Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Department of Endocrinology, |
RCV001794525 | SCV002032072 | pathogenic | 3-hydroxy-3-methylglutaryl-CoA synthase deficiency | criteria provided, single submitter | clinical testing | ||
Labcorp Genetics |
RCV001794525 | SCV002230146 | pathogenic | 3-hydroxy-3-methylglutaryl-CoA synthase deficiency | 2023-03-02 | criteria provided, single submitter | clinical testing | This variant is present in population databases (rs779321975, gnomAD 0.006%). This sequence change creates a premature translational stop signal (p.Asn465Thrfs*10) in the HMGCS2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in HMGCS2 are known to be pathogenic (PMID: 20346956, 23751782, 25511235). This premature translational stop signal has been observed in individual(s) with HMG-CoA synthase deficiency (PMID: 35308163). ClinVar contains an entry for this variant (Variation ID: 1327465). For these reasons, this variant has been classified as Pathogenic. |
Institute of Medical Genetics and Genomics, |
RCV001794525 | SCV002098041 | pathogenic | 3-hydroxy-3-methylglutaryl-CoA synthase deficiency | 2022-02-15 | no assertion criteria provided | clinical testing | The novel homozygous frameshift deletion variant c.1394delA (p. N465Tfs*9) has an allele frequency-0.0008% in gnomAD (aggregated) database and 0.0016% in 1000g. In-silico bioinformatic software mutation taster predicts this variant as Disease causing. Phenotype observed showed persistent metabolic acidosis, sudden onset fever, noisy breathing, altered sensorium. There was a clinical suspicion of inherited metabolic disorder. GCMS studies iterated similar clinical suspicion. HMG-CoA synthase-2 deficiency is an autosomal recessive disorder. Based on the phenotypic observation, we classify this variant as pathogenic. |