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PubMed2001

Deep venous thrombosis with suspected pulmonary embolism: detection with combined CT venography and pulmonary angiography.

PURPOSE: To determine the frequency and location of deep venous thrombosis at computed tomographic (CT) venography after CT pulmonary angiography in a large series of patients clinically suspected of having pulmonary embolism and to compare the accuracy of CT venography with lower-extremity venous sonography. MATERIALS AND METHODS: Venous phase images were acquired from the diaphragm to the upper calves after completion of CT pulmonary angiography in 650 patients (373 women, 277 men; age range, 18-99 years; mean age, 63 years) to determine the presence and location of deep venous thrombosis. Results of CT venography were compared with those of bilateral lower-extremity venous sonography in 308 patients. RESULTS: A total of 116 patients had pulmonary embolism and/or deep venous thrombosis, including 27 patients with pulmonary embolism alone, 31 patients with deep venous thrombosis alone, and 58 patients with both. Among 89 patients with deep venous thrombosis, thrombosis was bilateral in 26, involved the abdominal or pelvic veins in 11, and was isolated to the abdominal or pelvic veins in four. In patients in whom sonographic correlation was available, CT venography had a sensitivity of 97% and a specificity of 100% for femoropopliteal deep venous thrombosis. CONCLUSION: Combined CT venography and pulmonary angiography can accurately depict the femoropopliteal deep veins, permitting concurrent testing for venous thrombosis and pulmonary embolism. CT venography also defines pelvic or abdominal thrombus, which was seen in 17% of patients with deep venous thrombosis.

Adolescent↗
PubMed2006

Portal vein thrombosis and high factor VIII in Turner syndrome.

BACKGROUNDS/AIMS: Turner syndrome is not usually associated with thrombotic events. The aim of this study is to report 3 Turner syndrome patients with portal vein thrombosis and, in 2 of them, high factor VIII. These findings are compared to values in Turner syndrome patients without thrombosis and controls. METHODS: In different years, 3 patients with Turner syndrome were initially seen at the Gastroenterology Clinic of Hospital de Clínicas de Porto Alegre, Brazil, for portal vein thrombosis. After the most common causes of portal vein thrombosis and thrombophilias had been excluded, the 2 surviving patients were studied for clotting factors VIII, IX and von Willebrand factor. The same factors were also assessed in 25 Turner syndrome patients without thrombosis and 25 normal girls. RESULTS: One of the patients with portal vein thrombosis died before the study. In the 2 surviving patients, factors VIII and von Willebrand levels were >150 IU/dl, which is considered to be high. In Turner syndrome patients without thrombosis, the mean factor VIII level was 127.2 +/- 41.1 IU/dl and for von Willebrand factor 101.2 +/- 26.9 IU/dl, while in control girls these were 116.0 +/- 27.6 and 94.28 +/- 27.5 IU/dl, respectively. Factor VIII and von Willebrand factor were not different between these 2 groups. When non-O blood group Turner syndrome patients and normal girls were compared, the former had significantly higher levels of factor VIII. CONCLUSIONS: This is the first report on the unusual finding of portal thrombosis in patients with Turner syndrome in whom high levels of factor VIII and von Willebrand factor were found. Factor VIII is higher in the non-O blood group Turner syndrome patients without thrombosis when compared to normal girls.

Adolescent↗
PubMed2006

Haplotypes encoding the factor VIII 1241 Glu variation, factor VIII levels and the risk of venous thrombosis.

