Increased lipoprotein (a) levels as an independent risk factor for venous thromboembolism

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3364-3368 ◽  
Author(s):  
Mario von Depka ◽  
Ulrike Nowak-Göttl ◽  
Roswith Eisert ◽  
Christian Dieterich ◽  
Monika Barthels ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Independent Risk Factor ◽  
Elevated Serum ◽  
Prothrombin G20210a ◽  
Control Group ◽  
Healthy Controls ◽  
Lipoprotein A

Abstract Elevation of serum lipoprotein (a) (Lp[a]) is a known risk factor predisposing to cardiovascular and cerebrovascular disease. However, little is known about the role of increased Lp(a) in venous thromboembolism (VTE). This study evaluated the role of Lp(a) among a panel of established hereditary thrombogenic defects in patients with VTE. A total of 685 consecutive patients with at least one episode of VTE and 266 sex- and age-matched healthy controls were screened with regard to activated protein C resistance, protein C, protein S, and antithrombin deficiency, elevated serum levels of Lp(a), and the factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations. Elevated Lp(a) levels above 30 mg/dL were found in 20% of all patients, as compared to 7% among healthy controls (P < .001, odds ratio [OR] 3.2, 95% confidence interval [CI], 1.9-5.3). The coexistence of FV G1691A and elevated Lp(a) was significantly more prevalent among patients with VTE than in the control group (7% versus 0.8%; P < .001, OR 9.8, 95% CI, 2.4-40.7). No other established prothrombotic risk factor was found to be significantly combined with increased Lp(a). These data suggest that Lp(a) concentrations greater than 30 mg/dL are a frequent and independent risk factor for VTE. Furthermore, elevated Lp(a) levels might contribute to the penetrance of thromboembolic disease in subjects being affected by other prothrombotic defects, such as FV G1691A mutation.

Increased lipoprotein (a) levels as an independent risk factor for venous thromboembolism

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3364-3368 ◽  
Author(s):  
Mario von Depka ◽  
Ulrike Nowak-Göttl ◽  
Roswith Eisert ◽  
Christian Dieterich ◽  
Monika Barthels ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Independent Risk Factor ◽  
Elevated Serum ◽  
Prothrombin G20210a ◽  
Control Group ◽  
Healthy Controls ◽  
Lipoprotein A

Elevation of serum lipoprotein (a) (Lp[a]) is a known risk factor predisposing to cardiovascular and cerebrovascular disease. However, little is known about the role of increased Lp(a) in venous thromboembolism (VTE). This study evaluated the role of Lp(a) among a panel of established hereditary thrombogenic defects in patients with VTE. A total of 685 consecutive patients with at least one episode of VTE and 266 sex- and age-matched healthy controls were screened with regard to activated protein C resistance, protein C, protein S, and antithrombin deficiency, elevated serum levels of Lp(a), and the factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations. Elevated Lp(a) levels above 30 mg/dL were found in 20% of all patients, as compared to 7% among healthy controls (P < .001, odds ratio [OR] 3.2, 95% confidence interval [CI], 1.9-5.3). The coexistence of FV G1691A and elevated Lp(a) was significantly more prevalent among patients with VTE than in the control group (7% versus 0.8%; P < .001, OR 9.8, 95% CI, 2.4-40.7). No other established prothrombotic risk factor was found to be significantly combined with increased Lp(a). These data suggest that Lp(a) concentrations greater than 30 mg/dL are a frequent and independent risk factor for VTE. Furthermore, elevated Lp(a) levels might contribute to the penetrance of thromboembolic disease in subjects being affected by other prothrombotic defects, such as FV G1691A mutation.

Low Level of Circulating Activated Protein C Is a Risk Factor for Venous Thromboembolism

2001 ◽  
Vol 86 (12) ◽  
pp. 1368-1373 ◽  
Author(s):  
Amparo Vayá ◽  
Yolanda Mira ◽  
Pilar Medina ◽  
Amparo Estellés ◽  
Piedad Villa ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Independent Risk Factor ◽  
Activated Protein C ◽  
Control Group ◽  
Low Level ◽  
History Of ◽  
The Mean

