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PubMed2003

High prevalence of antiphospholipid antibodies in Asian cancer patients with thrombosis.

Thrombotic complications are a significant cause of morbidity and mortality in cancer patients. Studies in Caucasian populations have shown that up to one-third of such patients test positive to antiphospholipid antibodies. Our aim was to determine the prevalence and serotypes of antiphospholipid antibodies in an unselected group of Asian cancer patients with thrombosis. All patients with cancer-related thrombosis seen in the Department of Hematology-Oncology and Radiation Oncology were enrolled in this study. The study period was from April 2000 to May 2001. Antiphospholipid antibodies tests were performed, namely lupus anticoagulant screen, anticardiolipin antibodies (IgG and IgM) and anti-beta-2 glycoprotein I antibodies (B2 GPI) IgG, IgM and IgA. Thirty-three patients were recruited. There were 14 males and 19 females, with an age range of 35-78 years of age. Of those enrolled, there were 25 Chinese, five Malays and three Indians. The patients had several cancer types: 11 (36.7%) patients had adenocarcinoma as the histological cell type. Of the 33 patients, 75.8% had stage IV disease. Arterial thrombosis was seen in eight patients (24.2%), and venous thrombosis occurred in 29 patients (87.9%). Antiphospholipid antibodies were positive in 60.6% of the patients, of which anti-B2GPI IgA antibody was the most prevalent antiphospholipid present (46.9%). The presence of anti-beta-2 glycoprotein I IgA antibody was associated with strokes, extensive and recurrent venous thrombosis, and coincident arterial and venous thrombosis. A high prevalence of antiphospholipid antibodies (60.6%) was found in Asian patients with cancer-related thrombosis. The presence of antiphospholipid antibodies, particularly anti B2GPI IgA, may identify a subset of cancer patients who are at high risk of developing thrombotic complications, and further studies are warranted.

Adenocarcinoma↗
PubMed2005

A new model of reversible sinus sagittalis superior thrombosis in the rat: magnetic resonance imaging changes.

OBJECTIVE: The causes of cerebral sinus and vein occlusion and the accompanying parenchymal changes remain largely unexplained. The clinical variability and low incidence of the disease complicate systematic clinical investigations. Animal studies are indispensable; however, existing animal models of sinus thrombosis do not allow for long-term follow-up studies and are not suitable for pharmacological recanalization because sinus thrombosis is induced by ligation and injection of thrombogenic substances and does not resemble sinus thrombosis in humans. METHODS: We induced thrombosis of the superior sagittal sinus (SSS) by careful topical application of ferric chloride onto the SSS of rats, leading to highly reproducible occlusions. Magnetic resonance imaging was performed immediately after initiation of thrombosis and on postoperative Days 1, 2, and 7. Diffusion- and T2-weighted images allowed for calculation of the apparent diffusion coefficient and T2 relaxation time. Vascular status was assessed by venous magnetic resonance angiography. Neurological deficits were assessed with the rotarod test. RESULTS: Seven days after induction of thrombosis, partial recanalization (50.7% of the SSS remaining occluded) was accompanied by a resolution of early generalized changes of the apparent diffusion coefficient and of T2 relaxation time, indicating edema of the entire brain parenchyma. Compared with sham-treated animals, clinical skills in the experimental group improved over time, which was statistically independent from the degree of recanalization. Histopathological analysis revealed no signs of cerebral infarction. CONCLUSION: This is the first animal model of SSS thrombosis that offers the possibility to investigate pathophysiological aspects of the disease as well as the influence of therapy on the nature of disease progression.

Animals↗
PubMed1998

Central vein catheter-related thrombosis in intensive care patients: incidence, risks factors, and relationship with catheter-related sepsis.

