ライフサイエンスコーパス: factor V Leiden

1 tion in the factor V molecule: Arg506-->Gln (factor V Leiden).

2 sm (VTE), both alone and in combination with factor V Leiden.

3 E, particularly among those who co-inherited factor V Leiden.

4 agnitude than risk estimates associated with factor V Leiden.

5 protein-S deficiency, and 2.0 (0.5-7.7) with factor V Leiden.

6 eterozygous or homozygous (n=47) carriers of factor V Leiden.

7 VIIIa, and APC resistance is often caused by factor V Leiden.

8 resistance independently of the presence of factor V Leiden.

9 ociated with age, overweight or obesity, and factor V Leiden.

10 were not risk factors except in carriers of factor V Leiden.

11 trast, thrombogenic effects in patients with factor V-Leiden.

12 ls carried both the prothrombin mutation and factor V Leiden (5 controls and 4 cases).

13 A mutation in the Factor V gene (Factor V Leiden), a variant in the 5,10-methylenetetrahy

14 of 186 white control subjects possessed the factor V Leiden allele (P <.001; odds ratio, 17.1; 95% c

15 No factor V Leiden alleles were detected in 19 white TM pat

16 Studies examining the role of factor V Leiden among patients at higher risk of atherot

17 th VTE but was less common than heterozygous factor V Leiden and heterozygous prothrombin gene mutati

18 of synthetic nucleic acid targets including Factor V Leiden and methylenetetrahydrofolate reductase.

19 T and the presence or absence of coagulation factor V Leiden and prothrombin 20210 G-->A variants amo

20 Discovery of the factor V Leiden and prothrombin G20210A mutations has gr

21 genetic factors involved in thrombotic risk, factor V Leiden and prothrombin G20210A.

22 These data indicate that the prevalence of Factor V Leiden and the V allele of the MTHFR gene is lo

23 notyped for the prothrombin mutation and for factor V Leiden and were followed prospectively for recu

24 C associated with an abnormal factor V gene (factor V Leiden), and prothrombin gene variant 20210A, h

25 relation of moderate hyperhomocyst(e)inemia, factor V Leiden, and risk of VTE in the general populati

26 (1) report that thrombotic disorders such as factor V Leiden are often treated with drugs like low mo

27 Defects in this mechanism (eg, factor V Leiden) are associated with thrombosis but resu

28 ain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of veno

29 ge site and is the only mutation, other than factor V Leiden (Arg506-->Gln), that has been found in a

30 in the heterozygous form in combination with factor V Leiden (Arg506Gln).

31 The effect of prothrombotic polymorphism, factor V Leiden (Arg506Gln; FV Leiden), was examined in

32 Using a murine model of factor V Leiden-associated placental failure, we show th

33 d normal factor Va as well as membrane-bound factor V(LEIDEN) by APC at Arg(306) is required for the

34 -1.72), but double heterozygotes for HR2 and factor V Leiden carried an OR of idiopathic VTE of 16.3

35 As has already been shown, heterozygous factor V Leiden carrier status improves the survival of

36 The effect of the factor V Leiden carrier status in severe sepsis in the P

37 nvestigated the hypothesis that heterozygous factor V Leiden carrier status might protect against the

38 e survival benefit derived from heterozygous factor V Leiden carrier status was only evident at doses

39 vival advantage associated with heterozygous factor V Leiden carrier status.

40 The proportion of factor V Leiden carriers in patients with severe sepsis

41 Therefore, factor V Leiden carriers should not be excluded from thi

42 No homozygous factor V Leiden carriers were identified.

43 those without), and inherited thrombophilia (factor V Leiden carriers with a 10-year cumulative incid

44 tein C (drotrecogin alfa [activated]) as non-factor V Leiden carriers.

45 (95% CI, 2.20-6.12) in participants carrying factor V Leiden compared with noncarriers.

46 When the factor V(LEIDEN) concentration was varied from 50% to 15

47 A situation was found to be dependent on the factor V(LEIDEN) concentration.

48 in patients with severe sepsis suggest that factor V Leiden constitutes a rare example of a balanced

49 edication was rivaroxaban for her homozygous Factor V Leiden deficiency.

50 Previous findings in the mouse factor V Leiden endotoxemia model and in patients with s

51 Factor V Leiden enhanced the hormone-associated risk of

52 Factor V Leiden (F5(L) ) is a common genetic risk factor

53 Factor V Leiden (factor V Arg506Gln), the genetic defect

54 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210

55 m (hepatic lipase, APOE, PON1) and clotting (factor V Leiden, fibrinogen).

56 bolism (VTE) and potential interactions with factor V Leiden (FV:Q506) and prothrombin G --> A 20210,

57 Factor V(Leiden) (fV(Leiden)) predisposes to thrombosis

58 ysed for two specific common gene mutations, factor V Leiden (FVL) and prothrombin G20210A (PGM), whi

59 Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor fo

60 Factor V Leiden (FVL) is a common genetic risk factor fo

61 We describe a mouse model of fetal loss in factor V Leiden (FvL) mothers in which fetal loss is tri

62 The factor V Leiden (FVL) mutation is associated with vascul

63 n the second eye because of the heterozygous factor V Leiden (FVL) mutation.

