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PubMed2002

Factor V Leiden and prothrombin G20210A mutations in pregnancies with adverse outcome.

BACKGROUND: Inherited thrombophilia has been associated with obstetric complications through mechanisms that are not yet fully elucidated. The aim of this study was to investigate the relationship between specific obstetric adverse outcomes and factor V Leiden and prothrombin G20210A mutations. METHODS: Forty-five women with adverse pregnancy outcome defined as severe pre-eclampsia, abruptio placentae, intrauterine growth restriction and stillbirth, were tested for factor V Leiden and prothrombin G20210A mutations. The control group comprised 100 women with at least one normal pregnancy and no history of thrombosis. RESULTS: Overall, 13 women with one or more of the above-mentioned pregnancy complications (28%) had either thrombophilic mutation, as compared with six in the control group (6%) (p < 0.001, odds ratio (OR) 6.1; 95% confidence interval (CI) 1.9-20). The factor V Leiden mutation was detected in ten of the women with complicated pregnancies (22%) and in four of the controls (4%) (p < 0.001, OR 6.6; 95% CI 1.7-27.2). The prothrombin G20210A mutation was detected in three women in the group with complications (6%) and in two of the controls (2%) (p = 0.17, OR 3.4; 95% CI 0.4-30.5). Compared to controls, the prevalence of the factor V Leiden mutation was significantly higher in the subgroups of severe pre-eclampsia, abruptio placentae and fetal growth restriction. The prevalence of the prothrombin G20210A mutation does not appear to be significantly different from that in the controls in any of the groups studied. CONCLUSIONS: Our data suggest that inherited thrombophilia, and specifically the factor V Leiden mutation, may be associated with adverse pregnancy outcome. The role of the prothrombin G20210A mutation remains to be elucidated.

Abruptio Placentae↗
PubMed2000

Evaluation of the prothrombin gene polymorphism in patients with advanced retinopathy of prematurity.

It has been reported recently that a common genetic variant in the 3'-untranslated region of the prothrombin gene is associated with a significant fraction of premature births. The purpose of this study is to evaluate the prothrombin gene polymorphism in a large cohort of patients with preterm birth and advanced retinopathy of prematurity. For this purpose, the leukocyte DNAs were analyzed for the mutation (20210A) in the 3'-untranslated region of the prothrombin gene by PCR amplification, followed by restriction analysis and DNA sequencing. Our extensive analysis revealed a normal genotype (GG) in all patients as well as controls. These results suggest that the common genetic variant in the 3'-untranslated region of the prothrombin gene is not associated with advanced retinopathy of prematurity. Although more patients' samples should be evaluated, this genetic test does not support a relationship between prothrombin gene mutation and retinopathy of prematurity.

3' Untranslated Regions↗
PubMed1992

Imprecision of prothrombin time monitoring of oral anticoagulation. A survey of hospital laboratories.

Prothrombin time monitoring of oral anticoagulation is highly dependent on the tissue thromboplastin used. In the United States, patients have received a higher level of anticoagulation because of the use of a less sensitive thromboplastin. Many advocate the use of an International Normalized Ratio to rectify this problem. Laboratory supervisors from all acute care hospitals in Massachusetts were surveyed to determine the disparity in thromboplastin use and reporting practices for prothrombin time testing. Eighty-eight of 103 (86%) hospitals responded. Fifty-eight lots from six manufacturers of thromboplastin were in use. The International Sensitivity Index of these lots ranged from 1.89 to 2.74. Ninety-nine percent of hospitals reported prothrombin times in raw seconds. Only 5% reported an International Normalized Ratio. Sixteen different coagulation instruments were in use. Close to 70% of laboratory supervisors had little or no understanding of the significance of an International Sensitivity Index or an International Normalized Ratio. The management of oral anticoagulation appears far less precise than had been believed. Prothrombin times in the same individual from different laboratories may have poor correlation. Based on the level of understanding of laboratory supervisors, extensive education will be necessary to change practices and improve accuracy and comparability of prothrombin time testing.

Administration, Oral↗
PubMed2000

Factor V leiden and prothrombin G20210A mutations, but not methylenetetrahydrofolate reductase C677T, are associated with recurrent miscarriages.

