The risk of venous thrombosis in individuals with a history of superficial vein thrombosis and acquired venous thrombotic risk factors

Blood ◽  
2013 ◽  
Vol 122 (26) ◽  
pp. 4264-4269 ◽  
Author(s):  
Rachel E. J. Roach ◽  
Willem M. Lijfering ◽  
Astrid van Hylckama Vlieg ◽  
Frans M. Helmerhorst ◽  
Frits R. Rosendaal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thrombosis ◽  
Superficial Vein ◽  
Thrombotic Risk ◽  
Vein Thrombosis ◽  
Thrombotic Risk Factor ◽  
Key Points ◽  
Superficial Vein Thrombosis ◽  
History Of

Key Points Superficial vein thrombosis combined with an acquired thrombotic risk factor increases the risk of venous thrombosis 10- to 100-fold. If confirmed, these findings have important implications for the future prevention of venous thrombosis.

scholarly journals Increased risk of venous thrombosis in persons with clinically diagnosed superficial vein thrombosis: results from the MEGA study

Blood ◽  
2011 ◽  
Vol 118 (15) ◽  
pp. 4239-4241 ◽  
Author(s):  
Kirsten van Langevelde ◽  
Willem M. Lijfering ◽  
Frits R. Rosendaal ◽  
Suzanne C. Cannegieter
Keyword(s):  
Venous Thrombosis ◽  
Factor V Leiden ◽  
Population Based ◽  
Factor V ◽  
Superficial Vein ◽  
Vein Thrombosis ◽  
Increased Risk ◽  
Superficial Vein Thrombosis ◽  
History Of ◽  
Deep Vein

Abstract Superficial vein thrombosis (SVT) is regarded a self-limiting disorder, although the authors of recent studies showed that ultrasonographically diagnosed SVT is a precursor for venous thrombosis. We aimed to determine whether the same holds true for clinically diagnosed SVT and to what extent it is associated with thrombophilia in a population-based case-control study (ie, Multiple Environmental and Genetic Assessment of risk factors for venous thrombosis). We found that a history of clinical SVT was associated with a 6.3-fold (95% confidence interval [CI] 5.0-8.0) increased risk of deep-vein thrombosis and a 3.9-fold (95% CI 3.0-5.1) increased risk of pulmonary embolism. Blood group non-O and factor V Leiden showed a small increase in SVT risk in controls, with odds ratios of 1.3 (95% CI 0.9-2.0) and 1.5 (95% CI 0.7-3.3), respectively. In conclusion, clinically diagnosed SVT was a risk factor for venous thrombosis. Given that thrombophilia was only weakly associated with SVT, it is likely that other factors (varicosis, obesity, stasis) also play a role in its etiology.

scholarly journals On the Absence of Calreticulin (CALR) Mutations in Chronic Myeloprolierative Neoplasms (MPNs) with Splanchnic Venous Thrombosis (SVT): Experience from a Single Institution

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3198-3198 ◽  
Author(s):  
Bruno Martino ◽  
Corrado Mammì ◽  
Claudia Labate ◽  
Martino Enrica Antonia ◽  
Francesca Ronco ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thrombosis ◽  
Factor V Leiden ◽  
Factor V ◽  
Jak2 Mutation ◽  
Thrombotic Risk ◽  
Thrombotic Risk Factor ◽  
Prothrombotic Risk Factors ◽  
Calr Mutations

