BACKGROUND: Pancreatic trauma (PT) is rare among traumatic injuries and has a low incidence, but it can still lead to severe infectious complications, resulting in a high mortality rate. Acute pancreatitis (AP) is a common complication after PT, and when combined with organ dysfunction and sepsis, it will result in a poorer prognosis.
METHODS: We report a 25-year-old patient with multiple organ injuries, including the pancreas, due to abdominal trauma, who developed necrotising pancreatitis secondary to emergency caesarean section, combined with intra-abdominal infection (IAI). The patient underwent performed percutaneous drainage, pancreatic necrotic tissue debridement, and abdominal infection foci debridement on the patient.
CONCLUSIONS: We report a case of severe AP and IAI secondary to trauma. This patient was managed by a combination of conservative treatment such as antibiotic therapy and fluid support with surgery, and a better outcome was obtained.

UNASSIGNED: The objective of the study is to investigate the changes in the composition of intestinal microecology in severe acute pancreatitis (SAP) patients with or without intra-abdominal infection and also to analyze the expression of antibiotic resistance genes to provide evidence for early warning of infectious diseases and the rational use of antibiotics.
UNASSIGNED: Twenty patients with SAP were enrolled in the study. According to whether the enrolled patients had a secondary intra-abdominal infection, they were divided into two groups, each consisting of 10 patients. Stool specimens were collected when the patients were admitted to the emergency intensive care unit (EICU), and nucleic acid extraction was performed. Next-generation gene sequencing was used to compare the differences in intestinal microflora diversity and drug resistance gene expression between the two groups.
UNASSIGNED: The gut microbiota of patients in the infection group exhibited distribution on multiple clustered branches with some intra-group heterogeneity, and their flora diversity was compromised. The infected group showed an enrichment of various opportunistic bacteria in the gut microbiota, along with a high number of metabolic functions, stress functions to external signals, and genes associated with pathogenesis. Drug resistance genes were expressed in the gut microbiota of both groups, but their abundance was significantly lower in the non-infected group.
UNASSIGNED: The intestinal microbiota of patients in the infection group exhibited distribution on multiple clustered branches with some intra-group heterogeneity, and their flora diversity was compromised. Additionally, drug resistance genes were expressed in the gut microbiota of both groups, although their abundance was significantly lower in the non-infected group.

Severe acute pancreatitis (SAP) is an inflammatory disease with varying severity, ranging from mild local inflammation to severe systemic disease, with a high incidence rate and mortality. Current drug treatments are not ideal. Therefore, safer and more effective therapeutic drugs are urgently needed. 7α,14β-dihydroxy-ent-kaur-17-dimethylamino-3,15-dione DGA, a diterpenoid compound derivatized from glaucocalyxin A, exhibits anti-inflammatory activity. In this study, we demonstrated the therapeutic potential of DGA against SAP and elucidated the underlying mechanisms. Treatment with DGA markedly (1) inhibited death of RAW264.7 and J774a.1 cells induced by Nigericin and lipopolysaccharide, (2) alleviated edema, acinar cell vacuolation, necrosis, and inflammatory cell infiltration of pancreatic tissue in mice, and (3) inhibited the activity of serum lipase and the secretion of inflammatory factor IL-1β. DGA significantly reduced the protein expression of IL-1β and NLRP3 and inhibited the phosphorylation of NF-κB. However, DGA exhibited no inhibitory effect on the expression of caspase-1, gasdermin D (GSDMD), NF-κB, TNF-α, or apoptosis-associated speck-like protein (ASC) and on the cleavage of caspase-1 or GSDMD. Molecular docking simulation confirmed that DGA can bind to TLR4 and IL-1 receptor. In conclusion, DGA may effectively alleviate the symptoms of SAP in mice and macrophages by inhibiting the binding of TLR4 and IL-1 receptor to their ligands; therefore, DGA is a promising drug candidate for the treatment of patients with SAP.

BACKGROUND: Intestinal dysfunction plays an important role in the clinical progress and prognosis of severe acute pancreatitis (SAP). Qingyi decoction (QYD) has shown beneficial effects on intestinal function recovery, but the prevention actions of the QYD on intestinal paralysis and its mechanism have not been fully explored.
METHODS: The possible molecular mechanism was unraveled by network pharmacology, including active ingredients and potential target prediction, as well as GO, KEGG, and REATCOME pathway enrichment analyses. The potential interactions between the main active ingredients of the QYD and core genes were explored by molecular docking. A retrospective cohort study on 137 patients with SAP from Tianjin Nankai Hospital was conducted to evaluate the preventive effect of QYD on intestinal paralysis.
RESULTS: A total of 110 active ingredients in QYD were screened out, and 37 key targets were predicted by network pharmacology. GO, KEGG, and REATCOME enrichment analyses showed that bioinformatics annotation of the hub genes was mainly involved in intestinal epithelial functions and inflammatory response pathways. The main components of QYD possessed good affinity with IL-6, TNF, CASP3, CXCL8, and CRP by molecular docking. Patients who used QYD plus usual care seemed to have fewer intestinal paralysis rates, lower risk of renal insufficiency, ARDS and blood purification therapy, and shorter hospital and ICU stays. The multivariable regression analyses indicated that the mode of nasogastric and enemas administration of QYD (P = 0.010) and timely intervention with QYD (P = 0.045) were the independent protective factors for intestinal paralysis prevention in patients with SAP.
CONCLUSIONS: In conclusion, QYD can be used as an effective adjuvant procedure to prevent the occurrence and development of intestinal paralysis in patients with SAP. The mechanisms may be involved in the anti-inflammatory response and maintenance of intestinal epithelial function.

