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PubMed2002

[Effect of urokinase on morphological changes of vein wall after acute thrombosis in rabbits].

OBJECTIVE: To assess the effect of urokinase on morphological changes of vein wall after acute thrombosis in rabbits. METHODS: Forty-three rabbits were randomly divided into 3 groups: thrombolysis group (n = 20), non-thrombolysis group (n = 20) and control group (n = 3). The thrombosed femoral veins of four rabbits in thrombolysis group anf four rabbits in non-thrombolysis group were taken 1, 4, 7, 14, and 21 days after thrombosis. The expression areas of smooth muscle actin and collagen fiber were measured by histochemistry. Scanning electron microscopy was used to observe the damage of endothelial cells. RESULTS: The expression area of smooth muscle actin began to increase significantly since day 4 after thrombosis reached the peak value on day 7 in thrombolysis group and non-thrombolysis group; and then decreased in thrombolysis group but remained at a high level in non-thrombolysis group. The expression area of smooth muscle actin in thrombolysis group was always less that in non-thrombosis group (all P < 0.01). The expression area of collagen fiber began to remarkably increase since day 7 after thrombosis in both thrombolysis and non-thrombolysis groups, however, being less in the thrombolysis group, and then decreased in thrombolysis group and remained at a high level in non-thrombosis group. Different cellular damages were observed by SEM one day after thrombosis in both thrombosis groups. However, the injury cells began to be repaired since day 4 in thrombolysis group. CONCLUSION: Thrombolysis with urokinase effectively maintains the integrity of endothelium of vein wall and decreases the fibrocellular proliferation of the thrombosed vein, however, fails to stop the pathological changes caused by thrombosis.

Actins↗
PubMed2002

Management of venous thrombosis and thromboembolism: prevention and treatment.

Thrombosis is a common cause of death in the United States. More than two million people die each year from an arterial or venous thrombosis, or the consequences thereof. Approximately an equal number suffer non-fatal thrombosis; for example, deep venous thrombosis (DVT), non-fatal pulmonary embolus (PE), non-fatal cerebrovascular thrombosis (CVT), transient cerebral ischemic attacks (40% of these have a fatal or non-fatal CVT within one year), non-fatal coronary artery thrombosis, retinal vascular thrombosis (RVT), and other non-fatal thrombotic deaths. These numbers emphasize the scope of the problem. By contrast, approximately 550,000 people will die this year in the United States from cancer; thus, fatal thrombosis is approximately four times as prevalent as fatality from malignancy. Thrombosis, therefore, accounts for extraordinary morbidity, mortality, and cost of medical care.

Humans↗
PubMed2002

[The possibility of the investigation of portal vein thrombosis by means of ultrasonography].

Doppler-based sonography investigation of liver blood circulation plays major role in the modern diagnosis of portal hypertension that is frequently caused by portal vein thrombosis. Eight patients with portal vein thrombosis have been investigated. During the sonographic investigation we evaluated the size of liver, focal changes in liver, the diameters of the portal vein and its both branches, of the spleen vein, of the superior mesenteric vein, the direction and the characteristics of the blood flow, portaportic and portasystemic collaterals, and the size of spleen. The thrombosis of the trunk and both branches of the portal vein was detected in 4 patients, out of which there was one case of additional thrombosis of the spleen and the superior mesenteric veins, while in another case there was partial thrombosis of the spleen vein. A separate thrombus of the portal vein trunk was noticed in 1 patient. The thrombosis of the portal vein trunk and the right branch was diagnosed in 1 case. There were 2 cases of thrombosis of only left branch of the portal vein. The cause of the portal vein thrombosis remained undetected in 6 cases. The thrombosis of the portal vein developed as a consequence of pancreatitis in one patient, the cause of another case was hepatocellular carcinoma. In comparison to CT, sonography is able to determine additionally the direction of the blood flow and to record a variety of different sections in detecting the above-mentioned pathology. Doppler-based sonography investigation of liver blood circulation, especially the color-coded, is non-invasive, it can be carried out quickly and does not need expensive contrast medium.

Adolescent↗
PubMedDate not supplied

Link between anti-CD36 antibodies and thrombosis in the antiphospholipid syndrome.

