Treatment of Noncirrhotic Portal Hypertension Secondary to Portal Vein Thrombosis With Endovascular Mesocaval Shunt Creation.

Transjugular intrahepatic portosystemic shunt (TIPS) creation can be very beneficial to decrease high portal pressure and its consequent dreadful complications, such as variceal hemorrhage. However, some anatomical limitations such as portal vein thrombosis can make TIPS technically impossible to perform. Here, we describe a case of a 72-year-old female patient who previously had a Roux-En-Y choledochojejunostomy, which was complicated by portal vein thrombosis. The patient subsequently developed portal hypertension, and this was successfully treated with endovascular mesocaval shunt creation, given that TIPS was not a viable option.

Life threatening hemobilia after endoscopic retrograde cholangiopancreatography (ERCP).

Arterial vascular complication from endoscopic retrograde cholangiopancreatography (ERCP) is exceedingly rare. This report describes a life threatening hemobilia, from a pseudoaneurysm of the right hepatic artery (RHA), which occurred post ERCP. The pseudoaneurysm and the active bleed were diagnosed by selective angiography of the RHA, and successfully treated with stenting.

Locoregional and systemic therapy for hepatocellular carcinoma.

The management of hepatocellular carcinoma (HCC) remains challenging due to late presentation and the presence of accompanying liver dysfunction. As such, most patients are not eligible for curative resection and liver transplant. Management in this scenario depends on a number of factors including hepatic function, tumor burden, patency of hepatic vasculature and patients' functional status. Based on these, patients can be offered catheter based intra-arterial therapy for intermediate stage disease and in more advanced disease, sorafenib. Given recent data, regorafenib is now an option following failure of sorafenib. Catheter directed intra-arterial therapy takes advantage of tumor hypervascularity and the unique dual blood supply of the liver, as hepatic tumors receive arterial perfusion via the hepatic artery while the rest of the liver is supplied by the portal vein. This allows selective embolization and delivery of chemotherapeutic agents to the tumor. Compared to best supportive care, intra-arterial therapy offers a survival benefit in intermediate stage HCC and is the recommended approach for treatment. None of the catheter based approaches; including bland embolization, conventional trans-arterial chemoembolization (cTACE), drug eluting bead trans-arterial chemoembolization (DEB-TACE) or trans-arterial radioembolization (TARE) offers a clear advantage over the other, although DEB-TACE may be characterized by less systemic toxicity. All of these approaches are contraindicated in patients with portal vein thrombosis (PVT). On the other hand, intra-arterial, radio embolization, with Yttrium-90 (Y90) can be offered to patients with PVT. The place of this modality in management of HCC is still being investigated. The role of sorafenib in advanced HCC is not in doubt, as until recently, it was the only systemic therapy approved for the management in this setting. This is despite multiple trials evaluating other agents. The addition of sorafenib to catheter-based therapy in intermediate stage disease has also failed to show any benefit. The modest survival benefit with sorafenib and the failure of other targeted agents suggest that it is important to look beyond inhibition of angiogenesis in advanced HCC. Identification of key drivers and mediators of HCC remains paramount for successful drug development. In line with this, it is refreshing that the excitement that has followed developments in cancer immunotherapy is finding its way to HCC with early trials of anti-PD1 monoclonal antibodies showing sufficient activity that phase III trials are now ongoing for Pembrolizumab and Nivolumab in advanced HCC. Future drug development efforts will focus on defining the feasibility of combining different treatment approaches targeting multiple important modulators of HCC.