Acute Pancreatitis Group Research Articles

Clinical predictive value of control attenuation parameters in combination with miR-192-5p in patients with acute pancreatitis in nonalcoholic fatty liver disease.

Control attenuation parameters (CAP) can detect nonalcoholic fatty liver disease (NAFLD). Our previous study found that miR-192-5p could screen for acute pancreatitis (AP) in NAFLD patients. This study focused on the role of CAP and miR-192-5p in NAFLD of acute AP. AP patients and controls were enrolled. Classification of AP patients into NAFLD/AP patients and non-NAFLD/AP was made based on the CAP value. CAP was measured by liver transient elastography. Serum miR-192-5p was measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Logistic regression analysis was conducted to examine the risk factors for the development of NAFLD. Receiver operating characteristic (ROC) was assessed for the predictive value of AP severity. NAFLD was more common in the AP group than in the controls (35.00% vs. 8.75%). The CAP value was higher in AP patients with NAFLD than in non-NAFLD, whereas miR-192-5p was significantly lower in AP patients with NAFLD. Additionally, AP patients with NALFD are more likely to experience respiratory failure, systemic inflammatory response syndrome (SIRS), and pancreatic necrosis with longer hospitalisation and exacerbate the incidence of moderate to severe AP. Both miR-192-5p and TG are potential risk factors for the development of NAFLD in patients with AP. Furthermore, the CAP value gradually increased with increasing AP severity, while miR-192-5p gradually decreased. Finally, the sensitivity and specificity of CAP combined with miR-192-5p for the prediction of moderate to severe AP were scored as 82.61% and 82.43%, respectively. NAFLD exacerbated the progression of AP, and CAP combined with miR-192-5p could predict the severity of AP. Our study may provide more reference for AP disease progression and treatment.

Evaluation of the clinical usefulness of pancreatic alpha amylase as a novel biomarker in dogs with acute pancreatitis: a pilot study

Pancreatic alpha amylase (P-AMY) is used as a biomarker of acute pancreatitis (AP) in human medicine. To our knowledge, there are no studies evaluating the usefulness of P-AMY in dogs with AP. In this study, we evaluated the diagnostic value of P-AMY, currently not verified in veterinary medicine. The AP group (n = 40) consisted of dogs with AP diagnosed using clinical signs and laboratory examinations, including abnormal canine pancreatic lipase (cPL) concentration, and compatible abdominal ultrasound examination at first presentation. Evaluation of the canine AP severity (CAPS) score was performed. The control group (n = 38) was composed of normal dogs without any abnormalities in clinical findings, blood exams or diagnostic imaging. The correlation of P-AMY with cPL was confirmed by Pearson’s correlation analysis (r = 0.564, p < .001). The sensitivity and specificity for the most appropriate cut-off values of P-AMY were recorded similar to the values of DGGR. The dogs with AP and CAPS ≥11 had significantly higher serum P-AMY (p = .016) contrary to DGGR lipase and cPL. Furthermore, there was a significant difference in the median P-AMY dependent on the presence of systemic inflammatory response syndrome (p = .001). P-AMY showed similar level of diagnostic accuracy along with sensitivity and specificity compared to DGGR lipase. In addition, P-AMY showed a significant association with CAPS score, contrary to cPL and DGGR lipase. Along with other biomarkers associated with AP, P-AMY has the potential of usefulness as a supportive diagnostic and prognostic biomarker of AP in dogs.

Ameliorative Effects of Larazotide Acetate on Intestinal Permeability and Bacterial Translocation in Acute Pancreatitis Model in Rats.

