Explore the vast range of titles available.

To evaluate the clinical utility of PCT, CRP, IL-6, NLR, and TyG index in improving the early diagnosis and severity assessment of acute pancreatitis (AP). This retrospective study included 137 AP patients and 30 healthy controls from Hunan Provincial People’s Hospital (January 2021–September 2023). Univariate and multivariate logistic regression analyses assessed the associations between biomarkers and severe acute pancreatitis (SAP). Receiver operating characteristic (ROC) curves, DeLong test, and Bonferroni correction were used to evaluate predictive performance. Model robustness was validated via 5-fold cross-validation. PCT, CRP, IL-6, NLR, and TyG index levels were significantly elevated in AP patients compared to controls ( P  < 0.001) and correlated with disease severity ( P  < 0.05). CRP and NLR levels differed significantly among mild, moderate, and severe AP ( P  < 0.01). Alcohol consumption and hyperlipidemia were significantly linked to AP severity (P for trend < 0.0001). Multivariate analysis identified hyperlipidemia (OR = 3.030, P  = 0.040), CRP (OR = 1.011, P  < 0.001), and NLR (OR = 1.078, P  = 0.020) as independent SAP predictors. The combined model of CRP + NLR + TyG achieved the highest AUC (0.882, sensitivity = 77.2%, specificity = 88.5%), though it was not significantly better than CRP + NLR or CRP + TyG models ( P  > 0.05). 5-fold cross-validation confirmed consistent performance (mean AUC = 0.817 ± 0.118). PCT, CRP, IL-6, NLR, and TyG index are valuable in diagnosing and assessing AP prognosis. Hyperlipidemia, CRP, and NLR are reliable independent predictors of SAP. Combining multiple biomarkers enhances diagnostic precision and provides guidance for personalized treatment strategies in AP.

BackgroundAcute pancreatitis (AP) is one of the most common acute abdominal disorders; due to the lack of specific treatment, the treatment of acute pancreatitis, especially serious acute pancreatitis (SAP), is difficult and challenging. We will observe the changes of Interleukin -22 levels in acute pancreatitis animal models, and explore the mechanism of Interleukin -22 in acute pancreatitis.ObjectiveThis study aims to assess the potential protective effect of Interleukin -22 on caerulein-induced acute pancreatitis and to explore its mechanism.MethodsBlood levels of amylase and lipase and Interleukin -22 were assessed in mice with acute pancreatitis. In animal model and cell model of caerulein-induced acute pancreatitis, the mRNA levels of P62 and Beclin-1 were determined using PCR, and the protein expression of P62, LC3-II, mTOR, AKT, p-mTOR, and p-AKT were evaluated through Western blot analysis.ResultsInterleukin -22 administration reduced blood amylase and lipase levels and mitigated tissue damage in acute pancreatitis mice model. Interleukin -22 inhibited the relative mRNA levels of P62 and Beclin-1, and the Interleukin -22 group showed a decreased protein expression of LC3-II and P62 and the phosphorylation of the AKT/mTOR pathway. Furthermore, we obtained similar results in the cell model of acute pancreatitis.ConclusionThis study suggests that Interleukin -22 administration could alleviate pancreatic damage in caerulein-induced acute pancreatitis. This effect may result from the activation of the AKT/mTOR pathway, leading to the inhibition of autophagy. Consequently, Interleukin -22 shows potential as a treatment.

Acute pancreatitis (AP) is a common gastrointestinal disorder, and acute kidney injury (AKI) is a frequent and severe complication, significantly increasing mortality risk. Mean arterial pressure (MAP) is crucial for maintaining organ perfusion in critically ill patients. However, the optimal MAP target for minimizing mortality in AP patients complicated by AKI (AP-AKI) remains unclear. This retrospective cohort study analyzed data from the MIMIC-IV database, including 934 critically ill adult patients diagnosed with AP-AKI between 2008 and 2019. We investigated the relationship between MAP and in-hospital mortality using logistic regression models, adjusting for demographics, comorbidities, disease severity scores and intensive care interventions. Smooth curve fitting was used to explore potential non-linear associations. Subgroup analyses were performed to assess the impact of MAP across different clinical and demographic groups. Our analysis revealed a non-linear, L-shaped relationship between MAP and in-hospital mortality, with an inflection point at 71.32 mmHg. Below this threshold, increasing MAP was associated with significantly decreased odds of mortality (OR: 0.93, 95% CI: 0.87-0.99,  = 0.026). However, above this threshold, the association was no longer significant (OR: 1.015, 95% CI: 0.98-1.03,  = 0.699). Subgroup analyses showed consistent trends across most subgroups, with the benefit of maintaining MAP above the threshold being most pronounced in AKI stage 1 and 2 patients. This study suggests a potential association between maintaining specific MAP levels, particularly above 71.32 mmHg, and reduced in-hospital mortality in critically ill AP-AKI patients.

