[1] No specific treatment for SOS is currently available. Defibrotide is an antithrombotic agent reported to improve symptoms and signs of SOS in 42% of patients.[3] The diagnosis of SOS is established by liver biopsy, with histologic findings including endothelial cell damage, dilatation of

the sinusoids, hepatocyte necrosis, and collagen deposition in the sinusoids, Crizotinib with subsequent liver fibrosis.[4] In hepatocytes, FDG is taken up by surface glucose transporter-2 expressed by the sinusoidal endothelium. The prevailing hypothesis of SOS pathophysiology focuses on damage to the hepatic venular and sinusoidal endothelium as an initial event that activates the coagulation cascade. The venular and sinusoidal lumen is reduced due to concentric subendothelial zone edema.[1, 5] We suggest that PET findings in the

liver could be explained by trapping of FDG in dilated sinusoids; FDG cannot enter hepatocytes due to destruction of the sinusoidal endothelium. An inflammatory reaction is a less likely hypothesis, as no inflammatory cells http://www.selleckchem.com/products/Rapamycin.html were observed on liver biopsy. Interestingly, patient 2 presented more severe clinical features and histologic findings, but obtained complete recovery in response to treatment, while patient 1 had no significant clinical findings, only moderate damage on liver biopsy, and derived no benefit from treatment. Differences in sinusoidal injuries may be predictive of response to defibrotide, but this aspect requires further investigation. In conclusion, FDG-PET/CT imaging may be a useful tool to assess the prognosis of SOS

and the therapeutic efficacy of BCKDHB defibrotide, but further data need to be generated and validated by larger studies. “
“Due to improvement in the immunosuppression regimens and monitoring, chronic rejection (CR) represents only a minor cause for the allograft failure after liver transplantation. Excluding other causes of abnormal liver chemistry tests after liver transplantation is critical in differential diagnosis of CR. Proper recognition and staging of CR is essential for the long-term management of this condition. An active interaction with liver expert pathologist to identify features of late and early CR is critical. There are histological predictors of graft failure but none are pathognomonic. There are only limited options regarding treatment of CR and none have been compared in a randomized controlled trial. “
“A 19-year-old woman presented to her family physician with sharp right flank pain during deep inspiration or twisting of the upper body. An abdominal ultrasound showed a large mass in the right lobe of the liver. On contrast-enhanced computed tomography (Fig. 1A-C), a slight arterial enhancement was found in the center of the lesion (Fig. 1B), which was more pronounced during the portal venous phase (Fig. 1C).