Hemobilia from a right hepatic artery pseudoaneurysm due to chronic cholecystitis.

Splanchnic pseudoaneurysms are rare causes of hemobilia. Specifically, hepatic artery pseudoaneurysms from infectious or inflammatory etiology are even more rare. In this article, we describe our encounter with a 72-year-old female presenting with obstructive jaundice and acute blood loss anemia. Upper endoscopy indicated hemobilia and endoscopic retrograde cholangiopancreatography was completed with stent in place. Post endoscopic retrograde cholangiopancreatography, computed tomography angiogram indicated a right hepatic artery pseudoaneurysm which was the cause of her hemobilia. The patient was ultimately treated with selective coil embolization and interval cholecystectomy.

Chronic exposure to a high-fat diet induces hepatic steatosis, impairs nitric oxide bioavailability, and modifies the mitochondrial proteome in mice.

Obesity-related pathologies, such as nonalcoholic fatty liver disease, are linked to mitochondrial dysfunction and nitric oxide (NO) deficiency. Herein, we tested the hypothesis that a high-fat diet (HFD) modifies the liver mitochondrial proteome and alters proteins involved in NO metabolism, namely arginase 1 and endothelial NO synthase. Male C57BL/6 mice were fed a control or HFD and liver mitochondria were isolated for proteomics and reactive oxygen species measurements. Steatosis and hepatocyte ballooning were present in livers of HFD mice, with no pathology observed in the controls. HFD mice had increased serum glucose and decreased adiponectin. Mitochondrial reactive oxygen species was increased after 8 weeks in the HFD mice, but decreased at 16 weeks compared with the control, which was accompanied by increased uncoupling protein 2. Using proteomics, 22 proteins were altered as a consequence of the HFD. This cohort consists of oxidative phosphorylation, lipid metabolism, sulfur amino acid metabolism, and chaperone proteins. We observed a HFD-dependent increase in arginase 1 and decrease in activated endothelial NO synthase. Serum and liver nitrate + nitrite were decreased by HFD. In summary, these data demonstrate that a HFD causes steatosis, alters NO metabolism, and modifies the liver mitochondrial proteome; thus, NO may play an important role in the processes responsible for nonalcoholic fatty liver disease.