OBJECTIVE: Some studies have previously suggested the involvement of antibodies directed against CD36 (anti-CD36) in the pathogenesis of thrombosis. The aim of this study was to evaluate the prevalence of anti-CD36 in patients with antiphospholipid antibodies (aPL) and its relationship with thrombosis. METHODS: Anti-CD36 were tested using an indirect MAIPA assay in 62 patients with autoimmune aPL but without SLE; there were 38 with and 24 without thrombosis. Nineteen patients with thrombosis served as an aPL(-) control group and 58 healthy subjects as the normal control group. RESULTS: 15 of 62 aPL patients (24.2%) but only 1 of 58 (1.7%) normal controls had anti-CD36 (p < 0.0005). As compared to normal controls, the prevalence of anti-CD36 was significantly higher in aPL patients with (26.3%, p < 0.0005) or without thrombosis (20.8%, p < 0.01). Anti-CD36 were significantly more frequent in aPL patients with thrombosis than in thrombosis aPL(-) subjects (26.3% vs 0%, p = 0.02). The presence of anti-CD36 seems to be more frequent in aPL patients with recurrent thrombosis than in those with a single episode (36.8% vs 15.8%). CONCLUSION: The presence of anti-CD36 is highly prevalent in patients with autoimmune aPL with a trend to being more frequent in patients with recurrent episodes of thrombosis.

Adult↗
PubMed2005

[Postoperative vessel thrombosis and its management after free flap transfers in head and neck region].

OBJECTIVE: To analyze the rate of postoperative vessel thrombosis and its management after free tissue transfers in head and neck region. METHODS: Eight hundred and forty-nine consecutive free flap transfers were performed from May 1999 to September 2004. Among them, the flaps with postoperative vessel thrombosis were selected and reviewed. Data concerning each case included time of vessel thrombosis, kind of thrombosis, time of emergent exploration, and salvage of free flaps. RESULTS: Among the 849 free flaps, postoperative vessel thrombosis occurred in 28 free flaps, between 8 to 120 hours after operation. There were 5 arterial thrombosis, and 23 venous thrombosis. Thirteen flaps were salvaged after emergent exploration, and 15 flaps were lost. The rate of postoperative vessel thrombosis was 3.3% in this group, the salvage rate of flap was 46.4%, and the overall successful rate was 98.2%. CONCLUSION: Clinical monitoring after free flap transfer in head and neck region is very important and effective. In case of vessel thrombosis, emergent exploration is the only effective way to salvage the flap.

Adolescent↗
PubMedDate not supplied

Vascular endothelial growth factor and monocyte chemoattractant protein-1 in Behçet's patients with venous thrombosis.

OBJECTIVE: Vascular lesions can involve both arterial and venous systems which are often the major causes complicating the disease course of Behçet's disease (BD). Vascular endothelial growth factor (VEGF) is a stimulant of angiogenesis secondary to ischemia while monocyte chemoattractant protein 1 (MCP-1) is induced by shear stresses leading to vascular collateral development. MCP-1 has been also shown to contribute to the recanalization of venous thrombi. Tumor necrosis factor-alpha (TNF-alpha) is known to play a major role in the pathogenesis of BD. Furthermore, up-regulation of secreted MCP-1 and VEGF was observed following stimulation with TNF-alpha. In view of the above functions of VEGF, MCP-1 and TNF-alpha, we hypothesized that these factors may be important in the pathogenesis of thrombosis seen in BD. METHODS: A total of 36 patients with a diagnosis of BD were studied. BD patients were separated into 3 groups with respect to vascular involvement. Group BD-AT (n = 9) with acute thrombosis, BD-CT (n = 12) with chronic thrombosis and BD-MC (n = 15) with mucocutaneous involvement only. The control group (group H) was comprised of 20 healthy persons. In addition, patients with acute, DC-AT (n= 11) and patients with chronic DC-CT (n = 9) thrombosis without BD served as disease controls. Serum measurements of VEGF MCP-1 and TNF-alpha were performed by quantitative sandwich ELISA. The acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured. RESULTS: The levels of VEGF were significantly higher in the patients in group BD-AT than either in group BD-CT or BD-MC (p = 0.03 and p < 0.001, respectively). However, no significant difference was found for VEGF levels of thrombotic patients regarding the cause (BD-AT vs. DC-AT, p = 0.063; BD-CT vs. DC-CT, p = 0.084) or the stage of thrombosis (DC-AT vs. DC-CT, p > 0.05). Both BD patients and disease controls with acute thrombosis had significantly higher levels of MCP-1 as compared to corresponding chronic thrombosis patients (BD-AT vs. DC-CT; p < 0.001; DC-AT vs. DC-CT, p < 0.001). Patients with BD and disease controls had significantly higher serum TNF-alpha level when compared with healthy subjects. No significant difference with respect to serum TNF-alpha level was noted when patient subgroups with BD and disease controls were compared with each other Serum levels of VEGF, MCP-1, and TNF-alpha were not found to be correlated with either ESR or CRP (p > 0.05). CONCLUSIONS: Increased levels of VEGF and MCP-1 detected in BD thrombosis suggest the possible role of those angiogenic cytokines in the pathogenesis. Although not specific for BD, detection of VEGF or MCP-1 levels seems to serve as an assay for differentiation of BD patients with acute thrombosis from chronic.