Levels of factor VIII (FVIII) are associated with the risk of venous thrombosis. The FVIII variation D1241E has been reported to be associated with decreased levels of FVIII. Our objective was to study whether D1241E is associated with levels of FVIII and the risk of venous thrombosis and whether this association is caused by D1241E or another linked variation. We analyzed the association of three FVIII gene haplotypes encoding 1241E (further denoted as HT1, HT3, and HT5) with FVIII levels and thrombosis risk. This analysis was performed in the Leiden Thrombophilia Study (LETS). The control populations of two case-controls studies on arterial thrombosis in men and women, respectively, were used to confirm the effects observed on FVIII:C in the LETS. In men, HT1 was associated with a 6% reduction in FVIII:C and with a reduced risk of venous thrombosis [odds ratio 0.4 (CI95 0.2-0.8)]. Logistic regression showed that the risk reduction was only partially dependent of the reduction in FVIII levels. HT1 showed no effects in women on either FVIII:C or risk of thrombosis. The number of carriers of HT3 and HT5 was too low to make an accurate estimate of the risk of venous thrombosis. Neither HT3 nor HT5 showed effects on levels of FVIII:C. When we consider that all three haplotypes encoding 1241E show different effects on FVIII:C and thrombosis risk, it is possible that D1241E is not the functional variation. However, FVIII gene variations do contribute to both levels of FVIII and the risk of thrombosis.

Aged↗
PubMed1994

Interaction between plasma potassium and epinephrine in coronary thrombosis in dogs.

BACKGROUND: Both plasma potassium ([K]) and epinephrine concentrations have been known to increase during exercise and decrease rapidly shortly after exercise; in addition, it is also known that exercise can promote coronary thrombosis in human and animal subjects. Many studies have shown that epinephrine has a stimulatory effect on coronary thrombosis; however, little information is available concerning the effect of raising plasma [K] on coronary thrombosis. The present study was designed to investigate the effect of raising plasma [K] and its interaction with epinephrine infusion on coronary thrombosis. METHODS AND RESULTS: A canine model of coronary thrombosis was used, and the frequency of cyclic blood flow reductions (CFRs) resulting from thrombus formation in the circumflex artery was analyzed in the study. By acutely raising plasma [K] to approximately 6.0 mEq/L, the frequency of CFRs was reduced from 8.0 +/- 0.6 to 3.7 +/- 1.0 in 40 minutes (P < .01). Epinephrine infusion (0.5 microgram.kg-1 x min-1) stimulated the frequency of CFRs from 7.1 +/- 0.5 to 11.5 +/- 0.7 in 40 minutes (P < .01). However, if plasma [K] was raised to approximately 6.0 mEq/L while the epinephrine infusion was continued, the frequency fell from 11.5 +/- 0.7 to 7.7 +/- 1.1 in 40 minutes (P < .01). CONCLUSIONS: The present study demonstrated that acutely raising plasma [K] inhibited coronary thrombosis in dogs and also blocked the potentiating effect of epinephrine on coronary thrombosis. These findings may suggest that raising plasma [K] exerts a protective effect against coronary thrombosis and that a rapid decrease in plasma [K], such as that occurring shortly after exercise, facilitates coronary artery thrombosis when the artery has a preexisting pathological condition.

Animals↗
PubMed1995

Opposing effects of plasma epinephrine and norepinephrine on coronary thrombosis in vivo.