OBJECTIVE: To evaluate the incidence and risk factors for catheter-related central vein thrombosis in ICU patients. DESIGN: Observational prospective multicenter study. SETTING: An 8-bed surgical ICU, a 10-bed surgical cardiovascular ICU, and a 10-bed medical-surgical ICU. PATIENTS: During an 18-month period, 265 internaljugular or subclavian catheters were included. Veins were explored by duplex scanning performed just before or < 24 h after catheter removal. Suspected risk factors of catheter-related central vein thrombosis were recorded. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Fifty-seven catheters were excluded from the analysis. Therefore 208 catheters were analyzed. Mean age of patients was 64+/-15 years, simplified acute physiologic score was 12+/-5, organ system failure score at insertion was 1+/-1, and mean duration of catheterization was 9+/-5 days. A catheter-related internal jugular or subclavian vein thrombosis occurred in 33% of the cases (42% [95% confidence interval (CI), 34 to 49%] and 10% [95% CI, 3 to 18%], respectively). Thrombosis was limited in 8%, large in 22%, and occlusive in 3% of the cases. Internal jugular route (relative risk [RR], 4.13; 95% CI, 1.72 to 9.95), therapeutic heparinization (RR 0.47; 95% CI, 0.23 to 0.99), and age >64 years (RR, 2.44; 95% CI, 2.05 to 3.19) were independently associated with catheter-related thrombosis. Moreover, the risk of catheter-related sepsis was 2.62-fold higher when thrombosis occurred (p=0.011). CONCLUSIONS: Catheter-related central vein thrombosis is a frequent complication of central venous catheterization in ICU patients and is closely associated with catheter-related sepsis.

APACHE↗
PubMed1989

Thrombosis: the major Hickman catheter complication in patients with solid tumor.

Major complications of Hickman catheter placement (thrombosis and infection) were determined in 168 patients with solid tumor (lung, 79; head and neck, 56; esophagus, 24; and miscellaneous, 9). Catheter-related thrombosis was clinically detected in 22 individuals and was detected at autopsy in six (total 17 percent). The 17 percent figure underestimates the true incidence of thrombosis since only 25 percent of study patients had autopsies. Patients with adenocarcinoma of the lung constituted a high risk group. Nine of 20 (45 percent) of these patients had thrombosis compared to 25, 9, and 16 percent of patients with squamous cell cancers of lung, head and neck and esophagus, respectively (p less than 0.002). Three patients with thrombosis had pulmonary emboli and two died. Thrombosis occurred despite daily heparin catheter flushing. INfections occurred in 11 patients. One had suspected endocarditis, one had a subcutaneous tunnel infection, and nine had exit site infections. All responded to local or systemic antibiotics. Better methods to prevent thrombosis are needed.

Adenocarcinoma↗
PubMed1994

Deep venous thrombosis and pulmonary embolism after major reconstructive operations on the spine. A prospective analysis of three hundred and seventeen patients.

We performed a prospective study of 317 patients in order to determine the prevalence of deep venous thrombosis after reconstructive operations on the spine; 126 of the patients were examined with duplex ultrasound assessments of the lower extremities to ensure that no asymptomatic thrombi were being missed. Thigh-high stockings and sequential pneumatic compression of the lower extremities were used, in all patients, for prophylaxis against venous thrombosis. No antiplatelet agents or anticoagulant medications were administered. There was no evidence of thrombosis on any of the duplex ultrasound studies. Subsequently, venous thrombosis developed and was treated successfully in one of the 126 tested patients and in one of the 191 untested patients, and a fatal pulmonary embolus developed in one of the untested patients. The over-all clinical prevalence of thrombotic complications was 0.9 per cent (three complications in 317 patients). All three of the patients who had clinical evidence of thrombosis had had an anterior lumbar procedure because of a degenerative disorder or trauma; however, we could not prove that this approach or these diagnoses were significant risk factors for thrombosis (p < 0.05). While it is possible that some thrombi may have escaped both clinical and ultrasonic detection, such thrombi apparently were not enough of a danger to warrant the use of intensive prophylactic procedures that are associated with more risk. On the basis of this prospective study, therefore, we think that routine screening for the detection of asymptomatic thrombosis in patients who have had a procedure on the spine is unwarranted.

Adolescent↗
PubMed1995

Portal vein thrombosis after percutaneous ethanol injection for hepatocellular carcinoma: value of color Doppler sonography in distinguishing chemical and tumor thrombi.