Acute Disease↗
PubMed2006

Increased platelet and leukocyte activation as contributing mechanisms for thrombosis in essential thrombocythemia and correlation with the JAK2 mutational status.

BACKGROUND AND OBJECTIVES: The mechanisms accounting for the increased risk of thrombosis in patients with essential thrombocythemia (ET) are not well known. The aim of the present study was to ascertain the role of platelet and leukocyte activation in the thrombosis of ET. DESIGN AND METHODS: The activation status of platelets and leukocytes was assessed by flow cytometry studies in 49 patients with ET (22 with previous thrombosis and 27 without a history of thrombosis) and in a group of age- and sex-matched healthy individuals. The assessment included platelet P-selectin expression (measured both at baseline and after stimulation with ADP, thrombin, arachidonic acid (AA), and collagen), platelet-neutrophil and platelet-monocyte complexes, determination of CD11b in the neutrophils and monocytes, and expression of tissue factor in the monocytes (mTF). The JAK2 V617F mutation was studied and correlated with platelet and leukocyte activation. RESULTS: As compared with controls, ET patients had significantly higher values of baseline P-selectin and thrombin- and AA-induced platelet P-selectin expression, as well as higher platelet-neutrophil and platelet-monocyte complexes, neutrophil CD11b expression and baseline mTF expression. Platelet P-selectin, monocyte CD11b, and lipopolysaccharide-induced mTF expression was significantly higher in ET patients with a history of thrombosis than in patients without thrombosis. Patients with the JAK2 V617F mutation or thrombosis showed higher baseline and AA-induced platelet P-selectin expression than did those without thrombosis. INTERPRETATION AND CONCLUSIONS: These results would support a role for platelet and monocyte activation in the thrombosis of ET. In these patients, the presence of the JAK2 V617F mutation is associated with higher platelet activation.

Adult↗
PubMed2006

Factor V Leiden is associated with higher risk of deep venous thrombosis of large blood vessels.

AIM: To determine the prevalence of factor V Leiden mutation in patients with different presentation of venous thromboembolic disease and healthy individuals in the Republic of Macedonia. METHODS: The retrospective case control study involved 190 patients with venous thromboembolic disease and 200 healthy individuals, who were screened for the presence of factor V Leiden mutation, using a polymerase chain reaction-restriction fragment length polymorphism method. The prevalence of factor V Leiden was analyzed according to the localization of thrombosis, presence of risk factors, and family history of thrombosis. The odds of deep venous thrombosis were calculated with respect to the presence of factor V Leiden mutation. RESULTS: The prevalence of factor V Leiden mutation among patients with venous thromboembolic disease was 21.1%, compared with 5.5% in the healthy individuals. Factor V Leiden positive patients had the first episode of deep venous thrombosis at a younger age, and the prevalence of the mutation was the highest among patients with a positive family history of thrombosis (33.9%, P=0.003) and in patients with deep venous thrombosis affecting a large blood vessel (37.7%, P=0.001). The prevalence of factor V Leiden mutation was lower in patients with calf deep venous thrombosis and primary thromboembolism (13.3% and 13.1%, respectively; P>0.05). The odds ratio for iliofemoral or femoral deep venous thrombosis in factor V Leiden carriers was 10.4 (95% confidence interval, 4.7-23.1). CONCLUSION: The prevalence of factor V Leiden mutation was high in patients with venous thromboembolic disease and healthy individuals in the Republic of Macedonia. Factor V Leiden carriers have the highest odds of developing deep venous thrombosis affecting a large venous blood vessel.