SummaryThe levels of circulating activated protein C (APC) reflect in vivo protein C activation. The aim of this study was to determine whether a low APC level is an independent risk factor for venous thromboembolism (VTE). We measured APC in 160 patients with a history of VTE and without recognized thrombophilic defects, and in 199 healthy individuals. The mean (±SD) APC level was lower in patients (0.99 ± 0.44 ng/ml) than in controls (1.19 ± 0.41 ng/ml) (p <0.0001), and showed a different distribution in the two groups. Thirty-eight patients (23.7%) had APC levels below the 5th percentile of the control group (<0.69 ng/ml) and 57 patients (35.6%) had APC levels below the 10th percentile (<0.77 ng/ml). APC levels <0.69 ng/ml increased the risk of a single or recurrent episode of VTE 4.2-fold (95% confidence interval, 2.0-9.0) or 6.9-fold (2.6-17.9), respectively, and APC levels <0.77 ng/ml increased these risks 3.4-fold (1.9-6.2) or 5.1-fold (2.3-11.2), respectively, compared with controls. Familial studies revealed that in some cases the low APC phenotype seems to be hereditary. We conclude that a low level of circulating APC in individuals without any of the most recognized thrombophilic defects is a prevalent, independent risk factor for VTE, and that it predisposes to recurrent VTE.

Role of lipoprotein(a) and its autoantibodies in polyvascular atherosclerotic disease

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Tmoyan ◽  
O Afanasieva ◽  
M Ezhov ◽  
U Chubykina ◽  
E Klesareva ◽  
...  
Keyword(s):  
Risk Factor ◽  
Independent Risk Factor ◽  
Lower Limbs ◽  
Public Institution ◽  
Funding Source ◽  
Lipoprotein A ◽  
National Medical ◽  
Vascular Beds ◽  
Relationship Of

Abstract Background Lipoprotein(a) [Lp(a)] is an independent risk factor of cardiovascular disease. The role of Lp(a) and its autoantibodies in the development of atherosclerosis, depending on the severity of lesion, is uncertain. Purpose To define the relationship of Lp(a) level and autoantibodies to Lp(a) with atherosclerosis of different vascular beds. Methods The study included 1288 patients older than 18 years with instrumental examination of three vascular beds (coronary, carotid and lower limbs arteries). Patients were divided according to the number of affected vascular beds (stenosis ≥50%): 0 (n=339), 1 (n=470), 2 (n=315), 3 (n=164). Levels of lipids, Lp(a) and autoantibodies to Lp(a) were measured in serum of all patients. Results Lp(a) concentration steadily increased and the level of IgM autoantibodies decreased with the number of affected vascular beds (Figure). There was no any association between IgG autoantibodies to Lp(a) and stenotic atherosclerosis. In logistic regression analysis adjusted for age, sex, hypertension, diabetes mellitus, smoking, elevated Lp(a) level was an independent predictor of stenotic atherosclerosis and it was associated with severity of lesions (table). Conclusions Lipoprotein(a) is an independent risk factor of stenotic atherosclerosis and its concentration increases with the number of affected vascular beds, while IgM autoantibodies to Lp(a) possess cardioprotective properties. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): National Medical Research Center of Cardiology of Ministry of Health of the Russian Federation

scholarly journals A Retrospective Cross-sectional Study on Activated Protein C Resistance (Factor V Leiden): an Independent, Gender-dependent Risk Factor for Venous Thromboembolism

2021 ◽  
Author(s):  
Vahideh Takhviji ◽  
Kazem Zibara ◽  
Asma Maleki ◽  
Ebrahim Azizi ◽  
Sanaz Hommayoun ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Control Group ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Cross Sectional ◽  
Factor V Leiden Mutation

Abstract Background: Activated protein C resistance (APCR) due to factor V R506Q (Leiden) mutation is a major risk factor in patients with venous thromboembolism. The present study investigated the symptoms patterns and the risk for venous thromboembolism regarding multiple clinical, laboratory, and demographic properties in APCR patients.Material and Methods: A retrospective cross-sectional analysis was conducted on a total of 288 APCR patients with age interval ranging between 1 to 80 years. In addition, 288 control samples, reported healthy after confirmatory tests, were also randomly selected. Demographic information, clinical manifestations, family and treatment history were recorded, and specific tests applied.Results: APCR was found to be 2.3 times significantly more likely in men (OR: 2.1, p < 0.05) than women. The risk of DVT and PE in APCR patients was 4.5 and 3.2 times more than the normal group, respectively (p < 0.05). However, APCR could not be an independent risk factor for arterial thrombosis and pregnancy complications. Moreover, patients were evaluated for thrombophilia panel tests and showed significantly lower protein C and S than the control group and patients without DVT (p<0.0001).Conclusion: Factor V Leiden mutation and APCR abnormality are noticeable independent risk factors for venous thromboembolism. Screening strategies for factor V Leiden mutation in patients undergoing surgery, oral contraceptive medication, and pregnancy cannot be recommended, but a phenotypic test for activated protein C resistance should be endorsed in patients with venous thromboembolism.