Acute pancreatitis (AP) is characterised by an inflammatory response that in its most severe form can cause a systemic dysregulated immune response and progression to acute multi-organ dysfunction. The pathobiology of the disease is unclear and as a result no targeted, disease-modifying therapies exist. We performed a scoping review of data pertaining to the human immunology of AP to summarise the current field and to identify future research opportunities. A scoping review of all clinical studies of AP immunology was performed across multiple databases. Studies were included if they were human studies of AP with an immunological outcome or intervention. 205 studies met the inclusion criteria for the review. Severe AP is characterised by significant immune dysregulation compared to the milder form of the disease. Broadly, this immune dysfunction was categorised into: innate immune responses (including profound release of damage-associated molecular patterns and heightened activity of pattern recognition receptors), cytokine profile dysregulation (particularly IL-1, 6, 10 and TNF-α), lymphocyte abnormalities, paradoxical immunosuppression (including HLA-DR suppression and increased co-inhibitory molecule expression), and failure of the intestinal barrier function. Studies including interventions were also included. Several limitations in the existing literature have been identified; consolidation and consistency across studies is required if progress is to be made in our understanding of this disease. AP, particularly the more severe spectrum of the disease, is characterised by a multifaceted immune response that drives tissue injury and contributes to the associated morbidity and mortality. Significant work is required to develop our understanding of the immunopathology of this disease if disease-modifying therapies are to be established.

Previous researches have emphasized a trypsin-centered theory of acute pancreatitis (AP) for more than a century. With additional studies into the pathogenesis of AP, new mechanisms have been explored. Among them, the role of immune response bears great importance. Pro-inflammatory substances, especially damage-associated molecular patterns (DAMPs), play an essential role in activating, signaling, and steering inflammation. Meanwhile, activated neutrophils attach great importance to the immune defense by forming neutrophil extracellular traps (NETs), which cause ductal obstruction, premature trypsinogen activation, and modulate inflammation. In this review, we discuss the latest advances in understanding the pathological role of DAMPs and NETs in AP and shed light on the flexible crosstalk between these vital inflammatory mediators. We, then highlight the potentially promising treatment for AP targeting DAMPs and NETs, with a focus on novel insights into the mechanism, diagnosis, and management of AP.

BackgroundsAngiopoietin-2 (Ang-2) is a new predictor for acute pancreatitis (AP).AimsTo assess the predictive value of Ang-2 in determining the progress of AP and the subsequent acute gastrointestinal injury (AGI).MethodsThis was a prospective study that enrolled 170 patients with AP and 100 healthy controls. Blood samples were collected within 24 h of the onset of AP.ResultsThe majority (108) of the patients were categorized as having MAP with the rest (62) classified as suffering from SAP. Considering AGI grading, there were 118 grade 1 and 12 grade 4 patients; in grades 2 and 3, there were 20 patients each. AP was accompanied by MODS and pancreatic necrosis in 46 and 24 cases, respectively. Eighty patients were admitted to the ICU, while mortality was reported among 7.1% patients. The plasma Ang-2 levels were higher among patients with AP than in controls. A similar trend prevailed, in patients with SAP compared to those with MAP. Ang-2 was significantly increased from AGI grade 1 through to grade 4, showing a desirable positive predictive accuracy. Moreover, Ang-2 also showed strong correlations with intestinal permeability as evaluated by d-lactate (DLA), diamine oxidase (DAO), and intestinal fatty acid binding proteins (I-FABPs). Tools (Ranson and APACHE II scores, CRP), which are used more conventionally, could not effectively distinguish the various grades of AGI. Furthermore, Ang-2 predicted poor prognosis and adverse outcomes, including mortality, among patients with AP.ConclusionsThis study showed Ang-2 to be an accurate early predictor for SAP, AGI, and intestinal barrier dysfunction, outperforming conventional biomarkers. Ang-2 levels also predicted the adverse outcomes and mortality due to AP.

BackgroundThe interleukin-1 pathway has been linked to pancreatic diseases. We applied the Mendelian randomization approach to explore whether higher interleukin-1 receptor antagonist (IL-1RA) levels reduce the risk of acute and chronic pancreatitis and pancreatic cancer.MethodsGenetic variants associated with blood IL-1RA levels at the genome-wide significance level and located 5MB downstream or upstream of the IL1RN gene were extracted from a genome-wide meta-analysis of 21,758 participants. After pruning, genetic variants without linkage disequilibrium were used as genetic instrument for IL-1RA. Summary-level data on acute and chronic pancreatitis and pancreatic cancer were obtained from the UK Biobank and FinnGen studies. The associations were meta-analyzed for one outcome from two sources.ResultsGenetically predicted higher levels of IL-1RA were associated with a lower risk of acute and chronic pancreatitis and pancreatic cancer. In the meta-analysis of UK Biobank and FinnGen, the combined odds ratio was 0.87 (95% confidence interval [CI] 0.77-0.97, P =0.003) for acute pancreatitis, 0.73 (95% CI 0.65-0.82, P =2.93×10-8) for chronic pancreatitis, and 0.86 (95% CI 0.77-0.96, P =0.009) for pancreatic cancer per one standard deviation increment in genetically predicted levels of IL-1RA.ConclusionThis study suggests a protective role of IL-1RA in three major pancreatic diseases, which hints the therapeutic potentials of IL-1RA in pancreatic diseases.

