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PubMed1996

Progression of superficial venous thrombosis to deep vein thrombosis.

PURPOSE: We have evaluated the progression of isolated superficial venous thrombosis to deep vein thrombosis in patients with no initial deep venous involvement. METHODS: Patients with thrombosis isolated to the superficial veins with no evidence of deep venous involvement by duplex ultrasound examination were evaluated by follow-up duplex ultrasonography to determine the incidence of disease progression into the deep veins of the lower extremities. Initial and follow-up duplex scans evaluated the femoropopliteal and deep calf veins in their entirety; follow-up studies were done at an average of 6.3 days, ranging from 2 to 10 days. RESULTS: From January 1992 to January 1996, 263 patients were identified with isolated superficial venous thrombosis. Thirty (11%) patients had documented progression to deep venous involvement. The most common site of deep vein involvement was progression of disease from the greater saphenous vein in the thigh into the common femoral vein (21 patients, 70%), with 18 of these extensions noted to be nonocclusive and 12 having a free-floating component. Three patients had extended above-knee saphenous vein thrombi through thigh perforators to occlude the femoral vein in the thigh, three patients had extended below-knee saphenous disease into the popliteal vein, and three patients had extended below-knee thrombi into the tibioperoneal veins with calf perforators. At the time of the follow-up examination all 30 patients were being treated without anticoagulation. CONCLUSIONS: Proximal saphenous vein thrombosis should be treated with anticoagulation or at least followed by serial duplex ultrasound evaluation so that definitive therapy may be initiated, if progression is noted. More distal superficial venous thrombosis should be carefully followed clinically and repeat duplex ultrasound scans performed, if progression is noted or patient symptoms worsen.

Adult↗
PubMed1998

Proposal of a new nomenclature for Budd-Chiari syndrome: hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion.

Budd-Chiari syndrome (BCS) was initially defined as a symptomatic occlusion of the hepatic veins, but subsequent reports on various obliterative changes that occur in the hepatic portion of the inferior vena cava (IVC) and hepatic vein orifices have resulted in a broadened and ambiguous definition. Membranous obstruction of the inferior vena cava has been regarded by many as a congenital vascular malformation, but its relation to the classical BCS has remained obscure. With modern imaging and recent histological study of new cases, membranous obstruction of the IVC is now considered to be a sequela to thrombosis. How to classify various forms of occlusion and stenosis of the IVC and hepatic vein ostia is a major challenge. In this review, we emphasize that primary hepatic vein thrombosis (classical Budd-Chiari) and an obliterative disease predominantly affecting the hepatic portion of the IVC, both of which account for most patients with venous outflow block, are clinically quite different. In the West, the former is more common than the latter, which constitutes the vast majority of cases of outflow block in developing countries such as Nepal, South Africa, China, and India. The latter is frequently complicated by hepatocellular carcinoma (HCC), and primary hepatic vein thrombosis is not. The major cause of thrombosis is a hypercoagulable state in hepatic vein thrombosis, but more of the latter cases are idiopathic. The clinical presentation of the latter is milder, and onset is frequently inapparent, whereas the former is more severe, sometimes causing acute hepatic failure. Markedly enlarged subcutaneous veins over the body trunk characterize the latter. We propose that these two disorders be clinically distinguished with a suggested term "obliterative hepato-cavopathy" for the latter against classical BCS.

Budd-Chiari Syndrome↗
PubMed2000

Sudden infant death syndrome, childhood thrombosis, and presence of genetic risk factors for thrombosis.

