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PubMed2005

Matched case-control study on factor V Leiden and the prothrombin G20210A mutation in patients with ischemic stroke/transient ischemic attack up to the age of 60 years.

BACKGROUND AND PURPOSE: The role of the factor V Leiden mutation (FVL) and the G20210A mutation of the prothrombin (factor II [FII]) gene for arterial thrombosis is not clear. METHODS: We investigated the prevalence of these mutations in 468 patients with an acute stroke or transient ischemic attack (TIA) before the age of 60 years and in a healthy control population individually matched for age and gender. We also analyzed interactions between the mutations, gender, standard vascular risk factors, and stroke risk. RESULTS: The prevalence of the FVL did not differ significantly between patients and control subjects. However, we found a significant interaction between the FVL, smoking, and risk of stroke in women: female smokers without FVL had a somewhat increased risk of stroke of 2.6 (95% CI, 1.5 to 4.6; P=0.001) compared with nonsmoking noncarriers of the FVL. Stroke risk was markedly higher in female smokers who had the FVL (OR, 8.8; 95% CI, 2.0 to 38.0; P=0.004) after multivariate adjustment. No such interaction was observed in men. In contrast, the frequency of the FII G20210A mutation was significantly higher in male patients compared with controls (6% versus 1%; adjusted OR, 6.1; 95% CI, 1.3 to 28.3; P=0.021). In females, the prevalence of the mutation was 3% in both groups. We found no significant interactions of the FII G20210A mutation with other vascular risk factors and stroke risk. CONCLUSIONS: Our data indicate a highly increased risk of ischemic cerebrovascular events in women up to 60 years who smoke and have FVL. We also found evidence for an increased risk of stroke/TIA in men who have the FII G20210A mutation but not in women in this age group.

Alleles↗
PubMed2001

Eptifibatide and 7E3, but not tirofiban, inhibit alpha(v)beta(3) integrin-mediated binding of smooth muscle cells to thrombospondin and prothrombin.

BACKGROUND: Our objective was to determine whether abciximab, eptifibatide, or tirofiban inhibited ligand binding to alpha(v)beta(3) integrins on human aortic smooth muscle cells (HASMCs) or human umbilical vein endothelial cells (HUVECs). Abciximab binds alpha(IIb)beta(3) on platelets and alpha(v)beta(3) on HUVECs with similar affinity, whereas eptifibatide and tirofiban are thought to be highly specific for alpha(IIb)beta(3). The conclusion that eptifibatide does not bind vascular alpha(v)beta(3) integrins may be premature, however, because recent studies have demonstrated that the affinity of alpha(v)beta(3) for various ligands, including antagonists, is subject to modulation. METHODS AND RESULTS: Abciximab and 7E3, the anti-beta(3) integrin monoclonal antibody from which abciximab was derived, bound alpha(v)beta(3) on HASMCs in a specific and saturable manner and with an affinity similar to binding to alpha(IIb)beta(3) on platelets. 7E3 and eptifibatide inhibited alpha(v)beta(3)-mediated attachment of HASMCs to thrombospondin (TSP) and prothrombin but had no effect on alpha(v)beta(5)- or beta(1)-mediated HASMC attachment to vitronectin-, collagen-, or fibronectin-coated or noncoated tissue culture plates. The inhibitory effect of eptifibatide was similar in magnitude and not additive to that of 7E3. Eptifibatide and 7E3 inhibited alpha(v)beta(3)-mediated attachment of HUVECs. Tirofiban had only nonspecific effects on HASMC attachment to extracellular matrix proteins. In cell proliferation assays, eptifibatide inhibited alpha(v)beta(3)-mediated responses to soluble TSP by HASMCs and beta(3) integrin-expressing HEK cells. CONCLUSIONS: Eptifibatide and 7E3, but not tirofiban, specifically inhibit alpha(v)beta(3)-mediated binding of human smooth muscle and endothelial cells.

Abciximab↗
PubMed2000

Prothrombin gene 20210 G-->A and Factor V Arg 506 to Gln mutation in a patient with Buerger's disease--a case report.