Abstract Background: According to recent findings, the management of myeloproliferative neoplasms (MPNs) is highly dependent on presence or absence of thrombotic events. The JAK2 mutation has been identified as a marker of MPNs. It is also an occult marker in several patients with splanchnic venous thrombosis (SVT), but its contribution as an additional thrombotic risk factor in MPNs is still under discussion. Moreover, a pro-thrombotic risk factor, either inherited or acquired (Factor V Leiden mutation, deficiencies in protein C, protein S and Prothrombin mutation 20210) can be identified in these patients. Recently, another milestone in the molecular diagnosis of MPNs, somatic mutations in the CALR gene, has been reported. A total of 36 types of frame-shifting insertions and deletions were detected in the exon 9 of CALR gene, which encodes a Ca2+ binding protein in endoplasmic reticulum called calreticulin. Type-1, 52-bp deletion (p.L367fs*46), and type-2, 5-bp TTGTC insertion (p.K385fs*47) variants constitute more than 80% of these mutations These mutations were reported to have a incidence of over 60% to 80% in JAK2 and MPLmutation-negative Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF) patients. Compared to those with JAK2 mutation, CALR-mutated ET patients are younger and have a lower leukocyte count and higher platelet count. CARL mutations have been also reported as a favorable prognostic factor on thrombosis-free survival (TFS) for ET patients. Aims: In this study, we evaluated the incidence of SVT, JAK2 and CALR mutations, and prothrombotic risk factors in patients with MPNs observed in our center from January 2000 to January 2014. Methods: We performed a retrospective review of clinical charts of 466 Ph1 negative MPN patients followed in our center, classified according to the WHO 2008 classification. Patient and disease characteristics, including JAK2V617F, MPL and CALR mutations and thrombotic risk factors were recorded. Results: The median age of patients with diagnosis of MPN was 43 years. Fourteen patients (13 females, 1 male; 3%) of median age 46 years presented a SVT. Three had a Budd Chiari syndrome and 11 a portal venous thrombosis. According to a histological review, these patients were classified as follows: ET, 2 cases, PMF, 3 cases, Polycythemia Vera (PV) 1 case, Myelofibrosis in a prefibrotic phase (MF0) 8 cases. Classification of 11 cases with Myelofibrosis according to the IPSS identified 7 as INT1, 1 as INT2 and 3 as low risk. Among all 14 patients diagnosed with SVT, 12 were JAK2V617F positive with a median allelic burden of 30%, 1 patient was MPL positive, and 1 patient was triple-negative. CALR mutation was not observed in any of the patients. Two cases were diagnosed with MPN 30 months after SVT, 3 patients experienced SVT after a median follow-up of 108 months from MPN diagnosis while in 9 patients the diagnosis of MPN was concomitant to SVT. In the latter patients, median Hb levels were 12.4 g/dL , WBC 8260 /µL, HCT 36.3%, PLT 337.000/ µL and a modest hepatomegaly and splenomegaly were documented. Prothrombotic risk factors were found in 9 of 13 patients. Two patients experienced a thrombotic episode prior to the diagnosis of SVT and two subsequently during the follow-up. Interestingly, 9 (70%) of MPN patients with SVT exhibited at least one prothromobtic risk factor, such as factor V Leiden, Protein C deficiency, hyperhomocystinemia and 50% had two or more associated defects. Thirteen of the 14 patients are currently being treated as follows hydroxyurea (9), interferon (1), and ruxolitinib (3). All patients received oral anticoagulant treatment except for three who are on antiplatelet therapy. MPN patients without SVT had a lower prevalence of prothrombotic risk factors and developed venous thrombosis in different anatomical sites: in these cases WBC count, platelet values and the presence of JAK2V617F mutation correlated with the development of the thrombotic event. Conclusions: Although SVT has a low incidence in MPN patients, a potential benefit of testing for mutations in CALR gene and for additional prothrombotic risk factors is suggested in the whole MPN population for the prevention and treatment of this complication. Disclosures No relevant conflicts of interest to declare.

Risk factors for superficial vein thrombosis in patients with primary chronic venous disease

VASA ◽  
2016 ◽  
Vol 45 (1) ◽  
pp. 63-66 ◽  
Author(s):  
Dalibor Musil ◽  
Marketa Kaletova ◽  
Jiri Herman
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Positive Family History ◽  
Chronic Venous Disease ◽  
Venous Disease ◽  
Superficial Vein ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis ◽  
History Of ◽  
Primary Chronic Venous Disease