BACKGROUND: It is well known that plasma catecholamines and myocardial infarction have a close relation and that coronary artery thrombosis is a major cause of myocardial infarction. In addition, epinephrine is known to be a prothrombogenic agent in vivo. However, the role of the other major circulating catecholamine, norepinephrine, in the development of coronary thrombosis is somewhat uncertain, although the role of norepinephrine is often considered analogous to the role of epinephrine. Therefore, the present study was designed to investigate the effect of norepinephrine and its interaction with epinephrine on coronary thrombosis. METHODS AND RESULTS: To compare the effects of epinephrine and norepinephrine on coronary thrombosis, we analyzed the frequency of cyclic blood flow reductions (CFRs) in an anesthetized canine model of coronary thrombosis (n = 25). Three experiments were used in the present study. In the first experiment with epinephrine infusion, plasma epinephrine was elevated from 0.46 +/- 0.25 to 27.7 +/- 1.85 nmol/L. The frequency of CFRs increased by more than 60%, from 7.1 +/- 0.5 to 11.5 +/- 0.7 in 40 minutes (P < .01). The second experiment included three experimental periods: control, norepinephrine infusion, and norepinephrine infusion plus epinephrine infusion. Norepinephrine was infused to raise plasma norepinephrine from 1.3 +/- 0.2 to 32.4 +/- 4.3 nmol/L. The frequency of CFRs in the dogs was markedly reduced, from 7.89 +/- 0.42 to 2.41 +/- 1.08 in 40 minutes (P < .01), whereas arterial pressure was elevated from 88 +/- 3 to 118 +/- 5 mm Hg (P < .01). However, when epinephrine infusion was added to the norepinephrine infusion, the frequency of CFRs increased from 2.41 +/- 1.08 to 7.74 +/- 1.12 in 40 minutes (P < .01). In the third experiment, a servocontrol device was used during the norepinephrine infusion to prevent rises in coronary arterial pressure. As a result of the norepinephrine infusion, the frequency of CFRs was reduced from 7.47 +/- 0.71 to 0.83 +/- 0.65 in 40 minutes (P < .01), even though the coronary arterial pressure was not altered. CONCLUSIONS: The present study demonstrated that infusion of epinephrine stimulated coronary artery thrombosis, whereas infusion of norepinephrine inhibited coronary artery thrombosis. In addition, the inhibitory effect of norepinephrine on coronary thrombosis is independent of increases in coronary arterial pressure. Therefore, the present findings suggest that epinephrine and norepinephrine have opposing effects on coronary thrombosis in dogs.

Animals↗
PubMed2005

Infectious complications of central venous catheters increase the risk of catheter-related thrombosis in hematology patients: a prospective study.

PURPOSE: We studied whether the risk of central venous catheter (CVC) -related thrombosis increased after an episode of CVC-related infection in patients undergoing intensive chemotherapy. Secondly, we determined whether thrombosis can be predicted or excluded by CVC lock fluid surveillance cultures. PATIENTS AND METHODS: In a prospective setting, 105 consecutive patients were carefully examined for CVC-related infection and thrombosis. In all patients, microbial surveillance cultures of CVC lock fluid were taken every other day. All patients with clinical suspicion of CVC-related thrombosis underwent Doppler ultrasound or additional venography. RESULTS: The cumulative incidence of CVC-related infection was 24% (25 of 105 patients). Clinically manifest thrombosis occurred in 13 (12%) of 105 patients. In patients with CVC-related infection, the risk of thrombosis increased markedly in comparison to those without infection (relative risk, 17.6; 95% CI, 4.1 to 74.1). In patients having two or more positive subsequent CVC lock fluid cultures with identical micro-organisms, 71.4% developed thrombosis, as compared with 3.3% in patients with negative or a single positive culture. CONCLUSION: The risk of clinically manifest thrombosis is increased after an episode of CVC-related infection in patients undergoing intensive chemotherapy. Surveillance culturing of CVC lock fluid may be clinically useful in estimating the risk for thrombosis and the instigation of focused early intervention.

Adolescent↗
PubMed2006

Travel-related venous thrombosis: results from a large population-based case control study (MEGA study).

BACKGROUND: Recent studies have indicated an increased risk of venous thrombosis after air travel. Nevertheless, questions on the magnitude of risk, the underlying mechanism, and modifying factors remain unanswered. METHODS AND FINDINGS: We studied the effect of various modes and duration of travel on the risk of venous thrombosis in a large ongoing case-control study on risk factors for venous thrombosis in an unselected population (MEGA study). We also assessed the combined effect of travel and prothrombotic mutations, body mass index, height, and oral contraceptive use. Since March 1999, consecutive patients younger than 70 y with a first venous thrombosis have been invited to participate in the study, with their partners serving as matched control individuals. Information has been collected on acquired and genetic risk factors for venous thrombosis. Of 1,906 patients, 233 had traveled for more than 4 h in the 8 wk preceding the event. Traveling in general was found to increase the risk of venous thrombosis 2-fold (odds ratio [OR] 2.1; 95% confidence interval [CI] 1.5-3.0). The risk of flying was similar to the risks of traveling by car, bus, or train. The risk was highest in the first week after traveling. Travel by car, bus, or train led to a high relative risk of thrombosis in individuals with factor V Leiden (OR 8.1; 95% CI 2.7-24.7), in those who had a body mass index of more than 30 kg/m(2) (OR 9.9; 95% CI 3.6-27.6), in those who were more than 1.90 m tall (OR 4.7; 95% CI 1.4-15.4), and in those who used oral contraceptives (estimated OR > 20). For air travel these synergistic findings were more apparent, while people shorter than 1.60 m had an increased risk of thrombosis after air travel (OR 4.9; 95% CI 0.9-25.6) as well. CONCLUSIONS: The risk of venous thrombosis after travel is moderately increased for all modes of travel. Subgroups exist in which the risk is highly increased.

