Non-alcoholic fatty liver disease (NAFLD) is the predominant cause of chronic liver conditions, and its progression is marked by evolution to non-alcoholic steatosis, steatohepatitis, cirrhosis related to non-alcoholic steatohepatitis, and the potential occurrence of hepatocellular carcinoma. In our systematic review, we searched two databases, Medline (via Pubmed Central) and Scopus, from inception to 5 February 2024, and included 73 types of research (nine clinical studies and 64 pre-clinical studies) from 2854 published papers. Our extensive research highlights the impact of Berberine on NAFLD pathophysiology mechanisms, such as Adenosine Monophosphate-Activated Protein Kinase (AMPK), gut dysbiosis, peroxisome proliferator-activated receptor (PPAR), Sirtuins, and inflammasome. Studies involving human subjects showed a measurable reduction of liver fat in addition to improved profiles of serum lipids and hepatic enzymes. While current drugs for NAFLD treatment are either scarce or still in development or launch phases, Berberine presents a promising profile. However, improvements in its formulation are necessary to enhance the bioavailability of this natural substance.

Background: Biliary acute pancreatitis (AP) during pregnancy is a challenging situation, and current guidelines for AP, pregnancy care, and surgery do not specifically address its management. This study investigated the safety and effectiveness of cholecystectomy and endoscopic retrograde cholangiopancreatography (ERCP) during pregnancy in AP. Methods: This international retrospective multicenter cohort study encompassed questions related to demographic information, clinical presentation, management strategies, timing of cholecystectomy, approaches to the procedure, complications, and outcomes. Continuous variables were summarized as medians with interquartile ranges, and categorical variables as frequencies and percentages. Group comparisons used Welch's t ‐test, Pearson's chi‐squared, or Fisher's exact tests. Results: A total of 101 cases from 14 countries and 19 centers were enrolled. Cholecystectomy after mild AP during pregnancy had a lower rate of readmission due to recurrent AP or other gallstone‐related complications compared with those who did not undergo surgery after a mild AP during pregnancy (0% vs. 24%; n = 0/17 vs. n = 12/49, p = 0.027). Cholecystectomy performed during pregnancy was associated with a low surgical complication rate, identical to that seen in postpartum procedures (12% vs. 10%; n = 2/17 vs. n = 3/30; p > 0.999). Preterm birth occurred in 7.1% ( n = 1/14) of patients with cholecystectomy versus 11% ( n = 5/45) without. Fetal loss after surgery occurred only in the first trimester ( n = 3/17 vs. n = 1/49). No difference was seen in readmission (5%, n = 1/21 vs. 27%, n = 4/15; p = 0.138), fetal loss (5%, n = 1/21 vs. 27%, n = 4/15; p = 0.138) and preterm birth (6%, n = 1/17 vs. 8%, n = 1/12; p > 0.999) between the surgical and ERCP groups. The fetal loss (9.1%, n = 2/22 vs. 5.4%, n = 4/74; p = 0.618) and preterm birth rates (5.9%, n = 1/17 vs. 12%, n = 8/65; p = 0.677) did not significantly differ between patients with and without ERCP during pregnancy. Conclusion: Cholecystectomy is effective and safe in pregnant patients during the second or third trimester in cases of mild biliary pancreatitis. ERCP is safe in any trimester.

Pain is the most significant and debilitating symptom throughout all stages of pancreatitis, yet the precise mechanisms responsible for it remain only partially understood, and current pain relief methods often prove insufficient. To gain a clearer understanding, it is crucial to consider pancreatitis not as a singular condition but as comprising three distinct clinical types: acute pancreatitis (AP), recurrent acute pancreatitis (RAP), and chronic pancreatitis (CP), each of which may involve different pathways for pain perception. Notably, RAP has historically been overlooked as a distinct entity, resulting in a paucity of phenotype-specific data regarding its pain mechanisms. At the molecular level, pain in pancreatitis involves peripheral and central sensitization, neuroinflammatory signaling, and structural neural remodeling, processes driven by mediators such as substance P, CGRP, NGF, TRP channels, and pro-inflammatory cytokines. However, these mechanisms have been studied largely in isolation and within single phenotypes, leaving a critical gap in our understanding of how they evolve and interact across the full disease spectrum. This review aims to establish a comprehensive framework detailing the molecular mechanisms responsible for pain in all three pancreatitis phenotypes, with a particular focus on RAP as a less-studied clinical condition and to identify phenotype-specific targets for therapeutic development.