Acute pancreatitis (AP) is a disease characterized by an acute inflammatory response in the pancreas. This is caused by the abnormal activation of pancreatic enzymes by a variety of etiologic factors, which results in a localized inflammatory response. The symptoms of this disease include abdominal pain, nausea and vomiting and fever. These symptoms are induced by a hyperinflammatory response and oxidative stress. In recent years, research has focused on developing anti-inflammatory and antioxidative therapies for the treatment of acute pancreatitis (AP). However, there are still limitations to this approach, including poor drug stability, low bioavailability and a short half-life. The advent of nanotechnology has opened up a novel avenue for the management of acute pancreatitis (AP). Nanomaterials can serve as an efficacious vehicle for conventional pharmaceuticals, enhancing their targeting ability, improving bioavailability and prolonging their half-life. Moreover, they can also exert a direct therapeutic effect. This review begins by introducing the general situation of acute pancreatitis (AP). It then discusses the pathogenesis of acute pancreatitis (AP) and the current status of treatment. Finally, it considers the literature related to the treatment of acute pancreatitis (AP) by nanomaterials. The objective of this study is to provide a comprehensive review of the existing literature on the use of nanomaterials in the treatment of acute pancreatitis (AP). In particular, the changes in inflammatory markers and therapeutic outcomes following the administration of nanomaterials are examined. This is done with the intention of offering insights that can inform subsequent research and facilitate the clinical application of nanomaterials in the management of acute pancreatitis (AP). Graphical Abstract

Background There are few reports of postoperative acute pancreatitis (AP) in patients with acute type A aortic dissection (ATAAD), but we reported a case of ATAAD complicated by AP and later reoperation for intraperitoneal hemorrhage. We discussed the causes of AP in this patient and summarized some of the experiences of postoperative management of patients with ATAAD involving the celiac trunk and/or superior mesenteric artery. Case presentations A 44-year-old male patient was diagnosed with ATAAD and underwent partial resection of the ascending aorta with graft replacement and total aortic arch graft replacement with stented elephant trunk surgery 8 h after admission, and the operation was successful. Due to poor oxygenation function of acute respiratory distress syndrome (ARDS) after surgery, the patient was treated with mechanical ventilation for a long time, which was followed by bloodborne infection and systemic inflammatory response syndrome. Abdominal distension occurred 20 days after surgery, and was diagnosed as acute pancreatitis (AP), and intraperitoneal bleeding occurred on the 39th postoperative day during conservative treatment. On the 40th day after surgery, the patient underwent exploratory laparotomy, during which multiple abscesses around the pancreas were found, and the venous vessels in the tail of the pancreas were eroded, ruptured and hemorrhaged by infected lesions, and the abdominal abscess was cut and drained and the spleen was removed. The patient gradually recovered and was discharged on the 65th day after surgery. No special discomfort was reported during the outpatient follow-up. Conclusions This case suggests that for ATAAD patients involving the abdominal trunk and/or superior mesenteric artery, especially those with systemic inflammatory response syndrome, dynamic serum amylase and abdominal CT examination are necessary to help us diagnose AP earlier and detect its complications.

Background Intraductal papillary mucinous neoplasm (IPMN) is a cystic tumor of the pancreas arising from abnormal papillary proliferation of ductal epithelial cells, and is a precancerous lesion of pancreatic malignancy. This study aimed to evaluate associations between acute pancreatitis (AP) and histologic subtypes of IPMN. Methods In the clinical study, patients with IPMN confirmed by surgical resection specimens at our institute between 2009 and 2021 were eligible for inclusion. Associations and predictive accuracy of AP on the presence of HGD were determined by logistic regressions. In addition, a systematic review and meta-analysis was conducted through literatures upon search in PubMed, Embase, CENTRAL, China National Knowledge Infrastructure (CKNI), and Wanfang database, up to June, 2023. Pooled effects of the associations between AP and HGD and intestinal epithelial subtype subtype, shown as odds ratios (ORs) with 95% confidence intervals (CIs), were calculated using random effects model. Results The retrospective cohort study included 47 patients (32 males, 15 females) diagnosed with IPMN at our center between 2009 and 2021, including 11 cases with AP (median 62 years) and 36 cases (median 64.5 years) without. Accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of AP in predicting HGD were 78.7%, 57.1%, 82.5%, 36.4%, and 91.7%, respectively. Univariate logistic regression analysis showed that AP group had greater odds of presence of HGD (OR: 6.29,95% CI: 1.14–34.57) than non-AP group. Meta-analysis of five case-control studies in the literature included 930 patients and showed that AP-IPMN patients had higher odds for HGD (OR: 2.13, 95% CI 1.38–3.29) and intestinal epithelial subtype (OR: 5.38, 95% CI: 3.50–8.27) compared to non-AP IPMN. Conclusions AP is predictive of malignancy in patients with IPMN.