Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
NIHR Bioresource Rare Diseases, |
RCV000851604 | SCV000899355 | uncertain significance | Hypofibrinogenemia | 2019-02-01 | criteria provided, single submitter | research | |
OMIM | RCV000017817 | SCV000038096 | other | FIBRINOGEN LONGMONT | 2018-03-29 | no assertion criteria provided | literature only | |
Prevention |
RCV004724748 | SCV005339164 | likely pathogenic | FGB-related disorder | 2024-08-14 | no assertion criteria provided | clinical testing | The FGB c.586C>T variant is predicted to result in the amino acid substitution p.Arg196Cys. This variant has been reported in multiple individuals with congenital dysfibrinogenemia (Lounes et al. 2001. PubMed ID: 11468164; Chinni et al. 2018. PubMed ID: 30418131; Table S3, Downes et al. 2019. PubMed ID: 31064749; Table S3, Gindele et al. 2021. PubMed ID: 33807613; Simurda et al. 2024. PubMed ID: 38251440). In vitro studies suggest that this variant disrupts fibrinogen polymerization, leading to impaired clot formation (Lounes et al. 2001. PubMed ID: 11468164). This variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Taken together, this variant is interpreted as likely pathogenic. |