← Back to search
Literature record

Whole-Exomes Sequencing Delineates Gene Variants Profile in a Young Saudi Male with Familial Hypercholesterolemia: Case Report.

PMID 28764195 | PMCID PMC5535388 | DOI 10.7860/JCDR/2017/28156.10143 · Journal of clinical and diagnostic research : JCDR · 2017

View on PubMed ↗

Familial hypercholesterolemia is an autosomal dominant genetic disease characterized by earlier elevated Low-Density Lipoprotein (LDL) cholesterol levels and increased risk for premature Myocardial Infarction (MI). Albeit the diagnosis of some medical Familial Hypercholesterolemia (FH) cases are due to mutations in PCSK9, APOB, or LDLR, detection of mutation rate and profiles relies heavily on different gene pools and ethnicity. We ran exome sequencing on blood genomic DNA (gDNA) from a 26-year-old Saudi patient on Ion Proton Platform (Ion Torrent, Guilford, Connecticut, USA) as part of a pilot study preluding the establishment of the Saudi Human Genome project. The sequencing results were analysed using Ion suit Bioinformatics system. The patient was matched with a lady of lean body mass and Welsh descent, who suffered from hypercholesterolemia. The first analysis of known FH genes identified five mutations in APOB, 25 mutations of known genes linked to FH, six mutations in LPR2, one mutation in LDLR, and three mutations in PCSK9. Finally, using disease filter algorithms, we filtered out more than 2000 intronic synonymous variants with likely no biological functions. No major new locus was found in FH. However, via variant reduction and TVC protocols we detected 15 new variants, among which 14 genes are linked to hypercholesterolemia, type-I, and type-II diabetes. We also detected three mutations in PCSK9 and confirmed one by Sanger. Taken together, this report suggests that the genetic determinant of FH in this Saudi patient is likely to be heterogeneous, complicating the diagnostic and novel gene discovery process.

Validated evidence

TypeEntitySource evidenceConfidenceExtractor
genePCSK9“Albeit the diagnosis of some medical Familial Hypercholesterolemia (FH) cases are due to mutations in PCSK9, APOB, or LDLR, detection of mutation rate and profiles relies heavily on different gene pools and ethnicity.”0.98hgnc_dict_v1
geneAPOB“Albeit the diagnosis of some medical Familial Hypercholesterolemia (FH) cases are due to mutations in PCSK9, APOB, or LDLR, detection of mutation rate and profiles relies heavily on different gene pools and ethnicity.”0.98hgnc_dict_v1
geneLDLR“Albeit the diagnosis of some medical Familial Hypercholesterolemia (FH) cases are due to mutations in PCSK9, APOB, or LDLR, detection of mutation rate and profiles relies heavily on different gene pools and ethnicity.”0.98hgnc_dict_v1
phenotypefamilial hypercholesterolemia“Whole-Exomes Sequencing Delineates Gene Variants Profile in a Young Saudi Male with Familial Hypercholesterolemia: Case Report.”0.98phenotype_alias_lexicon_v2
phenotypemyocardial infarction“Familial hypercholesterolemia is an autosomal dominant genetic disease characterized by earlier elevated Low-Density Lipoprotein (LDL) cholesterol levels and increased risk for premature Myocardial Infarction (MI).”0.98phenotype_alias_lexicon_v2
phenotypediabetes mellitus“However, via variant reduction and TVC protocols we detected 15 new variants, among which 14 genes are linked to hypercholesterolemia, type-I, and type-II diabetes.”0.93phenotype_alias_lexicon_v2
populationSaudi Arabia“Whole-Exomes Sequencing Delineates Gene Variants Profile in a Young Saudi Male with Familial Hypercholesterolemia: Case Report. We ran exome sequencing on blood genomic DNA (gDNA) from a 26-year-old Saudi patient on Ion Proton Platform (Ion Torrent, Guilford, Connecticut, USA) as part of a pilot study preluding the establishment of the Saudi Human Genome project. Taken together, this report suggests that the genetic determinant of FH in this Saudi patient is likely to be heterogeneous, complicating the diagnostic and novel gene discovery process.”0.95saudi_context_rules_v1