Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1998

Predischarge two-dimensional echocardiographic evaluation of left ventricular thrombosis after acute myocardial infarction in the GISSI-3 study.

Left ventricular (LV) thrombosis can be found in patients with acute myocardial infarction (AMI). No wide multicenter trial on AMI has provided information about LV thrombosis until now. The protocol of the GISSI-3 study included the search for the presence of LV thrombosis in patients from 200 coronary care units that did not specifically focus on LV thrombosis. We examined the GISSI-3 database results related to 8,326 patients at low to medium risk for LV thrombi in which a predischarge echocardiogram (9 +/- 5 days) was available. LV thrombosis was found in 427 patients (5.1%): 292 of 2,544 patients (11.5%) with anterior AMI and in 135 of 5,782 patients (2.3%) with AMI in other sites (p <0.0001). The incidence of LV thrombosis was higher in patients with ejection fraction < or = 40% (151 of 1,432 [10.5%] vs 276 of 6,894 [4%]; p <0.0001) both in the total population and in the subgroup with anterior AMI (106 of 597 [17.8%] vs 186 of 1,947 [9.6%]; p <0.0001). Multivariate analysis showed that only the Killip class > I and early intravenous beta-blocker administration were independently associated with higher LV thrombosis risk in the subgroup of patients with anterior AMI (odds ratio 1.75, 95% confidence interval 1.28 to 2.39; odds ratio 1.32, 95% confidence interval 1.02 to 1.72, respectively). In patients with anterior AMI, oral beta-blocker therapy given or not given after early intravenous beta-blocker administration does not influence the occurrence of LV thrombosis. The rate of LV thrombosis was similar in patients treated or not treated with nitrates and lisinopril both in the total population and in patients with anterior and nonanterior AMI. In conclusion, in the GISSI-3 population at low to medium risk for LV thrombi, the highest rate of occurrence of LV thrombosis was found among patients with anterior AMI and an ejection fraction < 40%. Killip class > I and the early intravenous beta-blocker administration were the only variables independently associated with a higher predischarge incidence of LV thrombosis after anterior AMI.

Adrenergic beta-Antagonists↗
PubMed1999

Frequent factor II G20210A mutation in idiopathic portal vein thrombosis.

BACKGROUND & AIMS: Despite extensive investigations of portal vein thrombosis, no underlying cause is identifiable in up to 30% of patients. A recently described mutation of the prothrombin gene at nucleotide position 20210 is associated with history of venous thrombosis and was assessed in this study. METHODS: We compared the frequency of factor II G20210A and factor V G1691A (factor V Leiden) mutations in 10 patients with idiopathic portal vein thrombosis, 10 patients with nonidiopathic portal vein thrombosis, 60 patients with deep vein thrombosis of the legs, and 42 control subjects. RESULTS: The frequency of factor II G20210A mutation was increased in patients with idiopathic portal vein thrombosis (40.0%; confidence interval, 3.1%-76.9%) compared with controls (4.8%; confidence interval, 0%-11.5%) or patients with nonidiopathic portal vein thrombosis or deep vein thrombosis (P = 0.0001). In contrast, the frequency of the factor V G1691A mutation was similar in subjects with portal vein thrombosis and in controls but was increased in patients with deep vein thrombosis (P = 0.0001). CONCLUSIONS: The factor II G20210A mutation is frequent in patients with idiopathic portal vein thrombosis and should therefore be assessed under this circumstance.

Adult↗
PubMed1996

Central venous thrombosis after cardiac operations in children.

