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Purpose: Middle segment-preserving pancreatectomy (MSPP) is a relatively new parenchymal-sparing surgery that has been introduced as an alternative to total pancreatectomy (TP) for multicentric benign and borderline pancreatic diseases. To date, only 36 cases have been reported in English. Methods: We reviewed 22 published articles on MSPP and reported an additional case. Results: Our patient was a 49-year-old Japanese man diagnosed with Zollinger-Elison syndrome (ZES) caused by duodenal and pancreatic gastrinoma associated with multiple endocrine neoplasia syndrome type 1. We avoided TP and chose MSPP as the operative technique due to his relatively young age. The patient developed a grade B postoperative pancreatic fistula (POPF), which improved with conservative treatment. He was discharged without further treatment. To date, no tumor has recurred, and pancreatic function seems to be maintained. According to a literature review, the morbidity rate of MSPP is as high as 54%, mainly due to the high incidence of POPF (32%). In contrast, there was no perioperative mortality, and postoperative pancreatic function was comparable to that after conventional pancreatectomy. Conclusions: Despite the high incidence of POPF, MSPP appears to be safe, with low perioperative mortality and good postoperative pancreatic sufficiency. [ABSTRACT FROM AUTHOR]

INTRODUCTION: To investigate whether increased intrapancreatic fat deposition (IPFD) heightens the risk of diseases of the exocrine and endocrine pancreas. METHODS: A prospective cohort study was conducted using data from the UK Biobank. IPFD was quantified using MRI and a deep learning-based framework called nnUNet. The prevalence of fatty change of the pancreas (FP) was determined using sex- and age-specific thresholds. Associations between IPFD and pancreatic diseases were assessed with multivariate Cox-proportional hazard model adjusted for age, sex, ethnicity, body mass index, smoking and drinking status, central obesity, hypertension, dyslipidemia, liver fat content, and spleen fat content. RESULTS: Of the 42,599 participants included in the analysis, the prevalence of FP was 17.86%. Elevated IPFD levels were associated with an increased risk of acute pancreatitis (hazard ratio [HR] per 1 quintile change 1.513, 95% confidence interval [CI] 1.179-1.941), pancreatic cancer (HR per 1 quintile change 1.365, 95% CI 1.058-1.762) and diabetes mellitus (HR per 1 quintile change 1.221, 95% CI 1.132-1.318). FP was also associated with a higher risk of acute pancreatitis (HR 3.982, 95% CI 2.192-7.234), pancreatic cancer (HR 1.976, 95% CI 1.054-3.704), and diabetes mellitus (HR 1.337, 95% CI 1.122-1.593, P = 0.001). DISCUSSION: FP is a common pancreatic disorder. Fat in the pancreas is an independent risk factor for diseases of both the exocrine pancreas and endocrine pancreas. [ABSTRACT FROM AUTHOR]

Aim: Biallelic mutations in the PTRH2 gene have been associated with infantile multisystem neurological, endocrine, and pancreatic disease (IMNEPD), a rare autosomal recessive disorder of variable expressivity characterized by global developmental delay, intellectual disability or borderline IQ level, sensorineural hearing loss, ataxia, and pancreatic insufficiency. Various additional features may be included, such as peripheral neuropathy, facial dysmorphism, hypothyroidism, hepatic fibrosis, postnatal microcephaly, cerebellar atrophy, and epilepsy. Here, we report the first Italian family presenting only predominant neurological features. Methods: Extensive neurological and neurophysiological evaluations have been conducted on the two affected brothers and their healthy mother since 1996. The diagnosis of peripheral neuropathy of probable hereditary origin was confirmed through a sural nerve biopsy. Exome sequencing was performed after the analysis of major neuropathy‐associated genes yielded negative results. Results: Whole‐exome sequencing analysis identified the homozygous substitution c.256C>T (p.Gln86Ter) in the PTRH2 gene in the two siblings. According to American College of Medical Genetics and Genomics (ACMG) guidelines, the variant has been classified as pathogenic. At 48 years old, the proband's reevaluation confirmed a demyelinating sensorimotor polyneuropathy with bilateral sensorineural hearing loss that had been noted since he was 13. Additionally, drug‐resistant epileptic seizures occurred when he was 32 years old. No hepatic or endocrinological signs developed. The younger affected brother, 47 years old, has an overlapping clinical presentation without epilepsy. Interpretation: Our findings expand the clinical phenotype and further demonstrate the clinical heterogeneity related to PTRH2 variants. We thereby hope to better define IMNEPD and facilitate the identification and diagnosis of this novel disease entity. [ABSTRACT FROM AUTHOR]

The pancreas is an organ with both exocrine and endocrine functions, comprising a highly organized and complex tissue microenvironment composed of diverse cellular and non-cellular components. The impairment of microenvironmental homeostasis, mediated by the dysregulation of cell-to-cell crosstalk, can lead to pancreatic diseases such as pancreatitis, diabetes, and pancreatic cancer. Macrophages, key immune effector cells, can dynamically modulate their polarization status between pro-inflammatory (M1) and anti-inflammatory (M2) modes, critically influencing the homeostasis of the pancreatic microenvironment and thus playing a pivotal role in the pathogenesis of the pancreatic disease. This review aims to summarize current findings and provide detailed mechanistic insights into how alterations mediated by macrophage polarization contribute to the pathogenesis of pancreatic disorders. By analyzing current research comprehensively, this article endeavors to deepen our mechanistic understanding of regulatory molecules that affect macrophage polarity and the intricate crosstalk that regulates pancreatic function within the microenvironment, thereby facilitating the development of innovative therapeutic strategies that target perturbations in the pancreatic microenvironment. [ABSTRACT FROM AUTHOR]

Type 3c diabetes mellitus (T3cDM), also known as pancreatogenic or pancreoprivic diabetes, is a specific type of DM that often develops as a result of diseases affecting the exocrine pancreas, exhibiting an array of hormonal and metabolic characteristics. Several pancreatic exocrine diseases and surgical procedures may cause T3cDM. Diagnosing T3cDM remains difficult as the disease characteristics frequently overlap with clinical presentations of type 1 DM (T1DM) or type 2 DM (T2DM). Managing T3cDM is likewise challenging due to numerous confounding metabolic dysfunctions, including pancreatic endocrine and exocrine insufficiencies and poor nutritional status. Treatment of pancreatic exocrine insufficiency is of paramount importance when managing patients with T3cDM. This review aims to consolidate the latest information on surgical etiologies of T3cDM, focusing on partial pancreatic resections, total pancreatectomy, pancreatic cancer and trauma. [ABSTRACT FROM AUTHOR]

Severe acute pancreatitis (SAP) begins with premature activation of enzymes, promoted by the immune system, triggering a potential systemic inflammatory response that leads to organ failure with increased mortality and a bleak prognosis. Interleukin-22 (IL-22) is a cytokine that may have a significant role in SAP. IL-22, a member of the IL-10 cytokine family, has garnered growing interest owing to its potential tissue-protective properties. Recently, emerging research has revealed its specific effects on pancreatic diseases, particularly SAP. This paper provides a review of the latest knowledge on the role of IL-22 and its viability as a therapeutic target in SAP. Highlights: 1. Interleukin-22 (IL-22) is a member of the IL-10 family of cytokines. 2. IL-22 is a potential indicator for monitoring organ dysfunction and severity of severe acute pancreatitis (SAP). 3. IL-22 acts as a protective factor against acinar cell damage by suppressing autophagy and reducing the infiltration of inflammatory cells. 4. IL-22 alleviate SAP-induced multiorgan injury. 5. IL-22 protect SAP-induced intestinal barrier damage. [ABSTRACT FROM AUTHOR]

