Congenital anomaly of the inferior vena cava and factor V Leiden mutation predisposing to deep vein thrombosis.
Humans; Male; Young Adult; Ultrasonography; *Mutation; Risk Factors; Predictive Value of Tests; Genetic Predisposition to Disease; Activated Protein C Resistance/*complications/diagnosis/drug therapy/genetics; Anticoagulants/therapeutic use; deep vein thrombosis (DVT); DNA Mutational Analysis; Factor V/*genetics; inferior vena cava (IVC); lower extremities; Phlebography/methods; thrombophilic; Vascular Malformations/*complications/diagnosis; venography; Venous Thrombosis/diagnosis/drug therapy/*etiology/genetics; Mutation; Tomography; Human; X-Ray Computed; Sequence Analysis; Vena Cava; Inferior/*abnormalities/diagnostic imaging; Venous Thrombosis; Blood Coagulation Factors; Disease Susceptibility; Hematologic Diseases; Venous Thrombosis – Drug Therapy; Anticoagulants – Therapeutic Use; Hematologic Diseases – Complications; Hematologic Diseases – Diagnosis; Hematologic Diseases – Drug Therapy; Inferior – Abnormalities; Inferior – Radiography; Inferior – Ultrasonography; Phlebography – Methods; Vascular Malformations – Complications; Vascular Malformations – Diagnosis; Venous Thrombosis – Diagnosis; Venous Thrombosis – Etiology
A previously healthy 21-year-old man presented with back pain, bilateral extremity pain, and right lower extremity weakness, paresthesias, and swelling. Sonographic examination revealed diffuse deep vein thrombosis (DVT) in the femoral and popliteal venous system. CT imaging revealed hypoplasia of the hepatic inferior vena cava (IVC) segment with formation of multiple varices and collateral veins around the kidneys. Hematologic workup also discovered a factor V Leiden mutation, further predisposing the patient to DVT. The rare, often overlooked occurrence of attenuated IVC, especially in the setting of hypercoagulable state, can predispose patients to significant thrombosis.
Lamparello Brooke M; Erickson Cameron R; Kulthia Arun; Virparia Vasudev; Thet Zeyar
Vascular Health and Risk Management
2014
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.2147/vhrm.s66283" target="_blank" rel="noreferrer noopener">10.2147/vhrm.s66283</a>
Unique N-linked glycosylation of CasBrE Env influences its stability, processing, and viral infectivity but not its neurotoxicity.
*Protein Processing; Animals; Canavan Disease/pathology/virology; DNA Mutational Analysis; env/genetics/*metabolism; Gene Products; Glycosylation; Leukemia Virus; Mice; Murine/genetics/*pathogenicity/*physiology; Post-Translational; Virulence; Virus Replication
The envelope protein (Env) from the CasBrE murine leukemia virus (MLV) can cause acute spongiform neurodegeneration analogous to that induced by prions. Upon central nervous system (CNS) infection, Env is expressed as multiple isoforms owing to differential asparagine (N)-linked glycosylation. Because
Renszel Krystal M; Traister Russell S; Lynch William P
Journal of virology
2013
2013-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1128/JVI.00392-13" target="_blank" rel="noreferrer noopener">10.1128/JVI.00392-13</a>