To evaluate the incidence, mortality, late outcome, and cause of central venous thrombosis after pediatric heart operations and other operations performed with cardiopulmonary bypass, we identified patients with postoperative central venous thrombosis during a 10-year period at a single pediatric hospital. There had been 1591 open heart (with bypass) and 1086 closed heart (no bypass) procedures and 13 operations with cardiopulmonary bypass for extracardiac indications. There were 20 patients with central venous thrombosis, yielding incidences of 1.1% and 0.2% after cardiopulmonary bypass and after closed heart operations, respectively. When neonates were compared with older children (1 to 119 months of age) undergoing heart procedures, a tenfold increase (5.8% vs 0.6%) (p < 0.001) in the incidence of central venous thrombosis was observed. The mortality was eight of 20 (40%). Central venous thrombosis contributed to seven deaths and it was a direct cause of one death. Ten patients were reinvestigated 5 to 108 months after central venous thrombosis. The outcome of surgery was excellent in eight. Two had residual thrombosis, but this was not hemodynamically significant to the cardiorespiratory condition of the patients. During or preceding thrombosis, low levels of antithrombin III and/or protein C and high levels of the plasminogen activator inhibitor were observed in five of the patients. A congenital thrombotic risk factor, "resistance to activated protein C," was found in two of 12 tested patients with central venous thrombosis (17%). In conclusion, central venous thrombosis, especially in neonates, is an important cause of morbidity and mortality after cardiac operations. The cause is multifactorial, with contributions from multiple acquired thrombophilic coagulation abnormalities, and resistance to activated protein C may act as a risk factor for thrombosis already during neonatal period.

Blood Coagulation Tests↗
PubMed2003

Antiphospholipid thrombosis syndromes.

Antiphospholipid antibodies are associated strongly with thrombosis and are the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, numerous theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACLAs are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). Patients with type V disease are those with antiphospholipid antibodies and RMS. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of ACLAs in association with arterial and venous thrombosis strongly suggests that they should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I-VI) should be defined, if possible, because this identification may dictate both the type and the duration of immediate and long-term anticoagulant therapy. Unlike those patients with ACLAs, patients with primary LA-thrombosis syndrome usually have venous thrombosis. Because the aPTT is unreliable in patients with LA (prolonged in only approximately 40%-50% of patients) and usually is not prolonged in patients with ACLAs, definitive tests, including ELISA for ACLA, the dilute Russell's viper venom time for LA, hexagonal phospholipid-neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be ordered immediately when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these test results are negative, subgroups also should be assessedin the appropriate clinical setting. Most patients with antiphospholipid thrombosis syndrome will fail to respond to warfarin therapy, and except for retinal vascular thrombosis, may fail some types of antiplatelet therapy, so it is of major importance to make this diagnosis so patients can be treated with the most effective therapy for secondary prevention-LMWH or unfractionated heparin in most instances and clopidogrel in some instances.

Antiphospholipid Syndrome↗
PubMed2001

Kidney retransplants after initial graft loss to vascular thrombosis.

BACKGROUND: Vascular thrombosis early after a kidney transplant is an infrequent but devastating complication. Often, no cause is found. These recipients are generally felt to be good candidates for a retransplant. However, their ideal care at the time of the retransplant and their outcomes have not been well documented. We studied outcomes in 16 retransplant recipients who had lost their first graft early posttransplant (< 1 month) to vascular thrombosis. METHODS: Of 2,003 kidney transplants between I January 1984 and 30 September 1998, we identified 32 recipients who had lost their first graft early posttransplant to vascular thrombosis. Of these 32 recipients, 16 were subsequently retransplanted and detailed chart reviews were done. RESULTS: Of the 16 retransplant recipients, 12 lost their first graft to renal vein thrombosis and 4 to renal artery thrombosis. Thrombosis generally occurred early (mean, 3.6 d). Five recipients underwent a complete hematologic workup to rule out a thrombophilic disorder before their retransplant: 4 had a positive result (presence of antiphospholipid antibodies, n = 3; increased homocysteine levels, n = 1). These 4 recipients, along with 1 other recipient who had a strong family history of thrombosis, underwent thrombosis prophylaxis at the time of their retransplant. Prophylaxis consisted of low-dose heparin for the first 3-5 d posttransplant, followed by acetylsalicylic acid or Coumadin. Of the 16 retransplant recipients, none developed thrombosis. Of the 5 who underwent thrombosis prophylaxis, none had significant bleeding complications. At a mean follow-up of 5.4 yr, 10 (63%) recipients have functioning grafts. Causes of graft loss in the remaining 6 recipients were death with function (n = 5, 31%) and acute rejection (n = 1.6%). Graft and patient survival rates after these 16 retransplants were equivalent to results after primary transplants. The incidence of acute and chronic rejection was also no different (p = ns). CONCLUSION: Vascular thrombosis in the absence of obvious technical factors should prompt a workup for a thrombophilic disorder before a retransplant. Recipients with an identified disorder should undergo prophylaxis at the time of the retransplant. Results in these retransplant recipients are equivalent to those seen in primary transplant recipients.

