Shah, David Lee, M. Aloysius, Frank G. Gress Purpose: To evaluate retrospectively the safety, technical success and clinical efficacy of hepatic vein stenting in the management of clinically evident hepatic venous outflow obstruction complicating orthotopic liver transplantation. Material and methods: From 2003 to 2013, 24 patients BTK inhibitor ( 8 female and 16 male), including 23 adults and one adolescent

(17 years of age) underwent hepatic vein stent placement for hepatic venous outflow obstruction after orthotopic liver transplant. Pre and post stent deployment pressure gradients were measured. Results: Reduction of pressure gradient was achieved in 23 of 24 patients . Reduction of post stent placement to 3mmHg or below was achieved in 15 of 24 patients. Mean pressure gradient before stenting was 15.5 mmHg with SD of 3.5 mmHg and mean pressure gradient after stenting was 2 mmHg with SD of 2.8 mmHg with mean reduction in pressure of 13.5 mmHg with SD of 6.4 mmHg. There were no immediate major complications

in our population. Mean interval from transplantation to stenting was 570 days. Mean follow-up was 618 days. Analysis of pre and post liver function values is ongoing. Conclusion: Hepatic vein stenting for the treatment of post liver transplant clinically evident hepatic venous outflow obstruction is a safe and technically successful procedure. post stent placement venogram demonstrates resolution of stricture and rapid flow Disclosures: Matthew Johnson – Advisory LY2109761 Committees or Review Panels: Boston Scientific, Guerbet; Consulting: BTG, Bayer, Endoshape; Grant/Research Support: Argon, Bard, B Braun, BTG, ALN, Cook, Cordis; Speaking and Teaching: BTG, Bayer, Cook, Argon; Stock Shareholder: Endoshape The following people have nothing to disclose: Faiz Francis, Thomas Lowe, David Agarwal, Daniel E. Wertman, Sabah Butty, Thomas Casciani “
“Department of Pathology, Shanghai Medical College, Fudan University, Shanghai, China

Tau-protein kinase Department of Pathology, Public Health Care Laboratory, Leeuwarden, the Netherlands Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion. In addition to features that are predominantly found in either FNH or HCA (e.g., dystrophic vessels in FNH and single arteries in HCA), FNH and HCA share morphological vascular abnormalities such as dilated sinusoids. We hypothesized that these anomalous vascular features are associated with altered expression of growth factors involved in vascular remodeling.