Intestinal barrier dysfunction in acute pancreatitis (AP) may progress to systemic inflammatory response syndrome (SIRS) and multi-organ failures by causing bacterial translocation. Larazotide acetate (LA) is a molecule that acts as a tight junction (TJ) regulator by blocking zonulin (Zo) receptors in the intestine. In our study, we aimed to investigate the effects of LA on intestinal barrier dysfunction and bacterial translocation in the AP model in rats. Thirty-two male Sprague-Dawley rats were divided into 4 groups; control, larazotide (LAR), AP, and AP + LAR. The AP model was created by administering 250 mg/100 g bm L-Arginine intraperitoneally 2 times with an hour interval. AP + LAR group received prophylactic 0.01 mg/mL LA orally for 7 days before the first dose of L-Arginine. For intestinal permeability analysis, fluorescein isothiocyanate-dextran (FITC-Dextran) was applied to rats by gavage. The positivity of any of the liver, small intestine mesentery, and spleen cultures were defined as bacterial translocation. Histopathologically damage and zonulin immunoreactivity in the intestine were investigated. Compared to the control group, the intestinal damage scores, anti-Zo-1 immunoreactivity H-Score, serum FITC-Dextran levels and bacterial translocation frequency (100% versus 0%) in the AP group were significantly higher (all p < 0.01). Intestinal damage scores, anti-Zo-1 immunoreactivity H-score, serum FITC-Dextran levels, and bacterial translocation frequency (50% versus 100%) were significantly lower in the AP + LAR group compared to the AP group (all p < 0.01). Our findings show that LA reduces the increased intestinal permeability and intestinal damage by its effect on Zo in the AP model in rats, and decreases the frequency of bacterial translocation as a result of these positive effects.

The role of thiol/disulfide hemostasis in the diagnosis and severity prediction of acute pancreatitis

Objective: Reactive oxygen radicals are generated in the early stages of acute pancreatitis (AP) and are responsible for its progression. Thiol/disulfide homeostasis (TDH) is an important antioxidative mechanism. This study aimed to evaluate the role of TDH in the differential diagnosis of AP and predict its clinical severity.&#x0D; Methods: Patients admitted to the emergency department due to upper abdominal pain were evaluated. The study consisted of two groups: the AP group and the non-AP group (patients with diagnoses other than AP). The AP group was divided into mild and severe according to Acute physiology and chronic health evaluation II (APACHE-II) scores. TDH was measured with an automated assay from Erel et al. Statistical analyses were done with SPSS 16.0.&#x0D; Results: The results from 128 cases—58 in the AP group and 70 in the non-AP group—were evaluated. There was no difference in TDH parameters between the AP and non-AP groups. Among the AP subgroups, native thiol (sh) and total thiol (tt) were significantly lower in the severe AP group (sh: 313.9 μmol/L, 239.1 μmol/L; tt: 351.5 μmol/L, 303 μmo/L, respectively, in the mild and severe AP groups, P-value=0.006, P-value=0.013).&#x0D; Conclusion: TDH parameters change because of inflammatory processes in AP. Since this change does not occur for any specific reason, using TDH parameters for differential diagnosis of AP in patients with upper abdominal pain is not appropriate. However, in patients already diagnosed with AP, native and total thiol levels might be helpful in the prediction of clinical severity with a limited role.

The relationship between inflammatory cytokines and in-hospital complications of acute pancreatitis.

Acute necrotic collection (ANC), acute peripancreatic fluid collection (APFC), pleural effusion, and ascites are common early complications of acute pancreatitis. This study aimed to investigate the relationship between 12 serum cytokines and the early complications and severity of acute pancreatitis (AP). We retrospectively analyzed the clinical data of 307 patients with AP, and divided them into severe group and mild-to-moderate group according to the revised Atlanta classification. Propensity score matching was used to control for confounding factors. Binary logistic regression analysis was used to explore the relationship between cytokine levels and early complications of AP. Serum levels of interleukin (IL)-1β, IL-5, IL-6, IL-8, IL-10, IL-17, and tumor necrosis factor-α were significantly higher in the severe acute pancreatitis (SAP) group than in the non-SAP group (p < .05). After adjusting for confounding factors, the upper quartiles of IL-6, IL-8, and IL-10 were associated with an increased risk of ANC compared with those in the lowest quartile (IL-6: quartile 3, odds ratio [OR] = 3.99, 95% confidence interval [CI] = 1.95-8.16; IL-8: quartile 4, OR = 2.47, 95% CI = 1.27-4.84; IL-10: quartile 2, OR = 2.22, 95% CI = 1.09-4.56). APFC was associated with high serum levels of IL-6 (quartile 3, OR = 1.32, 95% CI = 1.02-1.72), pleural effusions were associated with high serum levels of IL-1β, IL-6, IL-8, and IL-10 (IL-1β: quartile 4, OR = 2.36, 95% CI = 1.21-4.58; IL-6: quartile 3, OR = 4.67, 95% CI = 2.27-9.61; IL-8: quartile 3, OR = 2.95, 95% CI = 1.51-5.79; IL-10: quartile 4, OR = 3.20, 95% CI = 1.61-6.36), and high serum levels of IL-6 and IL-10 were associated with an increased risk of ascites (IL-6: quartile 3, OR = 3.01, 95% CI = 1.42-6.37; IL-10: quartile 3, OR = 2.57, 95% CI = 1.23-5.37). Serum cytokine levels, including IL-1β, IL-6, IL-8, and IL-10 may be associated with the occurrence of early complications of AP. In daily clinical practice, IL-6 may be the most worthwhile cytokine to be detected.