The aim of this study was to investigate the relationship between recurrent miscarriages and factor V Leiden, prothrombin G20210A and C677T methylenetetrahydrofolate reductase (MTHFR) mutations. In this case-control study the prevalence of factor V Leiden, prothrombin G20210A and C677T methylenetetrahydrofolate reductase mutations was determined in a consecutive series of 80 recurrent miscarriage patients and 100 controls. Fifteen of 80 recurrent miscarriage patients and four out of 100 controls carried the factor V Leiden mutation (19 versus 4%, P = 0.003, odds ratio 5.5, 95% confidence interval (CI): 1.7-17). Seven of 80 recurrent miscarriage patients and two of 100 controls were carriers of the prothrombin G20210A mutation (9 versus 2%, P = 0.038, odds ratio 4.6, 95% CI: 0.9-23.2). Six of 80 recurrent miscarriage women and 15 of 100 controls were homozygotes for the C677T MTHFR mutation (8 versus 15%, P = 0.134, odds ratio: 0.4, 95% CI: 0.1-1.2). Our results suggest that the presence of factor V Leiden and prothrombin G20210A polymorphism, but not MTHFR C677T homozygosity, could be additional risk factors for recurrent miscarriages. Furthermore, it was suggested that the prevalence of factor V Leiden and prothrombin G20210A mutations is more prominent in second trimester, primary fetal losses and it is independent of the existence of additional pathology predisposing to recurrent fetal losses.

Abortion, Habitual↗
PubMed1996

Construction, properties and specific fluorescent labeling of a bovine prothrombin mutant engineered with a free C-terminal cysteine.

To define the role of phosphatidylserine-induced conformational changes in prothrombin activation during blood coagulation, a recombinant bovine prothrombin was constructed, characterized and shown to have a globally native-like conformation. We introduced a cysteine to replace the penultimate residue (Gly581) of a previously constructed active site mutant, and expressed the double mutant in Chinese hamster ovary cells at the level of 0.6 microgram/ml of cell culture medium. Specific labeling with fluorescein maleimide was accomplished by limited reduction with dithiothreitol to free the engineered cysteine while maintaining the native-like functional properties of the molecule. The average stoichiometry of labeling was 0.84 probe/protein. The location of the probe at the C-terminus was confirmed by proteolysis by native thrombin, by Taipan venom, and by carboxypeptidase Y. Both the double mutant and labeled prothrombin could be activated by snake venoms and the prothrombinase but, as expected, the double mutant meizothrombin did not autolyze as does native meizothrombin. Thus, for the first time, a native-like but specifically labeled prothrombin has been constructed. This molecule will be an essential tool for elucidating the structural role of membranes during prothrombin activation. In addition, the methods described might be usefully applied to labeling of an odd, engineered cysteine in other disulfide bond-containing proteins.

Amino Acid Sequence↗
PubMed1996

Activation of human prothrombin by porcine aortic endothelial cells--a potential barrier to pig to human xenotransplantation.

A potential solution to the shortage of human organs for transplantation lies in the use of animal organs with the pig as the most likely donor. Perfusion of porcine organs with human blood, however, results in hyperacute rejection (xenograft reaction) which occurs within minutes to hours and is characterised by intravascular thrombosis. The pathogenesis of this xenograft reaction is attributed to xenoreactive natural antibodies (XNA) binding to epitopes on porcine endothelium activating complement with subsequent haemostatic activation. We have investigated whether there is direct activation of human coagulation by porcine endothelium in the absence of XNA and complement. Previous experiments demonstrated possible pathological activation of the common pathway, thus human prothrombin and factor X were added separately to porcine endothelium and monitored for activation. Human prothrombin was activated by porcine but not human endothelium. There was no activation of factor X. Hirudin inhibited prothrombin activation suggesting that a conformational change may occur in prothrombin on binding to porcine endothelium, such that its catalytic centre is exposed with subsequent autocatalytic cleavages. If this in vitro observation of direct prothrombin activation is translated to the in vivo situation then this phenomenon may pose a non-immunological obstacle to pig to human xenotransplantation.

Animals↗
PubMed1998

Measurement of plasma fibrinogen concentration by the prothrombin-time-derived method: applicability and limitations.

