Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by Albert Wiegman
Total Records ( 3 ) for Albert Wiegman
  Sung Kee Ryu , Barbara A. Hutten , Maud N. Vissers , Albert Wiegman , John J.P. Kastelein and Sotirios Tsimikas


Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an independent risk factor of cardiovascular disease and a target of treatment. Lp-PLA2 levels in children have not been previously reported. The effect of statin therapy on Lp-PLA2 mass and activity in children with familial hypercholesterolemia (FH) is also not known.


Lp-PLA2 mass and activity levels were measured at baseline and after 2 years in 178 children with FH randomized to pravastatin or placebo and in 78 unaffected and untreated siblings. At the end of the randomized period, all FH children were then placed on pravastatin for an additional 2 years, and Lp-PLA2 mass and activity levels were correlated with changes in carotid intima-media thickness during 4 years of follow-up.


Baseline levels of Lp-PLA2 mass and activity were significantly greater in children with FH compared with unaffected siblings (mass: 240.3 ± 41.6 vs 222.1 ± 36.5 ng/mL, P = .002; activity: 205.7 ± 41.6 vs 124.3±23.0 nmol/min/mL, P < .0001). In the randomized FH cohort, after 2 years treatment, Lp-PLA2 mass (217.8 ± 35.0 vs 231.5 ± 34.8 ng/mL, P = .001) and activity (178.8 ± 37.3 vs 206.2 ± 33.5 nmol/min/mL, P < .0001) were significantly reduced by pravastatin compared with placebo. Change in Lp-PLA2 activity was related to change in low-density lipoprotein cholesterol (pravastatin: r = 0.53, P < .0001, placebo: r = 0.23, P < .001) but change in Lp-PLA2 mass was not related to change in low-density lipoprotein cholesterol. Baseline levels of Lp-PLA2 mass and activity were not significantly associated with carotid intima-media thickness at baseline or at 4 years.


Lp-PLA2 mass and activity are significantly elevated in children with heterozygous FH compared with unaffected siblings and are significantly reduced by pravastatin therapy.

  D. Meeike Kusters , Barbarba A. Hutten , Brian W. McCrindle , David Cassiman , Gordon A. Francis , Claude Gagne , Daniel Gaudet , Katherine M. Morrison , Gisle Langslet , John J. Kastelein and Albert Wiegman


Statin therapy is recommended for children with familial hypercholesterolemia (FH), but most children do not reach treatment targets.


Here we present the design and results at baseline of the ongoing CHARON study, to evaluate the safety and efficacy of rosuvastatin.


This study comprises an international 2-year open label, titration-to-goal study in 198 children with heterozygous FH aged 6 to 18 years, with rosuvastatin in a maximum dose of 10 mg (<10 years of age) or 20 mg (older children). In addition, 64 unaffected siblings were enrolled as controls. The primary efficacy outcome is the change from baseline in low-density lipoprotein cholesterol, and the secondary outcome is the change in carotid intima-media thickness (c-IMT) in patients with FH compared with their siblings. The primary safety outcomes are growth and sexual maturation; secondary outcomes are the change in other lipoprotein levels and the incidence of adverse events, discontinuation rates, and abnormal laboratory values.


At baseline, mean age of patients with FH was 12.1 ± 3.3 years, 44% were boys, and mean low-density lipoprotein cholesterol levels were 6.1 ± 1.3 mmol/L (235.9 ± 48.7 mg/dL). Mean c-IMT was 0.399 mm (95% CI, 0.392-0.406 mm) in children with FH versus 0.377 (95% CI, 0.366-0.388 mm) in unaffected siblings (P = .001).


At baseline, as expected according to on previous observations, children with FH proved to have a greater c-IMT than their healthy siblings. These differences had already occurred at a very young age, which emphasizes the importance of considering early statin initiation in this high-risk population.

  Gerald F. Watts , Samuel Gidding , Anthony S. Wierzbicki , Peter P. Toth , Rodrigo Alonso , W. Virgil Brown , Eric Bruckert , Joep Defesche , Khoo Kah Lin , Michael Livingston , Pedro Mata , Klaus G. Parhofer , Frederick J. Raal , Raul D. Santos , Eric J.G. Sijbrands , William G. Simpson , David R. Sullivan , Andrey V. Susekov , Brian Tomlinson , Albert Wiegman , Shizuya Yamashita and John J.P. Kastelein
  Familial hypercholesterolemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low-density lipoprotein cholesterol and causes premature coronary heart disease. There are at least 20 million people with FH worldwide, but the majority remains undetected, and current treatment is often suboptimal. To address this major gap in coronary prevention we present, from an international perspective, consensus-based guidance on the care of FH. The guidance was generated from seminars and workshops held at an international symposium. The recommendations focus on the detection, diagnosis, assessment, and management of FH in adults and children and set guidelines for clinical purposes. They also refer to best practice for cascade screening and risk notifying and testing families for FH, including use of genetic testing. Guidance on treatment is based on risk stratification, management of noncholesterol risk factors, and the safe and effective use of low-density lipoprotein-lowering therapies. Recommendations are given on lipoprotein apheresis. The use of emerging therapies for FH is also foreshadowed. This international guidance acknowledges evidence gaps but aims to make the best use of contemporary practice and technology to achieve the best outcomes for the care of FH. It should accordingly be used to inform clinical judgment and be adjusted for country-specific and local healthcare needs and resources.
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility