(1) Background: Functional abdominal bloating and distension (FAB/FAD) are common disorders of the gut–brain interaction. Their physiopathology is complex and not completely clarified, although gut microbiota imbalances play a central role. The treatment of FAB/FAD still represents a clinical challenge for both patients and healthcare providers. Gut microbiota modulation strategies might play a crucial role in their management. The aim of this narrative review was to update the current evidence on FAB/FAD, with a focus on gut microbiota. (2) Methods: In October 2023, a review was conducted through the Medline, PubMed, and Embase databases. Selected literature included all available English-edited studies (randomized controlled trials and cross-sectional, cohort, and case-control studies). (3) Results: Twelve studies were selected, most of which investigated the relationship between IBS and microbiota, with bloating being one of its symptoms. The studies suggest that restoring a balanced microbiome appears to be the most promising solution for better management of FAB/FAD. Targeted approaches, such as the use of probiotics, prebiotics, antibiotics such as rifaximin or dietary modifications, may hold the key to alleviating symptoms. Other therapeutic options, such as diet, neuromodulators, and brain–gut behavioral therapies (i.e., cognitive-behavioral therapy) have shown promising outcomes, but strong data are still lacking. (4) Conclusions: Targeted approaches that focus on the gut microbiota, such as the use of probiotics, prebiotics, and antibiotics, are essential in managing FAB/FAD. Understanding the complex relationship between gut microbiota and FAB/FAD is crucial for developing effective treatments. Further studies are needed to explore the specific roles of different microbial populations in patients with FAB/FAD to enhance therapeutic strategies.

Both Glycaemic index (GI) and Glycaemic Load (GL) were introduced to measure the impact of a carbohydrate-containing food on blood glucose. From this perspective, high-amylose (HA) flours, with a higher percentage of resistant starch (RS), may represent a suitable raw material to improve the glycaemic response. The present work aims to investigate the GI of HA bakery products (biscuits, taralli and bread) compared to products obtained from conventional flour. Ten healthy volunteers were enrolled and their capillary blood glucose was measured every 15 min for 2 h after the consumption of HA and control products containing 50 g of available carbohydrates. On average, in the three bakery products, the amount of total starch replaced by RS was equal to 12%. HA biscuits and HA bread showed significantly lower GI than their control counterparts (p = 0.0116 and p = 0.011, respectively) and better glycaemic control. From the survey to assess liking and willingness to pay on HA snacks, HA packages received an average premium of €0.66 compared to control products. Although HA flour results in lower GI in both biscuits and bread, further studies are needed to evaluate the correct composition of HA products to have beneficial effects on post-prandial glycaemia.

Autoimmune pancreatitis (AIP) is a steroid-responsive inflammatory disease of the pancreas. Few studies investigated pancreatic exocrine function (PEF) in patients suffering from AIP and no definitive data are available on the effect of steroids in PEF recovery. Aim of the study is the evaluation of severe pancreatic insufficiency (sPEI) prevalence in AIP at clinical onset and after steroid treatment. 312 Patients with diagnosis of AIP between January 1st^, 2010 and December 31st^, 2020 were identified in our prospectively maintained register. Patients with a pre-steroid treatment dosage of fecal elastase-1 (FE-1) were included. Changes in PEF were evaluated in patients with available pre- and post-treatment FE (between 3 and 12 months after steroid). One-hundred-twenty-four patients were included, with a median FE-1 of 122 (Q1-Q3: 15-379) μg/g at baseline. Fifty-nine (47.6 %) had sPEI (FE-1<100 μg/g). Univariable analysis identified type 1 AIP, radiological involvement of the head of the pancreas (diffuse involvement of the pancreas or focal involvement of the head), weight loss, age and diabetes as associated with a greater risk of sPEI. However, at multivariable analysis, only the involvement of the head of the pancreas was identified as independent risk factor for sPEI. After steroids, mean FE-1 changed from 64 (15-340) to 202 (40-387) μg/g (P = 0.058) and head involvement was the only predictor of improvement of sPEI. The inflammatory involvement of the head of the pancreas is associated with PEF severity, as well as PEF improvement after treatment with steroids in patients with AIP.