Chromatography, High Pressure Liquid↗
PubMed2001

Pathophysiology and diagnosis of deep venous thrombosis.

Lower-limb deep venous thrombosis (DVT) affects between 1% to 2% of hospitalized patients. These thrombi disrupt the vascular integrity of the lower limbs and are the source of emboli that kill approximately 200,000 patients each year in the United States. The causes of thrombosis include vessel wall damage, stasis or low flow, and hypercoagulability. These factors favor clot formation by disrupting the balance of the opposing coagulative and fibrinolytic systems. The symptoms and signs of venous thrombosis are caused by obstruction to venous outflow, vascular inflammation, or pulmonary embolization. About 70% of patients referred for clinically suspected venous thrombosis, however, do not have the diagnosis confirmed by objective testing. Among the 30% who have venous thrombosis, about 85% have proximal vein thrombosis, and the remainder have thrombosis confined to the calf. Physicians cannot rely on signs and symptoms to make the diagnosis of DVT and must depend on imaging studies to guide treatment. Patients with proximal vein thrombosis who are inadequately treated have a 47% frequency of recurrent venous thromboembolism over 3 months. In contrast, clinically detectable recurrence occurs in less than 2% of patients with proximal vein thrombosis if an adequate anticoagulant response is achieved. Of the diagnostic procedures for DVT, venography is the only invasive test of proven value, and ultrasonographic (US) studies are the most commonly used noninvasive modaity. Other procedures are occasionally used to diagnose DVT, including impedance plethysmography, computed tomography, and magnetic resonance imaging. US examinations are noninvasive, they are rapidly obtained, and they can be performed serially. In symptomatic patients, venous US is sensitive and specific for proximal DVT; however, US is insensitive to calf vein thrombosis and to asymptomatic DVT occurring after surgery. Patients with symptoms of recurrent DVT also can present a difficult diagnostic problem. Only about 20% to 30% of these individuals actually have the disease; the rest have symptoms arising from chronic venous insufficiency or from any of the causes of lower extremity pain. After an acute episode, up to 50% of patients have compression ultrasound abnormalities for 6 months that are indistinguishable from the original findings of DVT. Hence, there are a significant number of patients and clinical circumstances in which the diagnosis of DVT is difficult. 99mTc-radiolabeled peptides that target the molecular biology of thrombosis should aid in the management of the disease, particularly in asymptomatic patients at high risk, in patients with recurrent symptoms, in patients with active DVT in the calf and/or pelvis, and in patients with intermediate- or low-probability lung scans.

Blood Coagulation↗
PubMed1999

Antiphospholipid syndrome and thrombosis.

Antiphospholipid antibodies [such as anticardiolipin antibodies (ACLA)] are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with ACLA are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome) or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). Type V patients are those with antiphospholipid antibodies and fetal wastage syndrome. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of ACLA in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through VI) should be defined, if possible, as this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with ACLA, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the activated partial thromboplastin time (aPTT) is unreliable in patients with lupus anticoagulant (prolonged in only about 40 to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests including ELISA for ACLA, the dRVVT for lupus anticoagulant, hexagonal phospholipid neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these are negative, in the appropriate clinical setting, subgroups should also be assessed. Finally, most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, most will fail antiplatelet therapy, thus it is of major importance to make this diagnosis in order that patients can be treated with the most effective therapy for secondary prevention, low-molecular weight heparin (LMWH) or unfractionated heparin (UHF) in most instances.