64 nous thromboembolism (VTE) in relatives with factor V Leiden (FVL) or G20210A prothrombin (PT20210A)

65 A well-known example is the factor V Leiden (FVL) paradox: the FVL mutation poses a

66 rdiac surgery, we tested the hypothesis that factor V Leiden (FVL), a common coagulation factor polym

67 anticardiolipin antibodies and genotyping of factor V Leiden (FVL), factor II G20210A (FII), and meth

68 A polymorphism in coagulation factor V, factor V Leiden (FVL), is the major known genetic risk f

69 gle gene mutation in factor V, the so called factor V Leiden (FVL), is the most common cause of throm

70 The factor V Leiden (FVL; rs6025) and prothrombin G20210A (P

71 Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation

72 blood samples, which were used to determine factor V Leiden, G20210A prothrombin, and 677C>T MTHFR p

73 On a factor V(Leiden) genetic background, ZPI deficiency prod

74 show for the first time that a heterozygous factor V Leiden genotype is associated with improved 30-

75 rare familial homocystinuria who also carry factor V Leiden have an increased incidence of venous th

76 Tm estimates from melting curve analysis for factor V Leiden, hemoglobin C, hemoglobin S, the thermol

77 Compared with non-Leiden carriers, factor V Leiden heterozygous carriers may have a slightl

78 ation-based prospective studies, we measured factor V Leiden, HR2 haplotype, activated protein C (APC

79 No interaction was found for factor V Leiden in either hypertensive or nonhypertensiv

80 clinicians considering whether to screen for factor V Leiden in high-risk groups such as those with p

81 V(LEIDEN) level to understand the effect of factor V(LEIDEN) in hemophilia A patients.

82 We conclude that factor V Leiden increases the risk of MI in young women.

83 To assess whether factor V Leiden increases the risk of myocardial infarct

84 These data indicate that prevalence of factor V Leiden is greater among Caucasians than minorit

85 This mutation, factor V Leiden, is found in 4% to 6% of the U.S. popula

86 ied by a quantitative analysis of the plasma factor V(LEIDEN) level to understand the effect of facto

87 These findings suggest that factor V Leiden may be a pathogenic risk factor in TM pa

88 lerotic plaque rupture, we hypothesized that factor V Leiden may be a stronger risk factor for athero

89 The survival of homozygous factor V Leiden mice did not differ from that of normal

90 polysaccharide, the survival of heterozygous factor V Leiden mice did not differ from that of wild-ty

91 els (thrombomodulin-deficient TMPro mice and factor V Leiden mice), in which the endogenous protein C

92 factor V proteolysis by activated protein C (factor V Leiden mice), were employed.

93 relative survival advantage of heterozygous factor V Leiden mice.

94 e severity of the prothrombotic phenotype of factor V(Leiden) mice.

95 18.2%) as compared to those with an isolated factor V Leiden mutation (19.2%).

96 of this study was to investigate whether the factor V Leiden mutation (Arg506Gln) is associated with

97 with severe thrombophilia such as homozygous factor V Leiden mutation (FVL) depend on a positive fami

98 rvival was significantly associated with the factor V Leiden mutation (p = .049).

99 The factor V Leiden mutation (R506Q), a prothrombotic gene p

100 IBD controls (4%) were heterozygotes for the factor V Leiden mutation (relative risk, 14.00; 95% conf

101 The discoveries of the factor V Leiden mutation and the prothrombin gene varian

102 d risk of thrombosis for women who carry the factor V Leiden mutation and use oral contraceptive pill

103 reports suggest that younger carriers of the factor V Leiden mutation are at greater risk for venous

104 proved survival of mice heterozygous for the factor V Leiden mutation complements results from the an

105 Prevalence of factor V Leiden mutation determined by a second-generati

106 confirm that carriers of this prothrombotic factor V Leiden mutation do not have an increased risk o

107 Factor V Leiden mutation does not seem to increase risks

108 Among nonsmokers the factor V Leiden mutation had little effect (odds ratio 1

109 , we determined total homocysteine level and factor V Leiden mutation in baseline blood samples from

110 The high prevalence of the factor V Leiden mutation in certain populations has prom

111 ly relevant than genetic testing to detect a factor V Leiden mutation in identifying persons who are

112 differences between men with and without the factor V Leiden mutation increased significantly with ag

113 thromboembolism in heterozygous carriers of factor V Leiden mutation increased with age at a rate si

114 Factor V Leiden mutation is associated with three- to si

115 different species strongly suggest that the factor V Leiden mutation is indeed a potent modifier of

116 The factor V Leiden mutation is not a significant risk facto

117 data are compatible with the hypothesis that factor V Leiden mutation may play a role in some cases o

118 f APC activity, in mice either harboring the factor V Leiden mutation or infused with an APC-blocking

119 es of thromboembolic disease associated with factor V Leiden mutation or resistance to activated prot

120 The presence of factor V Leiden mutation predisposes patients to venous

121 In patients with IBD, inheritance of the factor V Leiden mutation results in a significant increa

122 ymerase chain reaction was used to determine factor V Leiden mutation status in 156 study participant