Adult↗
PubMed2003

Venous thrombosis after hallux valgus surgery.

BACKGROUND: Although surgery for the treatment of hallux valgus is frequently performed, the exact rate of deep vein thrombosis following this procedure is unknown. We performed a single-center, prospective, phlebographically controlled study to quantify the rate of venous thrombosis following operative correction of hallux valgus. METHODS: Consecutive patients undergoing chevron bunionectomy for correction of hallux valgus deformity were enrolled in the study. Patients with clinical or hematological risk factors for venous thrombosis were excluded. One hundred patients with a mean age of 48.9 years were operated on and did not receive medical prophylaxis against thrombosis. All patients were assessed with phlebography at a mean of twenty-nine days postoperatively. RESULTS: Venous thrombosis was found in four patients (4%). The mean age of these patients (and standard deviation) was 61.7 +/- 6.1 years compared with a mean age of 48.4 +/- 13.9 years for the patients in whom thrombosis did not develop (p = 0.034). CONCLUSIONS: Patients are at a low risk for venous thrombosis following surgical treatment of hallux valgus. The need for prophylaxis against thrombosis should be calculated individually for each patient according to his or her known level of risk. Routine medical prophylaxis against thrombosis might be justified for patients over the age of sixty years.

Age Distribution↗
PubMed1994

Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up.

OBJECTIVE: The purpose of this study was to determine the value of venous MR angiography as the sole procedure for the diagnosis and follow-up of dural sinus thrombosis. MATERIALS AND METHODS: Forty-two patients with clinical findings suggestive of dural sinus thrombosis were examined with venous MR angiography and spin-echo MR imaging. Maximum-intensity-projection reconstructions and individual sections of the MR angiograms were examined for direct and indirect signs of dural sinus thrombosis by assessing flow signal from the major sinuses, the jugular bulb, upper jugular veins, ascending cortical veins (occlusion or increased flow due to formation of collaterals), diploe (emissary) veins and extracranial veins, and the deep subcortical veins (Galen's and internal cerebral veins). Direct signs of dural sinus thrombosis on MR angiograms included lack of typical high flow signal from a sinus that did not appear aplastic or hypoplastic on single sections from MR angiography and the frayed appearance of the flow signal from a sinus after recanalization. Indirect signs of dural sinus thrombosis included evidence of formation of collaterals, unusually prominent flow signal from deeper medullary veins, cerebral hemorrhage, visualization of emissary veins, and signs of increased intracranial pressure. When available, conventional angiograms were evaluated by analogous criteria as appropriate. Digital subtraction or cut-film angiograms were available for correlation in nine patients. In nine patients, MR angiography was repeated up to eight times during the course of follow-up. The results of MR angiography for all patients were compared with results in 10 control subjects. Confirmation of the diagnosis of dural sinus thrombosis was based either on conventional angiographic findings or on the changes seen in follow-up examinations. RESULTS: Dural sinus thrombosis could be ruled out in 25 of the 42 patients on the basis of clinical and MR angiographic findings. In 17 patients with MR angiographic findings that indicated dural sinus thrombosis, conventional angiography confirmed the diagnosis in nine patients, and changes seen on repeat MR angiograms during follow-up confirmed the diagnosis in nine patients as well (one patient's diagnosis was confirmed by both techniques). Individual frames from two-dimensional fast low-angle shot sequences allowed direct visualization of thrombus. Limited spin-echo sequences as performed here provided inconsistent findings and were insufficient for diagnosis. In the 10 control subjects, attenuation of flow signal was seen in the torcular Herophili in all studies; one subject had a nonpathologic variant of the sinojugular system. CONCLUSION: MR angiography is the technique of choice for diagnostic evaluation and follow-up of dural sinus thrombosis, and it is reliable as the sole examination for this condition. When MR angiographic findings are unremarkable and other abnormalities must be ruled out, routine spin-echo MR imaging should be performed.