Thromboangiitis obliterans, or Buerger's disease, is a segmental occlusive inflammatory disorder of the arteries and veins most commonly affecting the lower extremities of young male cigarette smokers. The etiopathogenesis of the thromboangiitis obliterans is still obscure. The authors have identified heterozygosity for the recently described prothrombin gene 20210 G-->A variation and Factor V Arg 506 to Gln (Factor V Leiden) mutation in a patient with Buerger's disease. Both mutations confer a high risk of thrombosis. This coincidental observation may serve as further evidence that a thrombotic mechanism is involved in Buerger's disease.

Adult↗
PubMed1992

Within-subject and between-subject biological variation of prothrombin time and activated partial thromboplastin time.

The within-subject and between-subject biological variation of prothrombin time (PT) and activated partial thromboplastin time (APTT) have been studied in a group of 19 women and 20 men over a period of 9 months. All measurements were performed with a mechanical coagulometer. The between-subject coefficients of variation were 6.8% for PT and 8.9% for APTT. The medians and the 90th percentiles of within-subject coefficients of variation were 1.7% and 5.9%, respectively, for PT, and 0.0% and 6.1% for APTT. These data were used to calculate the critical difference for significant change detection and the desirable between-day imprecision.

Adult↗
PubMed2000

Value of prothrombin fragment 1.2 (F 1.2) in the diagnosis of stroke in young patients with antiphospholipid antibodies.

The presence in the serum of antiphospholipid antibodies (aPL) is associated with venous and arterial thrombosis. This observation has led to the search for these antibodies in young patients with ischemic neurologic syndromes. However, 1% to 5% of healthy people may be found to have circulating aPL without necessarily being at increased risk of thromboembolism. Thus, the finding of APLA in a patient with cerebral ischemia does not necessarily provide an explanation for the etiology of the clinical syndrome. The aim of this study was to determine whether the presence of aPL in young patients with stroke or transient ischemic attacks represents a possible cause of hypercoagulability as defined by ongoing thrombin formation with resultant elevation of prothrombin fragment 1.2 (F1.2) levels. This was a retrospective, case-control study involving 57 subjects. Twenty-seven patients had a recent cerebrovascular ischemic event--either TIA or a stroke. Fifteen were positive for aPL, and 12 were aPL-negative. Thirty subjects, matched for age and sex with no history of cerebrovascular disease, served as controls. Of this group, 20 were aPL-positive and 10 were aPL-negative. Causes of hypercoagulability other than aPL were excluded by laboratory testing. A positive test for aPL was repeated after a 6-week interval and two positive tests were required for a patient to be regarded as being aPL-positive. Levels of F1.2 were measured by an ELISA technique. There was a significant difference (p < 0.05) in the mean F1.2 levels between the aPL-positive group with a history of cerebrovascular disease (mean F1.2 = 2.3733) and each of the other study groups. There was no statistically significant difference between any of the other study groups. Our findings suggest that F1.2 levels are elevated in young patients with cerebrovascular syndromes who have aPL and in whom other causes of hypercoagulability and atherosclerotic vascular disease are absent. Elevated F1.2 in these patients may be a potential marker of the hypercoagulable state associated with aPL.

Adult↗
PubMed2000

Portal vein thrombosis associated to prothrombin G20210A mutation and protein C deficiency.

We describe a patient with left branch portal vein thrombosis involving two thrombophilic alterations, the prothrombin G20210A mutation and protein C deficiency. In spite of not being under anticoagulant treatment, the thrombus in the portal vein underwent complete and spontaneous lysis. No other risk factors were detected and no family history related to thrombosis was found.

Adenine↗
PubMed2001

Upper extremity deep vein thrombosis in a young patient double heterozygous for factor V Leiden and prothrombin G20210A mutation.

