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Objective: Bacterial translocation, causing intestinal inflammation, is one of the key mechanisms in the pathogenesis of hepatic encephalopathy (HE) and spontaneous bacterial peritonitis (SBP) The presence of fecal calprotectin quantitatively relates to intestinal neutrophil migration and is therefore considered as a marker of intestinal inflammation. We aimed to assess the role of fecal calprotectin concentrations (FCCs) in diagnosing the onset and severity of HE and SBP., Methods: Sixty-one cirrhotics were prospectively included. Forty-two subjects served as controls. Several complications of cirrhosis were diagnosed by reference methods. Stool samples were collected for measuring FCCs. Patients revealing other causes of abnormal calprotectin results, e.g. gastrointestinal bleeding or inflammatory bowel disease were excluded. Multivariate analysis of cirrhosis-associated complications and their relation to FCCs was performed., Results: Fecal calprotectin concentrations were higher in cirrhotics compared with controls (P<0.001). Among cirrhotics, FCCs were elevated dependent on the severity of liver disease as assessed by Child- and model for end-stage liver disease-scores. The corresponding correlation co-efficients by Spearman's were 0.577 (P<0.001) and 0.303 (P=0.018) respectively. A correlation emerged between elevated FCCs and HE grading as measured by West-Haven criteria and critical flicker frequency (both P<0.001; sensitivity=0.94 and 0.93, specificity=0.95 and 0.89 respectively) and SBP (P<0.02; sensitivity=0.71, specificity=0.79). FCCs were higher in cirrhotic subjects with additional extra-intestinal inflammation (P<0.01; sensitivity=0.65, specificity=0.8). The Pearsons correlation coefficients were 0.190 and 0.164 revealing no influence (P=0.142 and P=0.207) of laboratory parameters of systemic inflammation on FCCs in cirrhotic subgroup., Conclusions: Fecal calprotectin concentrations serve as a screening tool for HE and SBP. Assessment of FCCs may faciliate grading of HE-severity., (© 2011 John Wiley & Sons A/S.)

Background: Nonhepatic cancer risk of cirrhotic patients seems to be increased. Major surgery and chemotherapy in cirrhosis are associated with increased mortality and morbidity, which limits treatment., Aim: The aims of this study were analysis of (a) prevalence, (b) outcome after treatment, (c) of survival rate and (d) predictors of survival in a cirrhotic population., Patients and Methods: The study population was assembled retrospectively from a database of hospitalized patients (n=354). The Kaplan-Meier method was used to calculate the survival rate, and Cox regression analysis was performed to identify prognostic parameters., Results: Altogether, 84 neoplasms in 70 patients were observed. A total of 54 were nonhepatic (15.3%) mainly colorectal carcinoma, prostate cancer and tobacco-related neoplasms. TNM stage was the best prognostic parameter (p<0.0001). Low bilirubin (p=0.01), normal albumin (p=0.005) and absence of ascites (p<0.0001) were also related significantly to longer survival. The rate of postinterventional death after specific treatment was high. A proportion of patients received no specific therapy due to reduced physical performance, even in cases of limited disease., Conclusion: Our data confirm the increased risk of cirrhotic patients for developing nonhepatic cancer. Advanced TNM stage was associated with reduced long-term survival. Scoring systems, such as Child's classification and Model of Elevated Liver Disease (MELD) score, were suitable parameters to predict mortality. Oncological management in patients with cirrhosis must be on an individual basis, independent from TNM classification.

Objectives: Patients with liver cirrhosis are considered as high-risk population for cardiac surgery. The aim of this study was to review mortality and mid-term outcome of patients with liver cirrhosis requiring coronary artery bypass graft (CABG), valve replacement, or combined procedures., Methods: Between July 1997 and December 2006, 47 patients (mean age 65.4 ± 11.7 years) with liver cirrhosis were operated for CABG (21 patients), aortic valve replacement /mitral valve replacement (14 patients), CABG/VR (9 patients) or aortic dissection/tumorexstirpation (3 patients) (group I). Thirty-three patients were classified as Child-Pugh class A (subgroup A), 14 patients as Child-Pugh class B cirrhosis (subgroup B). Postoperative complications/mortality were analyzed retrospectively and compared with a propensity-score pair-matched control group of 47 patients (group II). Follow-up ranged from 0.1 to 11.5 years (mean 3.9 ± 0.25 years) and was complete for 100%., Results: Necessity of blood products was higher in group I (red cells, fresh frozen plama, platelets; P < 0.01). Chest-tube output (group I 1113 ± 857 vs. group II 849 ± 521; P = 0.15) and re-exploration rate (8.5 vs. 0%; P = 0.11) were slightly accelerated. Ventilation time and ICU-stay was prolonged (P < 0.015). Thirty-day mortality showed 19.1% (group I) versus 8.5% (group II) (P < 0.01), 6.1% (subgroup A) versus 50% (subgroup B) (P < 0.01). Operative risk in subgroup A was not significantly increased compared with control group (P = 0.68). In Child-B operative risk was 15.5-fold higher than in Child-A cirrhosis (P < 0.001). Postcardiotomy syndrome and pleurisy were more frequent in the cirrhosis group (4/47 vs. 0/47; P = 0.11). Actuarial survival after 3, 5 and 8 years was: group I 78.6, 75.6, and 70.2% versus group II 89.1, 85.7, and 85.7% (P = 0.08). Subgroup survival analysis was: group A 90.7, 86.6, and 78.5% versus group B 50, 50, and 50% (P < 0.01)., Conclusion: Cardiac surgery can be performed safely in patients with Child-Pugh class A and selected patients with Child-Pugh class B cirrhosis. Mid-term survival-rates within 8 years were not significantly different compared with a propensity-score pair-matched control group without cirrhosis.