Adult↗
PubMed1988

Thrombosis of the umbilical cord: analysis of 52 cases and literature review.

Fifty-two cases of umbilical cord thrombosis from 3 patients populations are analyzed and compared with 68 cases from the literature. The incidence of cord thrombosis is approximately 1/1300 deliveries, 1/1000 perinatal autopsies, and 1/250 high-risk gestations. There is a slight male predominance. Umbilical vein thrombosis occurs more frequently than thrombosis of one or both umbilical arteries, but poor fetal outcome is more likely with arterial thrombosis. The mechanism of fetal death when only one umbilical artery is thrombosed is illustrated and discussed. The strong association between cord thrombosis and perinatal morbidity and mortality is not noted among prospective cases but, when present, is related to additional umbilical cord abnormalities, obstetrical complications, or systemic fetal conditions that are the likely cause of both the thrombosis and the poor fetal outcome. The pathogenetic relationship between cord thrombosis and these associated conditions is discussed, and it is concluded that cord thrombosis is a marker of both the severity of these conditions and the likelihood of poor fetal outcome.

Female↗
PubMed1998

The role of venous ultrasonography in the diagnosis of suspected deep venous thrombosis and pulmonary embolism.

This paper describes the role of venous ultrasonography in the diagnosis of suspected deep venous thrombosis and pulmonary embolism. Inability to compress the common femoral or popliteal vein is usually diagnostic of a first episode of deep venous thrombosis in symptomatic patients (positive predictive value of about 97%). Full compressibility of both of these sites excludes proximal deep venous thrombosis in symptomatic patients (negative predictive value of about 98%). In patients with suspected deep venous thrombosis or in those who present with suspected pulmonary embolism but have a nondiagnostic lung scan, the subsequent risk for symptomatic venous thromboembolism is very low (<2% during 6 months of follow-up) provided that ultrasonography of the proximal veins remains normal in the course of 1 week (suspected deep venous thrombosis) or 2 weeks (suspected pulmonary embolism). Anticoagulation and further diagnostic testing can usually be safely withheld in these situations. Venous ultrasonography is much less reliable for the diagnosis of asymptomatic, isolated distal, and recurrent deep venous thrombosis than for the diagnosis of a first episode of proximal deep venous thrombosis in symptomatic patients. Clinical evaluation of the probability of deep venous thrombosis or pulmonary embolism, preferably by using a validated clinical model, complements venous ultrasonographic findings and helps to identify patients who would benefit from additional (often invasive) diagnostic testing. Thus, venous ultrasonography is thought to be a very valuable test for the diagnosis and management of patients with suspected deep venous thrombosis or pulmonary embolism.

Humans↗
PubMed1997

Primary vascular thrombosis after renal transplantation in children.

The aim of the study was to assess the incidence, causes, diagnostic and treatment modalities, and outcome of vascular thrombosis after kidney transplantation in children. Between 1984 and 1995 we performed 176 kidney transplants in pediatric recipients aged 1 to 18 years. Vascular thrombosis followed 7 transplants, 4 were renal vein and 3 arterial thromboses. Venous thromboses occurred 2 to 12 days after transplantation. All of the patients with a renal vein thrombosis lost their grafts. Arterial thrombosis developed in 2 cases of double renal arteries which were separately anastomosed into the recipient vessels. One graft was lost, but the other was saved by thrombolytic therapy (streptokinase). One child experienced intrarenal segmental artery thrombosis during acute vascular rejection, which resolved following combined anti-rejection and thrombolytic (intra-arterial streptokinase) treatment with full recovery of graft function. In all, vascular thrombosis complicated 7 out of 176 transplants (4.0%), and was the cause of 5 graft losses (2.8%). The incidence of vascular thrombosis was not increased in grafts with vascular anomalies (3/34 v. 4/142; p>0.05, chi sq.). We conclude that acute tubular necrosis, rejection and unstable volemia may predispose to vascular thrombosis. In selected cases, early diagnosis of vascular thrombosis may enable graft salvage by surgical or thrombolytic treatment.