Risk of Venous Thromboembolism Is Not Increased by Elevated TAFI Levels.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1484-1484
Author(s):  
Nienke Folkeringa ◽  
Jan Leendert P. Brouwer ◽  
Nic J.G.M Veeger ◽  
Jan van der Meer
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Absolute Risk ◽  
Large Family ◽  
Protein S ◽  
High Plasma ◽  
Prothrombin G20210a ◽  
Chromogenic Assay ◽  
Increased Risk

Abstract TAFI (Thrombin-activatable fibrinolysis inhibitor) is a suppressor of fibrinolysis and high plasma levels of TAFI are assumed to induce venous thromboembolism (VTE). A few studies published on this subject identified TAFI as a mild risk factor for VTE. The risk may be increased if high TAFI levels are combined with other trombophilic defects. We performed a retrospective study to asses the absolute risk of VTE associated with elevated levels of TAFI and the contribution of concomitant thrombophilic defects. Subjects were recruited from a previous large family cohort study, which was designed to estimate the risk of VTE in first degree relatives of probands with documented VTE and a hereditary deficiency of antithrombin, protein C or protein S. Probands were excluded from analysis. Blood samples of relatives were tested on deficiencies of antithrombin, protein C and protein S, prothrombin G20210A, factor FV Leiden, hyperhomocysteinemia and increased levels of factor VIII:C, IX:C and XI:C. TAFI activity was additional measured by chromogenic assay on plasma samples stored at minus 80 degrees Celsius. We analysed 350 of 457 relatives, who were tested on TAFI. TAFI levels observed in women were lower than in men (median 97 versus 106 U/dL) and increased with age (median from 95 U/dL at age 15–30 yr to 107 U/dL at age>60 yr). Relatives with TAFI levels above the 90th percentile (>128 U/dL) had the same absolute risk of VTE as relatives with TAFI levels below the 90th percentile. Annual incidences (AI) were 0.74 versus 0.72 % per year: relative risk (RR) 1.0; 95% CI.0.51–2.10 (Table). Concomitant thrombophilic defects were demonstrated in 82% of the relatives. These defects were equally distributed among relatives with TAFI levels of >90th versus <90th percentile. Relatives with TAFI levels above the 90th percentile and concomitance of at least one other thrombophilic defect were not at increased risk of VTE compared to relatives with lower TAFI levels and concomitant thrombophilic defects (RR 0.83; 95% CI 0.41–1.68). Our data do not support that eleveated TAFI levels are a risk factor for VTE. The high absolute risk of VTE among relatives is mainly due to the presence of other thrombophilic defects rather than elevated TAFI levels, as interactions between TAFI and other thrombophilic defects were not demonstrated. VTE (n) Observation years AI (95% CI) RR (95% CI) TAFI > 90th percentile 9 1209 0.74 (0.3–1.4) 1.0 (0.51–2.10) Concomitance 9 1147 0.78 (0.4–14.9) 0.83 (0.41–1.68) No concomitance 0 62 0 TAFI < 90th percentile 53 7364 0.72 (0.5–0.9) Ref Concomitance 53 5724 0.93 (0.7–1.2) Ref No concomitance 0 1426 0

The deletion polymorphism in the angiotensin-converting enzyme gene is a moderate risk factor for venous thromboembolism

2003 ◽  
Vol 89 (05) ◽  
pp. 847-852 ◽  
Author(s):  
Andreas Czwalinna ◽  
Cornelia Wermes ◽  
Roswith Eisert ◽  
Inge Scharrer ◽  
Arnold Ganser ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Independent Risk Factor ◽  
Blood Donors ◽  
Angiotensin Converting Enzyme Gene ◽  
Deletion Polymorphism ◽  
Moderate Risk ◽  
G20210a Mutation

