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A prothrombin gene mutation is significantly associated with venous thrombosis.

This case-control study examined the prevalence of a prothrombin gene mutation in the 3'-untranslated region (UTR) first reported by Poort et al in Dutch subjects with a history of venous thrombosis and in matched control subjects without a history of thrombosis. We tested the hypothesis that the presence of the 3'UTR prothrombin mutation would convey a higher risk of venous or arterial thrombosis and therefore would be found in a higher-than-normal percentage of subjects with a history of thrombosis. Our study included 100 subjects: 50 with a history of thrombosis (21 with venous thrombosis and 29 with arterial thrombosis, who had been recruited from an anticoagulation clinic) and 50 control subjects without a history of thrombosis. DNA from these subjects was analyzed by polymerase chain reaction and agarose gel electrophoresis. We found a statistically significant increase in the prevalence of the 3'UTR mutation in subjects with a history of venous thrombosis compared with subjects without thrombosis. The prevalence of the 3'UTR prothrombin mutation was 19% (4/21;3 heterozygous and 1 homozygous) in subjects with a history of venous thrombosis, 0% (0/29) in subjects with a history of arterial thrombosis, and 2% (1/50) in control subjects (P < .0245, by Fisher's exact test for comparison of subjects with versus those without a history of venous thrombosis). The G-->A mutation at nucleotide 20,210 in the 3'UTR was confirmed by direct DNA sequencing. The similar increased prevalence of the 3'UTR mutation in subjects with venous thrombosis in our population and in the Dutch population studied by Poort et al suggests that this mutation is an important risk factor for venous thrombosis in the general white population.

Adult↗

Risk factors for deep venous thrombosis of the upper extremities.

BACKGROUND: Hypercoagulable states and triggering factors (surgery, trauma, immobilization, pregnancy, and use of oral contraceptives) are associated with an increased risk for deep venous thrombosis of the lower extremities. In contrast, risk factors for deep venous thrombosis of the upper extremities have not been identified. OBJECTIVE: To evaluate the prevalence of hypercoagulable states and triggering factors in patients with primary deep venous thrombosis of the upper extremities. DESIGN: Frequency-matched case-control study. SETTING: Hemophilia and thrombosis center at a university hospital. PATIENTS: 36 patients who had primary deep venous thrombosis of the upper extremities, 121 patients who had primary deep venous thrombosis of the lower extremities, and 108 healthy controls. Patients who had deep venous thrombosis of the lower extremities and study controls were frequency-matched by age, sex, geographic origin, and social status with patients who had deep venous thrombosis of the upper extremities. MEASUREMENTS: Resistance to activated protein C was evaluated by a clotting method based on the activated partial thromboplastin time. If test results were abnormal or borderline, DNA analysis for substitution in coagulation factor V gene was done. Antithrombin, protein C, protein S, antiphospholipid antibodies, and total plasma homocysteine levels were also measured. RESULTS: Prevalences of abnormalities of the natural anticoagulant system (9%) and hyperhomocysteinemia (6%) in patients who had deep venous thrombosis of the upper extremities were similar to prevalences of both factors in controls (6% and 7%, respectively) but lower than in patients who had deep venous thrombosis of the lower extremities (31% and 14%, respectively). Antiphospholipid antibodies were found only in patients who had venous thrombosis of the lower extremities (7%). The overall prevalence of hypercoagulable states in patients who had thrombosis of the upper extremities (15%) was similar to that in controls (12%) but was significantly lower than that in patients who had thrombosis of the lower extremities (56%). A recent history of strenuous exercise of muscles in the affected extremity was the most frequent triggering factor for patients who had deep venous thrombosis in the upper extremities (33%). CONCLUSIONS: This preliminary study indicates that the prevalence of hypercoagulable states is low in patients who have primary deep venous thrombosis of the upper extremities.

Adult↗

[Thrombosis in childhood--etiologic role of congenital thrombophilic conditions].