Antibodies, Antiphospholipid↗
PubMed1999

Upper-extremity deep vein thrombosis after central venous catheterization via the axillary vein.

OBJECTIVE: To determine the frequency of central venous catheter-induced thrombosis of the axillary vein. DESIGN: Prospective, controlled study. SETTING: Tertiary care university center. PATIENTS: Sixty patients in a medical-surgical intensive care unit who required central venous catheterization via the axillary vein. INTERVENTIONS: Single-lumen, silicone elastomer or polyurethane catheters were inserted for a mean duration of 14.7+/-7.4 days (range, 4-33 days). On catheter removal, bilateral upper-extremity phlebographic examination was performed in each patient. The incidence of deep vein thrombosis in catheterized arms was compared with that in uncatheterized arms. MEASUREMENTS AND MAIN RESULTS: Of the 60 patients who underwent axillary vein cannulation, one patient had clinical signs of arm vein thrombosis, but no patient had clinical sign of pulmonary embolism. There were 35 patients (58.3%) who developed positive phlebographic examinations homolateral to the catheter. Fibrin sleeves that developed around the catheters were observed in 28 patients (47%). Five patients (8.3%) had phlebographic signs of partial axillary vein thrombosis: nonobstructive clots adherent to the vessel wall and/or the catheter. Two patients (3.3%) had phlebographic signs of complete axillary vein thrombosis. No thrombosis was observed in patients with catheterizations lasting < or =6 days, two cases were observed for duration of 7-14 days, and five cases were observed for duration of > or =15 days (p < .01). In the seven patients with axillary vein thrombosis, the vessel was cannulated with fewer than three puncture attempts, and the mean duration for catheter insertion (10+/-2.5 min) was not different from that of patients with no axillary vein thrombosis (14+/-9 min). CONCLUSIONS: Based on the data from the present study, we conclude that axillary vein catheterization is associated with a 11.6% frequency of upper-extremity deep vein thrombosis. This rate of vein thrombosis is similar to that observed after internal jugular or subclavian vein cannulation. Given the acceptable rate of this clinically important complication, axillary vein cannulation offers an attractive alternative site for catheter insertion to the internal jugular or subclavian vein in the critically ill. Because thrombosis is rare or absent in catheterizations lasting <15 days, it seems wise to withdraw axillary catheters after a maximum of 2 wks.

Arm↗
PubMed2004

Eversion thromboendovenectomy in organized portal vein thrombosis during liver transplantation.

Portal thrombosis is no longer considered a contraindication for transplantation because of the technical experience acquired in the field of liver transplantation and the development of various surgical techniques. All the same, the results obtained in portal thrombosis patients are at times suboptimal, and the surgical technique used (thromboendovenectomy or veno-venous bypass) is also controversial. Between May 1988 and December 2001, 455 liver transplants were performed, of which 32 (7%) presented portal vein thrombosis. Of these, eight belonged to the first 227 transplants (group I), and 24 to the other 228 (group II). Of the 32 cases with portal thrombosis, 20 (62%) were type Ib, seven (22%) type II/III and five (16%) type IV. Twenty-two were males (69%), with a mean age of 50 yr (range: 30-70 yr); the thrombosis in all cases developed over a cirrhotic liver: 15 cases of an ethanolic origin, 11 because of hepatitis C virus, two cases of autoimmune aetiology, one case of primary biliary cirrhosis, one case because of hepatitis B virus and two cases of a cryptogenic origin. Five cases had a history of surgical treatment for portal hypertension. The surgical method in all cases consisted of an eversion thromboendovenectomy (ETEV) under direct visual guidance, with occlusion of the portal flow using a Fogarty balloon. Once re-canalization was achieved, we performed local heparinization and end-to-end portal anastomosis. In no case was systemic post-operative heparinization performed. In the 32 cases in which thrombectomy was attempted it was achieved in 31 of them (96%), failing only in a case of type IV thrombosis, which was resolved by portal arterialization. Of the 31 successful cases, only one with type IV thrombosis re-thrombosed. The 5-yr survival rate of the patients in the series was 69%, with 10 patients dying, of whom only two from causes related to the thrombosis and the thrombosis treatment, both with type IV thrombosis. The ideal treatment for portal thrombosis during liver transplantation is controversial and depends on its extension and the experience of the surgeon. In our experience, ETEV resolves most thromboses (types I, II and III), but management of type IV, which occasionally can be treated with this technique, may require more complex procedures such as bypass, portal arterialization or cavoportal haemitransposition.