We report on a 19-year-old girl with upper extremity deep vein thrombosis after catheter indwelling whose thrombophilic study disclosed the coexistence of factor V Leiden and the prothrombin G20210A mutation. The family study identified five other members who were also heterozygous for both mutations. This is the first case of upper extremity deep vein thrombosis with the co-inheritance of both genetic defects. It provides further evidence that thrombophilic defects mostly require additional triggering factors to induce a thrombotic event and suggests that in young patients with this venous thrombotic location, a thrombophilic search should be performed even when there are other acquired thrombotic risk factors.

Adult↗
PubMed2001

Homozygous patients with the 20210 G to A prothrombin polymorphism remain often asymptomatic in spite of the presence of associated risk factors.

Patients who are homozygous for the G to A nontranslated prothrombin polymorphism only occasionally have venous thrombosis. An evaluation of all published papers on the subjects has disclosed that nine patients of the 35 so far reported remained asymptomatic in spite of the presence of associated congenital or acquired thrombotic risk factors. We saw an additional patient recently, bringing the total to 10 of 36 patients. Some of these patients remained asymptomatic in spite of multiple or repetitive risk factors (e.g., five pregnancies in the case of one patient). Twelve patients who were homozygous and who had this polymorphism developed symptoms only in the presence of the same risk factors. This may suggest that this abnormality played a small role, if any, in both groups of patients. The finding that several patients with this abnormality remained asymptomatic in spite of associated risk factors casts serious doubts about the prothrombotic significance of this polymorphism. Until this problem is clarified, the clinician must abstain from attributing a prothrombotic effect to this polymorphism.

Adolescent↗
PubMed2001

Factor V Leiden and prothrombin G20210A in relation to arterial and/or vein rethrombosis: two cases.

The factor V Leiden (FV Leiden) and prothrombin G20210A mutations, are the most common established genetic risk factors for deep vein thrombosis (DVT). However, the relationship between these mutations and arterial thrombotic syndromes (coronary heart disease, myocardial infarction, stroke) has not been established. Some studies have suggested a relationship between them, but other authors have considered it unlikely that these anomalies are a major risk factor for arterial thrombosis. From the clinical point of view, a question arises concerning the risk of repeated thrombosis in patients carrying one of these two mutations. The question is whether the recurrence is attributable to the mutations or to the presence of additional circumstantial risk factors. As the risk of repeated thrombosis varies considerably from one patient to another, decisions about long-term treatment require weighing the persistence of risk factors for vascular disease (venous and arterial), especially in selected cases such as young patients or patients with thrombosis of unusual localization.

3' Untranslated Regions↗
PubMed2002

Effects of extracorporeal circulation on thrombinantithrombin III and prothrombin fragment 1+2 levels.

Cardiopulmonary bypass may alter the factors responsible for normal hemostasis by exposing blood to nonendothelial surfaces, for example, extracorporeal circuits. To evaluate the probable effect of extracorporeal circulation on hemostasis, we measured thrombin-antithrombin III complex (TAT) and prothrombin fragment 1+2 (PF 1.2) plasma levels, which are the biologic markers of in vivo coagulation, in 20 patients who underwent coronary artery bypass grafting (CABG). Postoperative PF 1.2 levels were higher in comparison to the preoperative concentrations of the parameter. Preoperative and postoperative TAT concentrations showed no statistically significant difference. The increment in the PF 1.2 levels in CABG patients might suggest ongoing subclinical hemostatic activation associated with CABG. Further investigations are needed to clarify the exact relationship between increased PF 1.2 levels and thrombotic complications observed in CABG patients. Hemostatis in CABG is still an enigma and remains to be eluciated.

Adult↗
PubMed1999

Central retinal vein thrombosis associated with prothrombin 20210G/A gene variant.

We describe a patient with central retinal vein thrombosis associated with the prothrombin gene 20210G/A. The associated risk factors and the patient's personal and family history of thrombosis are dealt with. In addition, the literature on the cases reported up to now is reviewed as is the prevalence of this new mutation in patients with central retinal vein thrombosis.

Humans↗
PubMedDate not supplied

Branch retinal vein occlusion associated with the 20210 G-to-A prothrombin variant.