BACKGROUND: Increasing frequency of thrombosis in podiatry brings about high morbidity and mortality. From published sets of clinical cases with thromboembolic complications can be concluded, that contrary to adults, origin of thrombosis in children is more frequently based on congenital thrombophilic states. The main of the work is: 1. To identify prevalence of the congenital thrombophilic states in the set of patients with venous and arterial thrombosis. 2. Formulate recommendations for the laboratory investigation. 3. Evaluate results of the thrombosis treatment in our set of patients. METHODS AND RESULTS: Set of 24 patients of the average age 6.7 years at the time of thrombosis (16 time venous, 8 times arterial) was retrospectively investigated for the presence of the factor V-Leiden mutation, prothrombine 20210A mutation, deficiency of C and S protein, and antithrombin III. Presence of acquired risk factors was also evaluated. Congenital thrombophilic state was identified in 5 patients (31.2%) with venous thrombosis and in 1 patient (12.5%) with arterial thrombosis. Mutation of the factor V-Leiden was found most frequently. It was identified at 3 patients (18.7%) with venous thrombosis and 1 patient (12.5%) with arterial thrombosis. The central venous catheter was the most frequent acquired risk of thrombosis (50%). In 1 patient with venous thrombosis and in 4 patients with arterial thrombosis no acquired or congenital risks of thrombosis were identified. Results of treatment confirmed beneficial effects of heparinisation and subsequent wafarinszation for the period of increased risk of thrombosis. Systemic thrombolysis was done 3 times without complications. CONCLUSION: Congenital thrombophilic states play significant role in the manifestations of thromboses in children. In majority of children with manifesting thrombosis at least one risk factor was identified. Cerebral infarcts in infants remain largely unrevealed.

Adolescent↗

[Therapy and prevention of deep venous thrombosis and pulmonary embolism in gynecology and obstetrics].

AIM: The aim of this paper is to present the latest developments in therapy and prophylaxis of deep vein thrombosis in gynecology and obstetrics. DATA EXTRACTION: The data presented in the paper have been extracted from the Current Contents database. In the introduction, the coagulation cascade is described, and certain coagulation abnormalities caused by deficiency or decreased activity of coagulation factors are highlighted. The most prominent signs of deep vein thrombosis in pregnant women are swelling and tenderness of the affected leg, sometimes accompanied with fever and leucocytosis. In pelvic thrombosis, swelling of the leg is often absent and such a condition may be mistaken for other abdominal emergencies. The diagnostic algorithm for deep vein thrombosis starts with the clinical Wells criteria. To confirm the diagnosis it is necessary to visualize the thrombus by one of the imaging methods. The value of D-dimer is limited by its low positive predictive value, particularly in pregnant women. Low weight molecular heparin's have lately almost replaced standard heparin in the treatment of the deep vein thrombosis in pregnant women for providing advantages of subcutaneous application, no need of laboratory control of coagulation parameters, lower risk of bleeding, and lower incidence of osteoporosis and heparin-induced thrombocytopenia. We list the recommendations of the American College of Chest Physicians published in 1991, which stratify pregnant women with deep vein thrombosis according to their medical history and laboratory parameters. We have specified the proposed approach according to: history of deep vein thrombosis due to transient risk factors; previous idiopathic deep vein thrombosis without anticoagulant therapy; previous deep vein thrombosis with thrombophylia; previous idiopathic deep vein thrombosis on anticoagulant therapy; laboratory-proven thrombophilia with no history of deep vein thrombosis; and recurrent deep vein thrombosis. Pregnant women with artificial heart valves may undergo one of three proposed treatments. Long preoperative hospitalization, prolonged operative procedures, extensive injuries of blood vein vessels on radical procedures, frequently present accompanying malignant disease or previous irradiation therapy and postoperative bed-ridden period after major gynecologic procedures increase the risk of perioperative development of deep vein thrombosis. It is necessary to appraise this risk, classify patients in one of the four groups, and administer appropriate measures. Patients at a low risk of developing thromboembolic incidents are those younger than 40, undergoing procedures lasting less than 30 minutes and without other risk factors. The risk is moderate in patients aged 40-60 without other risk factors, or those aged under 40 having malignancy have high risk. Patients at a very high risk are those with a history of deep vein thrombosis, thrombophilia or pelvic exenteration. In the last decade there has been a great advancement in the diagnostics and treatment of deep vein thrombosis. The discovery of genetic disorders predisposing the patient to the development of a thromboembolic incident (thrombophilia) has changed our position concerning the duration of anticoagulant therapy, and nowadays it can last from several months to a lifetime regimen, depending on the underlying mechanism causing the incident. A significant improvement in therapy has occurred with the introduction of low molecular weight heparins in clinical practice. Their therapeutic value is equal to standard heparin, and their advantages include easier dosage and less nursing time as well as in a lower incidence of side effects such as haemorrhage. For these reasons, low molecular weight heparin has almost completely replaced standard heparin in the western world.

Adult↗

Deep-vein thrombosis and the incidence of subsequent symptomatic cancer.