A prothrombin-time-derived method was used to measure plasma fibrinogen concentration (PFC) in 286 samples from 242 normal and 44 orally anticoagulated subjects. Absorbance changes at 405 nm (deltaOD) during the clotting process were obtained by an automatic coagulometer and their relationship with plasma fibrinogen concentration (range 90-1090 mg/dl), measured by the Clauss method, was investigated. A weighted linear regression between the deltaOD and the Clauss-derived PFC values provided the best fit of the experimental data. The fitting equation was found to be reliable and accurate for PFC determination in normal subjects, whereas a systematic overestimate of fibrinogen level was demonstrated in plasma with high fibrinogen concentrations (> 400 mg/dl) and in plasma from anticoagulated patients. The systematic overestimate in the latter samples could be a result of an increased fibrin gel turbidity, as shown by in-vitro experiments using purified fibrinogen clotted by different thrombin concentrations. The PFC overestimate by the prothrombin-time-derived method could also be experimentally reproduced by competitively inhibiting thrombin-fibrinogen interaction by hirudin 54-65 peptide and the fibrinogen fragment E. A similar qualitative result was also found for the prothrombin-time-derived method in the presence of the Gly-Pro-Arg-Pro peptide, which competitively inhibits the end-to-end fibrin aggregation process. Notably, under both the above experimental conditions, the Clauss method underestimated the PFC. On the other hand, the 'clot recovery' method was minimally affected by the above inhibitors. These results indicate that the prothrombin-time-derived method is accurate and precise for most routine purposes. Its precision seems inadequate, however, under those conditions where the prothrombin time is prolonged (such as anticoagulant therapy) and in the presence of high fibrinogen levels.

Anticoagulants↗
PubMed1998

Variability in plasma prothrombin concentration: implications for use in epidemiology.

Recent evidence suggests a major role for prothrombin as a risk factor for thrombosis. However, estimating prothrombin levels from a deficient plasma-based clotting assay (factor IIc) is expensive and technically difficult in the setting of population-based research. We report the development of an enzyme-linked immunosorbent assay (ELISA) for prothrombin using purified antigen and polyclonal anti-prethrombin-1 IgG. Three different quality control plasmas had coefficients of variation (CV) of 6.5%, 4.9%, and 4.8%. Analytical recovery averaged 103.8%. Results from the ELISA correlated well with factor IIc results (r=0.75). The 5th-95th percentile range for healthy men (n=10) and women (n=16) was 97.7 pg/ml to 161.8 microg/ml. The assay exhibited no significant cross-reactivity with other vitamin-K-dependent proteins. Prothrombin showed no diurnal variation. In a study of biovariability the analytical variability, CV(A), was 3.1%; the within-subject variability, CV(I), was 7.3%; the between-subject variability, CV(G), was 14.5%. The critical difference for sequential values (i.e. the smallest percentage change unlikely to be due to CV(A) or CV(I)) significant at P=0.05 was 21.9%. The index of individuality, CV(I)/CV(G), was 0.50. On the basis of the overall biovariability data, primarily the index of individuality, prothrombin as measured in our ELISA is well suited for applications in population-based research.

Adult↗
PubMed1998

Ischemic stroke in a young patient with protein C deficiency and prothrombin gene mutation G20210A.

We report a patient who had an ischemic stroke aged 22 years, an inherited type I protein C deficiency and a heterozygous genotype of prothrombin gene 20210A. In view of recent reports of an increased risk for ischemic cerebral vascular disease in patients with the prothrombin 20210A mutation, we suggest that many of the reported cases of ischemic stroke and protein C deficiency may have had additional prothrombotic disorders such as the prothrombin mutation. The current data concerning the magnified risk for stroke in patients with the prothrombin 20210A mutation suggests the need to study all patients with premature stroke for this mutation and the other risk factors for thrombosis. This would include homocysteine, lupus inhibitor, anticardiolipin antibodies, and possibly the natural inhibitors of coagulation. It is possible that patients with the prothrombin 20210A mutation and ischemic cerebral vascular disease would benefit from long-term anticoagulation therapy in a similar way to patients with the antiphospholipid syndrome.

Adult↗
PubMed2000

The A20210 allele in the prothrombin gene enhances the risk of venous thrombosis in carriers of inherited protein S deficiency.