SummaryACE displays potent vasoconstrictive effects, attenuation of fibrinolysis, and platelet activation and aggregation, thus possibly promoting venous thromboembolism (VTE). The ACE gene contains an insertion (I) or deletion (D) polymorphism accounting for 50% of the variation in serum ACE concentration. To evaluate the role of the I/D polymorphism in VTE, its prevalence was determined in 931 patients with VTE and 432 blood donors. The prevalence of the DD genotype was 27.6% in patients and 21.3% in controls (OR 1.4; p <0.02). In multivariate analysis there was a trend of the DD genotype to be an independent risk factor (OR 1.4; p = 0.08). No differences in DD genotype prevalence according to exogenous risk factors were found. Coinheritance of FV G1691A, PT G20210A mutation, and PS deficiency with the DD genotype increased the relative risk of VTE. Thus, the ACE DD genotype is a moderate risk factor of hereditary thrombophilia. Exogenous risk factors did not alter the manifestation of VTE among carriers of the DD genotype, whereas coinheritance of the DD genotype with the aforementioned defects increased the risk for VTE considerably.

Evaluation of ProC Global assay in women with a history of venous thromboembolism on hormonal therapy

2006 ◽  
Vol 96 (11) ◽  
pp. 578-583 ◽  
Author(s):  
Irit Aberbach ◽  
Liliana Schliamser ◽  
Zeev Blumenfeld ◽  
Benjamin Brenner ◽  
Galit Sarig
Keyword(s):  
Risk Factors ◽  
Logistic Regression ◽  
Multivariate Analysis ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Hormonal Therapy ◽  
Protein C ◽  
Healthy Controls ◽  
Activation Time ◽  
History Of

SummaryThe risk of thrombosis in women increases significantly during treatment with hormonal therapy (HT). The aim of this study was to evaluate ProC Global assay in women with a history of venous thromboembolism (VTE) while using HT. Protein C activation time normalized ratio (PCAT-NR) levels were significantly lower in 32 women with a history ofVTE while using HT (0.72 ± 0.1) compared with 56 healthy controls without HT, matched by age at blood sampling (0.99 ± 0.2) and 40 healthy controls with HT, matched by age and HT at VTE event (0.94 ± 0.2) (P<0.001 for both). PCAT-NR lower than the cut-off level of 0.8 was found in 23/32 (72%) patients compared with 5/56 (9%) age-matched controls (OR=26, 95%CI: 7-106, P<0.001) and 9/40 (22.5%) of HT-matched controls (OR=9, 95%CI: 2.7-30, P<0.001). Any thrombophilic risk factor was found in 20/32 (62.5%) of patients compared with 12/56 (21.4%) of agematched controls (OR=6, 95%CI: 2.1-10, P<0.001) and 12/40 (30%) of HT-matched controls (OR=4, 95%CI: 1.3-11.8, P=0.006).Out of the variables that are risk factors of VTE as age, HT or thrombophilic risk factor, ProC Global assay was found in the multivariate analysis - logistic regression, as the parameter that was the most associated with patient group [Exp(B)=15.8, 95% CI: 4.2-59.0, P<0.001]. In conclusion, abnormal PCAT-NR is associated with VTE in women using HT. ProC Global assay may potentially serve asa diagnostic tool for evaluating the risk of VTE in women prior to administration of HT.

scholarly journals Moderate Hyperhomocysteinemia in Patients with Huntington's Disease

Pteridines ◽  
2002 ◽  
Vol 13 (4) ◽  
pp. 121-125 ◽  
Author(s):  
Andreas Laich ◽  
Friedrich Leblhuber ◽  
Bernhard Widner ◽  
Barbara Frick ◽  
Kurt Jellinger ◽  
...  
Keyword(s):  
Risk Factor ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Immune Activation ◽  
Independent Risk Factor ◽  
Control Group ◽  
Healthy Controls ◽  
Healthy Elderly ◽  
Serum Homocysteine ◽  
Vascular Type