Pancreatogenic diabetes is a type of diabetes mellitus secondary to exocrine pancreatic disease, and it was officially proposed by the American Diabetes Association in 2014, with chronic pancreatitis as the most common etiology, followed by pancreatic cancer. At present, the misdiagnosis rate of this disease is extremely high, and patients with pancreatogenic diabetes have a higher risk of death and readmission than patients with type 2 diabetes. Therefore, it is of great significance to fully understand, correctly identify, and diagnose pancreatogenic diabetes in the early state, so as to reduce the disability rate and mortality rate of this disease. This article reviews the advances in the possible pathogenesis, diagnosis, treatment, and management of pancreatic diabetes secondary to pancreatitis and pancreatic cancer. [ABSTRACT FROM AUTHOR]

The role of the intestinal microbiota in the diagnosis and treatment of pancreatic diseases is increasingly significant. Consequently, fecal microbiota transplantation (FMT) is emerging as a promising therapeutic avenue for various pancreatic disorders, including cancer, pancreatitis, and type 1 diabetes (T1D). This innovative procedure entails transferring gut microbiota from healthy donors to individuals affected by pancreatic ailments with the potential to restore intestinal balance and alleviate associated symptoms. FMT represents a pioneering approach to improve patient outcomes in pancreatic diseases, offering tailored treatments customized to individual microbiomes and specific conditions. Recent research highlights the therapeutic benefits of targeting the gut microbiota for personalized interventions in pancreatic disorders. However, a comprehensive understanding of the intricate interplay between gut microbiota and pancreatic physiology warrants further investigation. The necessity for additional studies and research endeavors remains crucial, especially in elucidating both adult and pediatric cases affected by pathological pancreatic conditions. [ABSTRACT FROM AUTHOR]

Background: Pancreatic fluid collections (PFCs) may recur after resolution with endoscopic transmural drainage (ETD) and standard stent removal (SSR). Herein, we compared the efficacy and safety of leaving long-term indwelling plastic stents (LTIS) vs. standard stent removal after PFC resolution with ETD. Methods: We performed a systematic review of MEDLINE, EMBASE, CINAHL, Scopus, and Cochrane databases from inception to September 2022. Full-text articles comparing long-term (> 6 months) outcomes of LTIS and SSR were eligible, as well as single-arm studies with ≥ 10 patients with LTIS. Two independent reviewers selected studies, extracted data, and assessed the risk of bias using the Newcastle–Ottawa Scale. Measured outcomes included the following: (A) PFC recurrence; (B) interventions for PFC recurrence; (C) technical success; and (D) adverse events (AEs). Meta-analysis was carried out using random-effects models. Results: We included 16 studies, encompassing 1285 patients. Compared to SSR after PFC resolution with ETD, LTIS was associated with significantly lower risk of PFC recurrence (3% vs. 23%; OR 0.22 [95%CI 0.09–0.52]; I2 = 45%) and need for interventions (2% vs. 14%; OR 0.35 [95%CI 0.16–0.78]; I2 = 0%). The superiority of LTIS on reducing PFC recurrence was found with walled-off necrosis, with or without disconnected pancreatic duct, and with placement of ≥ 2 LTIS. When using LTIS, the pooled proportion of AEs was 8% (95%CI 4–11%) and technical success was 93% (95%CI 86–99%). Conclusions: Our results show that LTIS after PFC resolution with ETD is feasible, safe, and superior to SSR in reducing the risk of PFC recurrence and need for interventions. [ABSTRACT FROM AUTHOR]

Background: The accumulation of fat in the pancreas has greater clinical significance. It is unclear, though, how much the intermediate variables influence the fat deposition in these depots. This study aimed to determine the relation of pancreatic steatosis to Diabetes Mellitus, Acute Pancreatitis and Pancreatic Cancer. Methods: This case-control study was conducted on fifty patients for pancreatic diseases in internal medicine department at Zagazig University Hospitals, equally divided into five groups; group I: 10 cases as a control group, group II: with fatty pancreas (FP), group III: with acute pancreatitis (AP), group IV: with Diabetes Mellitus (DM) and case group V: with pancreatic cancer (PC). Patients were subjected to full medical history, physical examination, laboratory investigations, and non-contrast Computed Tomography (CT). Results: Age and males were significant increased in group V (PValue= 0.003 and P=0.019 respectively). Body Mass Index (BMI) (P=0.001) and females (P=0.006) were higher among fatty pancreas patients. Pancreatic steatosis diagnosed by CT in FP representing 100%, in acute pancreatitis 60%, DM 80% and PC 70% of patients, and it was worse in FP group as 40% ware grade 4 (P <0.001). Fatty liver diagnosed by CT in 100% of FP patients, 70% in AP and DM groups and 60% in PC group and was worse in FP group as 80% grade 3 (P <0.001). grades of fatty liver and Low-Density Lipoprotein (LDL) cholesterol significantly independently associated with fatty pancreas (P<0.001). High lipids, diabetes and grades of fatty liver were significantly associated with fatty pancreas (P<0.001) and LDL and fatty liver are independent risk factors (P<0.001). Conclusion: Pancreatic steatosis is highly related to Diabetes Mellitus, Acute Pancreatitis and Pancreatic Cancer. [ABSTRACT FROM AUTHOR]

Syndromic surveillance (SyS) is an important tool for early warning and monitoring of health in human and animal populations, but its use in aquaculture has been limited. Our study objective was to design a SyS system for Atlantic salmon aquaculture and to evaluate its performance in detecting pancreas disease (PD) outbreaks caused by salmonid alphaviruses on farms. We defined SyS outbreak alarms as cases where monthly farm mortality exceeded predefined cutoffs or deviated significantly from expected values based on predictive generalized linear models. These models were trained for each salmon production area in Norway, using data from 2014 to 2017. The outcome variable was fish mortality per farm-month, and input variables were production and environmental predictors, as well as an offset for the number of fish at risk. We also added autoregressive components to explain temporal dependency within fish cohorts. Subsequently, data from 2018 to 2021 was used to parameterize and validate the SyS system's performance against the current national PD surveillance program, which relies on routine farm-screening tests using molecular techniques and reports of clinical findings. The study covered 19,119 farm-months, involving 1,618 fish cohorts. The performance of our SyS system varied across production areas, with sensitivity ranging from 80.5% to 87.4% and a false alarm rate of 45.3%–53.2%. The absence of alarms was usually observed in farms that were truly negative for PD, i.e., a negative predictive value range of 81.2%–94.0%. The median time for alarms being raised was either in the same month as the current PD surveillance program or 1 month prior or after it. Our results indicate that the SyS system is a valuable tool for monitoring mortality on salmon farms, but alarms are unspecific if evaluated against an individual disease (PD). Increasing the frequency and granularity of mortality reporting might improve the SyS system's performance. [ABSTRACT FROM AUTHOR]

Identifying biomarkers linked to pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP) is crucial for early detection, treatment, and prevention. Methods: Association analyses of 10 serological biomarkers involved in cell signalling (IFN-γ, IL-6, IL-8, IL-10), oxidative stress (superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities, total glutathione (GSH), malondialdehyde (MDA) levels), and intestinal permeability proteins (zonulin, I-FABP2) were conducted across PDAC (n = 12), CP (n = 21) and control subjects (n = 23). A Mendelian randomisation (MR) approach was used to assess causality of the identified significant associations in two large genetic cohorts (FinnGen and UK Biobank). Results: Observational results showed a downregulation of SOD and GPx antioxidant enzyme activities in PDAC and CP patients, respectively, and higher MDA levels in CP patients. Logistic regression models revealed significant associations between CP and SOD activity (OR = 0.21, 95% CI [0.05, 0.89], per SD), GPx activity (OR = 0.28, 95% CI [0.10, 0.79], per SD), and MDA levels (OR = 2.05, 95% CI [1.36, 3.08], per SD). MR analyses, however, did not support causality. Conclusions: These findings would not support oxidative stress-related biomarkers as potential targets for pancreatic diseases prevention. Yet, further research is encouraged to assess their viability as non-invasive tools for early diagnosis, particularly in pre-diagnostic CP populations. [ABSTRACT FROM AUTHOR]