123 k factors and indicate that determination of factor V Leiden mutation status should not be limited to

124 The presence of the factor V Leiden mutation was determined by coagulation a

125 The factor V Leiden mutation was found more often in women w

126 Prevalence of the factor V Leiden mutation was greater among case-patients

127 The factor V Leiden mutation was not associated with a signi

128 The factor V Leiden mutation was not significantly associate

129 A factor V Leiden mutation was present in 6 patients, prot

130 in III, and the translational product of the factor V Leiden mutation were isolated by recycling immu

131 rioperative prophylaxis in patients with the factor V Leiden mutation who are undergoing hip or knee

132 were similar in men with and men without the factor V Leiden mutation who were younger than 50 years

133 he incidence and possible association of the factor V Leiden mutation with the development of thrombo

134 Thus, some 80% of all carriers of the factor V Leiden mutation would be detected if screening

135 an Arg506Gln mutation in the factor V gene (factor V Leiden mutation) is the most common cause of fa

136 ithrombin III, to a translational product of factor V Leiden mutation, and to proteins C and S in chi

137 ratory abnormality of activated protein C or factor V Leiden mutation.

138 hemorrhagic stroke who are heterozygous for factor V Leiden mutation.

139 ic cerebral palsy, placental thrombosis, and factor V Leiden mutation.

140 Genotyping for the factor V Leiden mutation.

141 For idiopathic VTE, in addition to the factor V (Leiden) mutation (odds ratio [OR], 5.13; 95% c

142 esented data support the hypothesis that the factor V(LEIDEN) mutation can increase thrombin formatio

143 ate to severe hemophilia A combined with the factor V(LEIDEN) mutation in vitro in a reconstituted mo

144 severe hemophilia were heterozygous for the factor V(LEIDEN) mutation, which leads to the substituti

145 of thrombin formation was observed with the factor V(LEIDEN) mutation.

146 that the system successfully identified the factor V Leiden mutations from human blood specimens.

147 sk of venous thrombosis in IBD patients with factor V Leiden of 23 (95% confidence interval, 2-294; P

148 cts and fetal loss in a cohort of women with factor V Leiden or deficiency of antithrombin, protein C

149 first-degree relatives of an index case with factor V Leiden or the prothrombin 20210A gene variant,

150 g and old patients of both sexes, those with factor V Leiden or the prothrombin gene mutation, and th

151 3 (CI, 0.50 to 1.39) among women with either factor V Leiden or the prothrombin mutation and 1.36 (CI

152 Women with either factor V Leiden or the prothrombin mutation had a 49% ha

153 embolism risk to carriers of the established factor V Leiden p.R506Q and prothrombin G20210A mutation

154 onwhite ethnicity, heterozygous carriers for factor V Leiden (P=0.001) and obesity (P=0.002) are sign

155 sk, mass screening of asymptomatic women for factor V Leiden prior to prescribing oral contraceptive

156 nce of such genetic thrombophilia markers as factor V Leiden, prothrombin 20210A mutation, and antiph

157 d adjustment for sex, race, body mass index, factor V Leiden, prothrombin 20210A, and elevated factor

158 Available evidence indicates that factor V Leiden, prothrombin 20210A, and lipoprotein (a)

159 hereditary thrombophilic defects, including factor V Leiden, prothrombin G20210A defect, and deficie

160 philic risk factors prevalent in Caucasians (factor V Leiden, Prothrombin G20210A) are distinctly rar

161 rrent use of a panel of three genetic tests (factor V Leiden, prothrombin variant G20210A, and protei

162 hisms that increase coagulability, including factor V Leiden R506G, factor II (prothrombin) G20210A,

163 aller in magnitude than that associated with factor V Leiden (RR=3.0, P<0.001).

164 Participating studies genotyped factor V Leiden status and shared risk estimates for the

165 The combined data on factor V Leiden status from 3894 adult patients with sev

166 Routine assessment of factor V Leiden status is unlikely to improve atherothro

167 complements results from the analysis of the factor V Leiden subgroup of patients enrolled in the PRO

168 The striking magnitude of the factor V Leiden survival benefit in the initial PROWESS

169 roves pregnancy outcome in a murine model of factor V Leiden that is unrelated to its anticoagulation

170 he combination of high factor V antigen plus factor V Leiden the OR of idiopathic VTE was 11.5 (95% C

171 clinical risk factors for post-COVID-19 VTE; factor V Leiden thrombophilia was additionally associate

172 68 Caucasian Americans, carrier frequency of factor V Leiden was 5.27% (95% confidence interval [CI],

173 several pregnancy losses, the prevalence of factor V Leiden was increased 2.2-fold (P = 0.026).

174 Thus, prevalence of factor V Leiden was less among minority subjects (P=.001

175 Factor V Leiden was not associated with increased risk o

176 Factor V Leiden was not associated with the combined out

177 The prevalence of factor V Leiden was significantly increased among the wh

178 Factor V Leiden was unrelated to venous thrombosis, but

179 n the general population, APC resistance and factor V Leiden were important VTE risk factors; homozyg