ライフサイエンスコーパス: hypercholesterolaemia

1 y contribute to decreased NO production with hypercholesterolaemia.

2 the ongoing CVD risk in patients with severe hypercholesterolaemia.

3 ity of DNA testing in patients with familial hypercholesterolaemia.

4 to have been largely addressed for familial hypercholesterolaemia.

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

6 e is less common than in homozygous familial hypercholesterolaemia.

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

8 at abnormal platelet Abeta release occurs in hypercholesterolaemia.

9 statins) has revolutionised the treatment of hypercholesterolaemia.

10 ct in the majority of patients with familial hypercholesterolaemia.

11 subsequent type 2 diabetes, hypertension, or hypercholesterolaemia.

12 uction, with fewer MRAEs in individuals with hypercholesterolaemia.

13 earned from observing patients with familial hypercholesterolaemia.

14 icensed specifically for homozygous familial hypercholesterolaemia.

15 ncluded patients who had homozygous familial hypercholesterolaemia.

16 bottom-up proteomics approach in people with hypercholesterolaemia.

17 itor, in patients with heterozygous familial hypercholesterolaemia.

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

19 hypercholesterolaemia or homozygous familial hypercholesterolaemia.

20 nal diseases, diabetes mellitus and familial hypercholesterolaemia.

21 100 mug eprotirome in patients with familial hypercholesterolaemia.

22 rolaemia will improve management of familial hypercholesterolaemia.

23 inhibitor, can reverse the hypertension and hypercholesterolaemia.

24 25-50% in patients with homozygous familial hypercholesterolaemia.

25 rug in the management of homozygous familial hypercholesterolaemia.

26 LDL-C in patients with heterozygous familial hypercholesterolaemia.

27 rug in the management of homozygous familial hypercholesterolaemia.

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

29 (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.

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

31 29 men and women with homozygous familial hypercholesterolaemia, aged 18 years or older, were recr

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

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

34 tations in apoB100 or in LDLR cause familial hypercholesterolaemia, an autosomal dominant disease tha

35 Traditional risk factors, such as hypercholesterolaemia and (systolic) hypertension, are s

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

37 ic cholestasis-like condition with attendant hypercholesterolaemia and an emergent pro-fibrotic, pro-

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

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

40 d self-reported hypertension, heart disease, hypercholesterolaemia and diabetes).

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

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

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

44 l hypercholesterolaemia, autosomal recessive hypercholesterolaemia and familial defective apolipoprot

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

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

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

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

49 ed cardiovascular (CV) risk factors, such as hypercholesterolaemia and obesity, predispose to both IH

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

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

52 2 affected individuals have unusually severe hypercholesterolaemia and require more stringent treatme

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

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

55 the treatment of conditions such as familial hypercholesterolaemia and transthyretin amyloidosis.

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

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

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

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

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

61 Hypertension, hypercholesterolaemia, and type 2 diabetes all explained

62 200 people could have heterozygous familial hypercholesterolaemia, and up to one in 300 000 individu

63 fied and linked to the phenotype of familial hypercholesterolaemia approximately 15 years ago.

64 1000 different molecular causes of familial hypercholesterolaemia are documented in the University C

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

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

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

68 Primary dyslipidaemias, including familial hypercholesterolaemia, are underdiagnosed genetic disord

69 Autosomal recessive hypercholesterolaemia (ARH), characterized clinically by

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

71 ndomised clinical trial included adults with hypercholesterolaemia at high- or very high CV risk.

72 eases such as hypertension, aortic aneurysm, hypercholesterolaemia, atherosclerosis, diabetic vascula

73 included patients with heterozygous familial hypercholesterolaemia, atherosclerotic CV disease (ASCVD

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

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

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

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

78 n, smoking status, type 2 diabetes mellitus, hypercholesterolaemia, cancer and past history of TEE.

79 Undiagnosed familial hypercholesterolaemia carries a high risk of cardiovascu

80 linical case-finding algorithm, the familial hypercholesterolaemia case ascertainment tool (FAMCAT),

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

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

83 vity analyses for LCR restricted to familial hypercholesterolaemia-coded patients (n=581) found assoc

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

85 Systemic immune responses caused by chronic hypercholesterolaemia contribute to atherosclerosis init

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

87 rtension, cardiovascular diseases, diabetes, hypercholesterolaemia, current smoking, obesity, diet an

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

89 Vascular risk factors (hypertension, hypercholesterolaemia, diabetes, obesity, physical inact

90 Median age at familial hypercholesterolaemia diagnosis in adults with obesity w

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

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

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

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

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

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

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

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

99 the greatest number of people with familial hypercholesterolaemia (FH) across different countries.