Sudden infant death syndrome or "cot death" has until the late eighties been a significant cause of death in children between the ages of 1 month and 1 year. Approximately two per 1000 children born alive dies of sudden infant death syndrome each year in Western Europe, North America, and Australia. The vulnerability of the infant brain stem to ischemia has been suggested to be a conceivable cause of sudden infant death syndrome. This is compatible with a hypothesis that genetic risk factors for cerebral thrombosis could cause microinfarction in the brain stem during the first month of life, affecting vital centers or their blood supply. The presence of three common point mutations seen in families with thrombophilia (1691G-->A in the coagulation factor V gene, 677C-->T in the methylenetetrahydrofolate reductase gene, and the 20210G-->A mutation in the prothrombin gene) could increase the risk for thrombosis in the child. This prompted us to investigate these genetic markers of thromboembolic disease in 121 cases of sudden infant death syndrome and in relevant controls, in the expectation of a more frequent occurrence of these markers if thrombosis is an etiological factor in sudden infant death syndrome. The frequency of homozygous 1691G-->A mutation in SIDS cases was higher than expected (odds ratio: 7.3, 95% confidence interval, 1.2-45.8). The allele frequencies (theta;) in cases of sudden infant death syndrome of the 1691G-->A, 677C-->T, and 20210G-->A alleles was 2.6% (1.0-5.5), 32.6% (26.8-38.9), and 0.9% (0.1-3.4), respectively. None of the allele frequencies found in the background population (3.4% for the 1691G-->A allele, 29% for the 677C-->T allele, and 1% for the 20210G-->A allele) differed significantly from that in cases of sudden infant death syndrome. In 5,251,027 inhabitants in Denmark, the incidence of venous thromboembolism was 0.9 per 1000 per year in the background population, and less than one-thousandth of these were children. Consequently it is not likely that venous thrombosis is a major cause of sudden infant death syndrome. On the other hand, this does not exclude other known or unknown risk factors for thrombosis as possible etiological factors for sudden infant death syndrome. It is likely that we must continuously employ the exclusion principle on possible etiological causes in genetic material from a large group of victims of sudden infant death syndrome if the phenomenon of sudden infant death syndrome is to be ascribed to a specific hereditary disorder.

3' Untranslated Regions↗
PubMed1996

Hepatic artery thrombosis after liver transplantation: temporal accuracy of diagnosis with duplex US and the syndrome of impending thrombosis.

PURPOSE: To determine how the interval between ultrasonography (US) and a definitive diagnosis affects the accuracy of duplex US for the diagnosis of hepatic artery thrombosis after transplantation. MATERIALS AND METHODS: Retrospective chart review was performed in 202 patients with liver transplants. Results of duplex US were compared with those of angiography, surgery, or autopsy. RESULTS: Sensitivity for US was 54% up to 1 month before and 82% on the day of the definitive diagnostic study. Specificity remained relatively constant over time (86%-87%). Accuracy reached 85%, and negative predictive value reached 93%. Qualitative changes on the sonogram enabled prediction of subsequent thrombosis. Rejection, recurrent hepatitis, aberrant anatomy, hypotension, arterial collaterals, and operator error caused false-positive or false-negative results. CONCLUSION: Although duplex US remains a good screen for hepatic artery thrombosis, angiography is strongly recommended. Serial US studies are necessary for diagnosis. Sensitivity improves over time as the clinical picture clarifies. Qualitative changes on the sonogram (the syndrome of impending thrombosis) enable prediction of subsequent hepatic artery thrombosis.

Adult↗
PubMed1988

Experimental study of acute coronary sinus thrombosis--clinical references to coronary sinus thrombosis and coronary venography.

The study was carried out to ascertain the effects caused by thrombosis in the coronary venous system. The coronary sinus (CS) of 21 adult mongrel dogs was abruptly obstructed to produce acute CS thrombosis. These dogs were then tested for serial changes of ECG, coronary arterial blood flow (CBF), left ventricular pressure (LVP), serum enzymes originating from the injured myocardium and histological changes of myocardium. Furthermore, the clinical application of a new coronary venography procedure was investigated. The results obtained in these experiments were as follows; (1) When the CS thrombosis was produced by the abrupt obstruction of the sinus, ECG patterns and serum enzymes originating from the myocardium showed changes similar to those of acute myocardial infarction. (2) The histological examinations showed that the changes in myocardial infarction were characteristically similar to those of hemorrhagic infarction. (3) Despite the complete obstruction of the coronary-venous system by thrombosis, the development of thrombosis or obstruction was not observed on the coronary-arterial side. This phenomenon is probably due to the recirculation of blood flow through the Thebesian vessels. (4) The experiment confirmed that the clear coronary venograms were easily obtained, without any risk, by the fixation of a balloon-tipped catheter inside the CS.

Animals↗
PubMed1992

Hematological causes of venous thrombosis in young people: high incidence of myeloproliferative disorder as underlying disease in patients with splanchnic venous thrombosis.