Abstract. Background: Primary chronic venous disease (CVD) is associated with an increased risk of superficial vein thrombosis (SVT). While CVD is a predominant factor in SVT, there is a range of additional predisposing factors. The objective was to investigate the association between age, gender, BMI, smoking, oestrogen hormone therapy, family history of venous thromboembolism (VTE) and CEAP clinical classification in patients with CVD and a history of SVT. Patients and methods: In a retrospective observational study on consecutive patients with primary CVD, 641 outpatients were enrolled (152 men, 23.7 %; 489 women, 76.3 %). The prevalence of SVT was evaluated according to age, BMI, smoking, presence of family history of VTE, use of hormone therapy, and clinical class of CVD. Results: Risk of SVT was significantly increased in women (OR 1.68, 95 % CI = 1.02 - 2.76; p = 0.041), older patients (46 - 69 years, OR 1.57, 95% CI = 1.03 - 2.4; p = 0.036, ≥ 70 years, OR 2.93, 95 % CI = 1.5 - 5.76; p = 0.001), smokers (OR 1.69, 95 % CI = 1.1 - 2.58; p = 0.015) and in persons with first-degree siblings diagnosed with VTE (OR 2,28, 95 % CI = 1.28 - 4.05; p = 0.004). The risk was significantly increased in older male smokers (p - 0.042). In women, smoking and oestrogen therapy (p = 0.495) did not increase the risk of SVT even older women or in those with increased BMI. In CVD (C0 - C3), a history of episodes of SVT was found in 103/550 (18.7 %), in chronic venous insufficiency (CVI) in 27/91 (29.7 %). There was a significantly higher prevalence of SVT in patients with CVI (OR 1.70, 95% CI = 1.1 - 2.5; p = 0.016). Conclusions: In patients with primary CVD, SVT was significantly associated with female gender. In men, older age, smoking and positive family history of VTE were relevant SVT risk factors. In women, risk factors were older age, BMI ≥ 25 kg/m2 and positive family history of VTE. Compared with C0 - C3 clinical classes, CVI significantly increases the risk of SVT.

Hereditary Homozygous Heparin Cofactor II Deficiency and the Risk of Developing Venous Thrombosis

1999 ◽  
Vol 82 (09) ◽  
pp. 1011-1014 ◽  
Author(s):  
Piedad Villa ◽  
Amparo Vaya ◽  
Francisco España ◽  
Fernando Ferrando ◽  
Yolanda Mira ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thrombosis ◽  
Family Members ◽  
Specific Inhibitor ◽  
Heparin Cofactor Ii ◽  
Thrombotic Risk ◽  
Thrombotic Risk Factor ◽  
First Case ◽  
At Deficiency

SummaryHeparin cofactor II (HCII) is a specific inhibitor of thrombin in the presence of heparin or dermatan sulphate. Although there have been reports on families in which a heterozygous HCII deficiency is associated with thromboembolic events, several epidemiological studies revealed that heterozygous HCII deficiency is as prevalent among healthy subjects as it is among patients with deep venous thrombosis (DVT). It is therefore not yet clear whether HCII is or is not a thrombotic risk factor.We analyze and describe in an extended family the biochemical and genetic thrombophilic risk factors and evaluate the potential thrombotic risk involved in homozygous and heterozygous HCII deficiency, either alone or associated with other thrombotic or circumstantial risk factors. The propositus has had three episodes of DVT and a pulmonary embolism. During the first episode of DVT the patient was diagnosed as having AT deficiency. Later, a functional and antigenic HCII deficiency, compatible with the homozygous form, was detected. The family study shows that both the propositus and her sister have homozygous HCII deficiency and that 12 of the 27 family members have heterozygous HCII deficiency.This is possibly the first case report on a homozygous phenotype for the HCII deficiency with, in addition, partial AT deficiency. The propositus has suffered several thrombotic events, unlike the other 12 family members with heterozygous HCII deficiency and her sister, who is also homozygous for this disorder. We suggest that HCII deficiency may play a limited in vivo role as a thrombotic risk factor unless associated with AT deficiency or another congenital thrombotic risk factor.