Association of pancreatitis with risk of diabetes: analysis of real-world data.

Diabetes is a major cause of disease burden with considerable public health significance. While the pancreas plays a significant role in glucose homeostasis, the association between pancreatitis and new onset diabetes is not well understood. The purpose of this study was to examine that association using large real-world data. Utilizing the IBM® MarketScan® commercial claims database from 2016 to 2019, pancreatitis and diabetes regardless of diagnostic category, were identified using International Classification of Diseases, Tenth Revision [ICD-10] codes. We then performed descriptive analyses characterizing non-pancreatitis (NP), acute pancreatitis (AP), and chronic pancreatitis (CP) cohort subjects. Stratified Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) of diabetes across the three clinical categories. In total, 310,962 individuals were included in the analysis. During 503,274 person-years of follow-up, we identified 15,951 incident diabetes cases. While men and women had higher incidence rates of CP and AP-related diabetes, the rates were significantly greater in men and highest among individuals with CP (91.6 per 1000 persons-years (PY)) followed by AP (75.9 per 1000-PY) as compared to those with NP (27.8 per 1000-PY). After adjustment for diabetes risk factors, relative to the NP group, the HR for future diabetes was 2.59 (95% CI: 2.45-2.74) (P<0.001) for the CP group, and 2.39 (95% CI: 2.30-2.48) (P<0.001) for the AP group. Pancreatitis was associated with a high risk of diabetes independent of demographic, lifestyle, and comorbid conditions.

Efficacy of Agmatine Treatment in Experimental Acute Pancreatitis Rat Model.

Acute pancreatitis which is characterized by pancreatic inflammation can sometimes be difficult to treat because of limited therapeutic options. The purpose of the study was to assess the effects of agmatine in the acute pancreatitis experimental rat model. An acute pancreatitis model was created with the administration of cerulein in 40 female Sprague-Dawley rats. Agmatine was administered as a protective agent at 5 mg/kg (low dose) and 10 mg/kg (high dose). The rats were divided into 5 groups, each with 8 rats: group 1 (acute pancreatitis); group 2 (acute pancreatitis+low-dose agmatine 5 mg/kg); group 3 (acute pancreatitis+high-dose agmatine 10 mg/kg); group 4 (placebo, acute pancreatitis+saline); and group 5 (sham and saline infusion). All rats were sacrificed 24 hours after the last injection, and the levels of superoxide dismutase, interleukin-1 beta, and tumor necrosis factor-alpha were assessed in blood samples collected via cardiac puncture. Histopathological examination was performed by a pathologist, who was blind to the groups, according to the Schoenberg's pancreatitis scoring index. The amylase (16.67 and 37.89 U/L), glutathione peroxidase (13.62 and 18.44 ng/mL), tumor necrosis factor-α (39.68 and 64 ng/mL), interleukin-1 (484.73 and 561.83 pg/mL), and transforming growth factor-β (110.52 and 126.34 ng/L) levels were significantly lower and superoxide dismutase (1.29 and 0.98 ng/L) and malondialdehyde (0.99 and 0.96 nmol/mL) levels were significantly higher in group 3 compared to group 1 (P < .05). Moreover glutathione peroxidase, tumor necrosis factor-α, and transforming growth factor-β levels were lower, and malondialdehyde levels were higher in the group 3 compared to group 2 (P < .05). Although the Schoenberg's pancreatitis scoring index was not significantly different between the high- and low-dose treatment groups, rats who received high-dose treatment had significantly lower scores compared to those with acute pancreatitis group. This is the first study that evaluated the efficacy of agmatine in an experimental model of acute pancreatitis. Agmatine, an anti-inflammatory and antioxidant agent, had a protective effect in an experimental rat model of acute pancreatitis.