Adult↗
PubMed1987

[Deep venous thrombosis in Behçet's disease. 106 localizations in a series of 177 patients].

A retrospective study of 177 patients (137 male, 40 female) with a disease that fulfilled the criteria of complete or incomplete Behçet's disease showed 106 thrombotic lesions of a venous trunk in 62 (35%) of these patients, superficial phlebitis and retinal vein thrombosis excluded. The incidence of thrombosis was unrelated to race and sex. The venous lesions were single in 38 cases and multiple in 24 cases, including 4 with more than 4 territories involved. Arterial lesions were also present in 7 cases. The lesions were located in the sural (n = 63), iliofemoral (n = 14), inferior vena cava (n = 13), superior vena cava (n = 3), axillary (n = 2) and cerebral (n = 13) veins or territories. Thrombosis developed during the first 4 years of Behçet's disease in one half of the patients. It preceded the aphthosis by 1 to 10 years in 11 cases, was concomitant with it in 15 cases and appeared more than 10 years after the diagnosis in 8 cases. Pulmonary embolism occurred in 11 patients, requiring clipping of the vena cava in 2, but it was never lethal. However, 2 of the 5 patients who died had venous thrombosis (Hughes Stovin syndrome). Thirty-eight patients could be followed up for 12 to 192 months (mean 43) under anticoagulant or antiplatelet therapy. Five vascular recurrences (13%) were observed, 2 of them (1 arterial graft thrombosis, 1 cerebral thrombosis) under anti-vitamin K agents. Cerebral thrombosis (9 men, 4 women) accounted for 27% of the neurological lesions; its prognosis was favourable in the 7 patients successfully treated with anticoagulants. Thrombosis could not be explained. Haemostasis studies showed a decrease of fibrinolytic activity compared to a group of normal subjects and an increase in fibrinogen, factor VIII and Willebrand's factor levels; these abnormalities did not seem to be specific. Thus, phlebitis truly is an element of Behçet's disease. Until its mechanism is better understood, effective anticoagulant therapy in cases with proven thrombosis and preventive antiplatelet therapy in the other cases seem to be rational measures.

Adult↗
PubMed1995

The antiphospholipid and thrombosis (APL-T) syndromes. Clinical and laboratory correlates.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanisms by which antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with anticardiolipin antibodies are deep venous thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular-retinal vessel thrombosis (type III syndrome); occasionally, patients present with mixtures (type IV syndrome). 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 measured. Also, the type of syndrome (I through V) should be defined, if possible, as this may dictate both the type and duration of both immediate and long-term anticoagulant therapy. Unlike patients with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually sustain venous thrombosis. Because the aPTT is unreliable in patients with lupus anticoagulant (prolonged in approximately 40% to 50% of patients) and is seldom prolonged in patients with anticardiolipin antibodies, definitive tests (ELISA for anticardiolipin antibodies and the dRVVT for lupus anticoagulant) should be immediately ordered when antiphospholipid syndrome is suspected or when individuals present with otherwise unexplained thrombotic or thromboembolic events.

Antiphospholipid Syndrome↗
PubMed1998

Correlation of thrombosis with increased platelet turnover in thrombocytosis.

