Metabolic-associated steatohepatitis liver disease (MASLD) currently impacts a quarter of the global population, and its incidence is expected to increase in the future. As a result, hepatocellular carcinoma associated with MASLD is also on the rise. Notably, this carcinoma does not always develop alongside liver cirrhosis, often leading to a more advanced stage at diagnosis. The challenge lies in accurately identifying patients who are at a higher risk to tailor screening processes effectively. Additionally, several therapeutic approaches are being explored to prevent hepatocellular carcinoma, although there are no universally accepted guidelines yet.

Obesity and inflammatory bowel disease (IBD) are two chronic conditions whose prevalence continues to rise globally. Emerging evidence suggests a bidirectional interplay between them, mediated by shared pathophysiological pathways. This narrative review explores the mechanisms Ilinking obesity to IBD development and progression, focusing on the role of adipose tissue dysfunction. Both diseases exhibit intestinal dysbiosis, low-grade systemic inflammation, and impaired epithelial barrier integrity, contributing to immune activation. Visceral adiposity, particularly mesenteric fat, acts as an immunometabolic organ producing cytokines and adipokines that may exacerbate intestinal inflammation. In Crohn’s disease, mesenteric fat expansion, or “creeping fat”, is associated with transmural inflammation, fibrosis, and luminal narrowing. Epidemiological data on obesity as a risk factor for IBD remain inconsistent due to methodological heterogeneity and confounders. Similarly, the impact of obesity on IBD outcomes, including disease activity, phenotype, and the need for surgery, is debated. While mesenteric surgical approaches like Kono-S anastomosis showed initial promise in reducing recurrence, recent randomized trials offer conflicting results. Finally, metabolic drugs such as statins, metformin, and GLP-1 receptor agonists have demonstrated anti-inflammatory properties with potential utility in IBD management. Prospective studies are warranted to elucidate the clinical significance of obesity and metabolic dysfunction in IBD and evaluate targeted therapeutic strategies.

INTRODUCTION: Clinical trials are the key to research in inflammatory bowel disease therapeutics. However, their external validity has been poorly evaluated, as have the outcomes in patients who do not meet the inclusion criteria. METHODS: This retrospective observational study at Miguel Servet University Hospital, Zaragoza, Spain, included all consecutive patients diagnosed with Crohn's disease or ulcerative colitis who initiated biologic treatments between January 2017 and December 2022. Eligibility was assessed against the criteria of pivotal randomized clinical trials (RCTs) for adalimumab, infliximab, golimumab, ustekinumab, or vedolizumab. Clinical effectiveness and safety were evaluated at 14–16 weeks and 54 weeks, with treatment persistence assessed using survival analysis. Effectiveness and persistence were assessed to analyze whether patient selection has an impact on different clinical outcomes. RESULTS: A total of 631 biologic treatments were initiated in 477 patients. Only 16.9% met the RCT criteria according to pivotal RCTs and 8% with newer RCTs. Disease-related criteria were the most frequently unmet (57.3%). Patients with ulcerative colitis were less likely to meet the criteria compared with patients with Crohn's disease (23% vs 4%, P < 0.001). No significant differences were observed in response rates, remission rates, adverse events, or drug discontinuation between eligible and noneligible patients. Survival analysis showed no differences in treatment persistence between both groups (hazard ratio 1.01, 95% confidence interval 0.73–1.38). DISCUSSION: Only a minority of real-world patients with inflammatory bowel disease would qualify for corresponding RCTs, questioning the external validity of these trials. However, real-world use of biologics demonstrated similar effectiveness and safety in eligible and noneligible patients, underscoring the importance of practical clinical judgement in therapeutic decisions.

Background: Numerous scores are designed to predict outcomes of patients with liver cirrhosis. Our study aimed to evaluate the ability of the Liver Disease Undernutrition Screening Tool (LDUST) in predicting mortality and decompensation in outpatients with clinically significant portal hypertension (CSPH). We hypothesized that LDUST could help identify patients in need of nutritional supplementation and intervention. Methods: A prospective study of 57 CSPH patients (36.8% female, mean age: 63.5 ± 9.9 years) with a median follow-up of 41 months was conducted. Baseline liver function, nutrition, and sarcopenia were assessed, alongside LDUST. During follow-up, the occurrence of liver decompensation, hospital admission, need for emergency care, and mortality were evaluated. Results: A total of 56.1% of patients were Child A, and the most frequent etiology was alcohol (50.9%). Malnutrition risk according to LDUST raised mortality (HR: 25.96 (1.47–456.78)), decompensation (HR 9.78 (2.08–45.89)), and admission (HR 4.86 (1.09–21.61)) risks in multivariate Cox analysis. Combining LDUST with Child and MELD scores improved their decompensation prediction (0.936 vs. 0.811 and 0.866 vs. 0.700). Conclusions: The LDUST has a solid ability to predict complications in cirrhosis outpatients with CSPH, and its integration with Child and MELD models enhances their predictive power. LDUST implementation could identify individuals necessitating early nutritional support.

INTRODUCTION: The coexistence of HIV infection and inflammatory bowel disease (IBD) is uncommon. Data on the impact of HIV on IBD course and its management are scarce. The aim of this study was to describe the IBD phenotype, therapeutic requirements, and prevalence of opportunistic infections (OIs) in IBD patients with a coexistent HIV infection. METHODS: Case-control, retrospective study includes all HIV-positive patients diagnosed with IBD in the Nationwide study on genetic and environmental determinants of inflammatory bowel disease registry. Patients with positive HIV serology (HIV-IBD) were compared with controls (HIV seronegative), matched 1:3 by year of IBD diagnosis, age, sex, and type of IBD. RESULTS: A total of 364 patients (91 HIV-IBD and 273 IBD controls) were included. In the whole cohort, 58% had ulcerative colitis, 35% had Crohn's disease (CD), and 7% were IBD unclassified. The HIV-IBD group presented a significantly higher proportion of proctitis in ulcerative colitis and colonic location in CD but fewer extraintestinal manifestations than controls. Regarding treatments, nonbiological therapies (37.4% vs 57.9%; P = 0.001) and biologicals (26.4% vs 42.1%; P = 0.007), were used less frequently among patients in the HIV-IBD group. Conversely, patients with HIV-IBD developed more OI than controls, regardless of nonbiological therapy use. In the multivariate analysis, HIV infection (odds ratio 4.765, 95% confidence interval (CI) 2.48–9.14; P < 0.001) and having ≥1 comorbidity (OR 2.445, 95% CI 1.23–4.85; P = 0.010) were risk factors for developing OI, while CD was protective (OR 0.372, 95% CI 0.18–0.78; P = 0.009). DISCUSSION: HIV infection seems to be associated with a less aggressive phenotype of IBD and a lesser use of nonbiological therapies and biologicals but entails a greater risk of developing OI.

The eradication of the hepatitis C virus (HCV) has revolutionized the hepatology paradigm, halting the progression of advanced liver disease in patients with chronic infection and reducing the risk of hepatocarcinoma. In addition, treatment with direct-acting antivirals can reverse the lipid and carbohydrate abnormalities described in HCV patients. Although HCV eradication may reduce the overall risk of vascular events, it is uncertain whether altered lipid profiles increase the risk of cerebrovascular disease in certain patients. We have conducted a review on HCV and lipid and carbohydrate metabolism, as well as new scientific advances, following the advent of direct-acting antivirals.