Computed Tomography Assessment of Severity of Acute Pancreatitis in Bangladeshi Children.

Acute pancreatitis (AP) is common among children in Bangladesh. Its management depends mainly on risk stratification. This study aimed to assess the severity of pediatric AP using computed tomography (CT). This cross-sectional, descriptive study was conducted in pediatric patients with AP at the Department of Pediatric Gastroenterology and Nutrition, BSMMU, Dhaka, Bangladesh. Altogether, 25 patients with AP were included, of whom 18 (mean age, 10.27±4.0 years) were diagnosed with mild AP, and 7 (mean age, 10.54±4.0 years) with severe AP. Abdominal pain was present in all the patients, and vomiting was present in 88% of the patients. Etiology was not determined. No significant differences in serum lipase, serum amylase, BUN, and CRP levels were observed between the mild and severe AP groups. Total and platelet counts as well as hemoglobin, hematocrit, serum creatinine, random blood sugar, and serum alanine aminotransferase levels (p>0.05) were significantly higher in the mild AP group than in the severe AP group (p=0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of CT severity index (CTSI) were 71.4%, 72.2%, 50%, and 86.7%, respectively. In addition, significant differences in pancreatic appearance and necrosis were observed between the two groups on CT. CT can be used to assess the severity of AP. In the present study, the CTSI effectively assessed the severity of AP in pediatric patients.

Fabp5 is a common gene between a high-cholesterol diet and acute pancreatitis.

Hypercholesterolemia has been identified as risk factor for severe acute pancreatitis (AP). We aimed to identify the common differentially expressed genes (DEGs) between a high-cholesterol diet and AP. We retrived gene expression profiles from the GEO database. DEGs were assessed using GEO2R. For AP hub genes, we conducted functional enrichment analysis and protein-protein interaction (PPI) analysis. GeneMANIA and correlation analysis were employed to predict potential DEG mechanisms. Validation was done across various healthy human tissues, pancreatic adenocarcinoma, peripheral blood in AP patients, and Sprague-Dawley rats with AP. The gene "Fabp5" emerged as the sole common DEG shared by a high-cholesterol diet and AP. Using the 12 topological analysis methods in PPI network analysis, Rela, Actb, Cdh1, and Vcl were identified as hub DEGs. GeneMANIA revealed 77.6% physical interactions among Fabp5, TLR4, and Rela, while genetic correlation analysis indicated moderate associations among them. Peripheral blood analysis yielded area under the ROC curve (AUC) values of 0.71, 0.63, 0.74, 0.64, and 0.91 for Fabp5, TLR4, Actb, Cdh1 genes, and artificial neural network (ANN) model respectively, in predicting severe AP. In vivo immunohistochemical analysis demonstrated higher Fabp5 expression in the hyperlipidemia-associated AP group compared to the AP and control groups. Fabp5 emerged as the common DEG connecting a high-cholesterol diet and AP. Rela was highlighted as a crucial hub gene in AP. Genetic interactions were observed among Fabp5, TLR4, and Rela. An ANN model consisting of Fabp5, TLR4, Actb, and Cdh1 was helpful in predicting severe AP.

Acute pancreatitis in intraductal papillary mucinous neoplasm: a single-center retrospective cohort study with systematic review and meta-analysis

BackgroundIntraductal 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.MethodsIn 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.ResultsThe 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.ConclusionsAP is predictive of malignancy in patients with IPMN.

Critical evaluation of established risk prediction models for acute respiratory distress syndrome in adult patients: A systematic review and meta-analysis.