Adolescent↗
PubMed2000

Risk of venous thrombosis in carriers of the prothrombin G20210A variant and factor V Leiden and their interaction with oral contraceptives.

BACKGROUND AND OBJECTIVES: The prothrombin G20210A mutation and factor V Leiden have been found to be associated with an increased risk of venous thrombosis, but the reported prevalences of the prothrombin gene variant both in the normal population and in patients with deep venous thrombosis (DVT) vary greatly in the literature. Moreover, the influence of oral contraceptives (OC) on thrombotic events in patients with the prothrombin G20210A variant has not been well established. In this study we evaluate both circumstances. DESIGN AND METHODS: A case-control study was run on 229 patients with DVT and 246 healthy controls. The patients' history of thrombosis and acquired thrombotic risk factors, especially OC, were recorded. Prothrombin G20210A mutation, factor V Leiden, antithrombin, heparin II cofactor, plasminogen and proteins C and S were evaluated. RESULTS: Seven and a half percent of the patients and 2.9% of the controls were carriers of the prothrombin mutation, while 12.2% of the patients and 1.6% of the controls had factor V Leiden. Among the 229 DVT patients there were 130 patients with clinically suspected thrombophilia (first thrombotic event occurring before the age of 45 years or positive family history of thrombosis or recurrent venous thrombosis). Ten percent of these 130 patients were carriers of the prothrombin G20210A mutation and 18.5% had the factor V Leiden mutation. The odds ratios (OR) for DVT risk were: 2.4 (95% CI, 1.0-6.3) for the total DVT patients and 5.2 (95% CI, 1.4-19.5) for the patients with clinically suspected thrombophilia with the prothrombin mutation. The risk of thrombosis was 6.9 (95% CI, 2.3-20.6) for the DVT patients and 14.3 (95% CI, 3.3-64.6) for the patients with clinically suspected thrombophilia with factor V Leiden. Fifty-five percent of the patients with combined congenital defects (prothrombin mutation G20210A plus another congenital defect) had recurrent thrombosis. In women receiving OC the risk of DVT was 3.5 (95% CI, 1.5-8.2) that of the patients not receiving OC. When women with combined defects were also taking OC, the risk of thrombosis increased significantly. INTERPRETATION AND CONCLUSIONS: The prevalence of the prothrombin G20210A mutation in the healthy population in our study is similar to that observed in other southern European countries. The prothrombin G20210A mutation does not by itself seem to be a high thrombotic risk factor. However, when it is present together with other thrombotic risk factors, the predicted risk of thrombotic events increases. The use of OC by women with the prothrombin G20210A variant or FV Leiden, either alone or combined with other thrombotic risk factors, was associated with a significant increase in the risk of venous thrombosis.

Adult↗
PubMed2001

Risk factors associated with thrombosis in patients with antiphospholipid antibodies.

OBJECTIVE: To define risk factors associated with thrombosis in patients with antiphospholipid antibodies (aPL). METHODS: Ninety-nine patients with aPL, most of whom had prior thrombosis, were evaluated for the presence of acquired and inherited thrombophilic states. Genomic testing was performed for factor V(R506Q), 3' prothrombin (PTG) and methylene tetrahydrofolate reductase (MTHFR) polymorphisms. Clinical records were reviewed for the presence of acquired risk factors (RF) for thrombosis and events associated with aPL. Univariate statistical analysis was performed using Fisher's exact testing. A neural network statistical model was also used to identify which thrombophilic risk factors were most important in development of arterial and venous thrombosis. RESULTS: For arterial thrombosis, hypertension, tobacco use, hyperlipidemia, and diabetes mellitus were the most important predictors of thrombosis. By contrast, tobacco use, the 3' PTG and factor V(R506Q) polymorphisms, and previous cardiac surgery were the most important predictors of venous thrombosis. CONCLUSION: In this hypothesis-generating retrospective study, acquired risk factors were most important in arterial thrombosis, while the presence of factor V(R506Q) and 3' PTG polymorphisms were more important in the development of venous thrombosis. These findings are being validated in an ongoing, prospective study.

