Key result
Novel C122X LDLR mutation accounts for ~16% of familial hypercholesterolemia cases in Southern Belgium.
Cohort (n=70)
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In a cohort of 70 unrelated patients living in Southern Belgium with autosomal dominantly inherited hypercholesterolemia, 11 had a hitherto undescribed mutation in exon 4. It consisted in a C-->A mutation at nucleotide 366, resulting in a stop codon at residue Cys122. This C122X mutation is expected to cause a class I receptor defect. The biochemical and clinical data collected from the patients carrying the mutation were consistent with a severe form of familial hypercholesterolemia (FH). Some differences between generations were noted. Amongst the C122X carriers, those born after 1926 had cardiovascular complications earlier than those born before 1926. This raises the possibility that changes in environmental factors during the course of the century have had an unfavorable impact on the prognosis of the disease. The mutation was found in 16% of the suspected FH patients and less frequently (less than 3% of suspected FH) in Northern Belgium. The haplotype of the chromosomes carrying the mutation was the same in all C122X families, but extensive genealogical studies failed to reveal a common ancestor. We conclude that C122X is an old and common cause of FH in Belgium. Screening for this mutation may be useful in the diagnosis of FH in Belgium.
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Descamps et al. (1997) conducted a cohort in Familial hypercholesterolemia (n=70). C122X mutation in exon 4 of the LDL receptor gene was evaluated on Prevalence of the C122X mutation in suspected familial hypercholesterolemia patients. A novel C122X mutation in exon 4 of the LDL receptor gene was identified in 16% of a cohort of 70 unrelated patients with familial hypercholesterolemia in Southern Belgium.
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