The risk of lower-limb superficial vein thrombosis relative to lower-limb venous thrombotic events is not increased in winter months

2020 ◽  
Vol 35 (7) ◽  
pp. 533-537
Author(s):  
Samir Henni ◽  
Pierre Ramondou ◽  
Guillaume Duval ◽  
Jean Picquet ◽  
Georges Leftheriotis ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Lower Limb ◽  
Homogeneous Distribution ◽  
Superficial Vein ◽  
Chi Square ◽  
Venous Flow ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis ◽  
Chi Square Test

Objectives Ambient temperature (that impacts differently venous flow in superficial and deep veins) could have a different effect on the risk of superficial and deep venous thrombosis. We searched for a trimestral variation of the risk of superficial venous thrombosis among all lower-limb thrombotic events (lower-limb thrombotic events = superficial venous thrombosis + deep venous thrombosis). Methods We retrospectively analyzed the results of venous ultrasound investigations performed among 11,739 patients (aged 67 ± 19 years old, 56.1% males) referred for suspected lower-limb thrombotic events over a 12-year period. Chi-square test was used to compare the superficial venous thrombosis/lower-limb thrombotic events ratio observed by trimesters to a homogeneous distribution. Results The proportion of lower-limb thrombotic events were 30.7%, 28.8%, 31.1%, and 31.4% (Chi2: 0.133; p = 0.987) of total investigations, while that of superficial venous thrombosis among all lower-limb venous thrombotic events were 27.2%, 30.0%, 31.4%, and 31.0%, for the first, second, third, and fourth trimesters respectively (Chi2: 0.357; p: 0.949). Conclusion No trimestral variation of the superficial venous thrombosis/lower-limb venous thrombotic events ratio was observed.

Risk factors for recurrent events in subjects with superficial vein thrombosis in the randomized clinical trial SteFlux (Superficial Thromboembolism Fluxum)

2014 ◽  
Vol 133 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Benilde Cosmi ◽  
Massimo Filippini ◽  
Fausto Campana ◽  
Giampiero Avruscio ◽  
Angelo Ghirarduzzi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Clinical Trial ◽  
Randomized Clinical Trial ◽  
Recurrent Events ◽  
Superficial Vein ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis

Recurrence of superficial vein thrombosis in patients with varicose veins

2016 ◽  
Vol 31 (7) ◽  
pp. 489-495 ◽  
Author(s):  
Christos Karathanos ◽  
Konstantinos Spanos ◽  
Vassileios Saleptsis ◽  
Aspasia Tsezou ◽  
Despina Kyriakou ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Regression Analysis ◽  
Logistic Regression Analysis ◽  
Varicose Veins ◽  
Gene Mutations ◽  
Ratio Method ◽  
Superficial Vein ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis ◽  
History Of

Objective To investigate which factors other than history of superficial vein thrombosis (SVT) are associated with recurrent spontaneous SVT episodes in patients with varicose veins (VVs). Materials and methods Patients with a history of spontaneous SVT and VVs were followed up for a mean period of 55 months. Demographics, comorbidities, and thrombophilia screening test were analyzed. Patients were grouped according to the clinical–etiology–anatomy–pathophysiology classification. A multiple logistic regression analysis with the forward likelihood ratio method was undertaken. Results Thirteen patients out of 97 had a recurrence SVT episode during the follow-up period. All those patients were identified to have a thrombophilia defect. Protein C and S, antithrombin, and plasminogen deficiencies were more frequently present in patients without recurrence. Gene mutations were present in 38% in the nonrecurrence group and 77% in the recurrence group. After logistic regression analysis, patients with dislipidemia and mutation in prothrombin G20210A (FII) had an increased risk for recurrence by 5.4-fold and 4.6-fold, respectively. No deep vein thrombosis or pulmonary embolism occurred. Conclusions Dislipidemia and gene mutations of F II are associated with SVT recurrence in patients with VVs. A selection of patients may benefit from anticoagulation in the short term and from VVs intervention in the long term.

