Frequency of Low-Density Lipoprotein Receptor Gene Mutations in Patients With a Clinical Diagnosis of Familial Combined Hyperlipidemia in a Clinical Setting
Fernando Civeira, MD, PhD*,*,
Estibaliz Jarauta, MD*,
Ana Cenarro, PhD*,
Angel L. García-Otín, PhD*,
Diego Tejedor, PhD ,
Daniel Zambón, MD, PhD ,
Miguel Mallen, BSc ,
Emilio Ros, MD, PhD and
Miguel Pocoví, PhD
* Unidad de Lípidos and Laboratorio de Investigación Molecular, Hospital Universitario Miguel Servet, Instituto Aragonés de Ciencias de la Salud (I+CS), Zaragoza, Spain
Progenika Biopharma S.A., Derio, Spain
Unitat de Lípids, Servei d'Endocrinologia I Nutrició, Institut d'Investigacions Biomèdiques August Pi Sunyer, Hospital Clínic, and Ciber Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Spain
Departamento de Bioquímica, Biología Molecular y Celular, Universidad de Zaragoza, Zaragoza, Spain
View larger version (27K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1 Percentage of Subjects With Clinical Diagnosis of FCH and With LDLR Mutation
Percentage of subjects with clinical diagnosis of familial combined hyperlipidemia (FCH) and with low-density lipoprotein receptor (LDLR) gene mutation. Columns represent the percentage in the whole group and in several subgroups. Subgroups have been defined according to the factors independently associated with the presence of LDLR mutation in the regression analysis. apoB = apolipoprotein B; APOE(–) = subjects without the APOE E2/E2 genotype or other rare APOE allele associated with hyperlipidemia; chol = cholesterol; DM(–) = subjects without diabetes mellitus.
|
|
|
