ライフサイエンスコーパス: hypercholesterolaemia

1 icensed specifically for homozygous familial hypercholesterolaemia.

2 to have been largely addressed for familial hypercholesterolaemia.

3 ibed as a 'phenocopy' of homozygous familial hypercholesterolaemia.

4 e is less common than in homozygous familial hypercholesterolaemia.

5 abetes, end-stage renal failure and familial hypercholesterolaemia.

6 at abnormal platelet Abeta release occurs in hypercholesterolaemia.

7 statins) has revolutionised the treatment of hypercholesterolaemia.

8 ct in the majority of patients with familial hypercholesterolaemia.

9 ncluded patients who had homozygous familial hypercholesterolaemia.

10 bottom-up proteomics approach in people with hypercholesterolaemia.

11 itor, in patients with heterozygous familial hypercholesterolaemia.

12 holesterol (LDL-C) in patients with familial hypercholesterolaemia.

13 hypercholesterolaemia or homozygous familial hypercholesterolaemia.

14 nal diseases, diabetes mellitus and familial hypercholesterolaemia.

15 100 mug eprotirome in patients with familial hypercholesterolaemia.

16 rolaemia will improve management of familial hypercholesterolaemia.

17 inhibitor, can reverse the hypertension and hypercholesterolaemia.

18 25-50% in patients with homozygous familial hypercholesterolaemia.

19 rug in the management of homozygous familial hypercholesterolaemia.

20 LDL-C in patients with heterozygous familial hypercholesterolaemia.

21 rug in the management of homozygous familial hypercholesterolaemia.

22 y contribute to decreased NO production with hypercholesterolaemia.

23 the ongoing CVD risk in patients with severe hypercholesterolaemia.

24 ity of DNA testing in patients with familial hypercholesterolaemia.

25 ascular disease (0.27, 0.17-0.45; p<0.0001), hypercholesterolaemia (0.53, 0.40-0.70; p<0.0001), and h

26 (1.55 [1.42-1.71] vs 1.36 [1.24-1.50]), and hypercholesterolaemia (1.19 [1.07-1.33] vs 1.14 [1.03-1.

27 ed adverse events among the 54 patients were hypercholesterolaemia (39 [72%] of 54 patients), hypertr

28 29 men and women with homozygous familial hypercholesterolaemia, aged 18 years or older, were recr

29 S: 29 men and women with homozygous familial hypercholesterolaemia, aged 18 years or older, were recr

30 found in patients with the disease familial hypercholesterolaemia alter residues that directly coord

31 cholesterolaemia liver chimeric mice develop hypercholesterolaemia and a 'humanized' serum profile, i

32 e(-/-) and Ldlr(-/-) mice does not attenuate hypercholesterolaemia and atherosclerosis.

33 confirm their effects in homozygous familial hypercholesterolaemia and clinical endpoint trials will

34 ction in patients with heterozygous familial hypercholesterolaemia and elevated LDL-C treated with hi

35 B-19), which exhibits hypertriglyceridaemia, hypercholesterolaemia and elevated levels of plasma apoB

36 ed for identifying individuals with familial hypercholesterolaemia and exploring the implications tha

37 l hypercholesterolaemia, autosomal recessive hypercholesterolaemia and familial defective apolipoprot

38 im to define a phenotype for severe familial hypercholesterolaemia and identify people at highest ris

39 e treatment of choice in homozygous familial hypercholesterolaemia and in autosomal recessive hyperch

40 d in mendelian disorders, including familial hypercholesterolaemia and insulin-resistant diabetes.

41 e enrolled adults with heterozygous familial hypercholesterolaemia and LDL-C concentrations of 2.6 mm

42 ure to the inflammatory responses induced by hypercholesterolaemia and offers the hypothesis that inf

43 lipoprotein apheresis in homozygous familial hypercholesterolaemia and patients with coronary disease

44 2 affected individuals have unusually severe hypercholesterolaemia and require more stringent treatme

45 uce LDL-C levels in both homozygous familial hypercholesterolaemia and severe heterozygous familial h

46 patients - particularly those with familial hypercholesterolaemia and those with statin intolerance.

47 clinical criteria for heterozygous familial hypercholesterolaemia and were on stable lipid-lowering

48 older, diagnosed with heterozygous familial hypercholesterolaemia, and had not reached target LDL ch

49 to pathologies like cancer, atherosclerosis, hypercholesterolaemia, and infectious diseases.

50 with more fractures, musculoskeletal events, hypercholesterolaemia, and strokes with anastrozole and

51 ng DNA testing for the diagnosis of familial hypercholesterolaemia, and subsequent cascade testing ha

52 200 people could have heterozygous familial hypercholesterolaemia, and up to one in 300 000 individu

53 1000 different molecular causes of familial hypercholesterolaemia are documented in the University C

54 hological impacts of a diagnosis of familial hypercholesterolaemia are in line with the risks associa

55 cent advances in its application to familial hypercholesterolaemia are reviewed to identify potential

56 Mid-life diabetes, hypertension and hypercholesterolaemia are risk factors for the developme

57 Autosomal recessive hypercholesterolaemia (ARH), characterized clinically by

58 plementation of cascade testing for familial hypercholesterolaemia as being feasible and cost-effecti

59 agement of patients with homozygous familial hypercholesterolaemia, autosomal recessive hypercholeste

60 as a potential drug target for treatment of hypercholesterolaemia, because inhibition of ASBT reduce

61 tients with a clinical diagnosis of familial hypercholesterolaemia, but no identified rare mutation i

62 We assessed the hypothesis that familial hypercholesterolaemia can also be caused by an accumulat

63 Undiagnosed familial hypercholesterolaemia carries a high risk of cardiovascu

64 ing hepatocytes from a patient with familial hypercholesterolaemia caused by loss-of-function mutatio

65 no identified rare mutation in the familial hypercholesterolaemia-causing genes, LDL receptor, apoli

66 anagement of patients with severe homozygous hypercholesterolaemia continues to be a major challenge.

67 risation of individuals with severe familial hypercholesterolaemia could improve resource use.

68 utation in the LDL receptor gene in familial hypercholesterolaemia determines clinical variability ha

69 ce that some patients with clinical familial hypercholesterolaemia do not have detectable defects in

70 gnificant proportion of patients with severe hypercholesterolaemia do not reach treatment goals and c

71 itors of ASBT, and ASBT is thus a target for hypercholesterolaemia drugs.

72 Our results suggest that maternal hypercholesterolaemia during pregnancy induces changes i

73 fetuses and is greatly increased by maternal hypercholesterolaemia during pregnancy.

74 cular disease and may provide a link between hypercholesterolaemia, endothelial dysfunction, hyperten

75 subset of patients with homozygous familial hypercholesterolaemia enrolled in an open-label, non-ran

76 In patients with heterozygous familial hypercholesterolaemia, evolocumab administered either 14

77 Typically, autosomal dominant familial hypercholesterolaemia (FH) is caused by mutations in the

78 known to be the underlying cause of familial hypercholesterolaemia (FH), but mutations of this type c

79 veral metabolic diseases, including familial hypercholesterolaemia (FH).

80 recent guideline facilitated by the Familial Hypercholesterolaemia Foundation.

81 assembled a sample of patients with familial hypercholesterolaemia from three UK-based sources and co

82 vascular function of children with familial hypercholesterolaemia has been demonstrated, but extensi

83 Autosomal recessive hypercholesterolaemia has been described as a 'phenocopy

84 ore of the cardiovascular risk factors (e.g. hypercholesterolaemia, hypertension).

85 amily history of premature coronary disease, hypercholesterolaemia, hypertension, or diabetes.

86 nal and neuropsychiatric complaints, or with hypercholesterolaemia, hyponatraemia, hyperprolactinaemi

87 Patients with severe homozygous hypercholesterolaemia illustrate the natural history of

88 nt KIAA0196 (strumpellin) is associated with hypercholesterolaemia in humans.

