Perception of the role of food and dietary modifications in patients with inflammatory bowel disease: Impact on lifestyle

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

Sarcopenia is associated with severe liver fibrosis in patients with non-alcoholic fatty liver disease

Background: Sarcopenia recognises insulin resistance and obesity as risk factors, and is frequently associated with cardiometabolic disorders, including non-alcoholic fatty liver disease (NAFLD). Aim: To test the prevalence of sarcopenia and its relation with the severity of fibrosis (main outcome) and the entire spectrum of liver histology in patients with NAFLD. Methods: We considered 225 consecutive patients with histological diagnosis of NAFLD (Kleiner score). The skeletal muscle index (%) (total appendicular skeletal muscle mass (kg)/weight (kg) Ã\u97 100), a validated measure of sarcopenia, was assessed by bioelectrical impedance analysis. Sarcopenia was defined as a skeletal muscle mass index â\u89¤37 in males and â\u89¤28 in females. Results: The prevalence of sarcopenia showed a linear increase with the severity of fibrosis, and severe fibrosis (F3â\u80\u93F4) was more than doubled in sarcopenia (48.3% vs. 20.4% in fibrosis â\u89¤F2, P < 0.001). After adjusting for confounders, the association of sarcopenia with severe fibrosis was maintained (OR 2.36, CI 1.16â\u80\u934.77, P = 0.01), together with age > 50 (OR 6.53, CI 2.95â\u80\u9314.4, P < 0.001), IFG/Diabetes (OR 2.14, CI 1.05â\u80\u934.35, P = 0.03) and NASH (OR 13.3, CI 1.64â\u80\u93108.1, P = 0.01). Similarly, a significant association was found between sarcopenia and NASH (P = 0.01), steatosis severity (P = 0.006), and ballooning (P = 0.01), but only the association with severe steatosis was maintained (OR 2.02, CI 1.06â\u80\u933.83, P = 0.03) after adjusting for confounders. Conclusions: 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

Insulin resistance is a risk factor for esophageal varices in HCV-induced cirrhosis

Indirect methods for predicting the presence of esophageal varices (EV) in cirrhotic patients are not sensitive enough to be used as a surrogate for endoscopy. We tested the effectiveness of liver stiffness measurement (LSM) by transient elastography (TE) and the presence of insulin resistance (IR), a marker associated with fibrosis progression, in the non-invasive prediction of portal hypertension. One hundred and four consecutive patients with newly diagnosed Child A HCV cirrhosis underwent upper GI endoscopy to search for EV. Clinical, anthropometric, biochemical, ultrasonographic and metabolic features, including IR by the homeostasis model assessment (HOMA), and LSM by TE, were recorded at the time of endoscopy. EV were detected in 63 of 104 patients (60%). In 10 patients (16%) the EV were medium-large (&#8805; F2). By multivariate analysis presence of EV was independently associated with a low platelet count/spleen diameter ratio (OR 0.998; 95% CI; 0.996-0.999) and with a high HOMA score (OR 1.296; 95%CI; 1.018-1.649) but not with LSM (OR 1.009; 95%CI; 0.951-1.070). It is noteworthy that 9/10 patients with medium-large EV had a platelet/spleen ratio of &lt; 792 and/or a HOMA of > 3.5. The independent association between low platelet/spleen ratio (OR 0.998; 95%CI; 0.996-1.000), high HOMA score (OR 1.373; 95%CI; 1.014-1.859) and presence of EV was confirmed in the sub-group of 77 non-diabetic subjects. Conclusions: In patients with Child A HCV cirrhosis, a low platelet/spleen ratio and a high HOMA score, regardless of diabetes, are the strongest independent predictors of the presence of EV. In this specific setting LSM seems not contribute to the diagnosis of portal hypertension

Aminopyrine breath test predicts liver-related events and death in HCV-related cirrhosis on SVR after DAA therapy

