Rationale: The prevalence of malnutrition and the provided nutritional therapy were evaluated in all the patients with SARS-CoV-2 infection (COVID-19) hospitalized in a 3rd level hospital in Italy. Methods: A one-day audit was carried out recording: age, measured or estimated body weight (BW) and height, body mass index (BMI, kg/m 2), 30-day weight loss (WL), comorbidities, serum albumin and Creactive protein (CRP: nv < 0.5 mg/dL), hospital diet (HD) intake, oral nutritional supplements (ONS), enteral (EN) and parenteral nutrition (PN). Modified NRS-2002 tool and GLIM criteria were used for nutritional risk screening and for the diagnosis of malnutrition, respectively. Results: A total of 268 patients was evaluated; intermediate care units (IMCUs, 61%), sub-intensive care units (SICUs, 8%), intensive care units (ICUs, 17%) and rehabilitation units (RUs, 14%): BMI: <18.5, 9% (higher in RUs, p ¼ 0.008) and !30, 13% (higher in ICUs, p ¼ 0.012); WL ! 5%, 52% (higher in ICUs and RUs, p ¼ 0.001); CRP >0.5: 78% (higher in ICUs and lower in RUs, p < 0.001); Nutritional risk and malnutrition were present in 77% (higher in ICUs and RUs, p < 0.001) and 50% (higher in ICUs, p ¼ 0.0792) of the patients, respectively. HD intake 50%, 39% (higher in IMCUs and ICUs, p < 0.001); ONS, EN and PN were prescribed to 6%, 13% and 5%, respectively. Median energy and protein intake/kg BW were 25 kcal and 1.1 g (both lower in ICUs, p < 0.05) respectively. Conclusions: Most of the patients were at nutritional risk, and one-half of them was malnourished. The frequency of nutritional risk, malnutrition, disease/inflammation burden and decrease intake of HD differed among the intensity of care settings, where the patients were managed according to the severity of the disease. The patient energy and protein intake were at the lowest limit or below the recommended amounts, indicating the need for actions to improve the nutritional care practice.

Highlights Job/time constraints limit the engagement of patients with NAFLD in counseling programs. Web-and group-based programs promote similar calorie/physical activity changes. Surrogate markers indicate reduced fat in the liver and no changes in hepatic fibrosis. Web counseling results in clinically significant weight loss in motivated patients. Structured web-based program is as effective as groupcounseling in selected patients with NAFLD.

The long-term weight management of obesity remains a very difficult task, associated with a high risk of failure and weight regain. However, many people report that they have successfully managed weight loss maintenance in the long term. Several factors have been associated with better weight loss maintenance in long-term observational and randomized studies. A few pertain to the behavioral area (eg, high levels of physical activity, eating a low-calorie, low-fat diet; frequent self-monitoring of weight), a few to the cognitive component (eg, reduced disinhibition, satisfaction with results achieved, confidence in being able to lose weight without professional help), and a few to personality traits (eg, low novelty seeking) and patient–therapist interaction. Trials based on the most recent protocols of lifestyle modification, with a prolonged extended treatment after the weight loss phase, have also shown promising long-term weight loss results. These data should stimulate the adoption of a lifestyle modification-based approach for the management of obesity, featuring a nonphysician lifestyle counselor (also called “lifestyle trainer” or “healthy lifestyle practitioner”) as a pivotal component of the multidisciplinary team. The obesity physicians maintain a primary role in engaging patients, in team coordination and supervision, in managing the complications associated with obesity and, in selected cases, in the decision for drug treatment or bariatric surgery, as possible more intensive, add-on interventions to lifestyle treatment.

Non-alcoholic fatty liver disease is a very common medical condition, driven by a combination of genetic and lifestyle factors, ultimately producing a severe chronic liver disease and increased cardiovascular risk. Most people are asymptomatic for a long time, and their daily life is unaffected, leading to difficulty in identifying and managing people who slowly progress to non-alcoholic steatohepatitis (NASH), NASH-cirrhosis, and eventually hepatocellular carcinoma. Despite advances in the understanding of pathogenic mechanisms and the identification of liver fibrosis as the strongest factor in predicting disease progression, no specific treatments have been approved by regulatory agencies. Outside controlled trials, treatment is generally limited to lifestyle intervention aimed at weight loss. Pioglitazone remains the drug of choice to reduce progression of fibrosis in people with diabetes, although it is often used off-label in the absence of diabetes. Vitamin E is mainly used in children and may be considered in adults without diabetes. Several drugs are under investigation according to the agreed targets of reduced NASH activity without worsening of fibrosis or improving fibrosis without worsening of NASH. Anti-inflammatory, anti-fibrotic agents and metabolism modulators have been tested in either phase III or phase IIb randomized controlled trials; a few failed, and others have produced marginally positive results, but only a few are being tested in extension studies. The development of non-invasive, easily repeatable surrogate biomarkers and/or imaging tools is crucial to facilitate clinical studies and limit liver biopsy.