Abstract Hyperhomocysteinemia is considered to be an independent risk factor for cardiovascular diseases and atherosclerosis. Also patients with dementia, either of Alzheimer's or of vascular type, may present with elevated homocysteine levels. All these disorders are linked with older age and since hyperhomocysteinemia is also frequent in the healthy elderly, we were interested to determine homocysteine concentrations in a younger population of demented patients suffering from Huntington's disease. In 15 patients with Huntington's disease and in a control group of similar age, serum homocysteine concentrations were measured and changes were compared to concentrations of folate and neopterin, the latter being an indicator of immune activation. A subgroup of patients with Huntington's disease presented with elevated homocysteine concentrations compared to healthy controls of similar age. Moderate hyperhomocysteinemia was related to lower folate concentrations and also to higher neopterin levels which indicate increased immune activation. The correlation of homocysteine with neopterin concentrations points to a possible relationship between the development of hyperhomocysteinemia and immune activation in the patient

scholarly journals Cleaved Protein S (PS), Total PS, Free PS, and Activated Protein C Cofactor Activity as Risk Factors for Venous Thromboembolism

2003 ◽  
Vol 49 (4) ◽  
pp. 575-580 ◽  
Author(s):  
Delphine Borgel ◽  
Jean-Luc Reny ◽  
David Fischelis ◽  
Sophie Gandrille ◽  
Joseph Emmerich ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Activated Protein C ◽  
Hormonal Treatment ◽  
Protein S ◽  
Molecular Forms ◽  
Cofactor Activity ◽  
Control Study

Abstract Background: Although hereditary protein S (PS) deficiency is clearly associated with venous thromboembolism (VTE), the importance of low PS concentrations as a risk factor for VTE in other patients is still a matter of debate. To clarify this issue, we designed a case-control study to evaluate the role of different molecular forms of plasma PS. Methods: We quantified plasma cleaved, total, and free PS and activated protein C (APC) cofactor activity in 87 VTE patients and 174 controls matched for age, sex, and hormonal treatment. Free PS was measured by ELISA or by enzyme-linked ligand sorbent assay (ELSA). Cleaved and total PS were measured by ELISA. Results: In controls, the mean (SD) concentration of circulating cleaved PS was 39 (14) nmol/L, corresponding to 10% (3.5%) of total PS. Concentrations of cleaved PS and total PS were not significantly different in patients with VTE compared with controls. However, in our population, low free PS measured by ELISA or ELSA, as well as APC cofactor activity values were significantly associated with VTE with odds ratios (95% confidence intervals) of 2.9 (1.3–6.3), 2.5 (1.1–5.6), and 2.9 (1.3–6.4), respectively, in multivariate analyses. Conclusion: Phenotypic low PS detected by APC cofactor activity assay or by an assay specific for free PS should be considered a risk factor for VTE.

scholarly journals A case-control study on factor V Leiden: an independent, gender-dependent risk factor for venous thromboembolism

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Vahideh Takhviji ◽  
Kazem Zibara ◽  
Asma Maleki ◽  
Ebrahim Azizi ◽  
Sanaz Hommayoun ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Protein C ◽  
Activated Protein C ◽  
Clinical Manifestations ◽  
Factor V Leiden ◽  
Control Group ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Fvl Mutation

Abstract Background Activated protein C resistance (APCR) due to factor V Leiden (FVL) mutation (R506Q) is a major risk factor in patients with venous thromboembolism (VTE). The present study investigated the clinical manifestations and the risk of venous thromboembolism regarding multiple clinical, laboratory, and demographic properties in FVL patients. Material and methods A retrospective cross-sectional analysis was conducted on a total of 288 FVL patients with VTE according to APCR. In addition, 288 VET control samples, without FVL mutation, were also randomly selected. Demographic information, clinical manifestations, family and treatment history were recorded, and specific tests including t-test, chi-square and uni- and multi-variable regression tests applied. Results APCR was found to be 2.3 times significantly more likely in men (OR: 2.1, p < 0.05) than women. The risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) in APCR patients was 4.5 and 3.2 times more than the control group, respectively (p < 0.05). However, APCR could not be an independent risk factor for arterial thrombosis (AT) and pregnancy complications. Moreover, patients were evaluated for thrombophilia panel tests and showed significantly lower protein C and S than the control group and patients without DVT (p < 0.0001). Conclusion FVL mutation and APCR abnormality are noticeable risk factors for VTE. Screening strategies for FVL mutation in patients undergoing surgery, oral contraceptive medication, and pregnancy cannot be recommended, but a phenotypic test for activated protein C resistance should be endorsed in patients with VTE.

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