Thrombotic events occur frequently in myeloproliferative disorders, namely polycythaemia vera and essential thrombocythaemia. Standard diagnostic criteria are designed quite stringent, so that a number of patients could be underdiagnosed. Spontaneous erythroid colonies formation from bone marrow or peripheral blood in the absence of exogenous erythropoietin is considered a reliable index of myeloproliferative disorder even at early stages. Endogenous erythroid colonies (EECs) formation was assessed in 43 patients having recently suffered from venous thrombosis prior to 45 years and without a previous diagnosis of hematological disease favouring thrombosis. A screening for coagulative abnormalities associated with thrombophilia was also carried out: in 5 patients (11.6%) a plasmatic thrombogenic defect was found (quantitative deficiency of antithrombin III, 1 case, protein C, 2 cases, protein S, 1 case, and plasminogen, 1 case). In 10 patients (2 males and 8 females) (23.2%) EECs assay was positive, allowing diagnosis of myeloproliferative disease even though 7 of them did not fulfill standard diagnostic criteria. In the other 3 patients who met the criteria for diagnosis of overt myeloproliferative disease the thrombotic event was the inaugural manifestation. In all these EECs-positive patients thrombosis involved mesenteric and portal veins (n = 4), hepatic veins (n = 3), portal vein (n = 2), mesenteric vein (n = 1). One of them was simultaneously affected from congenital protein C deficiency. Thus latent or atypical forms of myeloproliferative disease as well as the overt stages were the most frequent recognized cause of splanchnic venous thrombosis, accounting for 55% of the cases of our series. On the contrary no EECs-positive subject was found among the 25 patients with other sites of thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

[Coronary atherosclerosis, coronary thrombosis and myocardial infarction in autopsy cases. 9th communication: relationship of coronary thrombosis and myocardial infarction (author's transl)].

The autopsy reports of the Pathological Institute Erfurt of the period from 1.1.1951 until 31.12.1969 were scored for cases of myocardial infarction and coronary thrombosis. Among 2,393 morphologically analysed myocardial infarctions 454 coronary thromboses (18.97 per cent) were found. Males were significantly more affected than females. Fresh infarcts showed significantly more thromboses than callous infarcts. We found fresh and occluding vessel thromboses more frequently in fresh infarctions. The analysis of age distribution yielded an increase of the rate of thrombosis in cases with myocardial infarction. On the other hand, the frequency of infarctions in cases with a coronary thrombosis was decreasing. It is suggested that the risk for infarctions is larger in younger people with coronary thrombosis than in older ones. No infarctions were detected in 165 cases of thrombosis. Preferably this group includes those cases in which the patients deceased within 6 to 8 hours and, therefore, the infarction was not morphologically detectable.

Adult↗
PubMed2003

Deep vein thrombosis followed by internal jugular vein thrombosis as a complication of in vitro fertilization in a woman heterozygous for the prothrombin 3' UTR and factor V Leiden mutations.

Thrombosis of the internal jugular vein is a rare event but one that can have serious consequences. Most cases reported in the literature have occurred in patients with indwelling central venous catheters, in association with head and neck sepsis, or in hypercoagulable states. However, a small number of cases have been associated with in vitro fertilization and more often with the ovarian hyperstimulation syndrome (OHSS). We report the case of a 30-year-old woman heterozygous for both the prothrombin 3' UTR mutation and for the factor V Leiden mutation who presented with a proximal deep vein thrombosis following in vitro fertilization. She subsequently developed an internal jugular vein thrombosis extending into the subclavian and axillary vein despite therapeutic anticoagulation with a low molecular weight heparin. Thromboembolic events can occur in the absence of other clinical features of OHSS, especially in patients with underlying prothrombotic abnormalities. Neck pain and swelling in a pregnant woman, especially one that has undergone in vitro fertilization, should be taken seriously and investigated with duplex scanning and/or MRI. Women with a personal or family history of thrombosis undergoing in vitro fertilization should be made fully aware of the potential thrombotic risks and should be considered for a thrombophilia screen.

3' Untranslated Regions↗
PubMed2002

Selectins influence thrombosis in a mouse model of experimental deep venous thrombosis.