To assess the performance of validated prediction models for acute respiratory distress syndrome (ARDS) by systematic review and meta-analysis. Eight databases (Medline, CINAHL, Embase, The Cochrane Library, CNKI, WanFang Data, Sinomed, and VIP) were searched up to March 26, 2023. Studies developed and validated a prediction model for ARDS in adult patients were included. Items on study design, incidence, derivation methods, predictors, discrimination, and calibration were collected. The risk of bias was assessed by the Prediction model Risk of Bias Assessment Tool. Models with a reported area under the curve of the receiver operating characteristic (AUC) metric were analyzed. A total of 25 studies were retrieved, including 48 unique prediction models. Discrimination was reported in all studies, with AUC ranging from 0.701 to 0.95. Emerged AUC value of the logistic regression model was 0.837 (95% CI: 0.814 to 0.859). Besides, the value in the ICU group was 0.856 (95% CI: 0.812 to 0.899), the acute pancreatitis group was 0.863 (95% CI: 0.844 to 0.882), and the postoperation group was 0.835 (95% CI: 0.808 to 0.861). In total, 24 of the included studies had a high risk of bias, which was mostly due to the improper methods in predictor screening (13/24), model calibration assessment (9/24), and dichotomization of continuous predictors (6/24). This study shows that most prediction models for ARDS are at high risk of bias, and the discrimination ability of the model is excellent. Adherence to standardized guidelines for model development is necessary to derive a prediction model of value to clinicians.

Low skeletal muscle quality extracted from CT is associated with poor outcomes in severe acute pancreatitis patients

PurposeTo evaluate the association between body composition parameters derived from computed tomography (CT) scans and clinical outcomes in patients with severe acute pancreatitis (AP). MethodsPatients who have been diagnosed AP with a CT scan at ICU admission were included. Body composition parameters were measured on a single slice at L2-3 of the unenhanced CT scans. The intermuscular adipose tissue (IMAT), visceral adipose tissue (VAT), skeletal muscle area (SMA) and skeletal muscle density (SMD) were assessed using HUs by image analysis software. Univariable and multivariable analyses were performed to analyze the association between body composition parameters and clinical outcomes including all-cause mortality or prolonged ICU stay. The area under the curve (AUC) of a receiver operating characteristic curve was used to explore the predictive value of the body composition on treatment clinical outcomes. ResultsA total of 158 patients were included. The IMAT (8.3 cm2 vs 6.0 cm2, P = 0.001) and VAT (190.3 cm2 vs 143.7 cm2, P < 0.001) were significantly higher in the severe AP group than in the moderately severe group, but were notassociatedwithoutcomes. For 1 HU of SMD increased, the risk of poor clinical outcomes decresed 11 % (adjusted OR 0.892, 95 %CI 0.806–0.987, P = 0.026), while an SMD below the median value (32.1 HU for males and 28.5 HU for females) was independently associated with worse outcomes in the multivariable analysis (adjusted OR 8.868, 95 % CI 2.146–36.650, P = 0.003). The SMD had a good predictive ability for clinical outcomes, AUC was 0.824 (95 % CI, 0.715–0.933) for males and 0.803 (95 % CI, 0.639–0.967) for females. ConclusionLow SMD was associated with poor outcomes in patients with severe and moderately severe AP and might be used as a novel marker to predict outcomes in patients suffering from severe and moderately severe AP.

Quantitative CT features on admission combined with laboratory biomarkers for predicting severe acute pancreatitis