BACKGROUND: In contrast to the established relation between overt cancer and subsequent venous thromboembolism, it is unclear whether symptomatic deep-vein thrombosis is associated with a risk of subsequent overt malignant disease. METHODS: Two hundred sixty consecutive patients with symptomatic, venographically proved deep-vein thrombosis were enrolled in a study, of whom 250 were followed during a two-year period. Among those assessed during follow-up, the incidence of subsequently detected cancer in the 105 patients with secondary venous thrombosis (i.e., thrombosis associated with a well-recognized risk factor other than cancer) was compared with the incidence of cancer in the 145 patients with idiopathic venous thrombosis. RESULTS: Routine examination at the time of diagnosis of the venous thrombosis revealed cancer in 5 of the 153 enrolled patients with idiopathic venous thrombosis (3.3 percent) and in none of the 107 enrolled patients with secondary venous thrombosis. During follow-up, overt cancer developed in 2 of the 105 patients with secondary venous thrombosis (1.9 percent) and in 11 of the 145 patients with idiopathic venous thrombosis (7.6 percent; odds ratio, 2.3; 95 percent confidence interval, 1.0 to 5.2; P = 0.043). Of the 145 patients with idiopathic venous thrombosis, 35 had confirmed recurrent thromboembolism. Overt cancer subsequently developed in 6 of the 35 (17.1 percent). The incidence of cancer in the patients with recurrent idiopathic venous thrombosis was higher than that in the patients with secondary venous thrombosis (P = 0.008; odds ratio, 9.8; 95 percent confidence interval, 1.8 to 52.2) or in the patients with idiopathic venous thrombosis that did not recur (P = 0.024; odds ratio, 4.3; 95 percent confidence interval, 1.2 to 15.3). CONCLUSIONS: There is a statistically significant and clinically important association between idiopathic venous thrombosis and the subsequent development of clinically overt cancer, especially among patients in whom venous thromboembolism recurs during follow-up.

Aged↗

Compression sonography in patients with indeterminate or low-probability lung scans: lack of usefulness in the absence of both symptoms of deep-vein thrombosis and thromboembolic risk factors.

OBJECTIVE: We sought to determine whether compression sonography could be eliminated in the evaluation of patients who lacked both thromboembolic risk factors and symptoms of deep-vein thrombosis and who had an indeterminate or low-probability lung scan. MATERIALS AND METHODS: The medical records of 155 consecutive patients who underwent bilateral lower-extremity sonography after an indeterminate or low-probability lung scan were reviewed. The presence of thromboembolic risk factors and deep-vein thrombosis symptoms and the result of sonography were recorded. Patients were divided into two groups: group 1 consisted of patients with either thromboembolic risk factors or deep-vein thrombosis symptoms, and group 2 consisted of patients without thromboembolic risk factors and without deep-vein thrombosis symptoms. The incidences of deep-vein thrombosis in groups 1 and 2 were compared by use of a two-tailed Fisher's exact test. RESULTS: Thromboembolic risk factors or deep-vein thrombosis symptoms were found in 109 of 155 patients (70%) (group 1). Deep-vein thrombosis was found in nine of 108 patients (8%) in group 1. Both thromboembolic risk factors and deep-vein thrombosis symptoms were absent in 47 of 155 patients (30%) (group 2). Deep-vein thrombosis was found in none of 47 patients (95% confidence interval, 0-8%) in group 2. The difference in the incidences of deep-vein thrombosis in groups 1 and 2 approached statistical significance (p = .0579). The negative predictive value of the absence of both thromboembolic risk factors and deep-vein thrombosis symptoms in excluding deep-vein thrombosis was 100% (95% confidence interval, 93-100%). CONCLUSION: If both symptoms of deep-vein thrombosis and thromboembolic risk factors are absent, the usefulness of lower-extremity sonography in detecting deep-vein thrombosis in patients with an indeterminate or low-probability lung scan is low. The manner in which these findings may be used to modify individual practice patterns will undoubtedly depend on the rate of detection of deep-vein thrombosis at a given institution.

Algorithms↗

[Late sequelae of deep venous thrombosis: a 13-year follow-up of 223 patients].

