Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mendelics | RCV000986600 | SCV001135632 | pathogenic | Mitochondrial trifunctional protein deficiency | 2019-05-28 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001869339 | SCV002238915 | pathogenic | Mitochondrial trifunctional protein deficiency; Long chain 3-hydroxyacyl-CoA dehydrogenase deficiency | 2023-12-26 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 16 of the HADHA gene. RNA analysis indicates that disruption of this splice site induces altered splicing and likely results in a shortened protein product. This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individual(s) with clinical features of long-chain 3-hydroxyacyl coenzyme A dehydrogenase deficiency (PMID: 17143551, 27014569). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 801655). Studies have shown that disruption of this splice site results in skipping of exon 16, but is expected to preserve the integrity of the reading-frame (PMID: 17143551). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003467541 | SCV004191771 | pathogenic | Long chain 3-hydroxyacyl-CoA dehydrogenase deficiency | 2023-07-12 | criteria provided, single submitter | clinical testing |