There are no readily applicable methods to routinely assess thrombosis risk and treatment response in thrombocytosis. Reticulated platelets (RP) define the most recently released platelets in the circulation, and the RP% has been shown to estimate platelet turnover in thrombocytopenic states. We examined whether increased RP values were associated with thrombotic complications in thrombocytosis. Platelet count, RP%, and absolute RP count were measured at presentation in 83 patients with chronic or transient thrombocytosis, 46 patients with deep vein (DVT) or arterial (ART) thrombosis and normal platelet counts, and 83 healthy controls with normal platelet counts. Chronic thrombocytosis patients presenting with thrombosis (n = 14) had significantly higher RP% (14.7% +/- 10. 1%, mean +/- SD) than asymptomatic chronic thrombocytosis patients (n = 23, RP% = 3.4% +/- 1.8%), healthy controls (3.4% +/- 1.3%), DVT patients (n = 21, 3.8% +/- 2.1%), or ART patients (n = 25, 4.5% +/- 4.1%, P < .05 for all comparisons). Chronic thrombocytosis patients with thrombosis also had significantly higher absolute RP counts than asymptomatic chronic thrombocytosis patients (98 +/- 64 x 10(9)/L [range, 54 to 249 x 10(9)/L] v 30 +/- 13 x 10(9)/L [range, 11 to 51 x 10(9)/L]; P = .0004), whereas healthy controls, DVT, and ART patients had similarly low absolute RP counts (6 +/- 6 x 10(9)/L, 9 +/- 7 x 10(9)/L, and 11 +/- 7 x 10(9)/L, respectively; P > .49). The RP% and absolute RP counts remained significantly higher in chronic thrombocytosis patients with thrombosis when patients were further subdivided into primary myeloproliferative disorders versus secondary thrombocytosis. Similarly elevated RP percentages and absolute counts were also noted in transient thrombocytosis patients with thrombosis (n = 6, 11.5% +/- 4.4% and 90 +/- 46 x 10(9)/L, respectively) when compared with asymptomatic transient thrombocytosis patients (n = 40, 4.5% +/- 2.7% and 35 +/- 16 x 10(9)/L, respectively) and to all control groups (P < .05 for all comparisons). In addition, 7 of 8 thrombocytosis patients who were studied before developing symptoms of thrombosis had elevated absolute RP counts compared with only 1 of 63 thrombocytosis patients who remained asymptomatic. Follow-up studies in seven chronic thrombocytosis patients showed that successful aspirin treatment of symptomatic recurrent thrombosis significantly reduced the RP% from 17.1% +/- 10.9% before therapy to 4.8% +/- 2.0% after therapy; absolute RP counts decreased from 102 +/- 67 x 10(9)/L to 26 +/- 10 x 10(9)/L (P < .01 for both). We conclude that thrombosis in the setting of an elevated platelet count is associated with increased platelet turnover, which is reversed by aspirin therapy. Measurement of reticulated platelets to assess platelet turnover may be useful in evaluating both treatment response and thrombotic risk in thrombocytosis.

Adolescent↗
PubMed1998

Incidence of venographically proved deep vein thrombosis after knee arthroscopy.

BACKGROUND: Deep vein thrombosis is a common, important complication of major orthopedic surgery, particularly knee arthroplasty. Knee arthroscopy is performed more frequently and in younger patients than knee arthroplasty. However, the true risk of deep vein thrombosis in patients who undergo this procedure is unknown. OBJECTIVE: To determine the incidence of deep vein thrombosis after knee arthroscopy in a large cohort of patients. METHODS: Consecutive patients scheduled for knee arthroscopy were eligible for the study. Enrolled study patients received no thromboprophylaxis. They were discharged home the day of surgery and underwent unilateral contrast venography approximately 1 week after their operation. The primary outcome measure was the incidence of venous thromboembolism. Risk factors for deep vein thrombosis were evaluated. RESULTS: Among the 184 patients who had adequate venography, deep vein thrombosis was detected in 33 (17.9%; 95% confidence interval, 12.7%-24.3%). Of these, 9 were proximal (4.9%; 95% confidence interval, 2.3%-9.1%). No patient died and no patient presented with clinically suspected pulmonary embolism. Of 33 patients, only 20 (60.6%) with deep vein thrombosis had symptoms while 13 (39.4%) were asymptomatic. The risk of deep vein thrombosis was significantly higher among patients who had a tourniquet applied for more than 60 minutes. CONCLUSIONS: The results of our study demonstrate that 17.9% of patients develop deep vein thrombosis after knee arthroscopy (most being either proximal or extensive). It is reasonable to perform a randomized trial to determine whether the incidence of deep vein thrombosis can be safely reduced in patients undergoing knee arthroscopy.

Adult↗
PubMed1992

Pattern and distribution of thrombi in acute venous thrombosis.

The location and extent of thrombosis in the deep venous system will determine immediate and long-term outcome. During the past 3 years, we have studied by duplex scanning 833 patients with suspected deep vein thrombosis. In this group, 209 patients (25%) had a positive study. The findings relative to location and extent of involvement are as follows. (1) The right leg was involved in 35% of patients, the left leg in 48%. Bilateral involvement was noted in 17%. (2) The veins most frequently affected by deep vein thrombosis were as follows: superficial femoral in 74%, popliteal in 73%, common femoral in 58%, posterior tibial in 40%, deep femoral in 29%, greater saphenous in 19%, and the inferior vena cava in 2%; multisegment involvement was common. (3) Total occlusion was present in 82% of the patients with deep vein thrombosis, and partial occlusion in 18%. (4) Isolated occlusion of single veins was uncommon. (5) The proximal (above-knee) area was involved in 95% of the cases with deep vein thrombosis, and the calf in 40% of the cases. Isolated calf deep vein thrombosis was found in 6% of the cases with right leg involvement and in 3% for the left. (6) Total leg involvement (iliocaval, femoropopliteal, and calf) occurred in 10% of the patients. Our data confirm the fallibility of the clinical diagnosis of deep vein thrombosis. The frequent involvement of both limbs stresses the importance of not examining just the symptomatic limb. Proximal venous thrombosis (popliteal to inferior vena cava) is much more common than isolated calf vein thrombosis as a cause for symptoms and the referral for study.