The quest for medications to reduce intra-pancreatic fat deposition is now quarter a century old. While no specific medication has been approved for the treatment of fatty change of the pancreas, drug repurposing shows promise in reducing the burden of the most common disorder of the pancreas. This leading article outlines the 12 classes of medications that have been investigated to date with a view to reducing intra-pancreatic fat deposition. Information is presented hierarchically—from preclinical studies to retrospective findings in humans to prospective interventional studies to randomised controlled trials. This lays the grounds for shepherding the most propitious drugs into medical practice through well-designed basic science studies and adequately powered randomised controlled trials. [ABSTRACT FROM AUTHOR]

Background: A grim prognosis of pancreatic cancer (PCa) was attributed to the difficulty in early diagnosis of the disease. Aims: Identifying novel biomarkers for early detection of PCa is thus urgent to improve the overall survival rates of patients. Methods: The study was performed firstly by identification of candidate microRNAs (miRNAs) in formalin-fixed, paraffin-embedded tissues using microarray profiles, and followed by validation in a serum-based cohort study to assess clinical utility of the candidates. In the cohorts, a total of 1273 participants from four centers were retrospectively recruited as two cohorts including training and validation cohort. The collected serum specimens were analyzed by real-time polymerase chain reaction. Results: We identified 27 miRNAs expressed differentially in PCa tissues as compared to the benign. Of which, the top-four was selected as a panel whose diagnostic efficacy was fully assessed in the serum specimens. The panel exhibited superior to CA19-9, CA125, CEA and CA242 in discriminating patients with early stage PCa from healthy controls or non-PCa including chronic pancreatitis as well as pancreatic cystic neoplasms, with the area under the curves (AUC) of 0.971 (95% CI 0.956–0.987) and 0.924 (95% CI 0.899–0.949), respectively. Moreover, the panel eliminated interference from other digestive tumors with a specificity of 90.2%. Conclusions: A panel of four serum miRNAs was developed showing remarkably discriminative ability of early stage PCa from either healthy controls or other pancreatic diseases, suggesting it may be developed as a novel, noninvasive approach for early screening of PCa in clinic. [ABSTRACT FROM AUTHOR]

The aryl hydrocarbon receptor (AHR) serves as a ligand-activated transcription factor crucial for regulating fundamental cellular and molecular processes, such as xenobiotic metabolism, immune responses, and cancer development. Notably, a spectrum of endocrine-disrupting chemicals (EDCs) act as agonists or antagonists of AHR, leading to the dysregulation of pivotal cellular and molecular processes and endocrine system disruption. Accumulating evidence suggests a correlation between EDC exposure and the onset of diverse pancreatic diseases, including diabetes, pancreatitis, and pancreatic cancer. Despite this association, the mechanistic role of AHR as a linchpin molecule in EDC exposure-related pathogenesis of pancreatic diseases and cancer remains unexplored. This review comprehensively examines the involvement of AHR in EDC exposure-mediated regulation of pancreatic pathogenesis, emphasizing AHR as a potential therapeutic target for the pathogenesis of pancreatic diseases and cancer. [ABSTRACT FROM AUTHOR]

Immune-mediated cerebellar ataxias (IMCAs) have diverse etiologies. Patients with IMCAs develop cerebellar symptoms, characterized mainly by gait ataxia, showing an acute or subacute clinical course. We present a novel concept of latent autoimmune cerebellar ataxia (LACA), analogous to latent autoimmune diabetes in adults (LADA). LADA is a slowly progressive form of autoimmune diabetes where patients are often initially diagnosed with type 2 diabetes. The sole biomarker (serum anti-GAD antibody) is not always present or can fluctuate. However, the disease progresses to pancreatic beta-cell failure and insulin dependency within about 5 years. Due to the unclear autoimmune profile, clinicians often struggle to reach an early diagnosis during the period when insulin production is not severely compromised. LACA is also characterized by a slowly progressive course, lack of obvious autoimmune background, and difficulties in reaching a diagnosis in the absence of clear markers for IMCAs. The authors discuss two aspects of LACA: (1) the not manifestly evident autoimmunity and (2) the prodromal stage of IMCA's characterized by a period of partial neuronal dysfunction where non-specific symptoms may occur. In order to achieve an early intervention and prevent cell death in the cerebellum, identification of the time-window before irreversible neuronal loss is critical. LACA occurs during this time-window when possible preservation of neural plasticity exists. Efforts should be devoted to the early identification of biological, neurophysiological, neuropsychological, morphological (brain morphometry), and multimodal biomarkers allowing early diagnosis and therapeutic intervention and to avoid irreversible neuronal loss. [ABSTRACT FROM AUTHOR]

MR is a powerful diagnostic tool in the diagnosis and management of most hepatic and pancreatic diseases. Thanks to its multiple sequences, the use of dedicated contrast media and special techniques, it allows a multiparametric approach able to provide both morphological and functional information for many pathological conditions. The knowledge of correct technique is fundamental in order to obtain a correct diagnosis. In this paper, different MR sequences will be illustrated in the evaluation of liver and pancreatic diseases, especially those sequences which provide information not otherwise obtainable with other imaging techniques. Practical MR protocols with the most common indications of MR in the study of the liver and pancreas are provided. [ABSTRACT FROM AUTHOR]

Background and Aim: More insight into the incidence of and factors associated with progression following a first episode of acute pancreatitis (AP) would offer opportunities for improvements in disease management and patient counseling. Methods: A long‐term post hoc analysis of a prospective cohort of patients with AP (2008–2015) was performed. Primary endpoints were recurrent acute pancreatitis (RAP), chronic pancreatitis (CP), and pancreatic cancer. Cumulative incidence calculations and risk analyses were performed. Results: Overall, 1184 patients with a median follow‐up of 9 years (IQR: 7–11) were included. RAP and CP occurred in 301 patients (25%) and 72 patients (6%), with the highest incidences observed for alcoholic pancreatitis (40% and 22%). Pancreatic cancer was diagnosed in 14 patients (1%). Predictive factors for RAP were alcoholic and idiopathic pancreatitis (OR 2.70, 95% CI 1.51–4.82 and OR 2.06, 95% CI 1.40–3.02), and no pancreatic interventions (OR 1.82, 95% CI 1.10–3.01). Non‐biliary etiology (alcohol: OR 5.24, 95% CI 1.94–14.16, idiopathic: OR 4.57, 95% CI 2.05–10.16, and other: OR 2.97, 95% CI 1.11–7.94), RAP (OR 4.93, 95% CI 2.84–8.58), prior pancreatic interventions (OR 3.10, 95% CI 1.20–8.02), smoking (OR 2.33, 95% CI 1.14–4.78), and male sex (OR 2.06, 95% CI 1.05–4.05) were independently associated with CP. Conclusion: Disease progression was observed in a quarter of pancreatitis patients. We identified several risk factors that may be helpful to devise personalized strategies with the intention to reduce the impact of disease progression in patients with AP. [ABSTRACT FROM AUTHOR]