Balloon Occlusion↗
PubMed2005

The presence of IgG antibodies against beta2-glycoprotein I predicts the risk of thrombosis in patients with the lupus anticoagulant.

BACKGROUND: Lupus anticoagulant (LA) is a strong risk factor of thrombosis. However, a subgroup of patients positive for LA is unaffected by thrombosis and currently no predictive markers are available to identify patients positive for LA at increased risk for thrombosis. OBJECTIVE: The aim of the study was to investigate whether anti-beta-2-glycoprotein I (anti-beta2GPI) or anticardiolipin antibodies (ACA) are associated with an increased risk of thrombosis in patients persistently positive for LA. PATIENTS AND METHODS: A cohort of 87 consecutive patients persistently positive for LA was investigated, 55 with and 32 without a history of thrombosis. Immunoglobulin G (IgG) and M (IgM) antibodies against beta2GPI and cardiolipin were determined by enzyme-linked immunoassay. RESULTS: Patients positive for LA with thrombosis had significantly higher levels of anti-beta2GPI IgG (median 16.7 standard units, interquartile range 3.0-75.2, P = 0.002) and of ACA IgG (41.1 IgG phospholipid units per mL, 8.9-109.0, P = 0.002) than those without thrombosis (2.6, 1.4-7.9 and 9.7, 4.6-22.1, respectively). Levels of anti-beta2GPI IgM and ACA IgM did not differ significantly between LA patients with and without thrombosis (P = 0.25 and 0.12, respectively). Elevated anti-beta2GPI IgG was associated with an increased risk for thrombosis (OR = 4.0, 95% CI 1.2-13.1), especially for venous thromboembolism (OR = 5.2, 95% CI 1.5-18.0). CONCLUSIONS: Increased levels of anti-beta2GPI IgG were associated with thrombosis. We conclude that anti-beta2GPI IgG levels above normal predict an increased risk of thrombosis in patients persistently positive for LA.

Adult↗
PubMedDate not supplied

Choline deficiency is associated with increased risk for venous catheter thrombosis.

BACKGROUND: Patients with intestinal failure who require long-term parenteral nutrition (PN) develop catheter thrombosis as a complication. This patient group may also develop choline deficiency because of a defect in the hepatic transsulfuration pathway in the setting of malabsorption. This study was undertaken to determine whether choline deficiency is a risk factor for development of catheter thrombosis. METHODS: Plasma free and phospholipid-bound choline concentrations were measured in a group of 41 patients that required long-term PN. Episodes of catheter thrombosis from onset of PN to the time of blood testing were recorded. RESULTS: Sixteen (39%) patients developed catheter thrombosis, and 5 of these had recurrent catheter thrombosis. Plasma free choline was 7.7 +/- 2.7 nmol/mL in patients with no history of catheter thrombosis and 6.2 +/- 1.7 nmol/mL in patients with previous catheter thrombosis (p = .076 by Wilcoxon rank-sum test). The partial correlation between plasma free choline concentration and the frequency of clots after controlling for catheter duration was r = -0.33 (p = .038). The relative risk for catheter thrombosis in subjects with a plasma free choline concentration <8 nmol/mL was 10.0, 95% confidence interval (1.134-88.167). Plasma phospholipid-bound choline concentration was 2191.7 +/- 679.0 nmol/mL in patients with previous catheter thrombosis and 2103.3 +/- 531.2 nmol/mL in patients without history of catheter thrombosis (p = NS). CONCLUSION: Choline deficiency is a significant risk factor for development of catheter thrombosis in patients with intestinal failure who require PN.