OBJECTIVE: The distinction between benign (chemical) and tumor thromboses of the portal vein after treat,ent with percutaneous injection of ethanol for hepatocellular carcinoma is crucial for the proper management of the patient. The purpose of this study was to determine whether color Doppler sonography can be used to differentiate between the two types of thrombi. SUBJECTS AND METHODS: Between October 1991 and April 1994, portal vein thrombosis was detected by color Doppler sonography in 19 patients (13 men and six women 59-77 years old; mean age, 67 years) who had hepatocellular carcinomas and who had received percutaneous ethanol injection (n = 11) or percutaneous ethanol injection after transcatheter arterial embolization (n = 8). The criterion for diagnosing tumor thrombosis by color Doppler sonography was the detection of pulsatile arterial flow in the thrombus. The benign or malignant nature of the thrombosis was subsequently established by percutaneous fine-needle biopsy of the thrombus; malignant thrombosis was seen in 13 patients, and chemical thrombosis was seen in six patients. RESULTS: Pulsatile arterial flow in the thrombus was observed by color Doppler sonography in 12 of the 13 malignant thrombi and in none of the bland thrombi. The flow was hepatopetal in seven cases and hepatofugal in five cases. The peak systolic frequency shift ranged from 0.59 to 2.65 kHz (mean, 1.35 kHz), and the resistive index ranged from 0.37 to 0.69 (mean, 0.55). The sensitivity and the specificity of color Doppler sonography for the detection of tumor thrombosis were 92% and 100%, respectively. CONCLUSION: Our study shows that color Doppler sonography is a reliable way to differentiate between chemical and tumor thromboses of the portal vein in patients with hepatocellular carcinomas treated by ethanol injection. When the sonogram shows pulsatile arterial flow within the thrombus, percutaneous biopsy of the thrombus is unnecessary. The finding is always indicative of malignant thrombosis.

Aged↗
PubMed1999

Clinical utility of a rapid whole-blood D-dimer assay in patients with cancer who present with suspected acute deep venous thrombosis.

BACKGROUND: Although D-dimer assays have high negative predictive values for the diagnosis of deep venous thrombosis, their accuracy in patients with cancer is uncertain. OBJECTIVE: To compare the clinical utility of a whole-blood D-dimer assay for the diagnosis of deep venous thrombosis in patients with and those without cancer. DESIGN: Retrospective analysis of three prospective studies. SETTING: Two tertiary care hospitals. PATIENTS: 1068 consecutive outpatients with suspected deep venous thrombosis. MEASUREMENTS: All patients underwent D-dimer testing and assessment with a priori diagnostic strategies that incorporated impedance plethysmography, compression ultrasonography, or contrast venography. Patients in whom deep venous thrombosis was not diagnosed initially were followed for 3 months for the development of thrombosis. Results of D-dimer testing were assessed according to the final diagnosis based on objective testing and clinical follow-up. Cancer status was identified at presentation. RESULTS: The prevalence of deep venous thrombosis was 48.8% in 121 patients with cancer and 14.6% in 947 patients without cancer. Although the sensitivity of the D-dimer assay was similar in patients with and those without cancer (86.4% [95% CI, 75.0% to 94.0%] and 82.6% [CI, 75.2% to 88.5%], respectively), the specificity was significantly lower in patients with cancer (48.4% [CI, 35.5% to 61.4%] and 82.2% [CI, 79.4% to 84.8%]), as was the negative predictive value (78.9% [CI, 62.7% to 90.4%] and 96.5% [CI, 94.9% to 97.8%]). In contrast, the likelihood ratios of a negative test result (0.28 [CI, 0.14 to 0.56] and 0.21 [CI, 0.15 to 0.31]) did not differ significantly. CONCLUSIONS: A negative D-dimer test result in patients with cancer does not reliably exclude deep venous thrombosis because the negative predictive value of the test is significantly lower in these patients than in patients without cancer.

Acute Disease↗
PubMed2001

Management of suspected deep venous thrombosis in outpatients by using clinical assessment and D-dimer testing.