For many years, it has been taught in medical textbooks that the endocrine and exocrine parts of the pancreas have separate blood supplies that do not mix. Therefore, they have been studied by different scientific communities, and patients with pancreatic disorders are treated by physicians in different medical disciplines, where endocrine and exocrine function are the focus of endocrinologists and gastroenterologists, respectively. The conventional model that every islet in each pancreatic lobule receives a dedicated arterial blood supply was first proposed in 1932, and it has been inherited to date. Recently, in vivo intravital recording of red blood cell flow in mouse islets as well as in situ structural analysis of 3D pancreatic vasculature from hundreds of islets provided evidence for preferentially integrated pancreatic blood flow in six mammalian species. The majority of islets have no association with the arteriole, and there is bidirectional blood exchange between the two segments. Such vascularization may allow an entire downstream region of islets and acinar cells to be simultaneously exposed to a topologically and temporally specific plasma content, which could underlie an adaptive sensory function as well as common pathogeneses of both portions of the organ in pancreatic diseases, including diabetes. [ABSTRACT FROM AUTHOR]

Congenital variants of the pancreas are being increasingly detected with the widespread use of modern imaging techniques. The underlying embryologic aberration predicts the final appearance of pancreatic development. It is essential to recognize these congenital variants, as many of these have been proven to be associated with pancreatic diseases like recurrent pancreatitis and chronic abdominal pain. Cross-sectional techniques like multidetector computed tomography and magnetic resonance cholangiopancreatography are the most used imaging techniques for the pancreas, where a radiologist comes across these variants. This pictorial aims to classify the type of variant anatomy of the pancreas, their imaging appearances, and their clinical significance. [ABSTRACT FROM AUTHOR]

Introduction: Serum amylase and lipase elevations are classically related to pancreatic diseases. Hyperamylasemia is noticed to various common non-pancreatic clinical conditions, however hyperlipasemia is considered the specific marker of pancreatic diseases. Methodology and Results: This paper set forth 3 cases of Diabetic Keto Acidosis that presented with abdominal pain which are initially misapprehended to be Acute Pancreatitis due to markedly raised serum amylase and lipase levels. Conclusion: Markedly raised amylase and lipase levels are also noticed in non-pancreatic diseases. Optimal clinical judgement plays an essential role in diagnosis. [ABSTRACT FROM AUTHOR]

The pancreas exerts endocrine and exocrine functions in energy balance. The neural innervation and immune milieu are both crucial in supporting pancreatic homeostasis. The neuronal network connects the pancreas with the central nervous system (CNS) and the enteric nervous system (ENS) and sustains metabolic activities. The nerves in the pancreas are categorized as spinal sensory afferent fibers, vagal sensory afferent nerves, autonomic fibers of both sympathetic and parasympathetic divisions, and fibers from the ENS and intrapancreatic ganglia. They innervate different regions and various cell types, which collectively determine physiological functions. Studies have established that the diverse pathological conditions, including pancreatitis, diabetes, and pancreatic tumor, are attributed to aberrant immune reactions; however, it is largely not clear how the neuronal network may influence the disease conditions. Enlightened by the recent advances illuminating the organ-wide neuronal architecture and the dysfunctions in pancreatic disorders, this review will highlight emerging opportunities to explore the cellular interrelationship, particularly the neuroimmune components in pancreatic health and diseases. [ABSTRACT FROM AUTHOR]

Purpose: Although venous drainage of the jejunal loop may be maintained after sacrifice of jejunal vein tributaries during pancreatoduodenectomy, risk of severe jejunal mesenteric congestion following division of these tributaries can be difficult to predict. This study considered how best to predict safety of jejunal vein tributary dissection. Methods: Preoperative imaging findings and results of intraoperative clamp tests of jejunal vein tributaries during pancreatoduodenectomy were analyzed in 121 patients with hepatobiliary and pancreatic disease to determine whether this information adequately predicted safety of resecting superior mesenteric vein branches. Results: Jejunal vein tributaries caudal to the inferior border of the pancreatic uncinate process tended to be fewer when tributaries cranial to this landmark were more numerous. Tributaries cranial to the border drained a relatively wide expanse of jejunal artery territory in the jejunal mesentery. The territory of jejunal tributaries cranial to the inferior border of the pancreas did not vary according to course of the first jejunal vein branch relative to the superior mesenteric artery. One patient among 30 (3%) who underwent intraoperative clamp tests of tributaries cranial to the border showed severe congestion in relation to a venous tributary coursing ventrally to the superior mesenteric artery. Conclusion: Jejunal venous tributaries drained an extensive portion of jejunal arterial territory, but tributaries located cranially to the inferior border of the pancreas could be sacrificed without congestion in nearly all patients. Intraoperative clamp testing of these tributaries can identify patients whose jejunal veins must be preserved to avoid congestion. [ABSTRACT FROM AUTHOR]

The intricate network of the pancreatic nervous system plays a fundamental role in physiologic functions of the endocrine and exocrine pancreas. Several pancreatic diseases affect the normal functionality of the pancreatic nervous system. This chronic derangement leads to anatomical alterations, such as neural hypertrophy and increased nerve density. Perineural invasion is a prominent feature of pancreatic cancer, contributing to cancer progression and metastasis. Despite the fact that these pathogenic mechanisms are still incompletely studied and understood, the constant occurrence of these alterations highlights their importance in the pathophysiology of the pancreatic diseases. The occurrence of anatomical changes is strictly linked to the appearance of pain. Pancreatic pain has peculiar features, and its management is complex in clinical practice. In the present review, the evidence on lifestyle, pharmacological and interventional approaches for the management of pancreatic pain is presented. Analgesic therapy is the cornerstone of pain treatment. However, it is important to identify the individual characteristic of the patients and personalize the approach to pain management. Nevertheless, the incomplete efficacy of these strategies makes this field an area of unmet needs. The study of neuroplasticity is crucial to understand the mechanisms that regulate the pathophysiology of pancreatic diseases. Several trials testing new drugs with specific neuromodulatory effects are ongoing. However, further studies are needed to investigate crucial targets to develop novel therapies for the modulation of the nervous system and the prevention of complications of pancreatic diseases. This comprehensive review summarizes the importance of the nervous system in pancreatic diseases with a special focus on its anatomy and physiology, its pathophysiological features and clinical relevance in pancreatic disease, the treatment of pancreatic pain, and the identification of future trends of research. [ABSTRACT FROM AUTHOR]

Simple Summary: The relation between biliary tree diseases and pancreatitis is not well-known in veterinary medicine. Anecdotally, hyperlipemia, pancreatic inflammation, and abnormalities of biliary flow are thought to play a role in the pathogenesis. The aim of the work was to study the frequency and features of pancreatic involvement in dogs with chronic biliary tree disease. We retrospectively included 81 dogs with both laboratory and ultrasound signs of chronic biliary tree disease. Medical records of the included dogs and their pancreatic involvement was recorded considering ultrasonographic features and/or biochemical alterations (Lipase DGGR). Fifty-eight dogs (72%) showed pancreatic involvement, suggesting that pancreatic status should be investigated in canine patients with chronic biliary tree disease. Canine chronic biliary tree disease (CBTD) is a suspected risk factor for pancreatic injury. The aim of this study was to evaluate the frequency and features of pancreatic involvement in canine CBTD, and their relationship with hyperlipemia and its severity. CBTD was defined as the increase in at least two of ALP, GGT, total bilirubin, cholesterol, and a biliary tree abnormal abdominal ultrasound (graded mild to severe). Pancreatic ultrasound appearance was recorded and classified as acute/chronic. Dogs were divided into a PBD group (pancreatic and biliary disease) and BD group (only biliary tree disease). PBD group was subgraded into a "pancreatic injury" and "pancreatitis" group. Eighty-one dogs were retrospectively included: 56 in the PBD group and 25 in the BD group. Of the PBD group, 20 had pancreatitis (15 chronic and 5 dogs acute). US score was mild in 64 dogs and moderate in 17 dogs, and it was not associated with evidence of pancreopathy. Sixty-six dogs had hyperlipemia (mild = 27 dogs; moderate-to-severe = 39 dogs) and no association with pancreopathy was found. Pancreatic injury was more frequent than pancreatitis in CBTD dogs. Although both acute and chronic pancreatic injury may be present, chronic forms were more frequent. Pancreatic injury should be considered in CBTD patients due its possible clinical significance. [ABSTRACT FROM AUTHOR]