89 nal antibody against PCSK9, in patients with hypercholesterolaemia in the absence of concurrent lipid

90 rther assessment of ALN-PCS in patients with hypercholesterolaemia, including those being treated wit

91 Early hypercholesterolaemia-induced vascular disease is charac

92 Since hypercholesterolaemia is a chronic condition, the long-t

93 Familial hypercholesterolaemia is a common autosomal-dominant dis

94 Familial hypercholesterolaemia is a common genetic disorder of li

95 Homozygous familial hypercholesterolaemia is a genetic disorder characterise

96 Hypercholesterolaemia is a major risk factor for cardiov

97 Homozygous familial hypercholesterolaemia is a rare, serious disorder caused

98 Hypercholesterolaemia is associated with endothelial dys

99 Familial hypercholesterolaemia is associated with lifelong elevat

100 Heterozygous familial hypercholesterolaemia is characterised by low cellular u

101 Familial hypercholesterolaemia is common in individuals who had a

102 characterized clinically by severe inherited hypercholesterolaemia, is caused by recessive null mutat

103 hypercholesterolaemia patients, our familial hypercholesterolaemia liver chimeric mice develop hyperc

104 o on to replace the missing LDLR in familial hypercholesterolaemia liver chimeric mice using an adeno

105 Individuals with severe familial hypercholesterolaemia might benefit in particular from e

106 luding cardiovascular disease (hypertension, hypercholesterolaemia, myocardial infarctions, and strok

107 clinical diagnosis of heterozygous familial hypercholesterolaemia, on optimum lipid-lowering treatme

108 (aged >/=12 years) with homozygous familial hypercholesterolaemia, on stable lipid-regulating therap

109 th darunavir, or who had homozygous familial hypercholesterolaemia or any condition causing secondary

110 to regular statin treatment in patients with hypercholesterolaemia or at high risk of cardiovascular

111 y in those with severe heterozygous familial hypercholesterolaemia or homozygous familial hypercholes

112 nd to have the most severe forms of familial hypercholesterolaemia or markedly elevated LDL cholester

113 In patients with heterozygous familial hypercholesterolaemia or statin intolerance antibody-bas

114 or more (or >/=28 kg/m(2) with hypertension, hypercholesterolaemia, or diabetes) registered online wi

115 ypes of heterozygous and homozygous familial hypercholesterolaemia overlap considerably; the response

116 rcholesterolaemia and in autosomal recessive hypercholesterolaemia patients in whom maximal drug ther

117 equally acceptable for relatives of familial hypercholesterolaemia patients to be contacted by health

118 Like familial hypercholesterolaemia patients, our familial hypercholes

119 level and on reducing lipid peroxidation in hypercholesterolaemia rabbit, thereby preventing the for

120 In patients with homozygous familial hypercholesterolaemia receiving stable background lipid-

121 ein S deficiency, haemophilia B and familial hypercholesterolaemia, respectively.

122 Patients with homozygous familial hypercholesterolaemia respond inadequately to existing d

123 phenotypes are similar, autosomal recessive hypercholesterolaemia seems to be less severe, more vari

124 aneurysms such as smoking, hypertension and hypercholesterolaemia should be part of the management o

125 eptor (LDLR), the many mutations in familial hypercholesterolaemia that map to the YWTD domain can no

126 ore than 90% of these clearly cause familial hypercholesterolaemia, the remainder require careful int

127 ful in reducing the risk for CHD in familial hypercholesterolaemia, there have been difficulties in g

128 sterolaemia and severe heterozygous familial hypercholesterolaemia, thus reducing the risk for premat

129 Abundant data link hypercholesterolaemia to atherogenesis.

130 There is abundant evidence that links hypercholesterolaemia to both vascular inflammation and

131 the strongest clinical suspicion of familial hypercholesterolaemia to more than 70-80%.

132 In patients with heterozygous familial hypercholesterolaemia, treatment with anacetrapib for 1

133 FINDINGS: 631 patients with hypercholesterolaemia were randomly assigned to AMG 145

134 rol concentrations in patients with familial hypercholesterolaemia when added to conventional statin

135 sease may share some risk factors, including hypercholesterolaemia which is associated with increased

136 d 12 years or older with homozygous familial hypercholesterolaemia who were on stable LDL cholesterol

137 ents with cardiovascular disease or familial hypercholesterolaemia whose LDL cholesterol levels are i

138 r availability of guidance to treat familial hypercholesterolaemia will improve management of familia

139 re distribution among patients with familial hypercholesterolaemia with no confirmed mutation, those

140 esterol in patients with homozygous familial hypercholesterolaemia, with or without apheresis.

141 tantial proportion of patients with familial hypercholesterolaemia without a known mutation, their ra