BACKGROUND: This study characterizes venous thrombosis in the mouse and examines the important role that the adhesion molecules P-selectin and E-selectin and the anti-inflammatory cytokine interleukin-10 (IL-10) play in the thrombotic process. MATERIALS AND METHODS: C57BL/6 (wild-type) mice in a natural history protocol (Phase I) and gene-targeted (KO) mice for P-selectin, E-selectin, P/E-selectin, and IL-10 in a follow-up protocol (Phase II) were studied. Inferior vena caval thrombosis was produced by ligation just below the renal veins, and mice were sacrificed and evaluated at various time points up to 12 days later. RESULTS: Phase I: A significant increase in neutrophils on day 2 and in monocytes on day 6 postthrombosis was found in ligated vs sham animals. An associated significant increase in vein wall P-selectin mRNA (6 h, day 2) and an increase in protein (6 h through day 6) were found, while E-selectin mRNA was significantly increased (day 2 through day 6), with a smaller increase in E-selectin protein. IL-10 mRNA increased significantly later (day 2 through day 9), with the values increasing progressively. A positive correlation existed (r = 0.77) between neutrophils and thrombosis at day 2. PHASE II: The E-selectin and P/E-selectin double-KO mice showed the least thrombus at day 2 vs wild-type clotted mice, P < 0.01. Additionally, P/E-KO mice demonstrated the lowest inflammatory cell extravasation into the vein wall at day 2. CONCLUSIONS: This study demonstrates an acute to chronic inflammatory response in the vein wall associated with venous thrombosis. Inhibition of selectins decreased thrombus formation.

Animals↗
PubMed1998

Thrombotic storm: when thrombosis begets thrombosis.

Patients with hypercoagulability may present with a single thrombosis and subsequently develop progressive thromboses at other sites. With inadequate therapy, the thrombotic process may self-perpetuate, leading to multiple thromboses and even death. Six cases are presented demonstrating key features of what may be termed thrombotic storm: (1) an underlying hypercoagulable disorder; (2) a provocation to initiate thrombosis; (3) rapid development of new thromboses; (4) response to prompt use of thrombolytic agent or anticoagulant therapy; and (5) remarkable good long-term prognosis if the cycle of thrombosis is interrupted. Continued activation of coagulation by fresh thrombosis is hypothesized as the cause of the syndrome, which may explain its control by anticoagulants. Whereas these unusual patients' courses most likely represent only an extreme of hypercoagulability and not a new disorder, their characteristic behavior warrants attention.

Adult↗
PubMed2001

Sleeve-related thrombosis: a new form of catheter-related thrombosis.

In a detailed study of central venous catheter-related sleeve and thrombosis in experimental animals, a new form of thrombosis was detected and termed sleeve-related thrombosis. A silastic catheter was placed in the jugular vein and the anterior vena cava of 22 rabbits and 54 rats. After intervals of 1, 3, 7 days, 2, 3, 4 weeks and 1, 2, 4, 6 months the veins were examined by light microscopy and by transmission electron microscopy. In about 50% of the rats a thrombus was observed at the end of the catheter sleeve. Consecutive cutting allowed the visualization of a transition from a sleeve via part of sleeve and part of thrombus to a pure thrombus. This thrombus was separated from the vein wall and could not be considered a mural thrombus. As the thrombus was only attached to the terminal part of the organized catheter sleeve we propose the name sleeve-related thrombosis.

Animals↗
PubMed2001

Comparison of 3 and 6 months of oral anticoagulant therapy after a first episode of proximal deep vein thrombosis or pulmonary embolism and comparison of 6 and 12 weeks of therapy after isolated calf deep vein thrombosis. Pinede L, Ninet J, Duhaut P et al for the Investigators of the 'Durée Optimale du Traitement Antivitamines K' (DOTAVK) study. Circulation 2001; 103: 2453-60.

