritance of the HR2 haplotype in the factor V gene confers an increased risk of venous thromboembolism to carriers of factor V R506Q (factor V Leiden). 1055 90

A new genetic anomaly predisposing to venous thrombosis was described in 1996, namely the transition of guanine (G) to adenine (A) at position 20210 in the 3-untranslated region of the prothrombin gene. This mutation is associated with high levels of plasma prothrombin and increased risk of thrombotic events in the venous system. We report the case of a man who, lacking known risk factors for thrombosis, suffered a massive pulmonary embolism and deep venous thrombosis in both lower legs. Thrombophilic analysis confirmed that the patient and close relatives were carriers of the heterozygotic 20210G/A variant of the prothrombin gene. Two relatives with the genetic defect had also suffered some type of deep venous thrombosis.
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PMID:[20210G/A mutation of prothrombin gene in a patient with deep venous thrombosis ad pulmonary embolism without other risk factors of thrombosis]. 1068 43

The authors report the case of a 30-year-old man who died from pulmonary embolism and multiorgan failure caused by mesenteric and inferior vena cava thrombosis. The patient was found heterozygous for the prothrombin gene variant (G 20210 A). The family study showed the same asymptomatic anomaly in his brother. This recently described mutation is associated with an increased risk for venous thrombosis. The investigations and treatment of mesenteric venous thrombosis are discussed.
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PMID:[Mesenteric vein and inferior vena cava thrombosis: disseminated intravascular coagulation and/or G 20210 A mutation of the prothrombin gene?]. 1075 55

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international norrmalized ratio (INR) of 2.5-6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.
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PMID:Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation. 1078 17

We examined various nonSTAT commercially available coagulation activation markers in an attempt to help diagnose or exclude the often subtle clinical presentations of proximal deep vein thrombosis (PDVT) and pulmonary embolism (PE). Fifty-five patients presenting to the Emergency Department were completely assessed. Eleven patients were diagnosed with PDVT, six patients were diagnosed with PE, and three patients were diagnosed with both PDVT and PE. Thrombus precursor protein (TpP) excluded the diagnosis in 19 of the 35 patients negative for PDVT and/or PE, D-Dimer in 15 patients, prothrombin fragment 1.2 in 17 patients, and thrombin-antithrombin (TAT) in 14 patients. Both the TpP and TAT enzyme-linked immunosorbent assay (ELISA) tests had 100% sensitivity and negative predictive value for evaluating PDVT and/or PE. The TpP ELISA had the highest specificity (54%) of all four markers studied.
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PMID:The use of thrombus precursor protein, D-dimer, prothrombin fragment 1.2, and thrombin antithrombin in the exclusion of proximal deep vein thrombosis and pulmonary embolism. 1084 25

We report a case of a 35-year-old male with a history of recurrent thromboembolic events, who presented to the emergency room with right sided weakness and difficulty with speech. The patient's past medical history included two myocardial infarctions, two deep vein thromboses, and a pulmonary embolism. Subsequent laboratory evaluation indicated that the patient was heterozygous for both the factor V Leiden and prothrombin G20210A mutations. This case report emphasizes the importance of evaluating patients with suspected hereditary thrombophilia for both of these mutations.
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PMID:Concurrent factor V Leiden and prothrombin G20210A gene mutations in a patient with a history of recurrent thrombosis. 1086 Feb 31

Plasma levels of prothrombin fragment 1+2 (Fl+2), thrombin-antithrombin complexes (TAT) and D-dimers were measured in 15 patients with pulmonary embolism during heparin therapy, oral anticoagulation, and after cessation of warfarin therapy. Each patient had a favorable outcome during anticoagulant therapy (3 months), but late venous thromboembolism occurred in six cases. The mean levels of the three markers were significantly increased on day 4 after the thrombotic event, and normalized during warfarin therapy. Nine months after the initial pulmonary embolism, mean levels of the three markers, as compared with a control population, were significantly higher in the patients with late recurrences, whereas only TAT were slightly higher in patients without recurrences as compared with controls. Only TAT levels were significantly higher in the patients with late recurrences than in those without late recurrences. Thus, the levels of the three markers 9 months after pulmonary embolism seem to be interesting to identify patients with high risk of recurrence and who might require longer anticoagulant treatment.
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PMID:Markers of hemostatic system activation in pulmonary embolism. Changes during and after cessation of anticoagulant treatment. 1087 Aug 5


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