Acute pancreatitis (AP) is an acute inflammatory process of the pancreas, the incidence of which is increasing, and the management of which requires multidisciplinary intervention. Our work is a prospective analysis of 356 cases of BP collected in the emergency services, Visceral A and B surgery, and resuscitation of the Hassan II teaching hospital in Fez over a 2-year period from April 2017 to May 2019. The goal of our job is to analyze the epidemiological aspects of PA and mainly to verify the reliability and the feasibility of the new SIRS score in the evaluation of the severity of PA in our context. The mean age was 55±17.29 with a clear female predominance. The diagnosis of BP was established in front of an evocative clinical picture associated with lipasemia> 3x normal in 91.5% of cases. Abdominal CT revealed a predominance of PA stage E balthazar with 37.5% followed by stage C with 32.5%. Biliary etiology is predominant in 78.4% of cases followed by origin Admission SIRS was present in 48% of cases and was persistent beyond 48 hours in 18% of cases. All of the patients who developed a complication during BP had a positive SIRS at admission. The superinfection of the necrosis flows was present in 75.8% of the patients having a persistent SIRS beyond 48h. The complications were mainly dominated by the superinfection of the necrosis flows found in 15% of the cases. According to the Atlanta classification, we found : Medical treatment was initiated in all patients while endoscopic and surgical treatment were much less common In the light of our study, it was concluded that the SIRS score is a simple, precise and specific means for predicting and evaluating the severity of acute pancreatitis taking into account the drawbacks of other multifactorial scores. [ABSTRACT FROM AUTHOR]

BACKGROUND: Postoperative healthcare use and readmissions are common among the hepatopancreatobiliary (HPB) population. We evaluated the surgical volume required to sustain advanced practice providers (APPs) in the perioperative setting for cost reduction. STUDY DESIGN: Using decision analysis modeling, we evaluated costs of employing dedicated perioperative APP navigators compared with no APPs navigators. Simulated subjects could: (1) present to an emergency department, with or without readmission, (2) present for direct readmission, (3) require additional office visits, or (4) require no additional care. We informed our model using the most current available published data and performed sensitivity analyses to evaluate thresholds under which dedicated perioperative APP navigators are beneficial. RESULTS: Subjects within the APP navigator cohort accumulated $1,270 and a readmission rate of 6.9%, compared with $2,170 and 13.5% with no APP navigators, yielding a cost savings of $905 and 48% relative reduction in readmission. Based on these estimated cost savings and national salary ranges, a perioperative APPs become financially self-sustaining with 113 to 139 annual HPB cases, equating to 2 to 3 HPB cases weekly. Sensitivity analyses revealed that perioperative APP navigators were no longer cost saving when direct readmission rates exceeded 8.9% (base case 3.7%). CONCLUSIONS: We show that readmissions are reduced by nearly 50% with an associated cost savings of $900 when employing dedicated perioperative APPs. This position becomes financially self-sufficient with an annual HPB case load of 113 to 139 cases. High-volume HPB centers could benefit from postdischarge APP navigators to optimize outcomes, minimize high-value resource use, and ultimately save costs. [ABSTRACT FROM AUTHOR]

Recent studies have shown that a pro-inflammatory diet and dysbiosis, especially a high level of trimethylamine-N-oxide (TMAO), are associated with various adverse health conditions. Cardiovascular diseases and pancreatic diseases are two major morbidities in the modern world. Through this narrative review, we aimed to summarize the association between a pro-inflammatory diet, gut microbiota, and cardiovascular and pancreatic diseases, along with their underlying mechanisms. Our review revealed that TMAO is associated with the development of cardiovascular diseases by promoting platelet aggregation, atherosclerotic plaque formation, and vascular inflammation. TMAO is also associated with the development of acute pancreatitis. The pro-inflammatory diet is associated with an increased risk of pancreatic cancer and cardiovascular diseases through mechanisms that include increasing TMAO levels, activating the lipopolysaccharides cascade, and the direct pro-inflammatory effect of certain nutrients. Meanwhile, an anti-inflammatory diet decreases the risk of cardiovascular diseases and pancreatic cancer. [ABSTRACT FROM AUTHOR]

It is currently thought that excess fatty acid-induced lipotoxicity in hepatocytes is a critical initiator in the development of nonalcoholic fatty liver disease (NAFLD). Lipotoxicity can induce hepatocyte death; thus, reducing lipotoxicity is one of the most effective therapeutic methods to combat NAFLD. Abundant evidence has shown that hesperidin (HSP), a type of flavanone mainly found in citrus fruits, is able to ameliorate NAFLD, but the molecular mechanisms are unclear. We previously reported that pyroptosis contributed to NAFLD development and that inhibiting pyroptosis contributed to blunting the progression of NAFLD in rat models. Therefore, we questioned whether HSP could contribute to ameliorating NAFLD by modulating pyroptosis. In this study, a high-fat diet (HFD) induced dyslipidemia and hepatic lipotoxicity in rats, and HSP supplementation ameliorated dyslipidemia and insulin resistance. In addition, the HFD also caused pyroptosis in the liver and pancreas, while HSP supplementation ameliorated pyroptosis. In vitro, we found that HSP ameliorated palmitic acid-induced lipotoxicity and pyroptosis in HepG2 and INS-1E cells. In conclusion, we showed for the first time that HSP has a protective effect against liver and pancreas damage in terms of pyroptosis and provides a novel mechanism for the protective effects of HSP on NAFLD. [ABSTRACT FROM AUTHOR]

Background: Endoscopic retrograde cholangiopancreatography (ERCP) is the preferred technique for treating pathologies of the bile duct. It has been suggested that this procedure, combined with sphincterotomy, may influence the subsequent development of long-term complications. The main objective of this study was to determine the long-term complications of biliopancreatic disease after ERCP and their potential association with the development of biliopancreatic neoplasms. Methods: This retrospective cohort study included 576 patients who underwent ERCP (referred to as index ERCP) with sphincterotomy for benign biliary disease, with a minimum follow-up period of more than 2 years. Results: The incidence of long-term benign and neoplastic pathologies after ERCP was analyzed. The most common findings were recurrence of choledocholithiasis in 70 patients (12.1%), cholangitis "sine materia" in 27 patients (4.7%), and acute pancreatitis in 8 patients (1.4%). Eight patients (1.4%) developed hepatobiliopancreatic neoplasms, including 4 cases of pancreatic neoplasms (0.7%), 1 cholangiocarcinoma (0.2%), 1 ampulloma (0.2%), and 2 intrahepatic neoplasms (0.3%). Multivariate analysis revealed that factors such as age over 50 years, previous biliary surgery, diversion of the bile duct (BD) to the digestive tract, dilation of the BD, stent placement, biopsy, and cholecystectomy were factors associated with an increased risk of long-term benign complications. Conclusion: Endoscopic retrograde chola ngiop ancre atogr aphy with sphincterotomy is associated with an increased long-term risk of subsequent benign biliopancreatic disease. However, our data do not allow us to establish a direct relationship with the development of biliopancreatic neoplasms. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Primary pancreatic lymphoma is a rare disease that can mimic acute pancreatitis. Since the prognosis and approaches differ, clinicians should differentiate it from other pancreatic diseases, especially autoimmune pancreatitis and adenocarcinoma. [ABSTRACT FROM AUTHOR]