UNASSIGNED: To evaluate the long-term efficacy and cost-efficiency of blood purification (BP) in severe acute pancreatitis (SAP) through single-center data.
UNASSIGNED: A total of 155 SAP patients were collected and followed up for 6 months. The participants were divided into control (49 cases) and BP group (106 cases) according to whether they received BP treatment or not. The primary outcomes were 6-month mortality, length of hospital stay, and hospitalization costs. Propensity score matching (PSM) analysis was performed based on various factors such as gender, age, etiology, SOFA score, JSS score, and creatinine value on day 1.
UNASSIGNED: There were significant differences in all baseline data between BP and control groups (p<0.05). However, there was a significant difference in the mortality, length of hospital stay, hospital costs and infection aggravation rate the in outcome data for 6-months (all p<0.05). BP was not considered a death factor in any adjusted models, with p-values ranging from 0.81 to 0.93. The results of subgroup analysis after PSM showed that BP mode had no significant impact on prognostic indicators, but the length of ICU stay and total costs were significantly increased (all p<0.001). There was no significant difference in mortality among the cases that did not require early intervention after 6 months (p=0.487). However, the patients in BP group had longer ICU stays (p=0.001) and higher hospitalization costs (p<0.001) compared to the control group.
UNASSIGNED: The utilization of BP therapy did not decrease the 6-month mortality in SAP patients. Additionally, BP therapy has a significant impact on the duration of ICU stay or hospitalization expenses. However, the effectiveness and cost-efficiency of this therapy are unsatisfactory, and early intervention does not enhance survival benefits. Furthermore, there was no substantial variation in survival benefits between continuous veno-venous hemofiltration (CVVH) alone and compound BP.

UNASSIGNED: Previous studies showed that MSCs could mitigate damage in the pancreas during acute pancreatitis (AP). However, acute mortality associated with AP was more often a result of persistent failure of remote organs, rather than local damage, especially in severe acute pancreatitis (SAP), and the effect of MSCs may vary depending on their origin.
UNASSIGNED: An SAP model was induced in 8-week C57BL/6 J male mice by retrograde injection of 5 % sodium taurocholate solution through the bile duct. SAP mice were divided into the SAP group, UC-MSCs group, and BMSCs group, which were treated with saline, 1 × 106 UC-MSCs, and 1 × 106 BMSCs respectively, through the tail vein. After treatment, serum markers, inflammation, and morphology were assessed in the pancreas, kidneys, lungs, and hearts.
UNASSIGNED: MSCs infusion ameliorated the systemic inflammatory response in SAP mice. In the MSCs-treated SAP mice, local tissue injury and inflammation response in the pancreas were alleviated. But more importantly, the renal and lung injury were all significantly and drastically mitigated, and the levels of pro-inflammatory factors such as IL-6, MCP-1, IL-1β, and TNF-α in the kidney, lung and heart were sharply decreased. In terms of origin, UC-MSCs exhibited superior efficacy compared with BMSCs. Furthermore, compared to the normal control mice, UC-MSCs showed an earlier appearance, higher distribution densities, and longer duration of presence in the injured tissue.
UNASSIGNED: This study provides compelling evidence supporting the therapeutic potential of MSCs in SAP treatment and particularly their ability to mitigate multi-organ failure. Our results also suggested that UC-MSCs may offer greater advantages over BMSCs in SAP therapy.

Introduction Acute pancreatitis is caused by multiple factors. The disease can progress to severe acute pancreatitis (SAP) rapidly, which is a fatal condition. SAP is associated with systemic inflammatory response and disturbances in microcirculation, which are responsible for the high rate of mortality. Low-molecular-weight heparin (LMWH), apart from preventing thrombus formation, also has a property of reducing the release of cytokines and inflammatory mediators. This aids in the improvement of microcirculation of the pancreas. Materials and methods A prospective hospital-based study was conducted on 60 patients diagnosed with SAP. Patients were randomly divided into two groups: conventional treatment group (C group consisting of 30 patients) and LMWH in addition to conventional treatment (L group, consisting of 30 patients). Clinical and laboratory parameters and computed tomography (CT) scores of pancreatic necrosis (CTSPN) were compared in the two study groups. Results No significant difference (p > 0.05) was observed in the clinical and laboratory parameters and CTSPN among the two study groups at the time of admission. On initiation of treatment, the rate of improvement in symptoms and laboratory parameters were significantly higher in the L group compared with the C group (p < 0.05). Acute physiology and chronic health evaluation (APACHE) II score and development of complications were significantly lower in the L group compared with the C group (p< 0.05). CTSPN was found to be very low in the L group compared with the C group (p < 0.05). After two weeks of treatment, the recovery rate in response to treatment was observed to be higher in the L group compared to the C group, and the mortality rate was very low in the L group (p <0.05, significant). Conclusion The addition of LMWH to conventional treatment in SAP augments the effect and improves the clinical response, improving the recovery rate and decreasing mortality. LMWH is highly effective for the treatment of SAP, with a good safety profile and easy availability and without high financial burden.

