To validate the LiMAx test, a new bedside test for the determination of maximal liver function capacity based on 13C-methacetin kinetics. To investigate the diagnostic performance of different liver function tests and scores including the LiMAx test for the prediction of postoperative outcome after hepatectomy. Liver failure is a major cause of mortality after hepatectomy. Preoperative prediction of residual liver function has been limited so far. Sixty-four patients undergoing hepatectomy were analyzed in a prospective observational study. Volumetric analysis of the liver was carried out using preoperative computed tomography and intraoperative measurements. Perioperative factors associated with morbidity and mortality were analyzed. Cutoff values of the LiMAx test were evaluated by receiver operating characteristic. Residual LiMAx demonstrated an excellent linear correlation with residual liver volume (r = 0.94, P < 0.001) after hepatectomy. The multivariate analysis revealed LiMAx on postoperative day 1 as the only predictor of liver failure (P = 0.003) and mortality (P = 0.004). AUROC for the prediction of liver failure and liver failure related death by the LiMAx test was both 0.99. Preoperative volume/function analysis combining CT volumetry and LiMAx allowed an accurate calculation of the remnant liver function capacity prior to surgery (r = 0.85, P < 0.001). Residual liver function is the major factor influencing the outcome of patients after hepatectomy and can be predicted preoperatively by a combination of LiMAx and CT volumetry.

Initial graft function is a major factor influencing the clinical outcome after liver transplantation (LTX), but a reliable method for assessing and predicting graft dysfunction directly after LTX is not available. Ninety-nine patients undergoing deceased-donor LTX were studied in a prospective pilot study to evaluate the LiMAx test, the indocyanine green test, and conventional biochemical parameters with respect to their sensitivity and prognostic power for the diagnosis of initial graft dysfunction. Patients suffering from initial graft dysfunction (defined as technical complications or primary nonfunction (n = 8)) had significantly decreased LiMAx readouts (43 ± 18 versus 184 ± 98 μg/kg/hour, P < 0.001) immediately after LTX. Univariate analysis also showed significant differences for serum bilirubin, ammonia, glutamate dehydrogenase, and the international normalized ratio (P < 0.05), but multivariate analysis revealed LiMAx as the single independent predictor of initial dysfunction (P = 0.008) with an area under the receiver operating characteristic curve (AUROC) of 0.960 (95% confidence interval = 0.921-0.998, P < 0.001). In addition, the diagnosis of primary nonfunction (n = 3) was evaluated with LiMAx and aspartate aminotransferase (AST) activity on the first postoperative day. The calculated AUROC values were 0.992 (0.975-1.0, P = 0.004) for LiMAx and 0.967 (0.929-1.0, P = 0.006) for AST. By a combination of test results obtained directly after LTX and on the first day, LiMAx indicated primary nonfunction with a sensitivity of 1.0 (0.31-1.0) and a positive predictive value of 1.0 (0.31-1.0), whereas AST classification showed a sensitivity of 0.67 (0.13-0.98) and a positive predictive value of 0.29 (0.05-0.70). In conclusion, the assessment of initial graft function using the LiMAx test might be effective for identifying critical complications that could threaten graft survival within 24 hours after LTX.

Objective: Adipose tissue-derived factors link non-alcoholic fatty liver disease (NAFLD) with obesity, which has also been reported for circulating chemerin. On the other hand, hepatic chemerin and chemokine-like receptor 1 (CMKLR1) mRNA expression has not yet been studied in an extensively characterized patient collective.Design: This study was cross-sectional and experimental in design.Methods: Liver tissue samples were harvested from 47 subjects and histologically examined according to the NAFLD activity score (NAS). The concentrations of chemerin and CMKLR1 were measured using semi-quantitative real-time PCR, and the concentration of serum chemerin was measured using ELISA. To evaluate potential effects of chemerin and CMKLR1, cultured primary human hepatocytes (PHHs) were exposed to selected metabolites known to play a role in NAFLD (insulin, glucagon, palmitoic acid, and interleukin-6 (IL6)).Results: Chemerin andCMKLR1mRNA levels were elevated in the human liver. Their expression was correlated with the NAS (R²=0.543;P<0.001 andR²=0.355;P=0.014 respectively) and was significantly elevated in patients with definite non-alcoholic steatohepatitis (NASH) (P<0.05 respectively). Linear regression analysis confirmed an independent association of liver fibrosis, steatosis, inflammation, and hepatocyte ballooning with hepatic chemerin mRNA expression (P<0.05 respectively). The expression of hepatic chemerin and CMKLR1 was correlated with the measures of obesity (P0.05). None of the other metabolites showed an influence (P>0.05).Conclusion: This is the first study to show that chemerin mRNA expression is significantly elevated in the liver of NASH patients and that CMKLR1 expression is upregulated in liver inflammation, whereby IL6 could play a causal role.

Colorectal cancer (CRC) is the third most common malignancy worldwide. Most patients with metastatic CRC develop liver or lung metastases, while a minority suffer from brain metastases. There is little information available regarding the presentation, treatment, and overall survival of brain metastases (BM) from CRC. This systematic review and meta-analysis includes data collected from three major databases (PubMed, Cochrane, and Embase) based on the key words “brain”, “metastas*”, “tumor”, “colorectal”, “cancer”, and “malignancy”. In total, 1318 articles were identified in the search and 86 studies matched the inclusion criteria. The incidence of BM varied between 0.1% and 11.5%. Most patients developed metastases at other sites prior to developing BM. Lung metastases and KRAS mutations were described as risk factors for additional BM. Patients with BM suffered from various symptoms, but up to 96.8% of BM patients were asymptomatic at the time of BM diagnosis. Median survival time ranged from 2 to 9.6 months, and overall survival (OS) increased up to 41.1 months in patients on a multimodal therapy regimen. Several factors including age, blood levels of carcinoembryonic antigen (CEA), multiple metastases sites, number of brain lesions, and presence of the KRAS mutation were predictors of OS. For BM diagnosis, MRI was considered to be state of the art. Treatment consisted of a combination of surgery, radiation, or systemic treatment.