To investigate late sequelae of deep vein thrombosis, 223 consecutive patients, 148 men, 75 women, aged 61.5 +/- 14.7 years, with phlebographically documented unilateral deep vein thrombosis were reexamined 13 years after the acute event. 29 had an isolated calf vein thrombosis, 45 a 2-level- (calf an popliteal), 72 a 3-level- (calf, popliteal and femoral), 62 a 4-level- (calf, popliteal, femoral and pelvic) thrombosis and 15 had a special location, for example an isolated popliteal or pelvic involvement. In the acute stage all patients were given full dose heparin followed by a six month period of oral anticoagulation. 144 were initially treated by thrombolytic treatment with streptokinase. Control phlebography 5-14 days after the onset of the treatment revealed no clearance in a so called negative group of 123 patients, aged 63.5 +/- 14.9 years, namely the 79 "only" anticoagulated and 44 unsuccessfully thrombolysed. In this negative group natural course of deep vein thrombosis can be studied. The positive group, comprising 100 patients, aged 59.4 +/- 13.9 years (25 with complete and 75 with partial lysis, after streptokinase), is compared with the negative group. The global incidence of postthrombotic syndrome in the natural course, 13 years after deep vein thrombosis, was 39%, 9.8% with and 29.2% without ulcer. Slight changes were noted in 25% and no change in 36%. The incidence of postthrombotic syndrome was correlated with the extent of the original thrombosis: 3.7% after isolated calf vein thrombosis vs. 55.2% after 4-level thrombosis. Moreover, the mortality after deep vein thrombosis and the frequency of recurrence in the interval and of venous symptoms were also correlated to the extent of the thrombosis. The incidence of post phlebitic syndrome in the positive group is significantly lower in patients with 3- and 4-level thrombosis (p = 0.01). Patients with complete and partial lysis also have less venous symptoms (for 3- and 4-level thrombosis p < 0.0001). Thus, the successful thrombolysis seems to be beneficial in long terms for patients with extended thrombosis. Therefore, in our hospital thrombolytic treatment is offered as an additional treatment to anticoagulation to patients with recent, less than 7 days old, 3- and 4-level-thrombosis without contraindications.

Adult↗

Frequency of and risk factors for stent thrombosis after drug-eluting stent implantation during long-term follow-up.

Despite concerns regarding the long-term safety of drug-eluting stent (DES) implantation because of late-onset stent thrombosis, the actual incidence of stent thrombosis after 1 year is unknown. We investigated the incidence, risk factors, and association of antiplatelet therapy interruption for the development of stent thrombosis after DES implantation during long-term follow-up. A total of 1,911 consecutive patients with DES implantation were enrolled (sirolimus-eluting stents in 1,545 patients, 2,045 lesions; paclitaxel-eluting stents in 366 patients, 563 lesions). During long-term follow-up (median 19.4 months, interquartile range 15.3 to 24.3), 15 patients (0.8%, 95% confidence interval 0.5% to 1.3%) developed stent thrombosis within 6 hours to 20.4 months. Eleven patients (0.6%, 95% confidence interval 0.3% to 1.0%) had late thrombosis (median 6.1 months). The incidence of stent thrombosis was 3.3% (4 of 121 patients) in patients with complete interruption of antiplatelet therapy (vs 0.6% in those without, p = 0.004) and 7.8% (5 of 64 patients) with premature interruption of aspirin or clopidogrel, or both (vs 0.5% in those without, p < 0.001). Independent predictors of stent thrombosis were premature antiplatelet therapy interruption, primary stenting in acute myocardial infarction, and total stent length. Stent thrombosis also developed while patients were on dual antiplatelet therapy (all patients with acute/subacute stent thrombosis and 36% of those with late stent thrombosis; 47% of total with stent thrombosis). In conclusion, stent thrombosis occurred in 0.8% after DES implantation during long-term follow-up. The incidence of late stent thrombosis was 0.6%, similar to that for bare metal stents. The predictors of stent thrombosis were premature antiplatelet therapy interruption, primary stenting in acute myocardial infarction, and total stent length.

Blood Vessel Prosthesis Implantation↗

Portal and hepatic vein thrombosis in liver abscess: CT findings.

OBJECTIVE: Our aim is to describe imaging findings of portal and hepatic vein thrombosis in pyogenic liver abscess on contrast-enhanced MDCT and to determine the incidence and evolving patterns on follow-up imaging. METHODS: Over a 5-year period, 67 patients with liver abscess underwent single-phase (n=30) or triphasic (n=37) contrast-enhanced CT. Images were reviewed for the presence of portal vein (PV) or hepatic vein (HV) thrombosis, regional parenchymal attenuation, and changes on follow-up CT. RESULTS: Venous thrombosis was seen in 28/67 patients (42%), involving PV in 16/67 (24%) and HV vein in 15/67 (22%); 3/67 (4%) had both PV and HV thrombosis. Thrombosis was seen as non-enhancing linear structures without expanding the lumen in all cases. Regional parenchymal attenuation during the portal-phase was hyperattenuating (10/16, 63%) or isoattenuating (6/16, 38%) in PV thrombosis, and mostly hypoattenuating (13/15, 87%) in HV thrombosis (P<.001). Of 27 patients with follow-up contrast-enhanced CT, venous thrombosis resolved in 10/27 (37%) within 6 months and persisted in 17/27 (63%) for 3-38 months, including 13 PV thrombosis and 4 HV thrombosis. Interval parenchymal atrophy was seen only in four all with persistent PV thrombosis. CONCLUSIONS: Both PV and HV thrombosis frequently occurs in liver abscess and is seen as non-enhancing linear structures without expanding the lumen on contrast-enhanced CT. Regional attenuation changes in hepatic vein thrombosis were often hypoattenuating whereas none with portal vein thrombosis showed hypoattenuation.