BACKGROUND: Guidelines must be interpreted comprehensively and correctly to standardize the clinical process. However, this process is challenging and requires interpreters to have a medical background and qualifications. In this study, the accuracy of ChatGPT3.5 in answering clinical questions related to the 2019 guidelines for severe acute pancreatitis was evaluated.
RESULTS: An observational study was conducted using the 2019 guidelines for severe acute pancreatitis. The study compared the accuracy of ChatGPT3.5 in English versus Chinese and found that it was more accurate in English (71%) than in Chinese (59%) (P value: 0.203). Additionally, the study assessed the accuracy of ChatGPT3.5 in answering short-answer questions versus true/false questions and found that it was more accurate in answering short-answer questions (76%) than in answering true/false questions (60%) (P value: 0.405).
CONCLUSIONS: For clinicians managing severe acute pancreatitis, ChatGPT3.5 may have potential value. However, it should not be relied upon excessively for clinical decision making.

Background/Objectives: Early identification of patients at risk of developing severe acute pancreatitis (SAP) is still an issue. Dynamic assessment of clinical and laboratory parameters within the first 48 h of admission may offer valuable insights into the prediction of unfavorable outcomes such as SAP and death. Methods: A prospective observational study was conducted on a cohort of patients admitted for AP at a tertiary referral hospital. Clinical and laboratory data were collected on admission and at 48 h. Patients were classified based on the Revised Atlanta classification. Logistic regression analysis was performed to identify independent risk factors for SAP. Likelihood ratios and post-test probabilities were calculated to assess the clinical usefulness of predictive markers. Results: 227 patients were included, with biliary etiology being the most common and a prevalence of SAP and death of 10.7% and 5.7%, respectively. BISAP ≥ 2 on admission, presence of SIRS after 48 h, rise in heart rate over 20 bpm, and any increase in BUN after 48 h were independent risk factors for SAP. The combination of these factors increased the post-test probability of SAP and death, with BISAP ≥ 2 combined with the presence of SIRS after 48 h showing the highest probability (82% and 73%, respectively). Conclusions: Dynamic assessment of BUN, heart rate, and SIRS within the first 48 h of admission can aid in predicting the development of SAP and death in patients with AP. These findings underscore the importance of continuous monitoring, although multicenter studies are warranted to refine predictive models for SAP.

BACKGROUND: Ferroptosis is a newly recognized form of regulatory cell death characterized by severe lipid peroxidation triggered by iron overload and the production of reactive oxygen species (ROS). However, the role of ferroptosis in severe acute pancreatitis(SAP) has not been fully elucidated.
METHODS: We established four severe acute pancreatitis models of rats including the sham control group, the SAP group, the Fer -1-treated SAP (SAP + Fer-1) group, the 3-MA-treated SAP (SAP + 3-MA) group. The SAP group was induced by retrograde injection of sodium taurocholate into the pancreatic duct. The other two groups were intraperitoneally injected with ferroptosis inhibitor (Fer-1) and autophagy inhibitor (3-MA), respectively. The model of severe acute pancreatitis with amylase crest-related inflammatory factors was successfully established. Then we detected ferroptosis (GPX4, SLC7A1 etc.) and autophagy-related factors (LC3II, p62 ect.) to further clarify the relationship between ferroptosis and autophagy.
RESULTS: Our study found that ferroptosis occurs during the development of SAP, such as iron and lipid peroxidation in pancreatic tissues, decreased levels of reduced glutathione peroxidase 4 (GPX 4) and glutathione (GSH), and increased malondialdehyde(MDA) and significant mitochondrial damage. In addition, ferroptosis related proteins such as GPX4, solute carrier family 7 member 11(SLC7A11) and ferritin heavy chain 1(FTH1) were significantly decreased. Next, the pathogenesis of ferroptosis in SAP was studied. First, treatment with the ferroptosis inhibitor ferrostatin-1(Fer-1) significantly alleviated ferroptosis in SAP. Interestingly, autophagy occurs during the pathogenesis of SAP, and autophagy promotes the occurrence of ferroptosis in SAP. Moreover, 3-methyladenine (3-MA) inhibition of autophagy can significantly reduce iron overload and ferroptosis in SAP.
CONCLUSIONS: Our results suggest that ferroptosis is a novel pathogenesis of SAP and is dependent on autophagy. This study provides a new theoretical basis for the study of SAP.