BACKGROUND: When deep venous thrombosis is suspected, objective testing is required to confirm or refute the diagnosis. OBJECTIVE: To determine whether the combination of a low clinical suspicion and a normal D -dimer result rules out deep venous thrombosis. DESIGN: Prospective cohort study. SETTING: Three tertiary care hospitals in Canada. PATIENTS: 445 outpatients with a suspected first episode of deep venous thrombosis. INTERVENTIONS: Patients were categorized as having low, moderate, or high pretest probability of thrombosis and underwent whole-blood D -dimer testing. Patients with a low pretest probability and a negative result on the D -dimer test had no further diagnostic testing and received no anticoagulant therapy. Additional diagnostic testing was done in all other patients. MEASUREMENTS: Venous thromboembolic events during 3-month follow-up. RESULTS: 177 (40%) patients had both a low pretest probability and a negative D -dimer result. One of these patients had deep venous thrombosis during follow-up (negative predictive value, 99.4% [95% CI, 96.9% to 100%]). CONCLUSION: The combination of a low pretest probability of deep venous thrombosis and a negative result on a whole-blood D -dimer test rules out deep venous thrombosis in a large proportion of symptomatic outpatients.

Ambulatory Care↗
PubMed2004

Venous sonography for the diagnosis of asymptomatic deep vein thrombosis in patients with cancer undergoing chemotherapy.

OBJECTIVE: Early detection of asymptomatic deep vein thrombosis by venous sonography may identify patients who may benefit from anticoagulant therapy and thus may prevent morbidity and mortality associated with deep vein thrombosis. The aim of this study was to examine the prevalence of deep vein thrombosis by venous sonography in asymptomatic ambulatory patients with cancer undergoing chemotherapy and to evaluate the correlation between procoagulant activity and asymptomatic deep vein thrombosis. METHODS: The study population included 62 patients (32 with lung cancer and 30 with lymphoma) receiving chemotherapy with an ambulatory performance status and without clinical evidence of deep vein thrombosis. Bilateral venous sonographic studies of the lower extremities were performed, covering the femoropopliteal venous system. The D-dimer level and acquired activated protein C resistance were determined in the patients and in 30 healthy control subjects. RESULTS: Sonographic evidence of deep vein thrombosis on the femoropopliteal axis was found in 0 (0%) of 62 patients (1-sided 95% confidence interval, 0%-4.8%). Acquired activated protein C resistance prevalence and D-dimer levels were increased in study patients compared with control subjects (34% versus 0%; P < .003; median, 0.72 versus 0.25 mg/L; P < .0001, respectively). CONCLUSIONS: Despite the procoagulant tendency, venous sonography did not detect asymptomatic deep vein thrombosis in patients with cancer undergoing chemotherapy. Thus, screening by venous sonography is not justified in this patient population.

Activated Protein C Resistance↗
PubMed1999

Application of a diagnostic clinical model for the management of hospitalized patients with suspected deep-vein thrombosis.

The purpose of this study was to evaluate whether the determination of pretest probability using a simple clinical model and the SimpliRED D-dimer could be used to improve the management of hospitalized patients with suspected deep-vein thrombosis. Consecutive hospitalized patients with suspected deep-vein thrombosis, had their pretest probability determined using a clinical model and had a SimpliRED D-dimer assay. Patients at low pretest probability underwent a single ultrasound test. A negative ultrasound excluded the diagnosis of deep-vein thrombosis whereas a positive ultrasound was confirmed by venography. Patients at moderate pretest probability with a positive ultrasound were treated for deep-vein thrombosis whereas patients with an initial negative ultrasound underwent a single follow-up ultrasound one week later. Patients at high pretest probability with a positive ultrasound were treated whereas those with negative ultrasound underwent venography. All patients were followed for three months for the development of venous thromboembolic complications. Overall, 28% (42/150), and 10% (5/50), 21% (14/71) and 76% (22/29) of the low, moderate and high pretest probability patients. respectively, had deep vein thrombosis. Two of 111 (1.8%; 95% CI = 0.02% to 6.4%) patients considered to have deep vein thrombosis excluded had events during three-month follow-up. Overall 13 of 150 (8.7%) required venography and serial testing was limited to 58 of 150 (38.7%) patients. The negative predictive value of the SimpliRED D-dimer in patients with low pretest probability was 96.2%, which is not statistically different from the negative predictive value of a negative ultrasound result in low pretest probability patients (97.8%). Management of hospitalized patients with suspected deep-vein thrombosis based on clinical probability and ultrasound of the proximal deep veins is safe and feasible.

Cohort Studies↗
PubMed1999

[Thrombosis and its therapeutic targets].