Adult↗
PubMed2001

Antiphospholipid thrombosis syndromes.

Antiphospholipid antibodies are strongly associated with thrombosis and are the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagutable state remain unclear, numerous theories, as previously discussed, have been advanced. The most common thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type II syndrome); occasionally, patients present with mixtures of these types (type IV syndrome). Type V patients are those with antiphospholipid antibodies and RMS. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through VI) should be defined if possible, as this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually experience venous thrombosis. Because the aPTT is unreliable inpatients with lupus anticoagulant (prolonged in only about 40 to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests, including ELISA for anticardiolipin antibodies, the dRVVT for lupus anticoagulant, hexagonal phospholipid neutralization procedure, and beta-2-GP-I (IgG, IgA, and IgM) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If results of these tests are negative, in the appropriate clinical setting, subgroups should also be assessed. Finally, most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, may fail some types of antiplatelet therapy; thus it is of major importance to make this diagnosis so that patients can be treated with the most effective therapy for secondary prevention--LMWH or UH in most instances, and clopidogrel in some instances.

Antibodies, Antiphospholipid↗
PubMed2002

Fibrin fragment D-dimer and the risk of future venous thrombosis.

Plasma D-dimer concentration rises more than 100-fold during acute deep vein thrombosis, but there are no prospective data concerning D-dimer as a risk factor for incident venous thrombosis in a general population. Incident venous thrombosis was ascertained in 2 prospective observational studies, the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study. Of 21 690 participants enrolled between 1987 and 1993, after 8 years of follow-up, D-dimer was measured using baseline stored plasma of 307 participants who developed venous thrombosis and 616 who did not. Relative to the first quintile of the distribution of D-dimer, the age-adjusted odds ratios for future venous thrombosis for the second to fifth quintiles of D-dimer were 1.6, 2.3, 2.3, and 4.2, respectively (P for trend <.0001). Following added adjustment for sex, race, body mass index, factor V Leiden, prothrombin 20210A, and elevated factor VIII coagulant activity (factor VIII:c), these odds ratios were 1.5, 2.1, 1.9, and 3.0, respectively (P for trend <.0001). Among those with idiopathic thrombosis or secondary thrombosis unrelated to cancer, the adjusted fifth quintile odds ratios were 3.5 and 4.8, respectively. By contrast, D-dimer in the fifth versus first quintile was not related to occurrence of cancer-associated thrombosis (odds ratio, 1.1). Odds ratios for elevated D-dimer were consistently elevated in subgroups defined by age, sex, race, duration of follow-up, and thrombosis type (deep vein thrombosis or pulmonary embolus). D-dimer is strongly and positively related to the occurrence of future venous thrombosis.

Aged↗
PubMed2002

Comparison of outcomes after hospitalization for deep venous thrombosis or pulmonary embolism.

Venous thrombosis and pulmonary embolism are commonly viewed as different manifestations of a single disease process, venous thromboembolism. Recent evidence suggests that there may be important differences between patients who manifest these two conditions. Using linked hospital discharge records we analyzed 71,250 patients hospitalized with a principal diagnosis of venous thrombosis alone or pulmonary embolism and analyzed predictors of rehospitalization within 6 months for venous thrombosis or pulmonary embolism. There were 51233 patients diagnosed with venous thrombosis alone and 21,625 diagnosed with pulmonary embolism. Comparing patients initially diagnosed with venous thrombosis alone to patients with pulmonary embolism, the relative risk of being rehospitalized with venous thrombosis within 6 months for venous thrombosis was 2.7. Conversely, when patients with pulmonary embolism were compared to patients with venous thrombosis alone, the relative risk of rehospitalization within 6 months with a diagnosis of pulmonary embolism was 4.2. In multivariate models the strongest predictor of recurrent thromboembolism manifest as pulmonary embolism was an initial diagnosis of pulmonary embolism and the strongest predictor of recurrence as venous thrombosis was an initial diagnosis of venous thrombosis. We conclude that the initial clinical manifestation of thromboembolism strongly predicts the manifestation of a recurrence. Venous thrombosis and pulmonary embolism appear to be distinct, albeit overlapping, clinical entities with different natural histories.