Sixteen families with inherited protein S deficiency and venous thromboembolism (VT) were screened for the presence of factor V (FV) Leiden mutation and for the G20210A allele in the prothrombin gene. While FV Leiden was not detected in any of the families, protein S deficiency and prothrombin mutation were present in five families. To assess the risk of VT in carriers of the combined defects, a total of 92 members of the 16 families, including propositi, were examined. Thirty subjects were normal, 40 showed protein S deficiency, 10 the prothrombin mutation and 12 showed both abnormalities. When index cases were excluded, thrombosis history were present in 40.7% of protein S-deficient patients, 75% of patients with combined abnormality, one out of the 10 (10%) with prothrombin mutation and only one (3.3%) of the normal subjects. Relatives with combined defects showed the highest incidence rate of VT in comparison with normal relatives (rate ratio = 32.4), those with protein S deficiency an intermediate degree (rate ratio = 15.7), and G20210A relatives the lowest (rate ratio = 3.4). Relatives with combined defects had an increased risk of VT in comparison with relatives with protein S deficiency (incidence rate ratio 2.1; 95% confidence interval, 0.7-5.41; P = 0.1). In conclusion, the presence of the prothrombin mutation seems to increase the risk of VT carriers of protein S deficiency, although additional families are required to fully estimate the magnitude of risk.

Adult↗
PubMed2000

Prevalence of factor V Leiden and the G20210A prothrombin-gene mutation in inflammatory bowel disease.

A hypercoagulable state has been hypothesized as a contributing factor in the pathogenesis of inflammatory bowel disease (IBD); moreover, such patients have an increased risk of thrombotic complications. The aim of the present paper was to study the prevalence of the two most important causes of inherited thrombophilia: factor V Leiden and the G20210A prothrombin-gene mutation in patients with Crohn's disease (CD) and ulcerative colitis (UC). Fifty-two patients affected by IBD (33 UC and 19 CD, 16 female and 36 male; mean age, 42 years) and 156 healthy controls (48 female and 108 male; mean age, 37 years) were studied. Seven out of 52 patients (13%) had previous thrombotic events. High molecular weight DNA was analysed for the presence of factor V Leiden and the G20210A prothrombin-gene mutation. One out of 52 IBD patients (1.9%) and three out of 156 control subjects (1.9%) were heterozygous for factor V Leiden. One IBD patient (1.9%) and four healthy controls (2.6%) were heterozygous for the prothrombin-gene mutation. The prevalence of the two mutations was similar in patients and controls. In the subgroup of IBD patients with previous thrombotic events, only one patient was heterozygous for the prothrombin-gene mutation. Factor V Leiden and the G20210A prothrombin-gene mutation do not seem to play a major role in the pathogenesis of IBD or be associated with an increased incidence of thrombotic complications, but with limited data.

Adult↗
PubMed2001

Prevalence of factor V Leiden and prothrombin 20210 A variant in Bulgarian patients with pulmonary thromboembolism and deep venous thrombosis.

Factor V Leiden mutation and prothrombin variant 20210 A are well-known risk factors for venous thrombosis (DVT). Recent papers have reported a lower prevalence of factor V Leiden in patients with pulmonary thromboembolism (PTE) than in patients with deep venous thrombosis. The aim of the present study was to compare the prevalence of factor V Leiden and the prothrombin 20210 G <-- A mutation in patients with DVT and in patients with PTE. We studied 128 consecutive patients (45 with DVT, 40 with PTE, and 43 with DVT and PTE) for factor V Leiden and prothrombin 20210 A. One hundred healthy persons matched by age and sex were used as controls. Factor V Leiden was present in five of the patients with PTE [12.5%; 95% confidence interval (CI), 1.5-23.5%; not significant], 15 of the patients with DVT (33.3%; 95% CI, 9.6-38.7%; P < 0.001), and 12 of the patients with DVT and PTE (27.9%; 95% CI, 4.8-33%; P = 0.001). Results for the prothrombin 20210 A mutation were as follows: four of 40 patients with PTE (10%; 95% CI, 0-13.3%; P = 0.46), nine of 45 (20%) of the patients with DVT (95% CI, 0.5-25.5%; P < 0.05) and eight of 43 with DVT and PTE were heterozygous (18.6%; 95% CI, 0-23.9%; P = 0.02). In conclusion, there is a significantly higher frequency of factor V Leiden among patients with DVT than in patients with PTE. However, there is no significant difference of factor V Leiden or 20210 A prothrombin mutation in patients with DVT than in patients with combined DVT/PTE, therefore patients with DVT, carriers of the mutations, do not appear to be at lower risk for pulmonary embolism.