Background &amp; Aims: In patients with hepatitis C virus (HCV)-related advanced cirrhosis, the effects of sustained virological response (SVR) by direct antiviral agents (DAAs) on decompensation and liver deaths are less clearcut, since up to 30% of patients do not improve, and no predictors of outcome have been identified. We used 13C-aminopyrine breath test (ABT) to assess whether its changes can predict liver-related outcomes after DAA treatment in patients with HCV cirrhosis. Methods: Fifty consecutive patients with HCV cirrhosis were enrolled. Patients were included if they had Child A cirrhosis at risk for decompensation – defined as Child A6 (N&nbsp;=&nbsp;22, 44%) or previous decompensation (N&nbsp;=&nbsp;7, 14%) – or Child B cirrhosis (N&nbsp;=&nbsp;21, 42%) eligible for DAA-based antiviral therapy. ABT was performed at baseline and 12&nbsp;weeks after the end of antiviral therapy. Patients received sofosbuvir-based regimens. Results: Aminopyrine breath test was available for all 50 patients at baseline. The 120’ cumulative dose was directly associated at regression analysis only with albumin levels (P&nbsp;=.001). ABT was available at follow-up week 12 for 41 patients (FUW12), all with SVR, and followed for a median of 25.2&nbsp;months (range 12.2-32.1&nbsp;months). Lower Ʌ ABT – defined as changes of 120’ cumulative dose from FUW12 to baseline – (HR 0.97, 95% CI 0.94-0.99; P&nbsp;=.02) and FUW12 hepatic encephalopathy (HR 19.0, 95% CI 1.16-310.3; P&nbsp;=.03) were the only independent predictors of liver events/death at multivariate Cox regression analysis. The AUC of Ʌ ABT was good (0.87, 95% CI 0.75-0.97), with a delta ≥0% well discriminating patients at lower vs patients at higher risk of liver-related events/death (P&nbsp;&lt;.001). Conclusions: In patients with advanced HCV cirrhosis who achieve SVR with DAA, Ʌ ABT assists in assessing the residual likelihood of liver-related events and deaths after viral cure

Time course of insulin resistance during antiviral therapy in non-diabetic, non-cirrhotic patients with genotype 1 HCV infection

BACKGROUND: Genotype 1 (G1) hepatitis C virus (HCV) is associated with insulin resistance (IR) and its clearance seems to improve insulin sensitivity. We aimed to evaluate the time course of IR in response to antiviral therapy in non-diabetic, non-cirrhotic G1 HCV patients and to assess the effect of metabolic factors on sustained virological response (SVR). METHODS: A total of 83 consecutive treatment-naive G1 chronic hepatitis C (CHC) patients were evaluated by anthropometric and metabolic measurements, including IR using the homeostasis model assessment (HOMA). Patients were considered to have IR if HOMA was >2.7. All cases had a liver biopsy scored for staging, grading and steatosis. Anthropometric parameters and HOMA were re-evaluated at the end of antiviral therapy and at follow-up. RESULTS: SVR was achieved in 46 (55.4%) patients. By logistic regression, female gender (odds ratio [OR] 0.132, 95% confidence interval [CI] 0.33-0.529), gamma-glutamyltransferase >50 IU (OR 0.217, 95% CI 0.066-0.720) and presence of steatosis (OR 0.134, 95% CI 0.028-0.654) were independent negative predictors of SVR, whereas low-density lipoprotein cholesterol >107 IU (OR 6.671, 95% CI 1.164-11.577) was a positive predictor of SVR. The proportion of patients with IR significantly decreased (P=0.02) during antiviral therapy and at follow-up in patients achieving SVR. A similar trend, even if not significant, was observed in relapsers and non-responders. CONCLUSIONS: In non-diabetic G1 HCV patients undergoing antiviral therapy, IR improved in all patients, independently of virological outcome. HCV viral clearance was an additional factor in IR improvement. Female gender, hepatic steatosis and other metabolic parameters, but not IR, were identified as negative predictors of SVR in this study

Industrial, not fruit fructose intake is associated with the severity of liver fibrosis in genotype 1 chronic hepatitis C patients

