Nutritional Assessment of Greek Liver Cirrhosis Patients: Mini Nutritional Assessment Predicts Mortality.

Malnutrition is highly prevalent in liver cirrhosis (LC). It increases as the severity of the disease progresses and it is related to poor survival. The objectives of the study were the nutritional assessment of Greek LC patients, using various nutritional assessment and screening tools, and the comparison of their predictive value for mortality. In total, 137 (77 male) consecutive LC patients (median age: 67 years) were assessed with subjective global assessment (SGA) and mini nutritional assessment (MNA) questionnaires, anthropometrics, handgrip strength (HGS) tests, and bioelectric impedance analysis (BIA), in comparison to a control group of 148 healthy people. Disease severity was assessed using the model for end-stage liver disease (MELD) scores. Patients were followed up for a median of 19 months. Survival curves were calculated using the Kaplan-Meier method. In total, 60% and 43% of patients were of adequate nutritional status by SGA and MNA, respectively, which was confirmed by most anthropometric measurements. MNA and SGA scores correlated significantly with anthropometrics and BIA-derived parameters. Besides the MELD score, mid-arm circumference (MAC), triceps skinfold (TSF), BIA's phase angle (Pha), and MNA predicted mortality in cirrhotic patients. The nutritional assessment demonstrated an unexpectedly high prevalence of well-nourished LC patients. MNA was a strong predictor of mortality.

Endoscopic management and outcome of non-variceal bleeding in patients with liver cirrhosis: A systematic review.

BACKGROUND: Acute non-variceal bleeding accounts for approximately 20% of all-cause bleeding episodes in patients with liver cirrhosis. It is associated with high morbidity and mortality therefore prompt diagnosis and endoscopic management are crucial. AIM: To evaluate available data on the efficacy of endoscopic treatment modalities used to control acute non-variceal gastrointestinal bleeding (GIB) in cirrhotic patients as well as to assess treatment outcomes. METHODS: Employing PRISMA methodology, the MEDLINE was searched through PubMed using appropriate MeSH terms. Data are reported in a summative manner and separately for each major non-variceal cause of bleeding. RESULTS: Overall, 23 studies were identified with a total of 1288 cirrhotic patients of whom 958/1288 underwent endoscopic therapy for acute non-variceal GIB. Peptic ulcer bleeding was the most common cause of acute non-variceal bleeding, followed by portal hypertensive gastropathy, gastric antral vascular ectasia, Mallory-Weiss syndrome, Dieaulafoy lesions, portal hypertensive colopathy, and hemorrhoids. Failure to control bleeding from all-causes of non-variceal GIB accounted for less than 3.5% of cirrhotic patients. Rebleeding (range 2%-25%) and mortality (range 3%-40%) rates varied, presumably due to study heterogeneity. Rebleeding was usually managed endoscopically and salvage therapy using arterial embolisation or surgery was undertaken in very few cases. Mortality was usually associated with liver function deterioration and other organ failure or infections rather than uncontrolled bleeding. Endoscopic treatment-related complications were extremely rare. Lower acute non-variceal bleeding was examined in two studies (197/1288 patients) achieving initial hemostasis in all patients using argon plasma coagulation for portal hypertensive colopathy and endoscopic band ligation or sclerotherapy for bleeding hemorrhoids (rebleeding range 10%-13%). Data on the efficacy of endoscopic therapy of cirrhotic patients vs non-cirrhotic controls with acute GIB are very scarce. CONCLUSION: Endotherapy seems to be efficient as a means to control non-variceal hemorrhage in cirrhosis, although published data are very limited, particularly those comparing cirrhotics with non-cirrhotics and those regarding acute bleeding from the lower gastrointestinal tract. Rebleeding and mortality rates appear to be relatively high, although firm conclusions may not be drawn due to study heterogeneity. Hopefully this review may stimulate further research on this subject and help clinicians administer optimal endoscopic therapy for cirrhotic patients.

Autophagy in liver diseases.

Autophagy is the liver cell energy recycling system regulating a variety of homeostatic mechanisms. Damaged organelles, lipids and proteins are degraded in the lysosomes and their elements are re-used by the cell. Investigations on autophagy have led to the award of two Nobel Prizes and a health of important reports. In this review we describe the fundamental functions of autophagy in the liver including new data on the regulation of autophagy. Moreover we emphasize the fact that autophagy acts like a two edge sword in many occasions with the most prominent paradigm being its involvement in the initiation and progress of hepatocellular carcinoma. We also focused to the implication of autophagy and its specialized forms of lipophagy and mitophagy in the pathogenesis of various liver diseases. We analyzed autophagy not only in well studied diseases, like alcoholic and nonalcoholic fatty liver and liver fibrosis but also in viral hepatitis, biliary diseases, autoimmune hepatitis and rare diseases including inherited metabolic diseases and also acetaminophene hepatotoxicity. We also stressed the different consequences that activation or impairment of autophagy may have in hepatocytes as opposed to Kupffer cells, sinusoidal endothelial cells or hepatic stellate cells. Finally, we analyzed the limited clinical data compared to the extensive experimental evidence and the possible future therapeutic interventions based on autophagy manipulation.

Portal vein thrombosis in cirrhosis: diagnosis, natural history, and therapeutic challenges.

Portal vein thrombosis (PVT) is a frequent complication in cirrhosis and its prevalence increases with disease severity. Several factors are involved in the development and progression of PVT. The challenge for the management of PVT is the precise evaluation of the bleeding risk as opposed to life-threatening extension of thrombosis. Nevertheless, the impact on the progression and outcome of liver disease is unclear. A critical evaluation of the available data discloses that treating PVT in cirrhotics is safe and effective. However, there are open issues, such as which anticoagulant could represent a safer therapeutic option, and when and for how long this treatment should be administered to cirrhotic patients with PVT.

Clinical outcomes of compensated and decompensated cirrhosis: A long term study.

AIM: To study these characteristics and prognostic patterns in a Greek patient population. METHODS: We analyzed a large cohort of cirrhotic patients referred to the department of Gastroenterology and Hepatology and the outpatient clinics of this tertiary hospital, between 1991 and 2008. We included patients with established cirrhosis, either compensated or decompensated, and further decompensation episodes were registered. A data base was maintained and updated prospectively throughout the study period. We analyzed differences in cirrhosis aetiology, time to and mode of decompensation, hepatocellular carcinoma (HCC) occurrence and ultimately patient survival. RESULTS: Five hundreds and twenty-two patients with median age 67 (range, 29-91) years and average follow up 9 years-10 mo (range, 1-206 mo) were studied. Commonest aetiology was hepatitis C virus (HCV, 41%) followed by alcohol (31%). The median survival time in compensated cirrhotics was 115 mo (95%CI: 95-133), whereas in decompensated patients was 55 mo (95%CI: 36-75). HCV patients survived longer while HBV patients had over twice the risk of death of HCV patients. The median time to decompensation was 65 mo (95%CI: 51-79), with alcoholics having the highest risk (RR = 2.1 vs HCV patients). Hepatitis B virus (HBV) patients had the highest risk of HCC, alcoholics the lowest. Leading causes of death: liver failure, hepatorenal syndrome, sepsis and HCC progression. CONCLUSION: Cirrhosis aetiology and decompensation at presentation were predictors of survival. Alcoholics had the highest decompensation risk, HBV cirrhotics the highest risk of HCC and HCV cirrhotics the highest decompensation-free time.