Pathophysiological factors of thrombosis (flow, exposed surface and blood reactivity) explain when, how and why a thrombosis does develop. The same factors associated to the fibrinolytic capacity of the vessel wall explain the spontaneous evolution of the thrombosis. Among these factors, blood flow determines the relative participation of platelets and that of coagulation cascade. In arterial thrombosis, atherosclerotic plaque rupture is the triggering factor and platelets are the main actors in the thrombotic reaction: in consequence platelets are the main target and antiplatelet agents the main drugs to use for preventing atherothrombotic ischaemic events. In venous thrombosis, flow (stasis) is the main factor (with an additional role of blood coagulability and of venous wall lesion), and blood coagulation is the main contributor: anticoagulants are the logical option to prevent venous thromboembolic events. Thrombolytic agents can be used in arterial thrombosis only when a fibrin network completes and stabilizes the occluding platelet thrombosis (in myocardial infarction and not in unstable angina) and this has to be applied very early so that the physiological dethrombosis can still be possible.

Blood Coagulation Disorders↗
PubMedDate not supplied

Spectrum of upper-extremity deep venous thrombosis in a community teaching hospital.

OBJECTIVE: The goal of this study was to characterize the spectrum of upper-extremity deep venous thrombosis in a community teaching hospital. DESIGN AND SETTING: A retrospective analysis was used at a large urban teaching hospital. MATERIAL AND METHODS: We reviewed the records of 90 patients with ultrasound-documented thrombosis of the internal jugular, subclavian, axillary, or brachial veins to determine clinical characteristics, risk factors, and outcome. RESULTS: The most common underlying conditions associated with upper-extremity deep venous thrombosis were the presence of a central venous catheter in 65 patients (72%), infection in 25 (28%), extrathoracic malignancy in 20 (22%), thoracic malignancy in 19 (21%), renal failure in 19 (21%), and a prior lower-extremity deep venous thrombosis in 16 (18%). Pain was noted in 31 (34%) patients, and 76 patients (84%) had edema of the involved extremity. The left subclavian vein was involved in 44 patients (49%), and 35 patients (39%) had a central venous catheter in the left subclavian vein. When a central venous catheter was present, the deep venous thrombosis was usually ipsilateral (P <.001). Heparin and warfarin were administered to 65 (72%) and 53 (59%) of the patients, respectively. Eleven patients (12%) died. Of these patients, 8 (73%) had an underlying infection, whereas only 22% of survivors had an infection (P =.0012). CONCLUSION: Upper-extremity deep venous thrombosis typically occurs in patients with a systemic illness in the presence of a central venous catheter. The left subclavian vein is frequently involved because this is a common site for placement of a central venous catheter. Pain is uncommon, but edema of the involved extremity is noted in the majority of patients. The mortality rate of patients in this study with an upper-extremity deep venous thrombosis was 12%; most patients who died had a central venous catheter and an underlying infection.

Aged↗
PubMed2000

Minor events and the risk of deep venous thrombosis.

BACKGROUND: Deep venous thrombosis is a common disease, with genetic and acquired risk factors. Many patients have a history of minor events (short periods of immobilisation such as prolonged travel, short illness, minor surgery or injuries) before onset of venous thrombosis. However, the role of these minor events has received little formal study. Also, we do not know how minor events might interact with the presence of genetic prothrombotic defects (factor V Leiden mutation, factor II mutation, protein C, S and antithrombin deficiency). PATIENTS AND METHODS: On the basis of case-control data from a thrombosis service in the Netherlands, we added a follow-up period for a case-cross-over analysis of minor events as risk factors, and a case-only analysis for the interaction with factor V Leiden. A total of 187 patients with first, objectively diagnosed venous thrombosis of the legs, aged 15-70, without underlying malignancies and without major acquired risk factors entered the study. For the analysis of minor events in the case-cross-over analysis, we used a matched odds ratio; in the case-only analysis, we used the multiplicative synergy index. RESULTS: In 32.6% of the 187 patients with deep venous thrombosis who did not have major acquired risk factors, minor events were the only external risk factors. Minor events increased the risk of thrombosis about 3-fold, as estimated in the case-cross-over analysis (odds ratio 2.9, 95% confidence interval 1.5-5.4). The synergy index between minor events and factor V Leiden mutation in the case-only analysis was 0.7 (95% confidence interval 0.3-1.5). Therefore, persons with factor V Leiden mutation who experience a minor event will have an estimated risk increase of about 17-fold, which exceeds the sum of the individual risk factors. CONCLUSIONS: Minor events are likely to play an important role in the development of deep venous thrombosis, especially in the presence of genetic prothrombotic conditions.