Background/Objectives: IPMNs are a possible cause of acute pancreatitis (AP). IPMN-associated-AP is considered a relative indication for surgery for the prevention of recurrent attacks of pancreatitis and for a hypothesized increased cancer risk. The literature is based on surgical series, and no data on the clinical features of AP associated with IPMNs and on the risk of recurrent pancreatitis and pancreatic cancer are available. This study aimed to describe the clinical/radiological features of BD-IPMN-associated AP. Moreover, BD-IPMN-associated risk factors for AP recurrence and risk of pancreatic cancer were investigated. Methods: Patients with AP associated with branch-duct IPMN (BD-IPMN) without “worrisome- features” and “high-risk-stigmata” evaluated in a Gastroenterology Unit (University of Verona) between 1 January 2012 and 31 December 2022 were retrospectively analyzed. Cox proportional hazard models were used to analyze the time to recurrence after the first occurrence of AP. Results: One hundred and thirty-five patients were included, with a mean age of 55.8 ± 12.5 years. Necrosis was diagnosed in 15 patients (11.1%) and 1 patient (0.7%) was admitted to the ICU. One hundred and two (75.6%) patients had recurrent pancreatitis. The median size of the largest BD-IPMN was 8 mm (Q1–Q3: 5–12). Eighteen patients (13.3%) developed main pancreatic duct dilation ≥ 5 mm. No patients developed dilation of the main pancreatic duct ≥ 10 mm, mural nodules, thickened cystic walls, or jaundice. In the unadjusted analysis, no BD-IPMN-related features were associated with an increased risk of recurrent pancreatitis. None of the patients developed pancreatic cancer. Conclusions: BD-IPMN-associated AP appears to have a benign clinical course. Cystic features related to increased risk of recurrence were not identified. The risk of cancer appears extremely low.

Background and Clinical Significance: Pancreatic neuroendocrine tumors (pNETs) rarely exhibit intraductal growth, a pattern that may mimic intraductal papillary mucinous neoplasms (IPMNs) or pancreatic ductal adenocarcinoma (PDAC). Preoperative recognition is challenging, particularly when associated with anatomic variants such as pancreas divisum. Case Presentation: A 63-year-old man with a history of pancreatic duct dilation presented with pruritus, weight loss, and lymphadenopathy. Cross-sectional imaging revealed a cephalopancreatic mass with upstream ductal dilatation. EUS demonstrated a hypervascular lesion with intraductal extension into the dorsal duct in the setting of pancreas divisum. EUS-FNB confirmed a well-differentiated pNET (G1) with loss of DAXX expression and preserved ATRX. Ga-68 PET/CT showed intense uptake in the primary lesion and lower-grade uptake in two additional nodules, later proven non-neoplastic. A multidisciplinary tumor board recommended preoperative optimization with somatostatin analog therapy and supervised weight reduction, followed by pylorus-preserving duodenocephalopancreatectomy. Final pathology confirmed NET G1 with intraductal growth and full concordance with preoperative EUS-FNB findings. Conclusions: in this case, a pNET showed intraductal growth within the dorsal duct in the context of pancreas divisus, further expanding the range of its reported presentations. It underscores the diagnostic value of EUS-FNB for morphologic, proliferative, and molecular characterization, and highlights the importance of multidisciplinary evaluation in guiding preoperative optimization and tailored surgical management.

Background and Aims: Pancreatic hyperenzymemia in inflammatory bowel disease (IBD) is an under-recognized and challenging condition, as elevated pancreatic enzymes may arise from heterogeneous mechanisms and do not necessarily reflect true pancreatic disorder. This multicenter study aimed to characterize the clinical spectrum, diagnostic work-up, and outcomes of hyperenzymemia in IBD. Methods: This retrospective multicenter study was conducted within the PANDORA network, including 34 international IBD centers. For the present analysis, only centers providing patient-level data on pancreatic hyperenzymemia were considered. Collected variables included demographic, clinical, biochemical, imaging, and therapeutic data. Cases were categorized into three predefined phenotypes: chronic asymptomatic pancreatic hyperenzymemia (CAPH), reclassified acute pancreatitis not meeting Atlanta criteria (recAP), and autoimmune pancreatitis (AIP). Results: A total of 148 IBD patients with elevated pancreatic enzymes were included (CAPH 54.7%, RecAP 35.1%, AIP 10.1%). Ulcerative colitis (UC) accounted for 56.8% of cases and Crohn’s disease (CD) for 43.2%. Overall, 73.6% of patients were asymptomatic at the time of enzyme elevation. Marked hyperenzymemia (≥3× ULN) occurred in 22.3% of patients and was more frequent in RecAP than in CAPH or AIP (50.0%, 6.2%, and 13.3%, respectively). IBD was clinically active in 48.6% of patients, with higher rates in CD. Notably, the clinical meaning of hyperenzymemia differed across IBD phenotypes: in CD it was more often associated with active inflammation, whereas in UC it more frequently prompted advanced imaging and led to the identification of AIP. Imaging strategies differed significantly across phenotypes, and drug withdrawal was common in CAPH and RecAP but unnecessary in AIP. Only two rechallenges confirmed a drug-related mechanism. Conclusions: Pancreatic hyperenzymemia in IBD encompasses a spectrum of conditions with different implications. A phenotype-oriented diagnostic approach is essential to avoid misclassification and unnecessary treatment changes.