Adolescent↗
PubMed1991

"Idiopathic" deep venous thrombosis: the value of routine abdominal and pelvic computed tomographic scanning.

Recent studies have demonstrated an increased incidence in the diagnosis of malignancy subsequent to the diagnosis of deep venous thrombosis or pulmonary embolus. We reviewed 237 patients with venographically proven deep venous thrombosis over eight years. Of these, 216 had at least one predisposing cause for deep venous thrombosis; of the remaining 21 patients, three had hemoglobin determinations revealing anemia and were subsequently shown to have a malignant disease. One patient had two chief complaints and was shown to have deep venous thrombosis and malignant disease. The 17 remaining patients underwent computed tomographic scan of the abdomen and seven (41%) had abnormalities which proved to be malignant in origin. One further patient was diagnosed with carcinoma of the cervix two months following the onset of deep venous thrombosis. The remaining 10 patients continued free of malignant disease. Five have died of circulatory causes in the follow-up period. Seven of the nine patients diagnosed with malignancy succumbed within six months of the diagnosis. We conclude that only a small group of patients with deep venous thrombosis will have no identifiable cause for deep venous thrombosis and be asymptomatic for malignancy. Complete blood count, physical examination and computed tomographic scan of the abdomen at the time of venographic diagnosis of deep venous thrombosis is useful in diagnosis of "occult" malignancy. The number of gynecologic tumors would suggest the need for pelvic examination as well as radiographic examination. The presence of deep venous thrombosis and malignant disease is an ominous prognostic sign.

Abdominal Neoplasms↗
PubMed1995

Role of clotting factor VIII in effect of von Willebrand factor on occurrence of deep-vein thrombosis.

To elucidate the roles of the ABO blood group, von Willebrand factor (vWF), and clotting factor VIII in the process of deep-vein thrombosis we undertook a population-based patient-control study in which 301 consecutive patients younger than 70 with a first, objectively diagnosed episode of venous thrombosis and without an underlying malignant disorder were compared with 301 healthy controls matched for age and sex. In univariate analysis, blood group, vWF concentration, and factor VIII concentrations were all related to deep-vein thrombosis. The risk of thrombosis increased with increasing vWF or factor VIII concentration and was higher in subjects of non-O blood groups than in those of group O. In multivariate analysis only factor VIII remained as a risk factor, and the dose-response relation between factor VIII concentration and risk of thrombosis persisted (subjects with factor VIII concentrations above 1500 IU/L had an adjusted odds ratio of 4.8 [95% Cl 2.3-10.0]). By contrast, the adjusted odds ratio for each vWF stratum did not differ from 1, and that for blood group was 1.5 (1.0-2.2). Our findings point to an effect on thrombosis risk of vWF and blood group, the former fully and the latter at least partly mediated through factor VIII. The 25% prevalence of factor VIII concentrations above 1500 IU/L among unselected consecutive thrombosis patients and the high adjusted relative risk for thrombosis lead to the conclusion that high factor VIII concentrations are common and represent a clear increase in risk of thrombosis, similar to the risks conferred by deficiencies of the coagulation-inhibiting proteins and activated protein C resistance.

ABO Blood-Group System↗
PubMed1996

Deep vein thrombosis after major reconstructive spinal surgery.