Background: The accumulation of fat droplets in the hepatic parenchyma is driven by several factors, synergistically acting to increase triglyceride flow to the liver (diet and metabolic factors, endotoxemia from gut microbiota, genetic factors). Key Messages: In the presence of unhealthy lifestyles and behavioral factors, leading to enlarged adipose tissue and insulin resistance (IR), both lipolysis and de novo lipogenesis are expected to increase the risk of hepatic lipid depots, in association with high calorie (either high-fat or high-carbohydrate) diets. The gut microbiota may also be involved via obesity, IR and hepatic inflammation generated by gut-derived toxic factors. Finally, several data also support a primary role of genetic factors. A few gene polymorphisms have also been associated with the risk of nonalcoholic fatty liver disease development and nonalcoholic steatohepatitis progression to more fibrosis and advanced liver disease. In a few cases (e.g., patatin-like phospholipase domain-containing 3/adiponutrin), steatosis carries a high risk of both liver disease and cardiovascular morbidity/mortality; in other cases (e.g., transmembrane 6 superfamily 2 human gene), dissociation has been observed between the increased risk of liver disease versus cardiovascular disease. Conclusions: A variable interplay between the genetic background and the metabolic milieu is the likely physiopathologic mechanism involved in individual cases, which must be considered for implementing effective treatment strategies.

Many prognostic systems have been devised to predict the outcome of liver transplantation (LT) candidates. Today, the Model for End-Stage Liver Disease (MELD) is widely used for organ allocation, but it has shown some limitations. The aim of this study was to investigate the performance of MELD compared to 5 different score models. We evaluated the prognostic ability of MELD, modified Child-Turcotte-Pugh, MELD-sodium, United Kingdom MELD, updated MELD, and integrated MELD in 487 candidates with cirrhosis for LT at the Bologna Transplant Centre, Bologna, Italy, between 2003 and. Calibration analysis by Hosmer-Lemeshow test, calibration curves, and concordance c-statistics (area under the receiver operating characteristic curve [AUC]) were calculated at 3, 6, and 12 months. Actual cumulative survival curves, taking into account the event of interest in the presence of competing risk, were obtained using the best cutoffs identified by AUC. For each score, the Hosmer-Lemeshow test revealed a good calibration. Integrated MELD showed calibration curves closer to the line of perfect predicting ability, followed by MELD-sodium at 3 months and modified Child-Turcotte-Pugh at 6 months. MELD-sodium AUCs at 3 and 6 months (0.798 and 0.765, respectively) and integrated MELD AUC at 6 months (0.792) were better than standard MELD (P < 0.05). Actual survival curves showed that these 2 scores were able to identify the patients with the highest drop-out risk. In conclusion, MELD-sodium and integrated MELD were the best prognostic models to predict drop-out rates among patients awaiting LT. The Model for End-Stage Liver Disease (MELD) was first described in 2000 to predict 3-month survival rates in patients with chronic liver disease undergoing transjugular intrahepatic portosystemic shunt.1 This model, which includes 3 objective measurements (serum creatinine, bilirubin, and prothrombin time international normalized ratio [INR]) was subsequently proved to predict waitlist mortality in the liver transplantation (LT) setting more precisely than the ChildTurcotte-Pugh (CTP) score.2,3 At present, MELD is widely used for organ allocation, 4 but it has shown some limitations. First, MELD was devised to predict short-term survival, 3 whereas the time spent on the LT waitlist has increased over the past decade, reaching almost 1 year in about 63% of cases. 5 Moreover, MELD benefits patients with cholestasis or renal failure and is not directly influenced by other complications of cirrhosis associated with poor survival, suchAbbreviations: AUC, area under the receiver operating characteristic curve; CI, confidence interval; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis delta virus; HR, hazard ratio; iMELD, integrated MELD; INR, international normalized ratio; LT, liver transplantation; mCTP, modified Child-Turcotte-Pugh; MELD, Model for End-Stage Liver Disease; MELD-Na, MELD and serum sodium; MESO, MELD to serum sodium ratio; NPV, negative predictive value; PPV, positive predictive value; ROC, receiver operating character...

Background & AimsThe immune impairment characterizing chronic hepatitis B (cHBV) infection is thought to be the consequence of persistent exposure to viral antigens. However, the immune correlates of different clinical stages of cHBV and their relation with different levels of HBsAg have not been investigated. The aim of the present study was to evaluate the relationship between HBV-specific T cells response and the degree of in vivo HBV control and HBsAg serum levels in HBeAg-HBeAb+ cHBV.MethodsPeripheral blood mononuclear cells from 42 patients with different clinical profiles (treatment-suppressed, inactive carriers and active hepatitis) of cHBV, 6 patients with resolved HBV infection and 10 HBV-uninfected individuals were tested with overlapping peptides spanning the entire HBV proteome. The frequency and magnitude of HBV-specific T cell responses was assessed by IFNγ ELISPOT assay. Serum HBsAg was quantified with a chemiluminescent immunoassay.ResultsThe total breadth and magnitude of HBV-specific T cell responses did not differ significantly between the four groups. However, inactive carriers targeted preferentially the core region. In untreated patients, the breadth of the anti-core specific T cell response was inversely correlated with serum HBsAg concentrations as well as HBV-DNA and ALT levels and was significantly different in patients with HBsAg levels either above or below 1000 IU/mL. The same inverse association between anti-core T cell response and HBsAg levels was found in treated patients.ConclusionsDifferent clinical outcomes of cHBV infection are associated with the magnitude, breadth and specificity of the HBV-specific T cell response. Especially, robust anti-core T cell responses were found in the presence of reduced HBsAg serum levels, suggesting that core-specific T cell responses can mediate a protective effect on HBV control.

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