Adult↗
PubMed1995

Prothrombin fragment 1 + 2 and thrombin-antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases.

OBJECTIVES AND METHODS: The aims of the present work were to assess the presence of thrombin generation in Crohn's disease and in ulcerative colitis by using the prothrombin fragment 1 + 2 and the thrombin-antithrombin III complex assays and to study the possible relationships between these markers and disease activity. RESULTS: Prothrombin fragment 1 + 2 and thrombin-antithrombin III complex were significantly raised in patients with Crohn's disease (n = 69) and with ulcerative colitis (n = 25) as compared with healthy controls (n = 50). In Crohn's disease these two markers of thrombin generation were correlated with the Van Hees index (P < 0.05 and P < 0.001, respectively); values were significantly different from controls even in the patient group displaying the lowest disease activity (P < 0.001). No correlation was found with tumour necrosis factor alpha and C-reactive protein; nevertheless patients with C-reactive protein less than or equal to 10 mg/l had significant lower values of prothrombin fragment 1 + 2 (P < 0.03). In ulcerative colitis prothrombin fragment 1 + 2 and thrombin-antithrombin III complex were significantly increased by comparison with controls, were higher in patients with pancolitis and correlated with C-reactive protein (P < 0.002 and P < 0.009, respectively). CONCLUSION: These data show that prothrombin fragment 1 + 2 and thrombin-antithrombin III complex are increased in inflammatory bowel diseases and suggest that thrombin generation might be an early event in their pathogenesis.

Adolescent↗
PubMed2001

An investigation of the association of the prothrombin G20210A gene mutation and inflammatory bowel disease: Factor II and IBD.

BACKGROUND: A thrombotic etiology for inflammatory bowel disease (IBD) has been proposed as a result of its association with thromboembolic complications, smoking, the oral contraceptive pill, and the response of ulcerative colitis (UC) patients to heparin. We have previously demonstrated an increased prevalence of the Factor V Leiden mutation in UC and wished to investigate the frequency of the recently discovered prothrombin G20210A gene mutation in IBD. The aim of the study was to investigate the hypothesis that the prothrombic state associated with the prothrombin G20210A gene mutation is involved in the etiology of IBD. PATIENTS AND METHODS: A prospective cohort study of patients attending the Bristol Royal Infirmary and Gloucestershire Royal Hospital's IBD clinics was performed. Thirty-nine patients with IBD (24 with Crohn's disease and 15 with UC) and 100 historical controls were screened for the presence of the prothrombin gene mutation using a heteroduplex-based polymerase chain reaction technique. None of the patients with IBD had a personal history of thromboembolism, while three of them had a family history. RESULTS: No IBD patients had the prothrombin gene mutation compared with four (4%) controls (allelic frequency 2%). CONCLUSION: There does not appear to be an association of the prothrombin gene mutation with IBD and therefore it is unlikely to be involved in the etiology of IBD.

Cohort Studies↗
PubMed1980

Characterization of a variant prothrombin in a patient congenitally deficient in factors II, VII, IX and X.

An 18-month-old child, who had no evidence of liver disease, malabsorption, or chronic ingestion of coumarin compounds, was found to have plasma deficiencies of factors II, VII, IX and X. Assays for factor II and X by immunological techniques (antibody neutralization and immunoelectrophoresis) revealed normal or elevated antigenic activity of these factors, suggesting the presence of abnormal protein variants in the patient's plasma. On two-dimensional immunoelectrophoresis of the patient's plasma in calcium, a normal and an abnormal population of prothrombin were seen. The abnormal prothrombin had a mobility more anodal than that of normal prothrombin, but less anodal than that of acarboxyprothrombin. The abnormal prothrombin, in contrast to acarboxyprothrombin, adsorbed readily to both aluminum hydroxide and barium citrate, and could be identified by two-dimensional immunoelectrophoresis of a barium citrate eluate. We suspect that the abnormal variant represents a partially carboxylated prothrombin.

