نتایج جستجو برای: familial hypercholesterolemia fh

تعداد نتایج: 68801  

2014
Michela Zanetti Mariagrazia Zenti Rocco Barazzoni Federica Zardi Annamaria Semolic Michele Giuseppe Messa Filippo Mearelli Gianpaolo Russi Maurizio Fonda Luca Scarano Enzo Bonora Luigi Cattin

BACKGROUND Pentraxin 3 (PTX3), a key component of the humoral arm of innate immunity, is secreted by vascular cells in response to injury, possibly aiming at tuning arterial activation associated with vascular damage. Severe hypercholesterolemia as in familial hypercholesterolemia (FH) promotes vascular inflammation and atherosclerosis; low-density lipoprotein (LDL) apheresis is currently the t...

2014
Pezhman Fard-Esfahani Shohreh Khatami

Background and Objective: Familial hypercholesterolemia (FH) is an autosomal trait, which is caused by mutations in Low Density Lipoprotein Receptor (LDLR) gene. FH penetrance is about 100% and worldwide prevalence for heterozygous subjects is almost 1 in 500 and for homozygous 1 in 1,000,000. The patients are at risk of premature coronary heart disease (CHD) due to defective LDLR and hence cho...

2016
Chen Zhao Mingxiang Kong Li Cao Qiong Zhang Yong Fang Weiwei Ruan Xiaofan Dou Xiaohui Gu Qing Bi

A 23-year-old male patient presented with multiple large masses in his elbows, buttocks, knees, Achilles tendons, feet, shoulders and hands. The large masses in the elbows and buttocks measured ~6×5×5 cm and ~7×5×4 cm, respectively. The patient presented with an elevated level of low-density lipoprotein cholesterol, and had been previously diagnosed with homozygous familial hypercholesterolemia...

2017
Alberico Luigi Catapano Angela Pirillo Giuseppe Danilo Norata

Heterozygous familial hypercholesterolemia (FH) is a genetic disorder characterized by high low-density lipoprotein cholesterol levels from birth, which exposes the arteries to high levels of atherogenic lipoproteins lifelong and results in a significantly increased risk of premature cardiovascular events. The diagnosis of FH, followed by an appropriate and early treatment is critical to reduce...

Journal: :Clinical chemistry 2015
Marta Futema Sonia Shah Jackie A Cooper KaWah Li Ros A Whittall Mahtab Sharifi Olivia Goldberg Euridiki Drogari Vasiliki Mollaki Albert Wiegman Joep Defesche Maria N D'Agostino Antonietta D'Angelo Paolo Rubba Giuliana Fortunato Małgorzata Waluś-Miarka Robert A Hegele Mary Aderayo Bamimore Ronen Durst Eran Leitersdorf Monique T Mulder Jeanine E Roeters van Lennep Eric J G Sijbrands John C Whittaker Philippa J Talmud Steve E Humphries

BACKGROUND Familial hypercholesterolemia (FH) is an autosomal-dominant disorder caused by mutations in 1 of 3 genes. In the 60% of patients who are mutation negative, we have recently shown that the clinical phenotype can be associated with an accumulation of common small-effect LDL cholesterol (LDL-C)-raising alleles by use of a 12-single nucleotide polymorphism (12-SNP) score. The aims of the...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2008
Joel D Morrisett Kasey C Vickers

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Awan and coworkers1 describe the study of 25 homozygous familial hypercholesterolemic (FH) patients aged 5 to 54 years. Eighteen of the patients had aortic calcification scores 1000. The inference of this study is a strong linkage between homozygous FH and premature aortic calcification. Bazan et al2 have recently described th...

2015
Chang Ho Ahn Sung Hee Choi

Statins have been shown to be very effective and safe in numerous randomized clinical trials, and became the implacable first-line treatment against atherogenic dyslipidemia. However, even with optimal statin treatment, 60% to 80% of residual cardiovascular risk still exists. The patients with familial hypercholesterolemia which results in extremely high level of low density lipoprotein cholest...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2000
H G Kraft A Lingenhel F J Raal M Hohenegger G Utermann

Lipoprotein(a) [Lp(a)] is a quantitative genetic trait that in the general population is largely controlled by 1 major locus-the locus for the apolipoprotein(a) [apo(a)] gene. Sibpair studies in families including familial defective apolipoprotein B or familial hypercholesterolemia (FH) heterozygotes have demonstrated that, in addition, mutations in apolipoprotein B and in the LDL receptor (LDL...

Journal: :Atherosclerosis 2017
Mafalda Bourbon Ana Catarina Alves Rodrigo Alonso Nelva Mata Pedro Aguiar Teresa Padró Pedro Mata

BACKGROUND AND AIMS Familial hypercholesterolemia (FH) is an autosomal dominant disease of cholesterol metabolism that confers an increased risk of premature atherosclerotic cardiovascular disease (ASCVD). Therefore, early identification and treatment of these patients can improve prognosis and reduce the burden of cardiovascular mortality. The aim of this work was to perform the mutational ana...

2015
Venkat M. Ramakrishnan Jeong-Yeh Yang Kevin T. Tien Thomas R. McKinley Braden R. Bocard John G. Maijub Patrick O. Burchell Stuart K. Williams Marvin E. Morris James B. Hoying Richard Wade-Martins Franklin D. West Nolan L. Boyd

Acquiring sufficient amounts of high-quality cells remains an impediment to cell-based therapies. Induced pluripotent stem cells (iPSC) may be an unparalleled source, but autologous iPSC likely retain deficiencies requiring correction. We present a strategy for restoring physiological function in genetically deficient iPSC utilizing the low-density lipoprotein receptor (LDLR) deficiency Familia...

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