Background & Aims: Unhealthy food intake, specifically fructose, has been associated with metabolic alterations and with the severity of liver fibrosis in patients with non-alcoholic fatty liver disease. In a cohort of patients with genotype 1 chronic hepatitis C (G1 CHC), we tested the association of fructose intake with the severity of liver histology. Methods: Anthropometric and metabolic factors, including waist circumference (WC), waist-to-hip ratio (WHR), dorso-cervical lipohypertrophy and HOMA were assessed in 147 consecutive biopsy-proven G1 CHC patients. Food intake, namely industrial and fruit fructose, was investigated by a three-day structured interview and a computed database. All biopsies were scored by an experienced pathologist for staging and grading (Scheuer classification), and graded for steatosis, which was considered moderate-severe if >= 20%. Features of non-alcoholic steatohepatitis (NASH) in CHC were also assessed (Bedossa classification). Results: Mean daily intake of total, industrial and fruit fructose was 18.0 +/- 8.7 g, 6.0 +/- 4.7 g, and 11.9 +/- 7.2 g, respectively. Intake of industrial, not fruit fructose, was independently associated with higher WHR (p = 0.02) and hypercaloric diet (p = F3) reported a significantly higher intake of total (20.8 +/- 10.2 vs. 17.2 +/- 8.1 g/day; p = 0.04) and industrial fructose (7.8 +/- 6.0 vs. 5.5 +/- 4.2; p = 0.01), not fruit fructose (12.9 +/- 8.0 vs. 11.6 +/- 7.0; p = 0.34). Multivariate logistic regression analysis showed that older age (OR 1.048, 95% CI 1.004-1.094, p = 0.03), severe necroinflammatory activity (OR 3.325, 95% CI 1.347-8.209, p = 0.009), moderate-severe steatosis (OR 2.421, 95% CI 1.017-6.415, p = 0.04), and industrial fructose intake (OR 1.147, 95% CI 1.047-1.257, p = 0.003) were independently linked to severe fibrosis. No association was found between fructose intake and liver necroinflammatory activity, steatosis, and the features of NASH. Conclusions: The daily intake of industrial, not fruit fructose is a risk factor for metabolic alterations and the severity of liver fibrosis in patients with G1 CHC

Retinol-binding protein 4: a new marker of virus-induced steatosis in patients infected with HCV genotype 1

Retinol-binding protein 4 (RBP4) is an adipocytokine associated with insulin resistance. We tested serum levels of RB4 to assess its link with steatosis in patients with genotype 1 (G1) chronic hepatitis C (CHC) or non-alcoholic fatty liver disease (NAFLD). Non-diabetic patients with CHC (n=143) or NAFLD (n=37) were evaluated by liver biopsy and anthropometric and metabolic measurements, including insulin resistance by the homeostasis model assessment (HOMA). Biopsies were scored by Scheuer classification for CHC, and Kleiner for NAFLD. Steatosis was tested as a continuous variable and graded as absent-mild &lt;30%, or moderate-severe &#8805;30%. Thirty non-diabetic, non-obese blood donors served as controls. RBP4 levels were measured by a human competitive ELISA kit (AdipoGen). Mean values of RBP4 were similar in NAFLD and CHC (35.3\ub19.3 \ub5g/L vs 36.8\ub117.6 p=0.47), and both significantly higher than in controls (28.9\ub112.1; p=0.02 and p=0.01, respectively). RBP4 was higher in CHC patients with steatosis than in NAFLD (42.1\ub119.7 vs 35.2\ub19.3; p=0.04). By linear regression, RBP4 was independently linked to steatosis only (p= 0.008) in CHC, and to elevated BMI (p= 0.01) and low grading (p= 0.04) in NAFLD. By linear regression, steatosis was independently linked to HOMA-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 (OR 1.045; 95%CI 1.020-1.070; p=0.0004), while waist circumference was associated with moderate-severe steatosis in NAFLD (OR 1.095; 95%CI 1.007-1.192; p=0.03). We conclude that in non-diabetic, non-obese patients with G1 CHC, serum RBP4 levels might be the expression of a virus-linked pathway to steatosis, largely unrelated to insulin resistance