Blood Coagulation Disorders↗
PubMed1984

Quantitation of prothrombin activation products in human urine.

Urine samples obtained from 37 normal individuals have been screened for the presence of prothrombin activation products using radioimmunoassays developed for fragment 1, fragment 2 and prothrombin derivatives bearing the thrombin region. The cross-reacting materials detected in urine were isolated by affinity chromatography on insolubilized antibodies, and analysed by SDS polyacrylamide gel electrophoresis. The only prothrombin derivatives detected were fragment 1 (37/37) and fragment 2 (22/37). The mean values of daily urinary fragment 1 and fragment 2 excretion were respectively 13.4 nM and 1.5 nM. The excretion of prothrombin derivatives has been quantitated in 14 normal pregnant women, during the third trimester of gestation. The mean values of urinary excretion were 47.2 nM per day for fragment 1 (P less than 0.005) and 6.4 nM per day for fragment 2 (P less than 0.05). The significant increase in fragment 1 and fragment 2 excretion observed in a condition known to be associated with the so-called hypercoagulable state suggest that the measurement of prothrombin derivatives in urine could be a useful tool for the non-invasive detection of thromboembolic diseases or prethrombotic states.

Adolescent↗
PubMed1999

Prothrombin and PIVKA-II levels in cord blood from newborn exposed to anticonvulsants during pregnancy.

PURPOSE: To determine whether anticonvulsant exposure during human pregnancy caused an increase of the abnormal form of prothrombin, known as PIVKA-II (prothrombin induced by vitamin K absence for factor II), and a decrease in total prothrombin, in the blood of the newborn. METHODS: Cord blood was collected from the placenta at the time of parturition from 12 women who had received anticonvulsant therapy during pregnancy and from 11 control women. RESULTS: PIVKA-II was present in cord blood from control mothers at low or nondetectable levels. In the same samples, total prothrombin concentrations were approximately 50% of adult levels, but there was wide variation between individuals. Exposure to carbamazepine (CBZ) alone during pregnancy was associated with markedly increased PIVKA-II levels in four of six samples and decreased total prothrombin levels for the whole group. High PIVKA-II levels also were recorded in one cord blood sample from a mother who received phenytoin (PHT) and vigabatrin (VGB). Two cases of PHT alone and one of valproic acid (VPA) alone were not associated with increased PIVKA-II levels. CONCLUSIONS: These results are consistent with the hypothesis that some anticonvulsants (particularly CBZ) interfere with vitamin K metabolism during pregnancy and may result in hematologic signs of vitamin K deficiency in the newborn.

Adult↗
PubMed2005

Vibrio vulnificus secretes a broad-specificity metalloprotease capable of interfering with blood homeostasis through prothrombin activation and fibrinolysis.

Vibrio vulnificus is a causative agent of serious food-borne diseases in humans related to the consumption of raw seafood. It secretes a metalloprotease that is associated with skin lesions and serious hemorrhagic complications. In this study, we purified and characterized an extracellular metalloprotease (designated as vEP) having prothrombin activation and fibrinolytic activities from V. vulnificus ATCC 29307. vEP could cleave various blood clotting-associated proteins such as prothrombin, plasminogen, fibrinogen, and factor Xa, and the cleavage could be stimulated by addition of 1 mM Mn2+ in the reaction. The cleavage of prothrombin produced active thrombin capable of converting fibrinogen to fibrin. The formation of active thrombin appeared to be transient, with further cleavage resulting in a loss of activity. The cleavage of plasminogen, however, did not produce an active plasmin. vEP could cleave all three major chains of fibrinogen without forming a clot. It could cleave fibrin polymer formed by thrombin as well as the cross-linked fibrin formed by factor XIIIa. In addition, vEP could also cleave plasma proteins such as bovine serum albumin and gamma globulin, and its broad specificity is reflected in the cleavage sites, which include Asp207-Phe208 and Thr272-Ala273 bonds in prothrombin and a Tyr80-Leu81 bond in plasminogen. Taken together, the data suggest that vEP is a broad-specificity protease that could function as a prothrombin activator and a fibrinolytic enzyme to interfere with blood homeostasis as part of the mechanism associated with the pathogenicity of V. vulnificus in humans and thereby facilitate the development of systemic infection.

Cations↗