Adolescent↗
PubMed1975

National Conference on Thrombosis and Hemostosis, Dallas, Tesas 20.-22. November 1974. Clinical Correlations.

There are two aspects which are clinically relevant in the relationships among thrombosis and arteriosclerosis. First, the relationship of thrombosis to atherogenesis. Thrombosis is closely related to endothelial injury and there is recent evidence that repeated or continuous endothelial damage leads to the development of all the lesions seen in human atherosclerosis. This occurs in the absence of dietary lipid supplement. The relative importance of the parts played by injury and thrombosis in this process need further delineation. Secondly, established arteriosclerotic disease is associated with thrombosis. This thrombosis is us ually mural, seldom occlusive. Embolism by platelet aggregates which has been well described in the retinal and cerebral circulations may affect other vascular territories such as the heart and the kidney. Such a mechanism may explain some cases of otherwise unexplained sudden cardiac death and some cases of hypertension. We need better clinical tool to detect the occurrence of thrombo-embolism and to monitor it's progress. Measures to modify thrombosis and embolism may be as useful or more useful than those wer currently employ in the clinical management of atherosclerotic disease.

Animals↗
PubMedDate not supplied

Thrombosis as a complication of extended stay at high altitude.

BACKGROUND: There is limited knowledge about the medical problems of long term stay at high (> 3000 m) and extreme (> 5000 m) altitudes, as these areas are generally considered uninhabitable. METHODS: Prospectively collected clinical records of all patients hospitalized at Command Hospital, Western Command between November 1998 and February 2000 were reviewed to identify thrombotic complications among patients from high and extreme altitude areas as well as those from non-high altitude areas who were < 45 years of age. RESULTS: Of 20,257 hospital admissions during the study period, 1692 were from high and extreme altitude areas. Forty-six patients from these areas had thrombosis-related diseases compared to 17 from non-high altitude areas (odds ratio: 30.49; 95% CI: 17.06-51.67; p < 0.001). The mean (SD) age of all patients with thrombotic complications was 32 (8) years and all were men. The mean duration of stay at high and extreme altitudes of such patients was 10.2 (5.6) months. Only 25 were smokers (mean 5.2 pack-years) and 39 consumed alcohol (mean 54 ml/day). Apart from frostbite in 5, no other medical condition was noted in these patients. The vascular events were deep vein thrombosis (20), pulmonary thromboembolism (6), stroke (15), thrombosis of the abdominal veins (8), and retinal artery and peripheral arterial thrombosis (1 each). The presenting complaint in all patients with thrombosis of the abdominal veins was poorly localized pain in the upper abdomen followed by ascites (6/8). Five of these patients also had a large spontaneous splenic haematoma. None of the patients investigated was found to have a procoagulant disorder. CONCLUSION: Long term stay at high and extreme altitudes is associated with a 30 times higher risk of spontaneous vascular thrombosis. Veins are common sites of such thrombotic events. We also encountered thrombosis of the portal, splenic and superior mesenteric veins in our patients who had stayed at high and extreme altitudes.

Adult↗
PubMed2001

Risk of pregnancy-related venous thrombosis in carriers of severe inherited thrombophilia.

Homozygous carriers of factor V Leiden have an approximately 80-fold increased risk of venous thrombosis. Also double heterozygous carriers of both the factor V Leiden and the prothrombin gene mutations are at high thrombotic risk. The magnitude of the risk of venous thrombosis in pregnant women with the two severe thrombophilic conditions has not been estimated so far. We performed a multicenter retrospective family study in women with homozygous factor V Leiden, double heterozygous factor V Leiden and the prothrombin gene mutation, and women with normal coagulation. Only relatives of index patients with thrombosis formed the study cohort. Fifteen homozygous and 39 double heterozygous women were compared to 182 women with normal coagulation. Venous thrombosis occurred in 3 of 19, 2 of 50 and 1 of 221 pregnancies, respectively. One thrombotic episode occurred in the third trimester, the remaining 5 in the postpartum. The prevalence of venous thrombosis was 15.8% (95% CI 3.4-39.6) for homozygotes. 4.0% (95% CI 0.5-13.7) for double heterozygotes and 0.5% for women with normal coagulation. The relative risk of pregnancy-related venous thrombosis was 41.3 (95% CI 4.1-419.7) for homozygous and 9.2 (95% CI 0.8-103.2) for double heterozygous carriers. In conclusion, homozygous carriers of factor V Leiden and, to a lesser extent, double heterozygous carriers of factor V Leiden and of the prothrombin mutation have an increased risk of venous thrombosis during pregnancy, particularly high during the postpartum period. On the basis of these findings we recommend that these women receive anticoagulant prophylaxis at least in the postpartum, that should perhaps be extended to the whole pregnancy in homozygous carriers.