Treatment of superficial vein thrombosis with intermediate dose of tinzaparin: A real word cohort study – The SeVEN EXTension study

2021 ◽  
pp. 026835552094730
Author(s):  
Christos Karathanos ◽  
Dimitrios Chatzis ◽  
Panagiotis Latzios ◽  
Ioannis Papakostas ◽  
Konstantinos Goumas ◽  
...  
Keyword(s):  
Treatment Duration ◽  
Prolonged Treatment ◽  
Bleeding Complications ◽  
Superficial Vein ◽  
Duration Of Treatment ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis ◽  
History Of ◽  
Deep Vein ◽  
Intermediate Dose

Background To assess the treatment of superficial vein thrombosis (SVT) with intermediate dose of tinzaparin in a setting of real world practice. Methods Prospective observational study of consecutive patients treated by vascular physicians in the private sector with tinzaparin (131 IU/Kg) once daily. Treatment duration was at the treating physician’s discretion. The outcomes of the study were symptomatic venous thromboembolism, extension of thrombus and bleeding complications. Results 660 patients were included and followed up for at least 3 months. Median duration of treatment was 30 days (14–120). History of prior deep vein thrombosis (HR 2.77; 95% CI= 1.18–6.49; p = 0.018) and current SVT above the knee (HR1.84; 95% CI = 1.33–3.53; p = 0.0002) were associated with prolonged treatment duration. Primary efficacy outcomes occurred in 20 (3%) patients. The median time to the event was 24 (6–92) days and was not related to treatment duration. Conclusions Tinzaparin at intermediate dose is an effective and safe treatment for SVT.

scholarly journals JAK2V617F Variant Allele Frequency Identifies Patients with Polycythemia Vera (PV) at High Risk for Venous Thrombosis

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1776-1776
Author(s):  
Paola Guglielmelli ◽  
Giacomo Coltro ◽  
Giuseppe Gaetano Loscocco ◽  
Benedetta Sordi ◽  
Francesco Mannelli ◽  
...  
Keyword(s):  
Risk Factors ◽  
High Risk ◽  
Venous Thrombosis ◽  
Allele Frequency ◽  
Variant Allele ◽  
Continuous Variables ◽  
Variant Allele Frequency ◽  
Thrombotic Risk ◽  
History Of ◽  
The Impact

