Bevacizumab plus Irinotecan,Fluorouracil,and Leucovorin for Metastatic Colorectal Cancer

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.27210

Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study Of Liver Diseases and the European Association for the Study of the Liver

https://www.journal-of-hepatology.eu/article/S0168-8278(13)00887-8/pdf

Altered profile of human gut microbiome is associated with cirrhosis and its complications

Evidence-based guidelines on the management of pancreatic cystic neoplasms (PCN) are lacking. This guideline is a joint initiative of the European Study Group on Cystic Tumours of the Pancreas, United European Gastroenterology, European Pancreatic Club, European-African Hepato-Pancreato-Biliary Association, European Digestive Surgery, and the European Society of Gastrointestinal Endoscopy. It replaces the 2013 European consensus statement guidelines on PCN. European and non-European experts performed systematic reviews and used GRADE methodology to answer relevant clinical questions on nine topics (biomarkers, radiology, endoscopy, intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm (MCN), serous cystic neoplasm, rare cysts, (neo)adjuvant treatment, and pathology). Recommendations include conservative management, relative and absolute indications for surgery. A conservative approach is recommended for asymptomatic MCN and IPMN measuring 5 mm, and MPD diameter >10 mm. Lifelong follow-up of IPMN is recommended in patients who are fit for surgery. The European evidence-based guidelines on PCN aim to improve the diagnosis and management of PCN.

/pdf/european-evidence-based-guidelines-on-pancreatic-cystic-1wsge9ovyy.pdf

European evidence-based guidelines on pancreatic cystic neoplasms

/pdf/international-consensus-document-icon-common-variable-2jatr2zj0y.pdf

International consensus document (icon): common variable immunodeficiency disorders

Basal energy production rate and substrate use in stable cirrhotic patients.

BACKGROUND/AIMS Common variable immunodeficiency (CVID) is an immunological disorder characterised by defective antibody production. Patients with CVID have a high risk of gastric cancer. It has been suggested that gastric cancer results from an interaction between environmental factors and a genetic predisposition. The role of Helicobacter pylori as an environmental factor in gastric carcinogenesis is of current interest. Moreover, p53 gene mutations have been reported in gastric cancer. This study focuses on the gastric pathology of patients with CVID and correlation with H pylori infection. METHODS Thirty four consecutive dyspeptic patients with CVID (mean age 49.6 years, range 14–72; 17 men) were included in the study. An upper gastrointestinal endoscopy was performed and biopsy specimens were taken from the antrum, incisura angularis, and gastric body. Biopsies were used for histological assessment, to identify the presence of H pylori, and to evaluate p53 overexpression. RESULTS H pylori infection was detected in 14/34 (41%) patients. Chronic active gastritis involving both antrum and body was observed more frequently in H pylori positive (79%) than H pylori negative (20%) patients (p = 0.001). Similarly, a histological feature of multifocal atrophic gastritis was found more frequently in infected (50%) than uninfected patients (10%) (p = 0.012). In addition, one case of gastric adenocarcinoma and another of notable dysplasia were observed in the H pylori positive group. Overexpression of p53 was found in six (18%) patients, including one with normal gastric mucosa. CONCLUSIONS It can be hypothesised that both H pylori and p53 alterations play a role in the gastric carcinogenesis of patients with CVID.

https://gut.bmj.com/content/gutjnl/45/1/77.full.pdf

Gastric pathology in patients with common variable immunodeficiency

A population of 70 patients with liver cirrhosis, most of whom were nonalcoholic, was studied. Distribution of ideal body weight and body mass index was below the median of controls, but very few patients were below the cut-off points for normalcy. Distribution of triceps skinfold and arm muscle circumference was also below the median and, in most patients, was also below the cut-off points. Serum visceral protein concentrations and anthropometric parameters each were reciprocally correlated with one another, but no correlation was observed between visceral proteins and anthropometric parameters. Serum visceral proteins appeared to correlate better with the degree of liver damage than with the degree of malnutrition. Therefore, anthropometric parameters seem preferable to serum visceral proteins for the assessment of nutritional status in patients with liver cirrhosis.

Optimal Nutritional Indexes in Chronic Liver Disease

Originally, colorectal cancer (CRC) tumorigenesis was understood as a multistep process that involved accumulation of tumor suppressor genes and oncogenes mutations, such as APC, TP53 and KRAS. However, this assumption proposed a relatively limited repertoire of genetic alterations. In the last decade, there have been major advances in knowledge of multiple molecular pathways involved in CRC pathogenesis, particularly regarding cytogenetic and epigenetic events. Microsatellite instability, chromosomal instability and CpG island methylator phenotype are the most analyzed cytogenetic changes, while DNA methylation, modifications in histone proteins and microRNAs (miRNAs) were analyzed in the field of epigenetic alterations. Therefore, CRC development results from interactions at many levels between genetic and epigenetic amendments. Furthermore, hereditary cancer syndrome and individual or environmental risk factors should not be ignored. The difficulties in this setting are addressed to understand the molecular basis of individual susceptibility to CRC and to determine the roles of genetic and epigenetic alterations, in order to yield more effective prevention strategies in CRC patients and directing their treatment. This review summarizes the most investigated biomolecular pathways involved in CRC pathogenesis, their role as biomarkers for early CRC diagnosis and their possible use to stratify susceptible patients into appropriate screening or surveillance programs.

Focus on genetic and epigenetic events of colorectal cancer pathogenesis: implications for molecular diagnosis

We compared the effect of lactulose or lactitol on the fecal flora of 21 cirrhotic patients without hepatic encephalopathy. All were treated with an individualized disaccharide dose to achieve and maintain two semiliquid bowel movements per day. Stool pH and fecal flora were determined before and 10 days after stabilizing the cathartic effect. Increased counts of lactobacilli were obtained with both treatments. This increase, which was related to the decreased stool pH, was more constant with lactulose. In addition, lactitol decreased certain proteolytic bacteria such as enterococci and enterobacteria. Both total aerobic and anaerobic bacterial counts showed little quantitative variations with either treatment.

Adriana Romiti

Papers

Basal energy production rate and substrate use in stable cirrhotic patients.

Gastric pathology in patients with common variable immunodeficiency

Optimal Nutritional Indexes in Chronic Liver Disease

Focus on genetic and epigenetic events of colorectal cancer pathogenesis: implications for molecular diagnosis

Effect of lactitol and lactulose administration on the fecal flora in cirrhotic patients.