Key Clinical Message: In this noteworthy case series regarding pancreatic pseudo tumors, we intend to spread knowledge among physicians for the diagnostic and therapeutic approach and eventual disease prognosis. Inflammatory pseudotumor of pancreatic head greatly mimics pancreatic head tumor. One of them is IgG4‐related pancreatic disease, which is commonly mistaken as neoplastic disease on imaging. In our novel case series, we report three cases of IgG4‐related pancreatic head pseudotumor with patients ranging from 35 to 72 years of age. Patients presented with jaundice and abdominal pain. Alongside initial laboratory workup, abdominal CTs and serum IgG4 levels were also obtained. Imaging features in conjunction with IgG4 levels confirmed the diagnosis of IgG4‐related autoimmune pancreatitis. Pancreatic pseudotumors are notorious for being often reported as real tumors. Through our noteworthy case series, we intend to highlight the imaging features and laboratory markers that are crucial in such cases to avoid invasive procedures. [ABSTRACT FROM AUTHOR]

Purpose: To highlight median arcuate ligament syndrome as a potential cause for celiac artery stenosis and pancreaticoduodenal artery aneurysm, and describe treatment options in this setting. Case Report: A 63-year-old male presented with a pancreaticoduodenal artery aneurysm and concomitant celiac artery stenosis that was treated with celiac artery stenting and aneurysm coiling. He subsequently developed stent fracture and celiac artery occlusion secondary to previously unrecognized median arcuate ligament syndrome causing reperfusion of the aneurysm. This was treated with open median arcuate ligament release and aorta to common hepatic artery bypass with good clinical result and stable 20-month surveillance imaging. Conclusion: It is critical to recognize median arcuate ligament syndrome as a cause of celiac artery stenosis in the setting of pancreaticoduodenal artery aneurysm given the high risk of failure of endovascular stenting. Open aorto-hepatic artery bypass and endovascular aneurysm coiling should be the preferred approach in these patients. [ABSTRACT FROM AUTHOR]

We report a case of postoperative pseudoaneurysm, successfully treated with selective arterial embolization, using a steerable microcatheter and triaxial system via retrograde approach. A pseudoaneurysm was detected in the dorsal pancreatic artery, a severely narrow and steeply inverted branch of the superior mesenteric artery, making microcatheter insertion via the antegrade approach challenging. However, a steerable microcatheter was advanced beyond the orifice and the tip was reversed, changing the route to retrograde allowing for easy insertion of the microguidewire. Subsequently, a small microcatheter was advanced beyond the pseudoaneurysm into the dorsal pancreatic artery, and arterial embolization was successfully completed without complications. [ABSTRACT FROM AUTHOR]

Background: Recent research increasingly highlights a strong correlation between gut microbiota and the risk of gastrointestinal diseases. However, whether this relationship is causal or merely coincidental remains uncertain. To address this, a Mendelian randomization (MR) analysis was undertaken to explore the connections between gut microbiota and prevalent gastrointestinal diseases. Methods: Genome-wide association study (GWAS) summary statistics for gut microbiota, encompassing a diverse range of 211 taxa (131 genera, 35 families, 20 orders, 16 classes, and 9 phyla), were sourced from the comprehensive MiBioGen study. Genetic associations with 22 gastrointestinal diseases were gathered from the UK Biobank, FinnGen study, and various extensive GWAS studies. MR analysis was meticulously conducted to assess the causal relationship between genetically predicted gut microbiota and these gastrointestinal diseases. To validate the reliability of our findings, sensitivity analyses and tests for heterogeneity were systematically performed. Results: The MR analysis yielded significant evidence for 251 causal relationships between genetically predicted gut microbiota and the risk of gastrointestinal diseases. This included 98 associations with upper gastrointestinal diseases, 81 with lower gastrointestinal diseases, 54 with hepatobiliary diseases, and 18 with pancreatic diseases. Notably, these associations were particularly evident in taxa belonging to the genera Ruminococcus and Eubacterium. Further sensitivity analyses reinforced the robustness of these results. Conclusions: The findings of this study indicate a potential genetic predisposition linking gut microbiota to gastrointestinal diseases. These insights pave the way for designing future clinical trials focusing on microbiome-related interventions, including the use of microbiome-dependent metabolites, to potentially treat or manage gastrointestinal diseases and their associated risk factors. [ABSTRACT FROM AUTHOR]

The autonomic nervous system innervates the pancreas by sympathetic, parasympathetic and sensory branches during early organogenesis, starting with neural crest cell invasion and formation of an intrinsic neuronal network. Several studies have demonstrated that signals from pancreatic neural crest cells direct pancreatic endocrinogenesis. Likewise, autonomic neurons have been shown to regulate pancreatic islet formation, and have also been implicated in type I diabetes. Here, we provide an overview of recent progress in mapping pancreatic innervation and understanding the interactions between pancreatic neurons, epithelial morphogenesis and cell differentiation. Finally, we discuss pancreas innervation as a factor in the development of diabetes. [ABSTRACT FROM AUTHOR]

Background: In the post-pandemic era, a wide range of COVID-19 sequelae is of growing health concern. However, the risks of digestive diseases in long COVID have not been comprehensively understood. To investigate the long-term risk of digestive diseases among COVID patients. Methods: In this large-scale retrospective cohort study with up to 2.6 years follow-up (median follow-up: 0.7 years), the COVID-19 group (n = 112,311), the contemporary comparison group (n = 359,671) and the historical comparison group (n = 370,979) predated the COVID-19 outbreak were built using UK Biobank database. Each digestive outcome was defined as the diagnosis 30 days or more after the onset of COVID-19 infection or the index date. Hazard ratios (HRs) and corresponding 95% confidence intervals (CI) were computed utilizing the Cox regression models after inverse probability weighting. Results: Compared with the contemporary comparison group, patients with previous COVID-19 infection had higher risks of digestive diseases, including gastrointestinal (GI) dysfunction (HR 1.38 (95% CI 1.26 to 1.51)); peptic ulcer disease (HR 1.23 (1.00 to 1.52)); gastroesophageal reflux disease (GERD) (HR 1.41 (1.30 to 1.53)); gallbladder disease (HR 1.21 (1.06 to 1.38)); severe liver disease (HR 1.35 (1.03 to 1.76)); non-alcoholic liver disease (HR 1.27 (1.09 to 1.47)); and pancreatic disease (HR 1.36 (1.11 to 1.66)). The risks of GERD were increased stepwise with the severity of the acute phase of COVID-19 infection. Even after 1-year follow-up, GERD (HR 1.64 (1.30 to 2.07)) and GI dysfunction (HR 1.35 (1.04 to 1.75)) continued to pose risks to COVID-19 patients. Compared to those with one SARS-CoV-2 infection, reinfected patients were at a higher risk of pancreatic diseases (HR 2.57 (1.23 to 5.38)). The results were consistent when the historical cohort was used as the comparison group. Conclusions: Our study provides insights into the association between COVID-19 and the long-term risk of digestive system disorders. COVID-19 patients are at a higher risk of developing digestive diseases. The risks exhibited a stepwise escalation with the severity of COVID-19, were noted in cases of reinfection, and persisted even after 1-year follow-up. This highlights the need to understand the varying risks of digestive outcomes in COVID-19 patients over time, particularly those who experienced reinfection, and develop appropriate follow-up strategies. [ABSTRACT FROM AUTHOR]

