A small tumor size may impact the diagnostic performance of endoscopic ultrasound-guided tissue acquisition (EUS-TA) for diagnosing solid pancreatic lesions (SPLs). We aimed to compare the diagnostic yield of EUS-guided fine-needle aspiration (FNA) and biopsy (FNB) in SPLs with a diameter ≤ 15 mm. Consecutive patients who underwent EUS-TA for SPLs ≤ 15 mm between January 2015 and December 2022 in a tertiary referral center were retrospectively evaluated. The primary endpoint was diagnostic accuracy. The final diagnosis was based on surgical pathology or disease evolution after a minimum follow-up of 6 months. Inadequate samples were all considered false negatives for the study. Secondary outcomes included sample adequacy, factors impacting accuracy, and safety. We included 368 patients (52.4% male; mean age: 60.2 years) who underwent FNA in 72 cases and FNB in 296. The mean size of SPLs was 11.9 ± 2.6 mm. More than three passes were performed in 5.7% and 61.5% of patients in the FNB and FNA groups, respectively (p < 0.0001). FNB outperformed FNA in terms of diagnostic accuracy (89.8% vs. 79.1%, p = 0.013) and sample adequacy (95.9% vs. 86.1%, p < 0.001). On multivariate analysis, using FNA (OR: 2.10, 95% CI: 1.07–4.48) and a final diagnosis (OR: 3.56, 95% CI: 1.82–6.94) of benign conditions negatively impacted accuracy. Overall, the adverse event rate was 0.8%, including one pancreatitis in the FNA group and one pancreatitis and one bleeding in the FNB group, all mild and conservatively managed. EUS-TA for SPLs ≤ 15 mm has a high diagnostic yield and safety. This study suggests the superiority of FNB over FNA, with better performance even with fewer passes performed.

Autoimmune diseases are often associated with human leukocyte antigen (HLA) haplotypes, indicating that changes in major histocompatibility complex (MHC)-dependent self-peptide or antigen presentation contribute to autoimmunity. In our study, we aimed to investigate HLA alleles in a large European cohort of autoimmune pancreatitis (AIP) patients. Hundred patients with AIP, diagnosed and classified according to the International Consensus Diagnostic Criteria (ICDC), were prospectively enrolled in the study. Forty-four patients with chronic pancreatitis (CP) and 254 healthy subjects served as control groups. DNA was isolated from blood samples and two-digit HLA typing was performed with sequence-specific primer (SSP-) PCR. HLA allele association strength to AIP was calculated as odds ratio. We uncovered a strong enrichment of HLA-DQB1 homozygosity in type 1 and type 2 AIP patients. Moreover, a significantly increased incidence of the HLA-DRB1∗16 and HLA-DQB1∗05 alleles and a concomitant lack of the HLA-DRB1∗13 allele was detected in AIP type 1 and type 2 patients. In contrast, the HLA-DQB1∗02 allele was underrepresented in the 'not otherwise specified' (NOS) AIP subtype. We detected no significant difference in the HLA-DRB3, HLA-DRB4 and HLA-DRB5 allele frequency in our cohort. Although AIP type 1 and type 2 are characterized by distinct histopathological characteristics, both subtypes are associated with the same HLA alleles, indicating that the disease might rely on similar immunogenic mechanisms. However, AIP NOS represented another subclass of AIP.

Acute pancreatitis (AP) is an inflammatory disease that can represent a challenge for clinicians, in fact, the early determination of its severity in the first 72 h is crucial for prognosis, recognizing the etiology and carrying out risk stratification to determine a more specific therapy. No accurate early prognostic scores for disease severity have been published, so the severity of AP often cannot be properly defined in the first few hours of the disease. This initial phase represents a "no man's land", in which there is no certainty in the stratification of the damage, prognosis is difficult to establish, therapy must be started promptly, although there is still no effective medical therapy against pancreatic enzymatic activation. Therefore, it is very difficult at this stage to make the correct decisions to achieve the best outcome for the patient with AP. Literature search was carried out using the PubMed database by entering early management of acute pancreatitis [title] or therapy of acute pancreatitis [title] and selecting the most relevant articles for the diagnosis and therapy of acute pancreatitis in clinical practice. This document provides suggestions on managing the key clinical decisions for patients suffering from AP before disease severity is defined, to achieve the best outcomes for patients with AP.

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: Many efforts have been made to improve accuracy and sensitivity in diagnosing chronic pancreatitis (CP), obtaining quantitative assessments related to functional data. Our purpose was to correlate a computer-assisted analysis of pancreatic morphology, focusing on glandular margins, with exocrine function—measured by fecal elastase values—in chronic pancreatitis patients. Methods: We retrospectively reviewed chronic pancreatitis patients who underwent fecal elastase assessment and abdominal MRI in our institute within 1 year. We identified 123 patients divided into three groups based on the fecal elastase value: group A with fecal elastase > 200 μg/g; group B with fecal elastase between 100 and 200 μg/g; and group C with fecal elastase < 100 μg/g. Computer-assisted quantitative edge analysis of pancreatic margins was made on non-contrast-enhanced water-only Dixon T1-weighted images, obtaining the pancreatic margin score (PMS). PMS values were compared across groups using a Kruskal–Wallis test and the correlation between PMS and fecal elastase values was tested with the Spearman’s test. Results: A significant difference in PMS was observed between the three groups (p < 0.0001), with a significant correlation between PMS and elastase values (r = 0.6080). Conclusions: Quantitative edge analysis may stratify chronic pancreatitis patients according to the degree of exocrine insufficiency, potentially contributing to the morphological and functional staging of this pathology.