Adult↗

Decreased venous thrombosis with an oral inhibitor of P selectin.

BACKGROUND: P-selectin inhibition with protein therapeutics such as antibodies or soluble ligands given intravenously can decrease thrombosis in a mouse ligation model of venous thrombosis. In this study, we hypothesized that oral inhibition of P selectin with a novel oral nonprotein inhibitor (PSI-697) would decrease thrombosis and circulating microparticle populations. This study evaluated the effects on thrombosis and circulating microparticle populations in this murine venous thrombosis model. METHODS: Mice underwent inferior vena cava ligation to induce thrombosis. Mice with high circulating level of P selectin, Delta Cytoplasmic Tail (CT), mice gene-deleted for both E- and P-selectin knockout (EPKO), and wild-type C57BL/6 mice (WT) were studied without and with administration of PSI-697 in food (100 mg/kg daily) from 2 days before thrombosis until the end of the study. Animals were killed 2 and 6 days later. Evaluations included thrombus weight (TW), vein wall morphometrics, microparticle quantification by using fluorescence-activated cell sorter analysis, and vein wall enzyme-linked immunosorbent assays for interleukin (IL)-10, P selectin, and monocyte chemotactic protein 1. RESULTS: PSI-697 significantly decreased TW in WT and CT mice, with a treated vs nontreated TW of 132 +/- 24 vs 228 +/- 29 x 10(-4) g (P = .014) and 166 +/- 19 vs 281 +/- 16 x 10(-4) g (P = .001), respectively. At day 6, the effect was significant only in the CT group (P < .05). Drug therapy at day 2 significantly increased vein wall monocytes in WT mice and increased monocytes and total inflammatory cells in CT animals. A significant decrease in neutrophils and total inflammatory cells was seen in EPKO mice at day 2 with therapy. Therapy significantly increased platelet-derived microparticles and total microparticles in CT mice on day 2. Changes in treated WT and treated EPKO animals were not significant compared with respective vehicle treatments at day 2. On day 6, therapy significantly decreased total microparticles in EPKO animals. Vein wall expression of IL-10 increased in all groups with therapy at day 2 (n = 18) and was significantly increased in WT (2687.5 +/- 903 pg/mL vs 636 +/- 108 pg/mL total protein; P = .038) and CT (2078 +/- 295 pg/mL vs 432 +/- 62 pg/mL total protein; P = .001) mice. Therapy significantly decreased vein wall P selectin, monocyte chemotactic protein 1, and IL-10 levels at day 6. CONCLUSIONS: PSI-697 decreased thrombosis. P-selectin inhibition allowed vein wall inflammatory cell extravasation in this model of complete ligation. Circulating microparticles (platelet-derived microparticles and total microparticles) increased with P-selectin inhibition, possibly because of decreased consumption into the thrombus. In summary, the oral administration of an inhibitor to P selectin provides significant TW reduction. CLINICAL RELEVANCE: Deep venous thrombosis is a significant national health problem in the general population. The average annual incidence of deep venous thrombosis is approximately 250,000 cases per year. The selectin family of adhesion molecules is thought to be largely responsible for the initial attachment and rolling of leukocytes on stimulated vascular endothelium. Recent studies have explored the possible therapeutic implications of P-selectin inhibition to modulate venous thrombosis. For example, prophylactic dosing of a recombinant P-selectin ligand decreases venous thrombosis in a dose-dependent fashion in both feline and nonhuman primate animal models. Additionally, treatment of 2-day iliac thrombi with a recombinant protein, P-selectin inhibitor, significantly improves vein reopening in nonhuman primates. It is interesting to note that P-selectin inhibition decreases thrombosis without adverse anticoagulation. On the basis of the results from these previous studies, the use of P-selectin antagonism is a logical therapeutic approach to treat venous thrombosis. All inhibitors developed to date are either proteins or small molecules with low oral bioavailability that require intravenous or subcutaneous injection. This study evaluates, for the first time, a novel orally bioavailable inhibitor of P-selectin (PSI-697).

Animals↗

Graduated compression stockings as prophylaxis for flight-related venous thrombosis: systematic literature review.