Ferroptosis is a newly discovered form of regulatory cell death characterized by excessive iron-dependent lipid peroxidation. In the past decade, significant breakthroughs have been made in comprehending the features and regulatory mechanisms of ferroptosis, and it has been confirmed that ferroptosis plays a pivotal role in the pathophysiological processes of various diseases, including tumors, inflammation, neurodegenerative diseases, and infectious diseases. The pancreas, which is the second largest digestive gland in the human body and has both endocrine and exocrine functions, is a vital organ for controlling digestion and metabolism. In recent years, numerous studies have confirmed that ferroptosis is closely related to pancreatic diseases, which is attributed to abnormal iron accumulation, as an essential biochemical feature of ferroptosis, is often present in the pathological processes of various pancreatic exocrine and endocrine diseases and the vulnerability of the pancreas to oxidative stress stimulation and damage. Therefore, comprehending the regulatory mechanism of ferroptosis in pancreatic diseases may provide valuable new insights into treatment strategies. In this review, we first summarize the hallmark features of ferroptosis and then analyze the exact mechanisms by which ferroptosis is precisely regulated at multiple levels and links, including iron metabolism, lipid metabolism, the GPX4-mediated ferroptosis defense system, the GPX4-independent ferroptosis defense system, and the regulation of autophagy on ferroptosis. Finally, we discuss the role of ferroptosis in the occurrence and development of pancreatic diseases and summarize the feasibility and limitations of ferroptosis as a therapeutic target for pancreatic diseases. [ABSTRACT FROM AUTHOR]

Objective Post-pancreatitis diabetes mellitus (PPDM) is a frequent complication of pancreatitis and is associated with an increased risk of adverse outcomes. Metformin is recommended for the treatment of PPDM, but evidence of its risk-benefit profile is limited. In a pharmaco-epidemiologic study, we investigated the association between metformin treatment and adverse outcomes in patients with PPDM. Design and Methods In a Danish nationwide population-based cohort study, we included adults (≥18 years) with incident PPDM or type 2 diabetes between 2009 and 2018. Post-pancreatitis diabetes mellitus was categorised into acute and chronic subtypes (PPDM-A and PPDM-C). Associations between metformin treatment and severe hypoglycaemia, major adverse cardiovascular events (MACE), and all-cause mortality were examined across the diabetes subgroups using Cox regression analysis. Treatments with metformin, insulin, and other glucose-lowering therapies were handled as time-varying exposures. Results We included 222 337 individuals with new-onset type 2 diabetes and 3781 with PPDM, of whom 2305 (61%) were classified as PPDM-A and 1476 (39%) as PPDM-C. Treatment with metformin was associated with a lower risk of severe hypoglycaemia (adjusted hazard ratio [HR] 0.41, 95% CI 0.27-0.62, P <.0001), MACE (HR 0.74, 95% CI 0.60-0.92, P =.0071), and all-cause mortality (HR 0.56, 95% CI 0.49-0.64, P <.0001) in patients with PPDM. In sensitivity analyses and among individuals with type 2 diabetes, metformin treatment exhibited comparable trends of risk reduction. Conclusions Metformin is associated with a lower risk of adverse outcomes, including all-cause mortality in patients with PPDM, supporting the use of metformin as a glucose-lowering therapy for these patients. [ABSTRACT FROM AUTHOR]

Endoscopic retrograde cholangiopancreatography (ERCP) is an advanced endoscopic technique used to diagnose and treat biliary and pancreatic diseases. It is one of the most technically demanding endoscopic procedures. ERCP training programs must ensure trainees have adequate knowledge of the anatomy and physiology associated with biliopancreatic diseases. The variety of ERCP procedures included in training programs should provide sufficient basic training for novice trainees and advanced training for experienced endoscopists. The main endoscopic procedures should be trained in ascending order of difficulty. Incorporating models capable of simulating various clinical and anatomical conditions could provide an effective means of fulfilling training requirements, although they are not easily available due to expensive facilities and void of standard assessment. Competency assessment is crucial in ERCP training to ensure trainees can independently and safely perform ERCP. Because of the rapid advancement of diagnostic and therapeutic methods, postgraduate training is critical for ERCP practitioners. Once certificates are attained, practitioners are solely responsible for maintaining their competency, credentialing, and quality. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a prominent risk factor for malignant and non-malignant pancreatic diseases. Furthermore, the presence of DM predicts an unfavourable outcome in people with pancreatic cancer. This retrospective observational study investigated 370 patients who underwent pancreatic resection surgery for various indications (84.3% in malignant indication) in a single surgery centre in Graz, Austria. The preoperative and postoperative diabetes statuses were evaluated according to surgery method and disease entity and predictors for diabetes development after surgery, as well as outcomes (survival and cancer recurrence) according to diabetes status, were analysed. In the entire cohort, the postoperative diabetes (postopDM) incidence was 29%. PostopDM occurred significantly more frequently in malignoma patients than in those with benign diseases (31.3% vs. 16.7%; p = 0.040, OR = 2.28). In the malignoma population, BMI, longer surgery duration, and prolonged ICU and hospital stay were significant predictors of diabetes development. The 1- and 2-year follow-ups showed a significantly increased mortality of people with postopDM in comparison to people without diabetes (HR 1-year = 2.02, p = 0.014 and HR 2-years = 1.56, p = 0.034). Local cancer recurrence was not influenced by the diabetes status. Postoperative new-onset diabetes seems to be associated with higher mortality of patients with pancreatic malignoma undergoing pancreatobiliary surgery. [ABSTRACT FROM AUTHOR]

Background: Jaundice occurs in some pancreatic disease. However, its occurrences and role in pancreatic neuroendocrine neoplasms (PNENs) has not been well studied. In this study we showed the association between jaundice and the risk of high grade and poorly differentiated PNENs. Methods: Ninety-three patients with head-neck PNENs were included. Poorly differentiated pancreatic neuroendocrine neoplasms were defined by a ki67 index > 55.0%. Logistic regression was used to show the association between demographic information, clinical signs and symptoms and the risk of poorly differentiated tumors. A nomogram model was developed to predict poorly differentiated tumor. Results: Eight of 93 PNEN patients (8.6%) had jaundice. The age and ki67 index in patients with jaundice were significantly higher than those patients without jaundice. All jaundice occurred in patients with grade 3 PNENs. Mutivariable regression analysis showed that age (odds ratio(OR) = 1.10, 95% confidence interval (CI):1.02–1.19), tumor size (OR = 1.42, 95%CI:1.01-2.00) and jaundice (OR = 14.98, 95%CI: 1.22-184.09) were associated with the risk of poorly differentiated PNENs. The age and size combination showed a good performance in predicting poorly differentiated PNENs (area under the curve (AUC) = 0.81, 95% CI: 0.71–0.90). The addition of jaundice further improved the age- and size-based model (AUC = 0.86, 95% CI: 0.78–0.91). A nomogram was developed based on age, tumor size and jaundice. Conclusion: Our data showed that jaundice was associated with the risk of high grade PNENs and poorly differentiated PNENs. [ABSTRACT FROM AUTHOR]

Background: Diffusion-weighted imaging (DWI) can confidently characterize the nature of a lesion. "Apparent diffusion coefficient" (ADC) has a role in evaluating malignant lesions of the pancreas when conventional sequences appear normal. Aims and Objectives: The aim of the study was to determine the role of DWI and ADC to differentiate benign from malignant pancreatic lesions. Materials and Methods: An observational study was carried out on 75 participants with a suggestion of pancreatic pathologies at a tertiary care institute. Twenty-five participants, who had normal parenchyma of the pancreas, were taken as controls. Magnetic resonance imaging protocol was done, including DWI and ADC. Data analysis was done using coGuide software. ADC was the primary outcome of interest. Results: Out of the 75 cases, 76.9 % (n=60) were males. 15.4 % (n=9) of pathologies were malignant. A significant decrease of ADC values in subjects with acute diffuse pancreatitis (1.12×10-3), acute on chronic pancreatitis (1.14×10-3), chronic pancreatitis (1.32×10-3) as well as adenocarcinoma pancreas (0.92×10-3) was seen in comparison to the controls (1.41×10-3). ADC values for acute pancreatitis, chronic pancreatitis, and acute on chronic pancreatitis were significantly higher than malignancy. Conclusion: DWI and ADC is a useful tools complementing conventional MR imaging and other imaging modalities in characterizing pancreatic pathologies. Mean ADC values of various pancreatic diseases can be determined without major overlap and a reasonable cutoff value can be obtained for differentiating benign and malignant lesions. [ABSTRACT FROM AUTHOR]

