Portal embolic agents

Occlusion of portal branches of the liver parenchyma to be resected redistributes the totality of its portal blood flow, and consequently all its hepatotrophic contents, towards the FRL. This is the basic rationale of the method that triggers off regenerative activity of the nonembolized portion of the liver. Moreover, PVE dilates the portal branches in the FRL, exposing liver vasculature to stretch stress which act as a trigger for IL-6 release from endothelial cells and contribute to the activation of regenerative cascade in the FRL [26]. Induction of heat shock protein in the nonembolized lobe is supposed to have similar effects [40]. PVE also acts through two potentially complementary pathways specifically related to embolization ischemia and inflammation. With most of the embolic agents, PVE induces a mild ischemia apoptosis or necrosis of some hepatocytes, and intercellular disjunction. 

Ko GY, Sung KB, Yoon HK et al. (2003) Preoperative portal vein embolization with a new liquid embolic agent. Radiology 227 407-413... 

Eligibility requirements for hepatic artery embolotherapy for neuroendocrine tumor metastases are summarized in Table 14.1. They include adequate hepatic and renal function, acceptable coagulation parameters, and hepatopedal portal venous flow. While what constitutes an adequate amount of residual uninvolved liver is not clear, in most published series 50% to 60% tumor replacement is considered as the acceptable upper limit. It is well recognized that over 75% tumor replacement is associated with higher incidence of hepatic failure post embolization [48]. In those patients with borderline liver and/or renal function, superselective embolization using smaller amounts of embolic agent and iodin-ated contrast could be considered. 

Hepatic arterial bland and chemo-embolization have also been utilized. This therapy is based on the anatomic vascular distribution of the blood supply for hepatic tumors. The hepatic artery serves tumors in the liver almost exclusively while the portal vein serves normal hepatic parenchyma. There is some crossover but it is only approximately 10%. Bland embolization uses particles placed in the hepatic artery only while chemoembolization mixes these particles with a variety of chemotherapeutic agents and lipiodol, an iodinated poppy seed oil, which has been shown to increase the uptake into the cell via a pump in the cell wall. This therapy has been utilized for the last 20 years but eventual re-growth and recurrence have also uniformly occurred. Repeated embolizations are necessary to keep the disease in check and to palliate the patient s symptoms. The mean response to embolization is approximately 12-18 months with eventual occlusion of the hepatic arterial supply to the tumor after multiple embolizations. Response to embolotherapy has been dramatic for palliation of symptoms, with 63% of patients reporting a reduction in symptoms and an objective response seen on CT to be 76% either partial or minimal response, with an additional 16% reporting stable disease [4]. The embolotherapy will rid the patient of much of their tumor burden but isolated islets of viable tumor will remain after the procedure, accounting for the resurgence of disease. 

Distal embolization is achieved with particulate agents, cyanoacrylate or other liquid agents. Proximal ligation is surgically performed or may be done percutaneously with steel coils or detachable balloons. Considering that the intrahepatic portal vasculature was classically considered as terminal... 

Kaneko T, Nakao A, Takagi H (2002) Clinical studies of new material for portal vein embolization comparison of embolic effect with different agents. Hepatogastroenterology 49 472-477... 

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