100 itor cells (HSPCs) of patients with familial hypercholesterolaemia (FH) and healthy normocholesterola

101 Familial hypercholesterolaemia (FH) is a highly prevalent monogen

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

103 Optimal care for familial hypercholesterolaemia (FH) requires patient-centred mana

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

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

106 cally focusing on Fabry Disease and Familial Hypercholesterolaemia (FH).

107 in Australia to detect heterozygous familial hypercholesterolaemia (FH).

108 recent guideline facilitated by the Familial Hypercholesterolaemia Foundation.

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

110 ers (2.2, 1.2-4.0; p=0.013), but not grade 1 hypercholesterolaemia, grade 1-2 hypertriglyceridaemia,

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

112 Autosomal recessive hypercholesterolaemia has been described as a 'phenocopy

113 ce in individuals with heterozygous familial hypercholesterolaemia (HeFH) and whether they confer add

114 Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disorder

115 Homozygous familial hypercholesterolaemia (HoFH) is a rare inherited disorde

116 es clinical guidance for homozygous familial hypercholesterolaemia (HoFH), explains the genetic compl

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

118 d high-sugar diet, are resistant to obesity, hypercholesterolaemia, hypertension, diabetes and athero

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

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

121 sed the ability of FAMCAT to detect familial hypercholesterolaemia (ie, its discrimination) and compa

122 Patients with severe homozygous hypercholesterolaemia illustrate the natural history of

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

124 tients with the highest likelihood of having hypercholesterolaemia in primary care.

125 ecommended methods for detection of familial hypercholesterolaemia in primary care.

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

127 e vast majority of individuals with familial hypercholesterolaemia in the general population remain u

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

129 Early hypercholesterolaemia-induced vascular disease is charac

130 0.93), sleep disorder (IRR 0.74, 0.68-0.80), hypercholesterolaemia (IRR 0.69, 0.60-0.80), diabetes (I

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

132 Familial hypercholesterolaemia is a common autosomal-dominant dis

133 Familial hypercholesterolaemia is a common genetic disorder of li

134 Homozygous familial hypercholesterolaemia is a genetic disorder characterise

135 Hypercholesterolaemia is a major risk factor for cardiov

136 Homozygous familial hypercholesterolaemia is a rare, serious disorder caused

137 Hypercholesterolaemia is an important risk factor for ca

138 Hypercholesterolaemia is associated with decrements in n

139 Hypercholesterolaemia is associated with endothelial dys

140 Hypercholesterolaemia is associated with further impairm

141 Familial hypercholesterolaemia is associated with lifelong elevat

142 Heterozygous familial hypercholesterolaemia is characterised by low cellular u

143 Familial hypercholesterolaemia is common in individuals who had a

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

145 e, which include hypertension, diabetes, and hypercholesterolaemia, is important for timely and effec

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

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

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

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

150 however, little is known about the impact of hypercholesterolaemia on the integrated responses to hea

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

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

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

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

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

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

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

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

159 cade testing has potential value in familial hypercholesterolaemia, or with family or personal histor

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

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

162 ibep were evaluated in heterozygous familial hypercholesterolaemia patients requiring additional LDL-

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

164 Like familial hypercholesterolaemia patients, our familial hypercholes

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

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

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

168 Patients with homozygous familial hypercholesterolaemia respond inadequately to existing d

169 .4% (26.3-28.6) of the 250 573 people in the hypercholesterolaemia sample met the WHO PEN criteria fo

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

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

172 iglyceridaemia (13 [19%] of 69 patients) and hypercholesterolaemia (ten [14%]).

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

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

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

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

177 Abundant data link hypercholesterolaemia to atherogenesis.

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

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

180 Lastly, we link hypercholesterolaemia to perturbed lipid homeostasis in

181 a contribution of diabetes, hypertension and hypercholesterolaemia to the pathophysiology of Alzheime

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

183 In contrast, hypercholesterolaemia was related to lower SUVr values i

184 f more than 1 in 500 (prevalence of familial hypercholesterolaemia), we also assessed sensitivity, sp

185 Smoking, diabetes, hypertension, and hypercholesterolaemia were major risk factors for periph

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

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

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

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

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

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

192 LDL-C in subjects with heterozygous familial hypercholesterolaemia with a safety profile similar to p

193 FAMCAT identifies familial hypercholesterolaemia with greater accuracy than current

194 high risk for ASVCD or heterozygous familial hypercholesterolaemia with LDL cholesterol concentration

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

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

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