Context.--Immunohistochemistry serves as an ancillary diagnostic tool for a wide variety of neoplastic and nonneoplastic disorders, including infections, workup of inflammatory conditions, and subtyping neoplasms of the pancreas/liver/gastrointestinal luminal tract. In addition, immunohistochemistry is also used to detect a variety of prognostic and predictive molecular biomarkers for carcinomas of the pancreas, liver, and gastrointestinal luminal tract. Objective.--To highlight an update on the role of immunohistochemistry in the evaluation of pancreatic/liver/gastrointestinal luminal tract disorders. Data Sources.--Literature review and authors' research data and personal practice experience were used. Conclusions.--Immunohistochemistry is a valuable tool, assisting in the diagnosis of problematic tumors and benign lesions of the pancreas, liver, and gastrointestinal luminal tract, and also in the prediction of prognosis and therapeutic response for carcinomas of the pancreas, liver, and gastrointestinal luminal tract. [ABSTRACT FROM AUTHOR]

Various pancreatic diseases can cause dyspepsia due to pancreatic exocrine insufficiency （PEI） caused by pancreatic parenchymal injury and/or pancreatic duct obstruction， which further leads to impaired digestive function and a series of severe clinical outcomes such as malnutrition， weight loss， and shortened survival time. Therefore， pancreatic disease-related dyspepsia should be taken seriously in clinical practice to improve its diagnosis and treatment rates， so as to improve the quality of life of patients with pancreatic diseases and prolong overall survival time. [ABSTRACT FROM AUTHOR]

Acute pancreatitis (AP) is an inflammatory disease of the pancreas. Iron is an essential element for life and is involved in many metabolic processes. Ferroptosis is a type of regulated cell death that is triggered by iron and oxidative stress. A well-established mouse AP model was adopted to study the role of iron and ferroptosis in the pathogenesis of pancreatitis. Mice were injected with cerulein to induce AP, and pancreatic tissue samples were analyzed to determine the pathology, cell death, iron deposition, expression of iron transporters, and lipid peroxidation. The role of iron was studied by giving mice extra iron or iron chelator. In vitro studies with acinar cells with ferroptosis activator and inhibitor were also performed to assess the inflammatory response. Iron was found accumulated in the pancreatic tissue of mice who suffered cerulein-induced pancreatitis. Cell death and lipid peroxidation increased in these tissues and could be further modulated by iron dextran or iron chelator. Mice given Hemin through gavage had reduced levels of GSH in pancreatic tissue and increased inflammatory response. Studies with acinar cells showed increased levels of lipid peroxidation and ferroptosis-specific mitochondrial damage when treated with ferroptosis inducer and inflammatory cytokines. [ABSTRACT FROM AUTHOR]

Salmonid alphavirus strain 3 is responsible for outbreaks of pancreas disease in salmon and rainbow trout in Norway. Although the extensive amount of research on SAV3 focused mainly on the heart and pancreas (of clinical importance), tropism and pathogenesis studies of the virus in other salmon tissues are limited. Here, we used a combination of RT-qPCR (Q_nsp1 gene) and in situ hybridization (RNAscope®) to demonstrate the tropism of SAV3 in situ in tissues of Atlantic salmon, employing a challenge model (by cohabitation). In addition, as previous results suggested that the pseudobranch may harbor the virus, the change in the expression of different immune genes upon SAV3 infection (RT-qPCR) was focused on the pseudobranch in this study. In situ hybridization detected SAV3 in different tissues of Atlantic salmon during the acute phase of the infection, with the heart ventricle showing the most extensive infection. Furthermore, the detection of the virus in different adipose tissues associated with the internal organs of the salmon suggests a specific affinity of SAV3 to adipocyte components. The inconsistent immune response to SAV3 in the pseudobranch after infection did not mitigate the infection in that tissue and is probably responsible for the persistent low infection at 4 weeks post-challenge. The early detection of SAV3 in the pseudobranch after infection, along with the persistent low infection over the experimental infection course, suggests a pivotal role of the pseudobranch in SAV3 pathogenesis in Atlantic salmon. [ABSTRACT FROM AUTHOR]

Background: The pancreatic index (PI) is a useful preoperative imaging predictor for pancreatic ductal adenocarcinoma (PDAC). In this retrospective study, we determined the predictive effect of PI to distinguish patients of pancreatic body/tail cancer (PBTC) with vascular involvement who can benefit from upfront surgery. Method: All patients who received distal pancreatectomy for PDAC from 2016 to 2020 at the Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiaotong University School of Medicine were considered for the study. A total of 429 patients with PBTC were assessed in relation to the value of PI. Fifty‐five patients were eventually included and divided into low PI group and 29 patients in the normal PI group. Results: The median overall survival (mOS) was significantly shorter in the low PI group (13.1 vs. 30.0 months, p = 0.002) in this study, and PI ≥ 0.78 (OR = 0.552, 95% CI: 0.301–0.904, p = 0.020) was an independent influencing factor confirmed by multivariate analysis. Subgroup analysis showed that PI was an independent prognostic factor for LA‐PBTC (OR = 0.272, 95% CI: 0.077–0.969, p = 0.045). As for BR PBTC, PI (OR = 0.519, 95% CI: 0.285–0.947, p = 0.033) combined with carbohydrate antigen 125 (CA125) (OR = 2.806, 95% CI: 1.206–6.526, p = 0.017) and chemotherapy (OR = 0.327, 95% CI: 0.140–0.763, p = 0.010) were independent factors. Conclusion: This study suggests that the PI can be used as a predictive factor to optimize the surgical indication for PBTC with vascular involvement. Preoperative patients with normal PI and CA125 can achieve a long‐term prognosis comparable to that of resectable PBTC patients. [ABSTRACT FROM AUTHOR]

Background: Pancreoprivic diabetes is a brittle form of diabetes arising from a pancreatic disease. It is often associated with glycemic variability, exocrine insufficiency and risk of hypoglycemia. Studies focusing on its profile are scarce in India. This study aims to understand the clinico-etiological profile of pancreoprivic diabetes. Methods: Eighty consecutive patients with pancreoprivic diabetes were evaluated in this cross-sectional, observational study for pancreatic exocrine and endocrine insufficiency, and complications of diabetes. Results: The mean age of the study group was 38.68 years and the mean HbA1c and stimulated C-peptide levels were 10.3% and 0.96 ng/ml, respectively. About 57.5% of the patients had BMI less than 18.5 kg/m2. Alcoholic pancreatic diabetes (APD) (70%, n = 56) and fibro-calculus pancreatic diabetes (FCPD) (13.75%, n = 11) were the commonest. Primary hyperparathyroidism (n = 5), familial hypertriglyceridemia (n = 3), hemochromatosis, pancreas divisum, autoimmune pancreatitis, acute pancreatitis and post pancreatectomy (n = 1, each) accounted for the remaining (16.25%, n = 13). Pancreatic calcifications, neuropathy, nephropathy, and retinopathy were seen in 69.6%, 52.5%, 8%, and 5% of patients respectively. Conclusion: Pancreoprivic diabetes has a distinct pancreatic pathology, poor glycemic status, and low BMI. A high prevalence of pancreatic calcifications and neuropathy is seen. Besides APD, there are many other rare metabolic and anatomical etiologies. [ABSTRACT FROM AUTHOR]