Biliary complication has been one of the most common complications after liver transplantation. Nonanastomotic strictures and dilatations involving the intrahepatic biliary tree have been recognized as biliary complications. These lesions were reported to be associated with hepatic artery thrombosis; prolonged preservation time; ABO-incompatible organs; and immunological injury, including injuries to vascular endothelial cells (chronic rejection) and the bile duct (primary sclerosing cholangitis). However, the etiology of these lesions appeared to be mostly related to ischemic injury. Anatomical research on the arterial supply of the bile duct has provided further insights into bile duct blood supply and its surgical implications. The biliary tract is supplied with arterial blood by a vasculature called the peribiliary vascular plexus. Any injury to the peribiliary vascular plexus may contribute to ischemic death of the biliary system mucosa. At many points, the process of liver transplantation exposes the endothelial cells and peribiliary vascular plexus to ischemic injury. The majority of intrahepatic biliary strictures (IHBS) are diffuse or bilateral. A percutaneous or an endoscopic approach has been used as the initial treatment. However, a low threshold for surgical intervention (retransplantation) should be adopted, because these patients demonstrate high mortality. The aim of this article is to review the anatomy, etiology, clinical picture, diagnosis, management, and prognosis of IHBS after liver transplantation.
BackgroundLiver regeneration (LR) involves an early inductive phase characterized by the proliferation of hepatocytes, and a delayed angiogenic phase distinguished by the expansion of non-parenchymal compartment. The interest in understanding the mechanism of LR has lately shifted from the proliferation and growth of parenchymal cells to vascular remodeling during LR. Angiogenesis accompanied by LR exerts a pivotal role to accomplish the process. Vascular endothelial growth factor (VEGF) has been elucidated as the most dynamic regulator of angiogenesis. From this perspective, platelet derived/Intra-platelet (IP) VEGF-A should be associated with LR.Material and MethodsThirty-seven patients diagnosed with hepatocellular carcinoma and undergoing partial hepatectomy (PH) were enrolled in the study. Serum and IP VEGF-A was monitored preoperatively and at four weeks of PH. Liver volumetry was determined on computer models derived from computed tomography (CT) scan.ResultsSerum and IP VEGF-A was significantly elevated at four weeks of PH. Preoperative IP VEGF-A was higher in patients with advanced cancer and vascular invasion. Postoperative IP VEGF-A was higher after major liver resection. There was a statistically significant correlation between postoperative IP VEGF-A and the future remnant liver volume. Moreover, the soluble vascular endothelial growth factor receptor-1 (sVEGFR1) was distinctly down-regulated suggesting a fine-tuned angiogenesis at the later phase of LR.ConclusionIP VEGF-A is overexpressed during later phase of LR suggesting its implications in inducing angiogenesis during LR.
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