In Western patients with NAFLD, with high prevalence of metabolic disorders and advanced liver disease, sarcopenia was associated with the severity of fibrosis and steatosis, independently of hepatic and metabolic risk factors. Studies are needed to assess the impact of interventions to reduce sarcopenia on NAFLD progression.

P ortal hypertension (PH), defined by a hepatic venous pressure gradient (HVPG) greater than 6 mmHg, 1 is a common complication of cirrhosis. The presence and the development of esophageal varices (EV) is a clinical manifestation of PH, 2,3 with a prevalence that can range from 40% to 80% in patients with cirrhosis. This prevalence increases progressively in relation to the severity of liver damage. 4,5 The presence of EV is also a clear indicator of a certain stage of cirrhosis. 6 The development of EV in patients with cirrhosis occurs when the HVPG is greater than 10 mmHg, 3,7 with an incidence of approximately 5% per year and a yearly rate of progression to larger varices of 5% to 15%. 4,5,8 The clinical relevance of EV is linked to the risk of bleeding that occurs when HVPG is greater than 12 mmHg, 7-9 with a mortality rate that exceeds 20% within 6 weeks from the bleeding episode, despite aggressive treatment. 10 The Baveno IV 2005 Consensus Workshop 11 and the American Association for the Study of Liver Diseases 2007 single-topic symposium on portal hypertension 12 recommended that endoscopic screening for esophageal and gastric varices should always be performed when a diagnosis of cirrhosis is made. Upper endoscopy should be repeated at 2-year to 3-year intervals in patients without varices, and at 1-year to 2-year intervals in those with small varices, to evaluate their development or progression. 11,12 These guidelines might not be ideal for clinical

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Retinol-binding protein 4 (RBP4) is an adipocytokine associated with insulin resistance (IR).We tested serum levels of RBP4 to assess its link with steatosis in patients with genotype 1 chronic hepatitis C (CHC) or nonalcoholic fatty liver disease (NAFLD). Nondiabetic patients with CHC (n ‫؍‬ 143) or NAFLD (n ‫؍‬ 37) were evaluated by liver biopsy and anthropometric and metabolic measurements, including IR by the homeostasis model assessment. Biopsies were scored by Scheuer classification for CHC, and Kleiner for NAFLD. Steatosis was tested as a continuous variable and graded as absent-mild <30%, or moderate-severe >30%. Thirty nondiabetic, nonobese blood donors served as controls. RBP4 levels were measured by a human competitive enzyme-linked immunosorbent assay kit (AdipoGen). Mean values of RBP4 were similar in NAFLD and CHC (35.3 ؎ 9.3 g/L versus 36.8 ؎ 17.6; P ‫؍‬ 0.47, respectively), and both were significantly higher than in controls (28.9 ؎ 12.1; P ‫؍‬ 0.02 and P ‫؍‬ 0.01, respectively). RBP4 was higher in CHC patients with steatosis than in NAFLD (42.1 ؎ 19.7 versus 35.2 ؎ 9.3; P ‫؍‬ 0.04). By linear regression, RBP4 was independently linked to steatosis only (P ‫؍‬ 0.008) in CHC, and to elevated body mass index (P ‫؍‬ 0.01) and low grading (P ‫؍‬ 0.04) in NAFLD. By linear regression, steatosis was independently linked to homeostasis model assessment score (P ‫؍‬ 0.03) and high RBP4 (P ‫؍‬ 0.003) in CHC. By logistic regression, RBP4 was the only variable independently associated with moderate-severe steatosis in CHC (odds ratio, 1.045; 95% confidence interval, 1.020 to 1.070; P ‫؍‬ 0.0004), whereas waist circumference was associated with moderate-severe steatosis in NAFLD (odds ratio, 1.095; 95% confidence interval, 1.007 to 1.192; P ‫؍‬ 0.03). Conclusion: In nondiabetic, nonobese patients with genotype 1 CHC, serum RBP4 levels might be the expression of a virus-linked pathway to steatosis, largely unrelated to IR. (HEPATOLOGY 2008;48:28-37.)

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Background: Diet has a relevant role in triggering symptoms in inflammatory bowel disease (IBD) from the patients’ perspective, but there is gap the between patients’ and doctors’ perceptions. Few studies have addressed this topic. The aim of this study was to evaluate food habits and nutrition knowledge in a homogeneous cohort of patients with IBD from southern Italy. Methods: 167 consecutive patients with IBD were recruited. The survey was based on the administration of a semi-structured questionnaire assessing demographics, disease features, dietary behavior, and food intolerance. Results: The majority of patients did not consider food a cause of their disease. However more than 80% changed their diet after the diagnosis and most report an improvement in symptoms. Spiced and seasoned foods, dairy products, vegetables, and fruit were often avoided. A dairy-free diet was adopted by 33.7%. Food choices were based on self-experience and not on medical counselling. Dietary modifications deeply impact on lifestyle. Conclusions: Most of the patients with IBD set diet and lifestyle on self-experience and give up many foods. This has an impact on psychosocial functioning and can lead to nutritional deficiencies. High quality studies are warranted to assess evidence-based dietary strategies and develop patient-targeted dietary recommendations.

Recent evidence suggests a link between Inflammatory Bowel Disease (IBD) and eating disorders, an emerging complex bidirectional association. Indeed, the overlap of symptoms and signs can lead to delayed diagnosis and misdiagnosis of both conditions, but also the fear of food-induced symptoms, commonly observed in patients with IBD, determines dietary restrictions which in predisposed individuals may induce an overt eating disorder. ARFID (Avoidant Restrictive Food Intake Disorder) and anorexia nervosa are the eating disorders more frequently reported, while disordered eating and orthorexia nervosa are emerging conditions. Disease worsening due to refusal of therapies in patients with anorexia is also a matter of concern and an increased awareness of the possible association of these conditions by gastroenterologists and dietitians is strongly warranted in order for patients to receive the appropriate counseling.