AIM: This paper reports a systematic review whose objective was to evaluate the effectiveness of graduated compression stockings as prophylaxis for flight-related venous thrombosis, including deep vein thrombosis and superficial venous thrombosis, after air travel in the general population. BACKGROUND: Despite the extended history of the use of graduated compression stockings, their application to prevent flight-related thrombosis was not explored until flight-related thrombosis was perceived as a preventable illness. Even now, their effectiveness in preventing flight-related thrombosis remains unresolved. METHODS: Generic terms including stocking/s, sock/s, or hosiery/hosieries were used to search a variety of electronic databases. Based on the selection criteria, decisions regarding inclusion and exclusion of primary studies were made. Using a meta-analysis software program, relative risk for the incidence of deep vein thrombosis, superficial venous thrombosis, and intention-to-treat analysis was calculated. RESULTS: A total of nine randomized controlled trials were included. In the treatment group, two of 1237 participants developed deep vein thrombosis in comparison with 46 of 1245 in the control group. The weighted relative risk for deep vein thrombosis was 0.08, with fixed 95% confidence interval 0.03-0.23. In the treatment group, four of 826 participants developed superficial venous thrombosis in comparison with seven of 823 in the control group. The weighted relative risk for superficial venous thrombosis was 0.67. with fixed 95% confidence interval 0.24-1.87 (non-significant difference). Using intention-to-treat analysis, the risk for participants in the treatment group was 0.53 times as great as that for those in the control group. CONCLUSIONS: This review demonstrates the effectiveness of medium compression pressure, below-knee graduated compression stockings in preventing flight-related deep vein thrombosis but not superficial venous thrombosis in low-medium- or high-risk participants.

Aerospace Medicine↗

Renal outcome of neonatal renal venous thrombosis: review of 28 patients and effectiveness of fibrinolytics and heparin in 10 patients.

OBJECTIVES: Neonatal renal venous thrombosis is a rare disorder that can result in severe renal damage. To evaluate the experience over 10 years and review the effectiveness of fibrinolytic and/or heparin therapy, chart reviews were performed for newborns with renal venous thrombosis. PATIENTS, INTERVENTIONS, AND OUTCOME MEASURES: Twenty-eight newborns with renal venous thrombosis were treated at Children's Hospitals and Clinics of Minnesota and Fairview University Medical Center from 1991 to 2001. RESULTS: Unilateral involvement was noted in 25 neonates (89%) and bilateral involvement in 3 (11%). Unilateral renal venous thrombosis affected mostly term infants, whereas 2 of 3 infants with bilateral renal venous thrombosis were <32 weeks' gestational age (birth weight: 745-1505 g). One mother had antiphospholipid syndrome. Of 11 neonates evaluated for congenital thrombophilia, 1 had the factor V Leiden mutation. Ten neonates received either unfractionated or low molecular weight heparin for 3 days to 7 months. Three infants with unilateral renal venous thrombosis treated with heparin alone did not seem to benefit from such therapy. Seven neonates were treated with fibrinolytics and unfractionated heparin (4 neonates with unilateral renal venous thrombosis and 3 with bilateral renal venous thrombosis). Treatment with fibrinolytics did not result in restoration of renal function in the 4 neonates with unilateral renal venous thrombosis but was associated with return of almost normal function in the 2 neonates with bilateral renal venous thrombosis who received fibrinolytics immediately after renal venous thrombosis diagnosis. Two neonates treated with fibrinolytics suffered bleeding complications at the area of adrenal hemorrhage. Two neonates (not treated for renal venous thrombosis) died as a result of underlying disease. CONCLUSIONS: Most neonatal renal venous thrombosis is unilateral and does not respond to fibrinolytic therapy and heparin. The use of fibrinolytics may prevent chronic renal failure in neonates with bilateral renal venous thrombosis if begun within 24 hours of diagnosis. Fibrinolytic therapy, however, is associated with a risk of bleeding, specifically if there is an associated adrenal hemorrhage.

Female↗

Thrombosis of the muscular calf veins--reference to a syndrome which receives little attention.

BACKGROUND: Thrombosis of the soleal and gastrocnemial veins seldom receive very much attention. It is thought that they are frequently the starting point for deep vein thrombosis of the lower extremity. PATIENTS AND METHODS: 125 patients with clinically suspected deep vein thrombosis of the leg were examined by means of duplex sonography and phlebography. The ultrasound examination was performed on the lower limb in the form of a compression sonography. RESULTS: From 137 legs examined, a total of 82 cases of deep vein thrombosis were diagnosed. Sonographically and/or phlebographically, the soleal and/or gastrocnemial veins were found to be involved in 65 cases of thrombosis, i.e. 79% of all thrombosis. 25% of all cases of deep vein thrombosis of the leg were isolated muscular vein thrombosis. Pain in the calf while walking, similar to muscular soreness after exertion, was typical of the isolated muscular vein thrombosis. The muscular veins were involved in all the deep vein thrombosis of the leg of the 3- and 4-layer type. Diagnosis of soleal and gastrocnemial vein thrombosis is quite possible by means of sonography and phlebography. The sensitivity and specificity of the compression sonography were 88% and 95% respectively, compared to the phlebography. CONCLUSION: In patients suffering from pain in the calf, the soleal and gastrocnemial veins should be carefully included in the sonographic or phlebographic assessment. Due to the risk of deep vein thrombosis, isolated muscular vein thrombosis should receive treatment appropriate for a deep vein thrombosis of the calf, and its development be checked.

