Blesa Sebastian, Garcia-Garcia Ana Barbara, Martinez-Hervas Sergio, Mansego Maria Luisa, Gonzalez-Albert Veronica, Ascaso Juan Francisco, Carmena Rafael, Real Jose Tomas, Chaves Felipe Javier
Laboratorio de Estudios Genéticos, Fundación de Investigación HCUV, Hospital Clínico Universitario de Valencia, Valencia, Spain.
Clin Chem. 2006 Jun;52(6):1021-5. doi: 10.1373/clinchem.2006.067645. Epub 2006 Apr 20.
Familial hypercholesterolemia (FH) is a frequent form of autosomal-dominant hypercholesterolemia that predisposes to premature coronary atherosclerosis. FH is caused by sequence variations in the gene coding for the LDL receptor (LDLR). This gene has a wide spectrum of sequence variations, and genetic diagnosis can be performed by 2 strategies.
Point variations and large rearrangements were screened along all the LDLR gene (promoter, exons, and flanking intron sequences).
We screened a sample of 129 FH probands from the Valencian Community, Spain, and identified 54 different LDLR sequence variations. The most frequent (10% of cases) was 111insA, and 60% of the variants had a frequency as low as 1%. A previously described method for detection of known sequence variations in the Spanish population by DNA array analysis allowed the identification of only approximately 50% of patients with a variant LDLR gene and approximately 40% of the screened samples.
Our results indicate that the adequate procedure to identify LDLR sequence variations in outbreed populations should include screening of the entire gene.