Background & Aims: Lifestyle modification is a well-established approach for improving metabolic health and reducing ectopic fat accumulation in the liver. The Melbourne Consensus has recently highlighted intrapancreatic fat deposition (IPFD) as an important fat depot, playing a key role in the development of both endocrine and exocrine pancreatic diseases. Nevertheless, the existing literature on the impact of lifestyle modification on IPFD has not been systematically synthesized. We conducted a comprehensive systematic review and meta-analysis to assess the effects of lifestyle modification on IPFD. Methods: A systematic literature search was conducted in PubMed and Embase databases to identify interventional studies evaluating the effects of lifestyle modification on IPFD measured by magnetic resonance-based techniques. Data were meta-analyzed using a random-effects model. Statistical heterogeneity was assessed using the I² statistic, and publication bias was evaluated with Egger’s test. Results: A total of 23 studies were included. Lifestyle modification resulted in a significant reduction in IPFD (standardized mean difference [SMD] -0.26, 95% CI -0.36 to -0.16; p<0.0001), with low heterogeneity (I ² =12.9%). The pooled absolute reduction in MRI-measured IPFD was −1.02 % (95% CI −1.30 to −0.73; p<0.0001), with no evidence of heterogeneity (I ² =0%). Subgroup analyses showed the largest numerical reduction in IPFD with combined diet-and-exercise interventions (SMD -0.41, 95% CI -0.81 to -0.02, I ² =29.4%), followed by exercise alone (SMD -0.26, 95% CI -0.36 to -0.15, I ² =0%) and diet alone (SMD -0.22, 95% CI -0.37 to -0.08, I ² =27.9%). However, differences between intervention types were not statistically significant (p=0.40). There was no evidence of publication bias (p = 0.78). Conclusion: Lifestyle modification is an effective non-pharmacological approach for reducing IPFD, with combined diet-and-exercise interventions showing the largest numerical effect. These findings support the potential of structured lifestyle modification programs to reduce IPFD and may have implications for the prevention and management of pancreatic diseases.

Background: Growing evidence supports a role for high intrapancreatic fat deposition (IPFD) in the pathogenesis of type 2 diabetes mellitus (T2DM); however, the magnitude of this association and the extent to which it is influenced by body mass index (BMI), liver fat content (LFC), and age remain uncertain. Objective: To quantitatively evaluate IPFD measured by magnetic resonance imaging (MRI) in individuals with T2DM and to investigate study-level factors contributing to between-study variability. Methods: We systematically searched PubMed and Embase for observational studies comparing MRI-measured IPFD in individuals with T2DM versus non-diabetic controls, excluding studies in which IPFD quantification was performed using AI-based models. Pooled standardized mean differences (SMDs) were estimated using a restricted maximum likelihood approach with Hartung-Knapp adjustment. Heterogeneity was explored through subgroup, meta-regression, and sensitivity analyses. Results: Thirty studies ( n =3,980) were included. Individuals with T2DM had significantly higher IPFD than non-diabetic controls (SMD 1.13, 95% CI 0.74 to 1.51), with no significant differences when stratified by pancreatic region, MRI technique, geographic region, sample size, and risk of bias. In multivariable models, BMI remained the only consistent moderating covariate, and the excess IPFD in T2DM persisted after adjusting for BMI, LFC, and age (intercept=0.797, p=0.010, false discovery rate-adjusted p=0.018). Advanced heterogeneity exploration identified no structural outliers, and the pooled effect size remained consistent across multiple sensitivity analyses. Conclusion: T2DM is associated with substantially higher MRI-quantified IPFD, independent of study-level differences in BMI, LFC, and age. Although causality cannot be inferred, these findings support the hypothesis that IPFD may be involved in the underlying mechanism of T2DM. They also suggest that high IPFD could represent a metabolic hallmark, with potential implications for risk stratification and therapeutic targeting.

Patients with chronic hepatitis B often require prolonged nucleos(t)ide analogue since functional cure is rarely achieved. Medication nonadherence can trigger life-threatening hepatitis B virus (HBV) reactivation. We report a 58-year-old Asian man with HBeAg-negative chronic hepatitis B and cirrhosis. After 10 years of entecavir therapy, he achieved undetectable HBV DNA and fibrosis regression, but quantitative hepatitis B surface antigen remained >1200 IU/mL. He self-discontinued medication and presented with severe hepatitis reactivation. Liver condition gradually improved on restarting nucleos(t)ide analogue. This case highlights that medication cessation with a high hepatitis B surface antigen titer can precipitate severe hepatitis and liver failure, even after long-term HBV DNA suppression.

Background/Aim: Hepatitis D virus (HDV) infection is the most severe form of viral hepatitis but is under-recognized. We evaluated HDV screening frequency and clinical characteristics of HDV-positive patients in our liver center in the United States. Method: Patients with chronic hepatitis B (CHB) evaluated between January 2021 and December 2023 were included. For those tested anti-HDV(+), HDV RNA was performed and clinical data were recorded. Results: Among 1,337 (M=716, F=621) CHB patients, 93.3% were foreign-born. The cohort included 74.9% Asians, 12.3% Blacks, 9.1% Whites and 1.3% Hispanics. HDV screening significantly increased after 2011 reflecting an increase in HDV awareness. Patients aged 18-40 years had the highest screening rate of 58%. Overall, 13 (1.95%) were tested HDV positive and 11 were repeatedly HDV RNA(+). PWID was noted in 5 of 11. Despite low HBV DNA levels, all had ≥stage 2 fibrosis, and 7 had advanced stage 3-4 disease. After a median follow-up of 8.75 years, 8 (73%) developed hepatic decompensation and 4 had hepatocellular carcinoma. Conclusion: HDV screening reached 51.3% among our predominantly foreign-born CHB patients. The high prevalence of advanced fibrosis at diagnosis underscores the importance of HDV screening. Early diagnosis and effective therapy are urgently needed for this challenging disease.