Adult↗

Transfemoral temporary pacing and deep vein thrombosis.

The incidence of deep vein thrombosis following transfemoral temporary pacing was prospectively assessed in 20 consecutive patients using serial 125I-fibrinogen scanning, impedance plethysmography, and measurements of fibrin degradation products. Four patients underwent venography. Of the twenty patients, five (25%) had definite evidence of deep vein thrombosis, six demonstrated equivocal abnormalities, and nine had no evidence of thrombosis. Thrombosis was found only in the legs used for pacing. Of the five with deep vein thrombosis, one had positive findings in all the noninvasive tests. Venography confirmed the diagnosis in the other four; one had thrombosis of the femoral vein, one had thrombosis of several calf veins, and one had thrombosis of both the thigh and calf veins; the fourth patient had thrombosis of the entire deep venous system of the leg. This latter patient was the only one who had clinical evidence of venous thrombosis. The patients with deep vein thrombosis did not differ in clinical characteristics from those without thrombosis. There was no relationship between the occurrence of deep vein thrombosis and the number of venepunctures, the state of the electrode, the presence of the introducer sheath in the femoral vein, or the duration of pacing. In conclusion, deep vein thrombosis is a common complication of transfemoral temporary pacing and the high incidence of its occurrence should be considered before deciding upon the site of entry for a temporary pacemaker.

Adult↗

Long-term follow-up of patients with suspected deep vein thrombosis of the upper extremity: survival, risk factors and post-thrombotic syndrome.

BACKGROUND: The outcome of upper extremity thrombosis in terms of morbidity, mortality and arm functionality is virtually unknown. We investigated mortality, risk factors, recurrent thrombosis and post-thrombotic syndrome (PTS) in patients with suspected upper extremity thrombosis. METHODS: Consecutive patients suspected of having deep vein thrombosis (DVT) of the upper extremity were followed for up to 53 months (mean 21 months). Venography and/or ultrasonography was used for diagnosis. Risk factors were identified from history and thrombophilia laboratory screening. PTS was assessed using a scoring system. Death, recurrent thrombosis and PTS were primary outcome measures. RESULTS: DVT of the upper extremity was diagnosed in 50 of 116 consecutive patients (43%). Malignancy and/or central venous lines were present in 37 of 50 (74%) patients with thrombosis. Inherited thrombophilia was diagnosed in 6 of 30 (20%) and 4 of 33 (12%) of the investigated patients with and without thrombosis, respectively (not significant). Twenty-five patients (50%) with thrombosis died during the follow-up period; this was associated with cancer in 84% of the deaths. Recurrent thrombosis was observed in four patients (8%) during follow-up. Symptoms of PTS were present in 4 of 22 patients (18%) with thrombosis and in 14 of 36 patients (39%) in whom thrombosis was excluded. CONCLUSIONS: Malignancy and central venous lines are major risk factors of upper extremity thrombosis. Thrombophilia seems to be unrelated to the presence or absence of upper extremity thrombosis. Thrombosis in combination with malignancy predicts poor survival. A scoring system can be used to assess the severity of PTS, but it does not discriminate PTS from other causes of arm complaints.

Journal Article↗

High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives.

BACKGROUND: Idiopathic cerebral-vein thrombosis can cause serious neurologic disability. We evaluated risk factors for this disorder, including genetic risk factors (mutations in the genes encoding factor V and prothrombin) and nongenetic risk factors (such as the use of oral contraceptive agents). We compared the prevalence of these risk factors in 40 patients with cerebral-vein thrombosis, 80 patients with deep-vein thrombosis of the lower extremities, and 120 healthy controls. The G1691A mutation in the factor V gene and the G20210A prothrombin-gene mutation, which are established genetic risk factors for venous thrombosis, were studied. We also assessed the use of oral contraceptives and other risk factors for thrombosis. RESULTS: The prevalence of the prothrombin-gene mutation was higher in patients with cerebral-vein thrombosis (20 percent) than in healthy controls (3 percent; odds ratio, 10.2; 95 percent confidence interval, 2.3 to 31.0) and was similar to that in patients with deep-vein thrombosis (18 percent). Similar results were obtained for the mutation in the factor V gene. The use of oral contraceptives was more frequent among women with cerebral-vein thrombosis (96 percent) than among controls (32 percent; odds ratio, 22.1; 95 percent confidence interval, 5.9 to 84.2) and among those with deep-vein thrombosis (61 percent; odds ratio, 4.4; 95 percent confidence interval, 1.1 to 17.8). For women who were taking oral contraceptives and who also had the prothrombin-gene mutation (seven patients with cerebral-vein thrombosis but only one control), the odds ratio for cerebral-vein thrombosis rose to 149.3 (95 percent confidence interval, 31.0 to 711.0). CONCLUSIONS: Mutations in the prothrombin gene and the factor V gene are associated with cerebral-vein thrombosis. The use of oral contraceptives is also strongly and independently associated with the disorder. The presence of both the prothrombin-gene mutation and oral-contraceptive use raises the risk of cerebral-vein thrombosis further.