3' Untranslated Regions↗
PubMed2001

Resistance to activated protein C--frequent etiologic factor for venous thrombosis.

The discovery of the resistance to activated protein C (APCR) has provoked a new insight into the etiopathogenesis of venous and arterial thrombosis. APCR is determined in 95% genetically by point mutation in the gene for factor V resulting in substitution of arginine in the position 506 by glutamine. This change makes the activated form of factor V (factor Va) resistant to the cleavage by protein C in the place, where the cleavage takes place most quickly under normal conditions. The mutant factor V is known as factor V Leiden. Factor V Leiden preserves its procoagulation activity for a longer period, resulting thus into thrombophilia with all its negative consequences. The inherited deficiencies of antithrombin III, protein C and protein S occur in 10% of patients suffering from venous thrombosis, whereas factor V Leiden is present in as many as 20 to 60%. Thus, it seems that factor V Leiden is the most important inherited risk factor of venous thrombosis. The results of several trials did not indicate the participation of APCR in the development of myocardial infarction. On the other hand, APCR seems to be a risk factor of cerebrovascular accidents, especially of stroke and transitory brain ischemia. Factor V Leiden is an important risk factor of abortions, especially those occurring in the second trimester of pregnancy. According to recent results, factor V Leiden is considered to play a role in the pathogenesis of venous and arterial thromboses in children. The significant risk potential of factor V Leiden with respect to venous thrombosis development and relatively simple diagnosis of this mutation predispose the investigation of this disorder to become the screening method in indicated groups of patients. The investigation of APCR is recommended in all patients with either first or reoccurring attacks of venous thrombosis or thromboembolism, in patients with positive family history of thrombosis and thromboembolism and in women with repeated abortions, particularly in the second trimester of pregnancy. The investigation of APCR in selected groups of patients and early prophylactic anticoagulation therapy may be important in thrombosis prevention in situations with an increased thrombotic potential. (Tab. 1, Ref. 78.)

Activated Protein C Resistance↗
PubMed2002

[Superior mesenteric venous thrombosis during treatment of malignant lymphoma and of pure red cell aplasia].

Mesenteric vein thrombosis is an uncommon type of intestinal ischemia that can be associated with significant mortality if its diagnosis is delayed. We experienced two patients with hematological disorders--non-Hodgkin's lymphoma (NHL) and pure red cell aplasia (PRCA)--who developed superior mesenteric vein (SMV) thrombosis during treatment. Neither of the patients had underlying disorders of the anticoagulant system that might have produced a hypercoagulable state. The first patient developed SMV thrombosis immediately after chemotherapy for NHL. This patient also had portal hypertension due to chronic hepatitis B. Direct injury to endothelial cells by the anti-cancer drugs and alteration of blood flow were the probable causes of the SMV thrombosis. The second patient with PRCA had regularly taken prednisolone, and this had induced a hypercoagulable state. The clinical symptoms of SMV thrombosis are usually non-specific, and in our patients vague, crampy abdominal pain without bloody diarrhea was the only complaint. Abdominal CT scan under a clinical suspicion of SMV thrombosis revealed the thrombi in the SMV. Urgent surgical resection of the infarcted bowel and immediate postoperative anticoagulation resulted in a favorable outcome. Clinicians should be aware of the vague symptoms of SMV thrombosis, as early diagnosis and urgent therapy are essential to prevent a fatal outcome.

Antineoplastic Combined Chemotherapy Protocols↗