PURPOSE: To describe a case of branch retinal vein occlusion (BRVO) in a patient who tested positive for the 20210 A allele of the prothrombin (PT) gene. METHODS: A 48-year-old man had visual loss in the right eye secondary to BRVO confirmed by ophthalmoscopy and fluorescein angiography. His medical history was not remarkable for common risk factors for retinal occlusive diseases. RESULTS: Laboratory tests for hypercoagulability were positive for PT 20210 A variant. The patient's family tested negative for the PT variant. CONCLUSIONS: Laboratory tests for coagulopathy, including the PT 20210 A variant, should be added to the examination of patients with central or BRVO, especially if most common risk factors for thrombosis have been excluded.

Blindness↗
PubMed2002

Combined carrier status of prothrombin 20210A and factor XIII-A Leu34 alleles as a strong risk factor for myocardial infarction: evidence of a gene-gene interaction.

Studies associating the prothrombin 20210G>A (FII 20210A), factor V Leiden (FVL), and factor XIII Leu34 (FXIII-A Leu34) alleles with myocardial infarction (MI) have yielded conflicting results. Complicated gene-gene interactions, small sample sizes, and heterogeneous genetic and environmental backgrounds may contribute to opposing findings. Simultaneous analysis of multiple gene variants in a large sample size from a genetically isolated population may overcome these weaknesses. Genotyping was performed in 500 MI patients and 500 control subjects from the genetically isolated Newfoundland population to determine the prevalence of the FII 20210A, FVL, and FXIII-A Leu34 variants and their association with MI. Gene-gene interactions were also analyzed. The prevalence of the FII 20210A allele was higher in MI patients (3.2%) than in control subjects (1.0%; P =.015). The FII 20210A allele was also 5.6-fold higher in MI patients younger than 51 years than in age-matched control subjects (P =.04). FVL showed 3.9-fold higher prevalence in young patients than in patients older than 50 years (P =.004) and 2.7-fold higher than in age-matched control subjects (P =.007). Furthermore, the prevalence of combined carriers of the FXIII-A L34 and FII 20210A alleles was 12-fold higher in MI patients than in control subjects (P =.002) and with 92% penetrance. There was disequilibrium of the FXIII-A Leu34 allele to MI patients carrying the FII 20210A allele as a genetic background. Based on our data, we determined that (1) the FII 20210A allele is a risk factor for MI, possibly important for early onset; (2) FVL may predispose for early-onset MI; (3) the FXIII-A Leu34 allele predisposes for MI in males only; however, (4) interaction between the FII 20210A and FXIII-A Leu34 alleles forms a synergistic coeffect that strongly predisposes for MI, placing combined carriers at high risk for MI.

5' Untranslated Regions↗
PubMed1994

In vitro reversal of heparin effect with heparinase: evaluation with whole blood prothrombin time and activated partial thromboplastin time in cardiac surgical patients.

This study was designed to evaluate the potential in vitro use of heparinase to eliminate functionally active heparin prior to performing whole blood (WB) prothrombin time (PT) and activated partial thromboplastin time (APTT) assays. A total of 250 U/kg of heparin for cardiopulmonary bypass (CPB) was administered to 30 cardiac surgical patients in three consecutive, divided doses (20, 80, and 150 U/kg) at 15-min intervals. Blood specimens were obtained prior to heparin administration (baseline) and 10 min after each heparin dose. After collection, blood specimens were fractionated into three aliquots of which the first was used for determination of heparin concentration. After gentle mixing, WB PT and APTT measurements were performed for heparinase (Aliquot 2)- and nonheparinase (Aliquot 3)-treated blood. With consecutive heparin doses of 20 and 80 U/kg, WB PT increased from a baseline of 12.3 +/- 0.1 s to 13.3 +/- 0.2 and 18.5 +/- 1.3 s, while WB APTT increased from a baseline of 28.3 +/- 1.1 s to 89.5 +/- 5.4 after the initial heparin dose (20 U/kg). When compared to baseline (no heparin) results, small, progressive increases in heparinase-treated WB PT (0.7 +/- 0.1, 1.5 +/- 0.1, 2.1 +/- 0.1 s) and APTT (2.3 +/- 0.3, 5.7 +/- 0.4, 9.5 +/- 0.5 s) were seen with increasing heparin concentration (0.23, 1.58, and 3.95 U/mL, respectively). Heparinase was highly effective in eliminating the anticoagulant effects of even large amounts of heparin in plasma from cardiac surgical patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

