Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
ARUP Laboratories, |
RCV000211443 | SCV000268443 | likely pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2015-02-20 | criteria provided, single submitter | clinical testing | |
Counsyl | RCV000211443 | SCV000485329 | likely pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2015-11-18 | criteria provided, single submitter | clinical testing | |
Invitae | RCV000211443 | SCV002230736 | pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2023-09-27 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 7 of the ACADM gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in ACADM are known to be pathogenic (PMID: 16121256, 20434380). This variant is present in population databases (no rsID available, gnomAD 0.0009%). Disruption of this splice site has been observed in individual(s) with medium chain acyl-CoA dehydrogenase (MCAD) deficiency (PMID: 20434380). ClinVar contains an entry for this variant (Variation ID: 226060). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV000211443 | SCV002808629 | likely pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2022-02-23 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000211443 | SCV004216252 | pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2023-10-12 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV003917863 | SCV004731922 | likely pathogenic | ACADM-related disorder | 2024-02-02 | criteria provided, single submitter | clinical testing | The ACADM c.599+1G>A variant is predicted to disrupt the GT donor site and interfere with normal splicing. To our knowledge, this variant was not reported in patients with MCAD deficiency. However, a different variant affecting this donor site has been reported, along with the recurrent c.985A>G pathogenic variant, in a patient with biochemical markers consistent with MCAD deficiency (c.599+3A>G; Navarrete et al. 2019. PubMed ID: 30626930). The c.599+1G>A variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/1-76205796-G-A). Variants that disrupt the consensus splice donor site in ACADM are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Natera, |
RCV000211443 | SCV001461465 | likely pathogenic | Medium-chain acyl-coenzyme A dehydrogenase deficiency | 2020-09-16 | no assertion criteria provided | clinical testing |