Abstract Background. Cardiovascular (CV) events are leading cause of morbidity and mortality in PV. Current risk stratification is based on variables predicting thrombotic risk, ie age >60y and history of thrombosis. Recent studies focused on additional thrombotic risk factors in PV, including generic CV factors and leukocytosis. PV patients (pts) are JAK2V617F mutated, and present wide heterogeneity in variant allele frequency (VAF); it was shown that a VAF >75% was associated with higher number of thrombotic events after diagnosis (Vannucchi AM, Leukemia 2007), but the prognostic role of JAK2 VAF is still debated. Aim. The aim of the study was to evaluate the impact of JAK2V617F VAF on rate of thrombosis in WHO-2016 defined PV pts. Patients and Method. In the CRIMM (Florence) database, a total of 577 pts with a JAK2VF VAF determined within 3 years from diagnosis, who met the 2016 WHO criteria for PV, were identified. All pts had information regarding thromboembolic events, including history of thrombosis, occurrence, type and date of thrombosis in the follow-up (FU) and presence of CV risk factors (smoking, hypertension, and diabetes mellitus). Thrombosis‐free survival (TFS) was determined from the time of diagnosis to the time the first thrombotic event occurred. Pts in whom thrombosis did not occur were censored at the time of last FU. Pre-receiver operating characteristic (ROC) plots were used to determine cutoff levels for continuous variables of interest. Differences in the distribution of continuous variables between categories were analyzed by Mann-Whitney or Kruskal-Wallis test. Pts' groups with nominal variables were compared by χ2 test. TFS was estimated by Kaplan Meier analysis; log rank test was used to compare TFS difference between groups. Cox proportional hazards regression was used for multivariable analysis. A two tailed P ≤ 0.05 was considered statistically significant. Results. The median age of pts at diagnosis was 61y, 308 (53.4%) were above 60y; 57.2% were males. All pts were mutated for JAK2V617F with a median VAF 43% (range 1-100%), 62% had at least one CV risk factor; 83 (14.4%) pts suffered from an episode of thrombosis within 3 yr from, or coincident with, diagnosis. The median FU was 7.3y (0.6-35.9y) during which 87 pts (15.1%) developed thrombosis. (50 arterial and 45 venous thrombosis). During the FU, 110 pts (19.1%) died. A JAK2VAF of ≥60% cutoff level, as determined by ROC analysis, correlated with measurements of stimulated erythropoiesis (higher hematocrit, lower mean cell volume and serum ferritin; all P<.01), leukocytosis (P<.0001), lower platelets count (P=.02) and elevated serum lactate dehydrogenase (LDH) (P<.03). Pts with ≥60% JAK2V617F VAF were at higher relative risk (RR) of having splenomegaly (RR 3.1; P<0.001), suffering from pruritus (RR 2.5; P<0.001) or constitutional symptoms (RR 1.9; P=0.01), harboring a BM fibrosis grade-1 (RR 3.1; P<0.001). Additionally, pts with a VAF>60% had greater risk to progress to PPV-MF (RR 8.5, P<.0001) and acute leukemia (RR 4.4, P=0.04) or to die (RR 3.8, P<0.0001). The JAK2VF VAF (continuous or ≥60%) did not correlate with occurrence of thrombosis at diagnosis, while the rate of thrombosis during FU was significantly increased in pts with VAF ≥60% (23.4% vs 11.0%, RR 2.4, 95%CI = 1.4-4.0; P<0.0001), more marked for venous (RR 3.7, 95%CI = 2.0-6.8; P<0.0001) than arterial (RR 1.8, 95%CI = 0.9-3.3; P=0.05) thrombosis. The impact of VAF on thrombosis during FU was then estimated according to the conventional risk category. In low risk pts (LR) (n=236), factors significantly associated with occurrence of FU thrombosis were CV risk factors (dyslipidemia (RR 3.3, P = 0.02) and hypertension (RR 1.8, P=0.048)), a G1 BM fibrosis (RR 5.3, P=0.006), presence of splenomegaly (RR, 3.2, P=0.001) or constitutional symptoms (RR 3.3, P=0.003) and a VAF ≥60% (RR 2.2, P = 0.024). In high risk pts (HR) (n=341), factors significant for FU thrombosis were splenomegaly (RR 2.0, P=0.03), elevated LDH (RR 4.0, P=0.009) and a VAF ≥60% (RR 2.3, P = 0.012). A VAF ≥60% was correlated with shortened venous TFS after diagnosis in HR (P = 0.01, HR = 3.2, 95%CI = 1.2−8.3; fig.) but not in LR pts (P = 0.20, HR = 1.1, 95%CI = 0.5−2.9). Conclusions. This study indicates that conventionally-defined high-risk PV pts with a JAK2V617F VAF ≥60% suffer from increased rate of venous events and might be worthwhile of more intensive antithrombotic prophylaxis. Figure. Figure. Disclosures No relevant conflicts of interest to declare.

Venous thromboembolism

2020 ◽  
pp. 363-372
Author(s):  
Charlotte Frise ◽  
Sally Collins
Keyword(s):  
Risk Factors ◽  
Molecular Weight ◽  
Venous Thromboembolism ◽  
Low Molecular Weight Heparin ◽  
Superficial Vein ◽  
Mortality And Morbidity ◽  
Vein Thrombosis ◽  
Superficial Vein Thrombosis ◽  
Maternal Mortality And Morbidity ◽  
Deep Vein

Venous thromboembolism is a major cause of maternal mortality and morbidity. This chapter discusses thromboprophylaxis (including low-molecular-weight heparin and doses by patient weight), risk factors, deep vein thrombosis, pulmonary embolism, associated investigations, and management. Anticoagulants and bleeding while anticoagulated are both covered. Finally, superficial vein thrombosis in the first month postpartum is described.

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