European concerted action on anticoagulation. Minimum numbers of lyophilized plasma samples for ISI calibration of CoaguChek and TAS point-of-care whole blood prothrombin time monitors.

International sensitivity index (ISI) calibration of whole blood prothrombin time (PT) monitors is too complex. We previously simplified the method by using European Concerted Action on Anticoagulation (ECAA) lyophilized plasma samples with the TAS PT-NC (Bayer AG, Leverkusen, Germany) and the CoaguChek Mini (Roche Diagnostics, Mannheim, Germany) whole blood PT monitoring systems. The TAS PT-NC required a correction derived from the line of equivalence. Monte Carlo bootstrap analysis of reducing numbers of test samples was performed with both systems. Plasma samples from patients receiving coumarin (coumarin samples), healthy subjects (normal samples), and plasma samples artificially depleted of coagulation factors were used. With the TAS PT-NC, 20 coumarin samples or 20 artificially depleted samples with 7 normal samples gave reliable ISI and international normalized ratio and satisfactory precision. With the CoaguChek Mini, 30 coumarin and 10 normal samples were required. Simplification of ISI calibration of the 2 monitoring systems is possible using fewer ECAA lyophilized plasma samples than the 80 required according to the World Health Organization guidelines for conventional PT systems and previously recommended for fresh plasma samples tested on the same 2 monitoring systems.

Animals↗
PubMed2003

International sensitivity index calibration of the near-patient testing prothrombin time monitor, ProTime.

Near-patient testing devices (monitors) capable of measuring prothrombin time on an unmeasured drop of blood would be suitable alternatives to centralized laboratory monitoring of patients receiving oral anticoagulants. The essential prerequisite for the use of these monitors is their conformity to the international sensitivity index (ISI) calibration model recommended by the World Health Organization. We report on the ISI calibration of the ProTime monitor (International Technidyne, Edison, NJ) designed and approved for patient self-testing. According to our results, this monitor can be calibrated by adopting the model already used for other monitors. The apparent ISI was close to unity. Overall, the international normalized ratio values displayed by the monitor agreed with those measured with the international reference preparation for thromboplastin. Confirmation of these results in a large multicenter study is warranted.

Administration, Oral↗
PubMed2003

Diagnostic single nucleotide polymorphism analysis of factor V Leiden and prothrombin 20210G > A. A comparison of the Nanogen Eelectronic Microarray with restriction enzyme digestion and the Roche LightCycler.

Genetic thrombosis risk factors include a sequence variant in the prothrombin gene (20210G > A) and factor V Leiden (1691G > A). These single nucleotide polymorphisms can be diagnosed with restriction fragment length polymorphism (RFLP) analysis, fluorescent genotyping on the LightCycler (Roche Diagnostics, Indianapolis, IN), and microarray-based testing on the novel NanoChip electronic microarray (NanoChip Molecular Biology Workstation, Nanogen, San Diego, CA). We compared these methods for accuracy, time to results, throughput, and interpretation. Results from 789 of 800 individual amplicons analyzed on the NanoChip were in complete agreement with the other assays. Eleven were "no calls" (uninterpreted by the NanoChip system) resulting from failed polymerase chain reaction amplifications. Although the NanoChip System, when used in a low-throughput setting, requires more overall time than the LightCycler, it is nearly equivalent per genotyping call. Owing to minimal sample handling, assay results are more reliable on the NanoChip platform and on the LightCycler than with RFLP. The NanoChip assay is reliable and may be especially valuable to laboratories with a large volume of thrombophilia test requests.

Factor V↗