Aged↗
PubMed2002

Splenectomy after portal thrombosis in patients with polycythemia vera and essential thrombocythemia.

BACKGROUND AND OBJECTIVES: Polycythemia vera (PV) and essential thrombocythemia (ET) are two rare acquired myeloproliferative disorders (MPD) with frequent thrombotic and hemorrhagic complications. The occurrence of thrombosis in unusual sites, e.g. splanchnic vasculature, is a severe complication of these diseases. We describe a single-institution experience in patients with ET and PV, diagnosed in agreement with the Polycthemia Vera Study Group criteria, with portal vein thrombosis who did or did not undergo splenectomy. DESIGN AND METHODS: The medical records and the follow-up outcome of 16 MPD patients with portal thrombosis who underwent splenectomy (group A1) and 16 who did not (group A2) were evaluated. Their median follow-up was, respectively, 13.45 and 10.49 years. The overall survival of these patients was compared with that of a population of 32 patients with MPD and no portal thrombosis (group B) matched for sex, age, diagnosis and duration of follow-up. RESULTS: In group A1, 2 patients developed deep vein thrombosis, 1 patient had a surgical hemorrhage and 2 patients died early, one from acute infection, the other from bone marrow aplasia. Among the survivors, one male had a deep vein thrombosis and 1 developed a new portal thrombosis. Four patients died during the follow-up (median 9.48 years, range 3.17-25.1; 1 stroke, 2 gastrointestinal bleedings, 1 leukemic conversion). No difference was observed in the incidence of thrombotic or hemorrhagic complications or in the rate of deaths when group A1 was compared to the other groups. The use of antiplatelets drugs was statistically increased in group A1 after splenectomy, because portal vein thrombosis induced per se an increased use of therapeutic agents. No statistical difference was observed in overall survival between the different groups. INTERPRETATION AND CONCLUSIONS: 1) Bleeding and thrombosis are the leading causes of morbidity and mortality in ET and PV patients with portal vein thrombosis both with or without splenectomy. 2) Portal vein thrombosis, and sometimes splenectomy, requires increased use of drugs which may enhance the risk of leukemic transformation. In spite of this, the patients who survive the first post-splenectomy period may have a long and safe life.

Adolescent↗
PubMedDate not supplied

Extensive portal and splenic vein thrombosis: differences in hemodynamics and management.

BACKGROUND/AIMS: To assess the incidence of extensive portal and splenic vein thrombosis in patients with extrahepatic portal vein obstruction and determine the differences in presentation, portal hemodynamics and management as compared to patients with portal vein thrombosis alone. METHODOLOGY: 118 patients of extrahepatic portal vein obstruction presenting with variceal hemorrhage, having received no definitive treatment prior to presentation were divided into two groups--with portal and splenic vein thrombosis and with portal vein thrombosis, based on ultrasonography and splenoportography. Collateralization patterns on splenoportography were studied. Results of endoscopic variceal sclerotherapy were compared. RESULTS: Portal and splenic vein thrombosis was seen in 39 patients. Collateralization in case of portal and splenic vein thrombosis, in contrast to portal vein thrombosis, was predominantly left sided (74% vs. 9%, p < 0.0001). Fundal gastric varices were seen more often in patients with portal and splenic vein thrombosis (28% vs. 11%, p = 0.02), developing even after variceal obliteration, though obliteration was achieved in fewer sessions. Surgery for control of variceal bleed was performed more in the portal and splenic vein thrombosis group (33% vs. 15%, p = 0.02), especially for gastric varices (28% vs. 9%, p = 0.006). CONCLUSIONS: Portal and splenic vein thrombosis is present in 33% of patients with extrahepatic portal vein obstruction. Hemodynamic patterns differ, accounting for the preponderance of gastric varices on presentation in patients with portal and splenic vein thrombosis and an increased need for surgery.

