Aflatoxin exposure may not play a role in liver cancer development in Mongolia.

Background/aims: The incidence of hepatocellular carcinoma (HCC) in Mongolia is growing at an alarming rate. Traditional dried food was suggested as the major reason for high HCC numbers, due to possible aflatoxin contamination during manufacturing. We thus aimed to measure aflatoxin concentrations in Mongolian food samples.

Non-invasive separation of alcoholic and non-alcoholic liver disease with predictive modeling.

Background & Objective: Currently, a major clinical challenge is to distinguish between chronic liver disease caused by metabolic syndrome (non-alcoholic fatty liver disease, NAFLD) from that caused by long term or excessive alcohol consumption (ALD). The etiology of severe liver disease affects treatment options and priorities for liver transplantation and organ allocation. Thus we compared physiologically similar NAFLD and ALD patients to detect biochemical differences for improved separation of these mechanistically overlapping etiologies.

A positive feedback loop between RIP3 and JNK controls non-alcoholic steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD) represents the most common liver disease in Western countries and often progresses to non-alcoholic steatohepatitis (NASH) leading ultimately to liver fibrosis and liver cancer. The occurrence of hepatocyte cell death-so far characterized as hepatocyte apoptosis-represents a fundamental step from benign steatosis toward progressive steatohepatitis. In contrast, the function of RIP3-dependent "necroptosis" in NASH and NASH-induced fibrosis is currently unknown.

Tacrolimus as a reasonable alternative in a patient with steroid-dependent and thiopurine-refractory autoimmune pancreatitis with IgG4-associated cholangitis.

Background: More recently, autoimmune pancreatitis (AIP) in association with IgG4-positive cholangitis (IAC) has been recognised as a new and challenging entity. Currently, initiation of high dose steroids (e.g.

Osteopontin neutralisation abrogates the liver progenitor cell response and fibrogenesis in mice.

Background: Chronic liver injury triggers a progenitor cell repair response, and liver fibrosis occurs when repair becomes deregulated. Previously, we reported that reactivation of the hedgehog pathway promotes fibrogenic liver repair. Osteopontin (OPN) is a hedgehog-target, and a cytokine that is highly upregulated in fibrotic tissues, and regulates stem-cell fate.

NLRP3 inflammasome activation is required for fibrosis development in NAFLD.

NLR inflammasomes, caspase 1 activation platforms critical for processing key pro-inflammatory cytokines, have been implicated in the development of nonalcoholic fatty liver disease (NAFLD). As the direct role of the NLRP3 inflammasome remains unclear, we tested effects of persistent NLRP3 activation as a contributor to NAFLD development and, in particular, as a modulator of progression from benign hepatic steatosis to steatohepatitis during diet-induced NAFLD. Gain of function tamoxifen-inducible Nlrp3 knock-in mice allowing for in vivo temporal control of NLRP3 activation and loss of function Nlrp3 knockout mice were placed on short-term choline-deficient amino acid-defined (CDAA) diet, to induce isolated hepatic steatosis or long-term CDAA exposure, to induce severe steatohepatitis and fibrosis, respectively.

Endoscopic management is the treatment of choice for bile leaks after liver resection.

Background: Despite improvements in surgical techniques and postoperative patient care, bile leaks still occur postoperatively in as many as 15% of liver resections (LRs) and are associated with high mortality. There is a paucity of outcome data on endoscopic treatment of complex bile leaks.

Objective: The aim of this retrospective study was to evaluate the efficacy of interventional endoscopy in the treatment of bile leaks after LR.

[Drug-induced liver injury as predominant cause of acute liver failure in a monocenter study].

Background And Aim: Clinical course and mortality of acute liver failure (ALF) are determined by its causes. Traditionally, fulminant hepatitis B infection (HBV) was thought to be the predominant etiology of ALF in Germany. However, recent studies, conducted in American and European cohorts pointed to drug-induced liver injury (DILI) as the major cause.

(Cleaved) CK18 serum and tissue expression levels differentiate acute HCV reinfection from acute rejection in liver allografts.

Background & Aims: Orthotopic liver transplantation (OLT) is the sole therapeutic option to cure end-stage liver diseases including HCV-related cirrhosis. Timely and precise differentiation of relevant acute HCV reinfection from acute rejection after OLT is vital for appropriate therapy. Aim of this study was to evaluate the usefulness of (non-) invasive apoptosis (M30) and necrosis (M65) determination in the differential diagnosis of acute (and chronic) HCV reinfection vs.

Transcatheter coil embolization of a coronary artery-left ventricular fistula associated with single coronary artery anomaly.

Single coronary artery anomaly associated with coronary fistula is a rare entity. Transcatheter coil embolization is the treatment of choice for coronary artery fistulas. In this case report, we describe a patient with both single coronary artery anomaly and coronary fistula who was successfully treated with coil embolization.

[Cytokeratin 18 as marker for non-invasive diagnosis and prognosis of acute and chronic liver diseases].