Adolescent↗
PubMed2001

IgM anticardiolipin antibodies are associated with stenosis of vascular access in hemodialysis patients but do not predict thrombosis.

AIM: The prevalence of anticardiolipin antibodies (ACA) is elevated amongst hemodialysis patients as compared with the general population. Previous studies have disagreed as to whether the presence of ACA represents a risk factor for access thrombosis. Other risk factors for access thrombosis (decreased blood flow, elevated venous pressure) have also been described. MATERIALS AND METHODS: We performed a combination retrospective and prospective cohort study of a single outpatient dialysis unit to assess the association between these potential risk factors and access thrombosis. ACA, access blood flow, presence of stenosis, and venous pressures were measured in 100 patients. Information on episodes of access thrombosis was gathered for 12 months prior to and 12 months after ACA measurement. RESULTS: ACA were present in 19% of patients with equal numbers of IgG- and IgM-ACA. The presence of IgM-ACA was significantly associated with the use of aspirin and the presence of stenosis by Doppler at the time of ACA testing (p < 0.05). A logistic regression model was used to estimate the association between clinical factors and access thrombosis. In this multivariate analysis, the presence of access stenosis and a history of access thrombosis were both significantly associated with the development of access thrombosis. Adjusted for these variables, neither IgG- nor IgM-ACA was significantly associated with access thrombosis. The presence of an ACA was not associated with episodes of access thrombosis in either the prospective or retrospective analyses. CONCLUSION: Further investigation is required to determine if the association between aspirin use and IgM-ACA, or of IgM-ACA and access stenosis, has implications for underlying pathogenetic mechanisms of access stenosis.

Adult↗
PubMed2000

[Antiphospholipid thrombosis syndrome and acquired activated protein C resistance].

OBJECTIVE: To explore the correlation between antiphospholipid antibodies (APA) activated protein C resistance (APCR) and antiphospholipid thrombosis (APL-T) syndrome and investigate the mechanism of thrombosis in APL-T syndrome. METHODS: ELISA, APTT-LA and APTT+/-APC methods were used to detect anticardiolipin antibodies (ACA), lupus anticoagulants (LA) and APCR in 20 APL-T syndrome patients respectively. RESULTS: Twenty patients were diagnosed as APL-T. The patients were classified in three ways. According to etiology, 14 of 100 systemic lupus erythematosus (SLE) patients were diagnosed as "secondary" APL-T, and 6 of 16 "unexplained" thrombosis and spontaneous abortion as "Primary" APL-T syndrome. According to antibodies, 12 of 20 patients with positive LA were diagnosed as lupus anticoagulant thrombosis syndrome (LA-T), 12 of 20 patients with positive ACA as anticardiolipin antibodies thrombosis syndrome (ACA-T). According to clinical presentation: 7 of 20 patients with deep vein thrombosis were classified as type I APL-T, 3 of 20 patients with cerebrovascular thrombosis as type II, 1 of 20 patients with vein cerebrovascular thrombosis and spontaneous abortion as type IV (mixing), and 9 of 20 patients with spontaneous abortion as type V (fetal wastage type). The ACAs and LA are strongly associated with APL-T. There is close relationship between APCR and APL-T. CONCLUSION: The acquired APCR might be an important reason for thrombosis in APL-T caused by APA and LA.

Activated Protein C Resistance↗
PubMed2002

Venous thrombosis in patients with solid tumors: determination of frequency and characteristics.