QUESTION: Is anticoagulant treatment for calf vein thrombosis for 6 weeks duration associated with acceptable recurrence and safety outcomes? Is anticoagulant therapy for 3 months duration for proximal deep vein thrombosis (DVT) or pulmonary embolism (PE) associated with acceptable recurrence and safety outcomes? POPULATION: Men and women with a first episode of symptomatic calf vein thrombosis or proximal DVT confirmed by ultrasound or venography, or PE confirmed by lung scan or angiography. Patients with pregnancy, thrombophilia, severe PE, and cancer were excluded. DESIGN AND METHODS: After treatment with heparin and oral anticoagulants targeting an INR of 2-3, patients with calf DVT were randomized to 6 weeks (n = 105) versus 3 months (n = 92) of treatment, and patients with proximal DVT and/or PE were randomized to 3 months (n = 270) versus 6 months (n = 269) of treatment. The outcome events were recurrences and major, minor, or fatal bleeding complications. The mean follow-up time was 12 months. RESULTS: A total of 736 patients were enrolled. For calf vein thrombosis the recurrence of DVT or PE after 6 weeks of therapy was 2/105 (2.0%) versus 3/92 (3.4%) with 3 months of therapy, relative risk of 0.58 (95% CI: 0.10-3.36). The rates of major bleeding were 1/105 (1.0%) and 3/92 (3.4%) respectively, relative risk of 0.29 (95% CI: 0.03-2.72). For proximal DVT or PE, the recurrence rate after 3 months of therapy was 21/270 (8.1%) versus 23/269 (8.7%) after 6 months of treatment, relative risk of 0.93 (95% CI: 0.53-1.65). The rates of major bleeding were 5/270 (1.9%) versus 7/269 (2.6%) respectively, relative risk of 0.73 (95% CI: 0.24-2.27). CONCLUSION: After isolated calf vein DVT, 6 weeks of oral anticoagulation is sufficient. For proximal DVT or PE, 3 and 6 months of anticoagulant therapy is equivalent. For patients with temporary risk factors who have a low risk of recurrence, 3 months of treatment seems to be sufficient.

Administration, Oral↗
PubMed1997

[Colored Doppler ultrasound-guided fine-needle aspiration biopsy of portal vein thrombosis: value in diagnosis and assessment of therapeutic efficacy for portal vein thrombosis].

OBJECTIVE: To investigate the value of colored Doppler ultrasound-guided fine-needle aspiration(FNA) biopsy of portal vien thrombosis(PVT) in diagnosis and assessment of therapeutic efficacy for PVT. METHODS: Cytologic findings from 25 portal vien thrombosis patients who underwent FNA were reviewed before and after hepatic arterial chemo-embolization(HAE) and portal vien chemotherapy. RESULTS: 1. Biopsy specimens sufficient for histologic analysis were obtained in all cases (100%). No complications resulted from this procedure. 2. The blood flow within the portal vien with thrombosis could be detected by colored Doppler systems in 25 cases before the patients accepted the treatment. The proliferation and a trabecular cellular arrangement presented in all the cell blocks. Of the 25 cases, 4 (16.0%) demonstrated necrosis of the tumor thrombi and the disappearance of blood flow within portal vein thrombi three weeks after the treatment. Among the 4, 2 were followed-up clinically and underwent second stage resection. 21 (84.0%) cases had no significant change in portal vein thrombosis pathologically and ultrasonically after the treatment. CONCLUSION: Colored Doppler ultrasound-guided FNA biopsy of portal vein thrombi is a safe, accurate, sampling-reliable biopsy technique.

Adult↗
PubMed1989

[Biventricular thrombosis in dilated cardiomyopathy. Echocardiographic and pathophysiologic study of intra-cardiac thrombosis].

The paper reports on the observations of biventricular intracardiac thrombosis in dilated cardiomyopathy. The diagnosis was made with the aid of two-dimensional echocardiography used as the method of choice in suspected intracardiac thrombosis. In the authors' opinion, the principal hemostatic disorder in intracardiac thrombosis in dilated cardiomyopathy can be caused by insufficient fibrinolysis whose degree of reduction was confirmed with stimulations tests, some of which were developed at the authors' department. Adequate treatment of intracardiac thrombosis in dilated cardiomyopathy is open to discussion. At present, apart from the standard therapy, the authors mainly suggest anti-coagulation treatment as this can prevent embolization affecting the greater or lesser blood circulation.

Blood Coagulation Disorders↗
PubMed1984

Carrageenin-induced thrombosis in the rat and mouse as a test model of substances influencing thrombosis.

Kappa-carrageenins cause disseminated intravascular coagulation with thrombosis of the tail in rats and mice. Frequency and extent of tail thrombosis were used for determining antithrombotic effects after systemic and local external administration of substances. Inhibitors of cyclooxygenase and thromboxane synthetase caused irregular inhibition of thrombosis after relatively high doses. The cyclooxygenase/lipoxygenase inhibitor BW755C was ineffective after 50 mg/kg. Hitherto, no effective substances could be found after external administration on the tail of mice. At present, no convincing explanation for thrombogenic activity of kappa-carrageenin can be given. The advantages of the thrombosis model are discussed.