Adolescent↗
PubMedDate not supplied

[Thrombophilic disorders in children and adolescents with portal vein thrombosis].

OBJECTIVE: To determine the frequency of protein C, protein S and antithrombin deficiency, and factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations in children and adolescents with portal vein thrombosis, as well as assessing the hereditary character of this disorders. METHODS: A two-year study was carried out to determine the frequency of thrombophilic disorders in children and adolescents with portal vein thrombosis (n = 14), their parents (n = 24), and two control groups, one age-matched children and adolescents free of liver disease (n = 28) and another group with cirrhosis (n = 24). The portal vein thrombosis patients were investigated by clinical and laboratory means, esophagogastroduodenal endoscopy and liver biopsies. The presence of portal vein thrombosis was assessed by Doppler ultrasonography and/or angiographic analysis. RESULTS: The frequency of protein C, protein S and antithrombin deficiency was 6/14 (42.9%) (p < 0.05 versus controls), 3/14 (21.4%) (p > 0.05) and 1/14 (7.1%) (p > 0.05) of children and adolescents with portal vein thrombosis, respectively. The frequency of protein C, protein S and antithrombin deficiency in cirrhotic patients was 14/24 (58.3%), 7/24 (29.2%) and 11/24 (45.8%), respectively (p < 0.05 versus controls free of liver disease). None of the portal vein thrombosis parents or controls presented protein C, protein S or antithrombin deficiency. One portal vein thrombosis patient and one control (p = 0.999) presented prothrombin G20210A mutation. The homozygous form of methylenetetrahydrofolate reductase C677T mutation was observed in 3/14 (21.4%) patients with portal vein thrombosis and in 5/28 (17.9%) (p = 0.356) controls. None of the patients or controls presented the factor V Leiden. CONCLUSION: Half of the children and adolescents with portal vein thrombosis presented deficiency of one or more coagulation inhibitor proteins, mainly protein C, but this deficiency does not seem to be an inherited condition. The hereditary prothrombotic disorders do not seem to play a vital role in thrombosis in patients with portal vein thrombosis of this study. In the cirrhotic patients, there was a higher frequency of protein deficiency when the disease was more intense.

Adolescent↗
PubMed2004

The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis.

BACKGROUND AND OBJECTIVES: The purpose of this study was to assess the incidence of central venous catheter (CVC)-related thrombosis and the contribution of two common inherited coagulation disorders (factor V Leiden, prothrombin G20210A mutation) to this complication in a large hospital population. DESIGN AND METHODS: In a prospective setting, patients were assessed daily for signs and symptoms suggestive of thrombosis. Routine Doppler-ultrasound was performed weekly in all patients until CVC removal. Doppler-ultrasound examinations were stored on videotape and assessed by two blinded observers. In the case of clinically suspected thrombosis the physicians followed routine diagnostic and therapeutic procedures. The presence of factor V Leiden and prothrombin G20210A mutation and other potential risk factors were assessed in all patients. RESULTS: In 252 consecutive patients the cumulative incidence of-CVC related thrombosis was 30% (clinically manifested thrombosis: 7%). The relative risk of factor V Leiden or prothrombin G20210A mutation for thrombosis was 2.7 (CI95% 1.9 to 3.8). In addition, a personal history of venous thrombosis was associated with CVC-related thrombosis, whereas the severity of thrombosis was affected by the absence of anticoagulants and the presence of cancer. INTERPRETATION AND CONCLUSIONS: Thrombosis is frequently observed after central venous catheterization. Common inherited abnormalities in blood coagulation contribute substantially to CVC-related thrombosis. In view of physicians' reluctance to prescribe prophylactic anticoagulant treatment in vulnerable patients, a priori determination of common inherited and acquired risk factors may form a basis to guide these treatment decisions.

5' Untranslated Regions↗