Introduction: Currently liver biopsy represents the gold standard to assess severity and fibrosis grade in liver diseases. Since this laborious, costly, and invasive procedure is associated with possible complications, non-invasive methods and biomarkers, which allow for an easy, reliable, and repeatable assessment of liver disease are warranted. Cytokeratin (CK) 18 is an intermediary filament protein, expressed in hepatocytes, which is proteolytically cleaved during liver damage.

Liver transplantation for acute liver failure: are there thresholds not to be crossed?

Factors predicting survival after liver transplantation (LT) for irreversible acute liver failure (ALF) are rare. The aim of this study was to identify prognostic preoperative factors of patients with ALF that predict mortality after LT to avoid futile transplantation. From chart review, we identified 57 patients receiving transplants for ALF from 12/2000 to 09/2010.

Mini-laparoscopy is superior in detecting liver cirrhosis and metastases in liver cancer: an over 10-year experience in 1,788 cases.

Background/aims: Mini-laparoscopy has, since its first description in 1998, proven to be a valuable diagnostic method in liver diseases. We re-evaluated the significance of mini-laparoscopy for diagnosis and staging of liver disease and primary liver and bile duct cancer.

Patients And Methods: 1,788 consecutive patients who received a diagnostic mini-laparoscopy between 10/1998 and 06/2011 were included in this retrospective cohort study.

Clinical relevance and cellular source of elevated soluble urokinase plasminogen activator receptor (suPAR) in acute liver failure.

Background & Aims: Acute liver failure (ALF) is a life-threatening condition with a high mortality rate. The expression of urokinase plasminogen activator receptor (uPAR, CD87) and release of its shedded receptor into serum as soluble uPAR (suPAR) have been closely related to immune activation and prognosis in systemic inflammation and cirrhosis. We now aimed at investigating the clinical relevance and cellular source of uPAR and circulating suPAR in ALF.

A non-interventional study of the genetic polymorphisms of NOD2 associated with increased mortality in non-alcoholic liver transplant patients.

Background: Infections after liver transplantation are the main cause of death in the first year. Recent reports indicate that NOD2 gene mutations increase the risk for inflammatory bowl disease and the severity of graft-versus-host disease in bone marrow transplant patients. Data on polymorphisms in liver transplant patients are sparse.

Donor information based prediction of early allograft dysfunction and outcome in liver transplantation.

Background & Aims: Poor initial graft function was recently newly defined as early allograft dysfunction (EAD) [Olthoff KM, Kulik L, Samstein B, et al. Validation of a current definition of early allograft dysfunction in liver transplant recipients and analysis of risk factors. Liver Transpl 2010; 16: 943].

Oil Red O-assessed macrosteatosis in liver transplant donor biopsies predicts ischemia-reperfusion injury and clinical outcome.

Steatosis in donor livers is an accepted adverse prognostic factor after liver transplantation. While its semiquantitative assessment shows varying reproducibility, it is questioned as a standard method. Additionally, the influence of hepatic steatosis on ischemia/reperfusion injury (I/R injury) has not been evaluated in biopsies after reperfusion.

Delicate balance of bleeding and thrombosis in end-stage liver disease and liver transplantation.

Liver transplantation in cirrhotic patients is accompanied by severe bleeding. Indeed, the first 100 recipients of liver allografts transplanted by Thomas E. Starzl died mainly by uncontrolled bleeding.

Extrahepatic complications of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease, and is strongly associated with the metabolic syndrome. In the last decade, it has become apparent that the clinical burden of NAFLD is not restricted to liver-related morbidity or mortality, and the majority of deaths in NAFLD patients are related to cardiovascular disease (CVD) and cancer. These findings have fuelled concerns that NAFLD may be a new, and added risk factor for extrahepatic diseases such as CVD, chronic kidney disease (CKD), colorectal cancer, endocrinopathies (including type 2 diabetes mellitus [T2DM] and thyroid dysfunction), and osteoporosis.

Adiponectin attenuates osteolysis in aseptic loosening of total hip replacements.

Joint replacements have a longer durability in patients with high serum levels of adiponectin (APN) than in patients with low levels. We aimed to characterize the unknown pathophysiological effects of APN on wear particle-induced inflammation, apoptosis and osteolysis. Immunohistochemistry was performed to detect APN, its receptors and apoptosis in patients with and without aseptic loosening.

From NAFLD to NASH to cirrhosis-new insights into disease mechanisms.

NAFLD has evolved as a serious public health problem in the USA and around the world. In fact, NASH-the most serious form of NAFLD-is predicted to become the leading cause of liver transplantation in the USA by the year 2020. The pathogenesis of NAFLD and NASH, in particular the mechanisms responsible for liver injury and fibrosis, is the result of a complex interplay between host and environmental factors, and is at the centre of intense investigation.

NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice.

Unlabelled: Inflammasome activation plays a central role in the development of drug-induced and obesity-associated liver disease. However, the sources and mechanisms of inflammasome-mediated liver damage remain poorly understood. Our aim was to investigate the effect of NLRP3 inflammasome activation on the liver using novel mouse models.