To assess the association of quantitative computed tomography (CT) features on admission with acute pancreatitis (AP) severity, and to explore the performance of combined CT and laboratory markers for predicting severe AP (SAP). Data from 208 AP patients were reviewed retrospectively. Pancreas volume, the area of extrapancreatic inflammation, extrapancreatic fluid collection volume, and number were calculated based on CT images on admission. Laboratory biomarkers within 24 h of admission were collected. Interobserver agreement for CT measurements was measured by calculating interclass correlation coefficient (ICC). The associations of quantitative CT features with AP severity were evaluated. Predictive models for SAP were constructed based on CT and laboratory markers. Performances of single marker and the models were evaluated using receiver operating characteristic (ROC) curve and area under the ROC curve (AUC). Pancreas volume, area of extrapancreatic inflammation, extrapancreatic fluid collection volume, and number were significantly different between severe and non-severe AP groups. In predicting SAP, the AUCs of quantitative CT indicators ranged from 0.72 to 0.79; the AUCs of laboratory biomarkers were between 0.53 and 0.66. The combined model of area of extrapancreatic inflammation, serum calcium, and haematocrit yielded an AUC of 0.84, significantly higher than that of the laboratory model, single CT, or laboratory marker. Interobserver agreements for quantitative CT indicators were excellent, with ICC ranging from 0.91 to 0.98. Quantitative CT features on admission were significantly associated with AP severity; the combination of extrapancreatic inflammation area, serum calcium, and haematocrit could be taken as a new method for predicting SAP.

Clinical value of BISAP score combined with CRP and NLR in evaluating the severity of acute pancreatitis.

To investigate the clinical value of bedside index for severity in acute pancreatitis (BISAP) score combined with serum C-reactive protein (CRP) and neutrophil-to-lymphocyte ratio (NLR) in predicting the severity of early acute pancreatitis. A total of 113 patients with acute pancreatitis admitted to the Department of Gastroenterology, Second Affiliated Hospital of Nantong University from September 2019 to September 2022 were retrospectively collected and divided into mild acute pancreatitis group (51 cases), moderately severe acute pancreatitis group (32 cases) and severe acute pancreatitis group (30 cases) according to the severity of the disease. The general clinical data, laboratory test indicators, and imaging data within 72 hours were collected and compared among the 3 groups. The sensitivity, specificity, and accuracy of BISAP score, BISAP combined with CRP, BISAP combined with NLR, and BISAP combined with CRP and NLR in predicting the severity of acute pancreatitis were analyzed by receiver operating characteristic curve. 1. BISAP score (0.9608 ± 0.1119, 1.688 ± 0.1225, 2.6 ± 0.1135), CRP (74.77 ± 8.336, 142.9 ± 11.44, 187.6 ± 13.04), and NLR (8.063 ± 0.7781, 13.69 ± 1.023, 18.06 ± 1.685) increased sequentially in mild acute pancreatitis group, moderately severe acute pancreatitis group, and severe acute pancreatitis group, and the differences in BISAP score, CRP and NLR among the 3 groups were statistically significant (P < .05). BISAP score was positively correlated with CRP and NLR (R = 0.5062, 0.5247, P < .05). The area under the receiver operating characteristic curve of BISAP score, CRP, NLR, BISAP combined with NLR, and BISAP combined with CRP in predicting the severity of acute pancreatitis were 0.885, 0.814, 0.714, 0.953, respectively. The specificity and sensitivity of combined diagnosis were higher than those of BISAP score or CRP and NLR alone. BISAP score combined with CRP and NLR can effectively evaluate the severity of acute pancreatitis, and their combination has a higher predictive value for early severity assessment.

Profile of Pancreatic and Ileal Microbiota in Experimental Acute Pancreatitis.

Acute pancreatitis (AP) is accompanied by gut microbiota dysbiosis. However, the composition of the pancreatic and ileal microbiota associated with AP is still unknown. This study aims to examine the alterations in the microbial composition of the pancreas and ileum in the context of experimental acute pancreatitis, as well as explore the potential interplay between these two regions. Methods: Caerulein (CAE), caerulein+lipopolysaccharide (CAE+LPS), and L-arginine (ARG) were used to induce AP in mice. The pancreas and ileum were collected for histological study and bacterial 16S rRNA gene sequencing. The results showed microbial structural segregation between the AP and control groups and between ARG and the two CAE groups (CAE, CAE+LPS) in the pancreas and ileum. Taxonomic analysis at the genus level and linear discriminant analysis effect size (LEfSe) at the operational taxonomic units (OTUs) level illustrated that AP mice exhibited a marked increase in the relative abundance of Muribaculaceae and a decrease in that of Dietzia both in the pancreas and ileum, and a reduction in Bifidobacterium only in the ileum; in addition, Roseburia was enriched in the two CAE groups in the pancreas and/or ileum, while Escherichia-Shigella expanded in the pancreas of the ARG group. Spearman correlation analysis between pancreatic and ileal microbiota revealed that the abundance of Muribaculaceae and Dietzia in the pancreas was related to that in the ileum. These findings demonstrated that caerulein and L-arginine differentially disturbed the pancreatic and ileal microbiota when inducing AP. Furthermore, these findings provide preliminary support for an association between the microbiota of the pancreas and ileum, which could be caused by AP-induced microbial translocation.