Adolescent↗

Risk factors for acute and subacute stent thrombosis after high-pressure stent implantation: a study by intracoronary ultrasound.

BACKGROUND: In the era of coronary stenting with high-pressure expansion, stent thrombosis remains a major life-threatening risk. Because of its superior imaging mode, intracoronary ultrasound could provide insight into potential risk factors for stent thrombosis. PATIENTS AND METHODS: In 215 patients with stent implantations controlled by intracoronary ultrasound, four occurrences of subacute stent thrombosis, two complete acute thrombotic occlusions, and four occurrences of incomplete acute thrombosis were observed. All stents were expanded with inflation pressures of at least 14 atm ( 17+/-3 atm). The clinical data and the qualitative and quantitative ultrasound information were compared between stents with thrombosis and stents without thrombosis. The luminal area and the plaque border of the reference segments, and of the smallest and largest site of the stented segment after the initial and final expansion, were measured. RESULTS: Stents in the left anterior descending artery were more often involved in stent thrombosis than other vessels, but the vessel dimensions in this target vessel were smaller than in the right coronary artery. The plaque burden was considerably larger after stent implantation with subsequent thrombosis compared with no thrombosis (74.1+/-8.8% vs 63.6+/-8.0%; p < 0.001), and the stent area was smaller (4.80%+/-1.33 mm2 vs 6.86+/-2.08 mm2; p < 0.01 ). In stents with thrombosis the plaque burden of the stent site with the smallest and largest lumen differed by 15.2%, whereas the difference in plaque burden in stents without thrombosis was 2.7%. Intracoronary ultrasound showed that the best risk predictor of thrombosis was the residual plaque burden of the stented segment (odds ratio 15.7 [confidence interval 2.4 to 104.7]), and a small stent area after implantation (odds ratio 6.8 [confidence interval 1.9 to 24.3]). CONCLUSION: In a multivariate risk analysis plaque burden was the strongest independent risk factor for stent thrombosis. The amount of residual plaque mass around the stent might be a potential trigger for thrombus formation.

Acute Disease↗

Serum anti-beta2-glycoprotein-I and anticardiolipin antibodies during thrombosis in systemic lupus erythematosus patients.

PURPOSE: Antibodies to beta2-glycoprotein-I are more strongly associated with clinical antiphospholipid syndrome than are anticardiolipin antibodies. We previously found a decrease in anticardiolipin antibodies at the time of thrombosis in 6 patients with systemic lupus erythematosus (SLE). We therefore sought to determine the prevalence and levels of antibodies to beta2-glycoprotein-I and to cardiolipin before, during, and after thrombosis in patients with SLE, and to compare them with patients who did not have thrombosis. METHODS: We studied 24 patients with SLE who had at least one episode of thrombosis and 102 patients with SLE without thrombosis. Serum anticardiolipin antibodies were measured by conventional enzyme-linked immunosorbent assay (ELISA) using newborn calf serum as the blocking agent. Serum anti-beta2-glycoprotein-I antibodies were measured by ELISA on nonirradiated plates, using purified human beta2-glycoprotein-I without phospholipid. RESULTS: All patients with thrombosis had anti-beta2-glycoprotein-I antibodies, compared with only 17% of controls (P <0.0001). We observed a significant decrease in serum anti-beta2-glycoprotein-I levels at the time of thrombosis, as compared with previous and subsequent samples. The prevalence and levels of IgG and IgM anticardiolipin antibodies were similar in patients with and without thrombosis. A decrease in IgG or IgM anticardiolipin titers occurred during thrombosis in 6 patients. Anticoagulant, corticosteroid, and immunosuppressive treatments did not appear to affect anti-beta2-glycoprotein-I levels at the time of thrombosis. CONCLUSION: Anti-beta2-glycoprotein-I antibodies are strongly associated with thrombosis in patients with SLE. The decrease of anti-beta2-glycoprotein-I levels at the time of thrombosis may indicate a pathogenic role. This antibody may also be a marker of predisposition for thrombosis in these patients.

Adolescent↗