Although hepatic steatosis is seen with increasing frequency in clinical practice, its prevalence and risk factors are unknown. To investigate the prevalence of and risk factors for hepatic steatosis, such as alcohol consumption and obesity. Cross-sectional, observational study. Participants in the Dionysos Study. 257 participants assigned to one of four categories (67 controls, 66 obese persons, 69 heavy drinkers, and 55 obese heavy drinkers). Ethanol intake, assessed by a validated questionnaire and expressed as daily (g/d) and lifetime (kg) consumption, and body mass, expressed as body mass index. Biochemical tests of liver and metabolic function and hepatic ultrasonography were done. The prevalence of steatosis was increased in heavy drinkers (46.4% [95% CI, 34% to 59%]) and obese persons (75.8% [CI, 63% to 85%]) compared with controls (16.4% [CI, 8% to 25%]). Steatosis was found in 94.5% (CI, 85% to 99%) of obese heavy drinkers. Compared with controls, the risk for steatosis was higher by 2.8-fold (CI, 1.4-fold to 7.1-fold) in heavy drinkers, 4.6-fold (CI, 2.5-fold to 11.0-fold) in obese persons, and 5.8-fold (CI, 3.2-fold to 12.3-fold) in persons who were obese and drank heavily. In heavy drinkers, obesity increased the risk for steatosis by twofold (CI, 1.5-fold to 3.0-fold) (P < 0.001), but heavy drinking was associated with only a 1.3-fold (CI, 1.02-fold to 1.6-fold) increase in risk in obese persons (P = 0.0053). Elevated alanine aminotransferase and triglyceride levels are the most reliable markers of steatosis. Steatosis is frequently encountered in healthy persons and is almost always present in obese persons who drink more than 60 g of alcohol per day. Steatosis is more strongly associated with obesity than with heavy drinking, suggesting a greater role of overweight than alcohol consumption in accumulation of fat in the liver.

Research conducted during the past 30 years has increased our understanding of the mechanisms involved in colorectal cancer initiation and development. The findings have demonstrated the existence of at least three pathways: chromosomal instability, microsatellite instability and CpG island methylator phenotype. Importantly, new studies have shown that inflammation and microRNAs contribute to colorectal carcinogenesis. Recent data have demonstrated that several genetic and epigenetic changes are important in determining patient prognosis and survival. Furthermore, some of these mechanisms are related to patients’ response to drugs, such as aspirin, which could be used for both chemoprevention and treatment in specific settings. Thus, in the near future, we could be able to predict disease behavior based on molecular markers found on tumors, and direct the best treatment options for patients.

Commensal bacteria inhabiting the human intestine (i.e., intestinal microflora) participate in the development and maintenance of gut sensory and motor functions, including the promotion of intestinal propulsive activity. On the other hand, intestinal motility represents one of the major control systems of gut microflora, through the sweeping of excessive bacteria from the lumen. There is emerging evidence indicating that changes in this bidirectional interplay contribute to the pathogenesis of gut diseases, such as small intestinal bacterial overgrowth and intestinal pseudo-obstruction. Recent interest has also been directed to the potential role of intestinal microflora in the pathogenesis of the irritable bowel syndrome. Although the status of intestinal microflora in the irritable bowel syndrome remains unsettled, small intestinal bacterial overgrowth (as detected with breath testing) and increased fermentation of foods with gas production, provide indirect evidence that microflora may contribute to symptom generation in irritable bowel syndrome. The potential benefit of antibiotic and probiotic therapy is currently under investigation and opens new perspectives in irritable bowel syndrome treatment.

Biliary tract cancer (BTC) represents the second most frequently diagnosed primary liver cancer worldwide following hepatocellular carcinoma, and the overall survival of patients with unresectable disease remains poor. In recent years, the advent of immune checkpoint inhibitors (ICIs) has revolutionized the therapeutic landscape of several malignancies with these agents, which have also been explored in advanced BTC, as monotherapy or in combination with other anticancer agents. However, clinical trials evaluating ICIs in BTC have shown conflicting results, and the clinical benefit provided by immunotherapy seems limited to a small subgroup of BTC patients. Thus, the identification of reliable predictors of the response to immunotherapy represents a significant challenge in this setting. This review provides an overview of the available evidence on the biomarkers predictive of the response to ICIs in patients with advanced BTC, especially focusing on programmed death-ligand 1 (PD-L1), tumor mutational burden (TMB), microsatellite instability (MSI), and other emerging biomarkers.