Animals↗
PubMed1996

[Fibrinolysis of deep venous thrombosis on implantable perfusion devices. Apropos of a consecutive series of 57 cases of thrombosis and 32 cases of fibrinolysis].

The main complication of totally implantable venous access devices is deep venous thrombosis on catheter. It may dramatically reduce the already limited venous capacity of patients undergoing chemotherapy and obturate catheters, causing pulmonary embolism or functional disorders. These thromboses usually involve veins of the superior vena cava system where the catheters are implanted. Generally, they occur early, are extensive and often asymptomatic. Doppler ultrasonography is the diagnostic investigation of choice, phlebography being reserved for particular cases or to specify the limits of the thrombus. In a series of 412 vein access devices implanted and systematically monitored by Doppler ultrasonography, we found 57 thromboses (13.8%), 15 partial and 42 complete. The lowest thrombosis rate was observed in the right internal jugular vein (10% vs 20 to 23%, p = 0.006). Thirty-two patients received a systemic fibrinolytic treatment, 16 with streptokinase (SK), five with urokinase (UK), four with tissue plasminogen activator (rt-PA) and seven with SK/UK association. No serious side effects were observed. Sixteen repermeabilizations (50% of fibrinolysis) were obtained. There were no significant differences with respect to the fibrinolytic, the initial characteristics of thrombosis or the patients. Patients without fibrinolysis received 3 weeks of low molecular weight heparin (curative doses) then warfarin. Only one patient was repermeabilized with this treatment (significative difference with fibrinolysis: p = 0.009). Fibrinolysis is indicated in symptomatic thrombosis and/or in cases of extension to the innominate vein or the superior vena cava. Systematic monitoring by Doppler ultrasonography and prophylactic anti-thrombotic treatment are recommended in patients with implantable venous access devices in order to decrease the occurrence of thromboses, to detect asymptomatic patients at an early stage and to increase the effectiveness of fibrinolysis.

Adult↗
PubMed1996

Prevalence and distribution of calf vein thrombosis in patients with symptomatic deep venous thrombosis: a color-flow duplex study.

PURPOSE: This retrospective study was performed to identify the patterns of calf vein thrombosis in patients in whom deep vein thrombosis (DVT) was suspected and to better define the role of color-flow duplex scanning (CDS) in the evaluation of this patient population. METHODS: Over a recent 9-month period, we reviewed the vascular laboratory charts of 540 symptomatic patients (696 limbs) who underwent CDS for clinically suspected acute DVT. Patients who had a previous episode of DVT were excluded. RESULTS: CDS satisfactorily visualized all three paired calf veins in 655 of the limbs (94%). Inadequate scans (n = 41) were attributed to edema in 29, excessive calf size in eight, and anatomic inaccessibility in four. Peroneal veins were the most difficult to visualize (n = 29), followed by posterior tibial (n = 10) and anterior tibial (n = 9) veins. CDS identified acute DVT in 159 of 655 limbs (24%) that had adequate scans. Calf vein thrombi were detected in 110 of the 655 limbs (17%) and in 69% of the 159 limbs with DVT. Clots were confined to the calf veins in 53 limbs with DVT (33%). Isolated calf vein thrombi were found in 45% of outpatient limbs and in 27% of inpatient limbs with DVT. The peroneal (81%) and posterior tibial veins (69%) were more frequently involved (p < 0.001) than the anterior tibial veins (21%). In limbs with calf DVT, the prevalence of thrombosis isolated to the peroneal and posterior tibial veins was similar (37% and 25%, respectively); no limb had an isolated anterior tibial DVT (p = 0.02). CONCLUSION: CDS is a reliable method for evaluating calf veins for DVT. Calf vein thrombosis is common in patients who have acute DVT and often occurs as an isolated finding. The peroneal and posterior tibial veins are involved in the majority of cases; thrombi occur much less frequently in the anterior tibial veins. We conclude that CDS should be the noninvasive method of choice for the initial evaluation of patients in whom DVT is suspected, and we recommend that calf veins should always be studied but that routine scanning of the anterior tibial veins may not be necessary.

Acute Disease↗
PubMed1999

[20210G/A mutation of prothrombin gene in a patient with deep venous thrombosis ad pulmonary embolism without other risk factors of thrombosis].

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.

Adult↗