STUDY DESIGN: A prospective study was performed. OBJECTIVES: The goals of the study were to determine the incidence of deep vein thrombosis after major adult spinal surgery and the optimal mode of prophylaxis in this surgical population. SUMMARY OF BACKGROUND DATA: Few studies have evaluated deep vein thrombosis incidence and prophylaxis after major adult spinal surgery. Incidence rates have ranged from 0.9-14%. METHODS: Three hundred twenty-nine patients were evaluated. One hundred ten patients were randomized to 3 different deep vein thrombosis prophylaxis groups. These patients had duplex doppler scans between the fifth and seventh postoperative days. The remaining 219 patients formed a nonrandomized group and received either thrombosis embolic deterrent stockings alone or thrombosis embolic deterrent stockings and pneumatic compression boots for deep vein thrombosis prophylaxis. The type of deep vein thrombosis prophylaxis in this group was based on surgeon preference. All 329 patients were followed for clinical signs and symptoms of thromboembolic disease. Patients were followed clinically for a minimum of 1 year. RESULTS: All 110 prophylaxis study group patients were clinically asymptomatic and 109 duplex scans were normal. One scan was indeterminate and a follow-up venogram was negative. Two patients in the coumadin group (5.7%) experienced excessive blood loss. One of the 219 patients from the nonrandomized group developed a clinically detectable proximal deep vein thrombosis which was confirmed by duplex ultra-sonography. The overall clinical incidence of deep vein thrombosis was 0.3% (1 in 329 patients). CONCLUSIONS: This low 0.3% rate is in agreement with recent studies that focus on thromboembolic disease. Given the low incidence, routine screening for asymptomatic thrombi appears unwarranted. In addition, mechanical prophylaxis with graduated compression stockings and pneumatic compression boots is preferable to anticoagulation therapy.

Adolescent↗
PubMed1997

Poor prognosis and limited therapeutic options in patients with Budd-Chiari syndrome and portal venous system thrombosis.

OBJECTIVES: Therapeutic options in Budd-Chiari syndrome (BCS) are highly dependent on the site and extent of hepatic vein thrombosis. The aim of this study was to evaluate the effect of additional portal venous system thrombosis on the clinical presentation, treatment and outcome in patients with BCS. PATIENTS: Clinical notes of 51 patients with BCS admitted to our centre were evaluated. We identified 13 patients (25%) with BCS and additional portal venous system thrombosis. Ten patients were female and three male with a mean age at presentation of 42 years (range 32-67). RESULTS: An underlying haematological aetiology was identified in 10 of the 13 patients. Only four patients (31%) were anticoagulated before referral to our centre. In addition to hepatic vein thrombosis seven patients had portal vein thrombosis (PVT), three had PVT, splenic vein (SV) and superior mesenteric vein (SMV) thrombosis and three had either SV, SMV or inferior vean cava (IVC) thrombosis. The presentation was acute in three patients, subacute in six and chronic in four with a high incidence of encephalopathy (6/13; 46%). Treatment included liver transplantation (four), mesoatrial shunt (one) and balloon dilatation of hepatic veins (two). Six patients were treated medically as all other options were considered too risky or technically impossible. Nine of 13 patients (70%) died either after surgery or before any treatment could be instituted (median survival 1 month), compared to 14/38 (37%) in patients with isolated hepatic vein thrombosis (median survival 6.3 years). CONCLUSION: We conclude that patients with BCS and portal venous system thrombosis constitute a unique group with limited therapeutic options and poor prognosis. The importance of early recognition and anticoagulation of patients with BCS is emphasized.

Adolescent↗
PubMed1991

Liquid crystal thermography as a screening test for deep vein thrombosis in patients with cerebral infarction.

Pulmonary embolism secondary to deep vein thrombosis is a frequent cause of death in stroke patients. In a multicentre study of deep vein thrombosis prophylaxis, 112 patients with cerebral infarction and leg paresis were given aspirin 300 mg three times a day (t.d.s.) alone or with dipyridamole 100 mg t.d.s. To screen for deep vein thrombosis liquid crystal thermography of the legs was performed daily for 15 days on all patients. Those patients with positive thermography underwent immediate X-ray venography of the appropriate limb as the definitive investigation for venous thrombosis. Twenty-two patients had positive thermograms, of whom 16 had confirmed deep vein thrombosis as demonstrated by X-ray venography. Only 8 of the 22 had clinical signs of deep vein thrombosis and 2 of those had a negative venogram. Of the 14 patients with positive thermography but negative clinical signs 10 had positive venograms. Difference in the incidence of deep vein thrombosis in the two treatment groups was not demonstrated. It is concluded that occult deep venous thrombosis is common after ischaemic stroke and it can occur without clinical signs. Liquid crystal thermography is a simple, rapid and cheap screening test that will allow the detection of clinically unrecognized thrombosis.

Aged↗