Deep venous thrombosis (DVT) and pulmonary embolism (PE) are well recognized complications of cancer. However, our current knowledge of this association is derived from studies conducted more than a decade ago. In light of the changes in medical practice and the improvement in cancer care in recent years, a re-evaluation of the relationship between malignancy and venous thrombosis is in order. Of a total of 1041 patients with solid tumors admitted to 3 major medical centers, there were 81 (7.8%) diagnosed with DVT/PE. Patients were more likely to develop DVT/PE during chemotherapy (p = .0001). Advanced malignancies (p = .001), renal carcinoma (p = .005), pancreatic (p = .001), gastric (p = .014) and brain tumors (p = .001) were independent variables strongly associated with the occurrence of venous thrombosis. The occurrence of thrombotic events in the population tested in this study did not adversely affect survival (p = .082). The study identifies subset of patients with cancer at high risk for venous thrombosis. Early prophylaxis with anticoagulants in these patients may be warranted. Most importantly, further clinical trials are desperately awaited to detect possible new trends in the frequency and types of thrombotic events and to better define prevention strategies in cancer patients at risk for thrombosis. The association between venous thromboembolic disease (VTD) and malignant neoplastic disorders is well known and has been the subject of several reports for more than a century. There is a general agreement among investigators that thrombotic complications in patients with cancer occur at a rather high frequency, and that other circumstantial factors such as surgery or chemotherapy potentiates this risk. However, several important considerations pertaining to cancer and thrombosis continue to be shrouded in controversy. For example, there are inexplicable differences in the proportion of patients with cancer diagnosed with deep venous thrombosis (DVT) or pulmonary embolism (PE) reported in the literature. In the absence of large well-controlled studies, one may only postulate on the reasons that contributed to these differences. The inclusion of different types of VTD such as superficial, venous, arterial or vascular access device-induced thrombosis may have led to overestimation of the incidence of these events in patients with underlying malignancy. Another possible explanation for this discrepancy relates to the use of a variety of diagnostic and methodological criteria ranging from observation and clinical suspicion to more invasive procedures resulting in considerable differences in the rate of reported clotting events. Along the same line of discussion, one may argue whether VTD is a random event or constitutes a complication that occurs more commonly in patients with distinct characteristics and certain tumor types. To further investigate the association between malignancy and thrombosis, we evaluated 1041 patients with solid tumors for the risk of DVT/PE. The main objectives of the study were to determine the frequency of DVT/PE based on validated diagnostic criteria and to identify patients with cancer at high risk for developing these thrombotic episodes. Also, we evaluated the impact of VTD on the survival of these patients.

Adult↗
PubMed2002

Treatment of deep vein thrombosis with oral anticoagulants in patients with malignancy: prospective cohort study.

AIM: To assess the outcome of deep vein thrombosis in patients with malignancy after 6 months of oral anticoagulant therapy, and to compare it with international normalized ratio (INR). METHOD: Thirty-one patients with malignancy (13 with hematological and 18 with solid tumors) and deep vein thrombosis (29 leg thrombosis and 2 upper extremity thrombosis) were included into a prospective cohort study that lasted from March 2000 until May 2001. The presence of malignant tumors was histologically proved and documented, and deep vein thrombosis was proved by ultrasound or venography. Patients were treated with heparin during the acute phase, and with oral anticoagulant therapy during further 6 months. INRs and ultrasound examination performed during the acute event were repeated one month and 6 months afterwards for the needs of analysis. RESULTS: Twenty-four patients concluded the study. Clot resolution was achieved in 13 patients after 6 months of therapy. The patients with INR>2 (n=10) had better clot resolution than those with INR<2 (n=3); p=0.012. There was no statistically significant difference in the outcome of thrombosis with regard to the INR level after a month of therapy (p=0.555). Three patients experienced bleeding, one patient had recurrent thrombosis, and two patients suffered pulmonary embolism. CONCLUSION: Appropriate anticoagulation during 6 months after the acute deep vein thrombosis enhances the rate of the complete clot resolution. The INR values can be used as predictive of complete recovery from the thrombosis. Complications are comparable with those reported for patients without malignancy.

Administration, Oral↗