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 agnitude than risk estimates associated with factor V Leiden.

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

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

5 resistance independently of the presence of factor V Leiden.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 -1.72), but double heterozygotes for HR2 and factor V Leiden carried an OR of idiopathic VTE of 16.3

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

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

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

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

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

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

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

38 No homozygous factor V Leiden carriers were identified.

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

40 (95% CI, 2.20-6.12) in participants carrying factor V Leiden compared with noncarriers.

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

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

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

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

45 Factor V Leiden enhanced the hormone-associated risk of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 relative survival advantage of heterozygous factor V Leiden mice.

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

86 18.2%) as compared to those with an isolated factor V Leiden mutation (19.2%).

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

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

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

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

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

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

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

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

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

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

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

98 Factor V Leiden mutation does not seem to increase risks

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 The factor V Leiden mutation was not significantly associate

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

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

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

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

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

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

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

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

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

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

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

130 Genotyping for the factor V Leiden mutation.

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

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

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

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

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

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

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

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

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

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

141 3 (CI, 0.50 to 1.39) among women with either factor V Leiden or the prothrombin mutation and 1.36 (CI

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 68 Caucasian Americans, carrier frequency of factor V Leiden was 5.27% (95% confidence interval [CI],

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

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

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

162 Factor V Leiden was unrelated to venous thrombosis, but

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