Pancreas volumes in pediatric patients following index acute pancreatitis and acute recurrent pancreatitis

Background/objectivesPancreas volume derived from imaging may objectively reveal volume loss relevant to identifying sequelae of acute pancreatitis (AP) and ultimately diagnosing chronic pancreatitis (CP). The purposes of this study were to: (1) quantify pancreas volume by imaging in children with either (a) a single episode of AP or (b) acute recurrent pancreatitis (ARP), and (2) compare these volumes to normative volumes. MethodsThis retrospective study was institutional review board approved. A single observer segmented the pancreas (3D Slicer; slicer.org) on n = 30 CT and MRI exams for 23 children selected from a prospective registry of patients with either an index attack of AP or with ARP after a known index attack date. Patients with CP were excluded. Segmented pancreas volumes were compared to published normal values. ResultsMean pancreas volumes normalized to body surface area (BSA) in the index AP and ARP groups were 38.2 mL/m2 (range: 11.8–73.5 mL/m2) and 27.9 mL/m2 (range: 8.0–69.2 mL/m2) respectively. 43 % (6/14) of patients post-AP had volumes below the 25th percentile, 1 (17 %) of which was below the 5th percentile (p = 0.3027 vs. a normal distribution). Post-ARP, 44 % (7/16) of patients had volumes below the 5th percentile (p < 0.001). ConclusionsA significant fraction (40 %) of children with ARP have pancreas volumes <5th percentile for BSA even in the absence of CP. A similar, but not statistically significant, fraction have pancreas volumes <25th percentile after an index attack of AP. Pancreatic parenchymal volume deserves additional investigation as an objective marker of parenchymal damage from acute pancreatitis and of progressive pancreatitis in children.

Incidence and risk of pancreatic cancer in patients with acute or chronic pancreatitis: a population-based cohort study

We aimed to evaluate the incidence and risk of pancreatic cancer (PC) in pancreatitis. We identified patients with acute pancreatitis (AP) (n = 225,811, 50.0%) and chronic pancreatitis (CP) (n = 225,685, 50.0%) from Korean population-based data and matched them with age- and sex-matched controls (n = 4,514,960). We analyzed the incidence and adjusted hazard ratios (aHRs) of PC among patients followed for more than 2 years or 5 years, and assessed risk changes over time in single episode of AP (SAP), recurrent AP (RAP), CP with AP, and CP without AP groups. We also performed subgroup analysis for both sexes. The incidences (per 104 person-years) and risks (aHR) of PC were higher in the RAP (12.69, 5.00) or CP with AP (12.12, 5.74) groups compared to the SAP (2.31, 1.32) or CP without AP (2.28, 1.57) groups. The risks of PC decreased over time, however, the risk of PC remained elevated in the RAP and CP with AP groups for more than 8 years. Females with RAP, SAP, and CP with AP had higher risks of PC than males. The risk of PC is higher and persists for longer duration in patients with RAP and CP with AP compared to those with SAP or CP without AP.

Ketogenic Diet Exacerbates L-Arginine-Induced Acute Pancreatitis and Reveals the Therapeutic Potential of Butyrate.

The ketogenic diet (KD) has emerged as a popular weight-loss regimen in recent years. However, it has been confirmed to elicit a mild inflammatory response in the intestinal epithelium and exacerbate various digestive disorders. The severity of acute pancreatitis (AP) is closely associated with the permeability of the intestinal epithelium and gut microbiota, yet the impact of KD on acute pancreatitis remains unclear. In this study, we induced acute pancreatitis using L-arginine in mice fed with KD. The consumption of KD resulted in an elevation of lipopolysaccharide-binding protein (LBP), accompanied by upregulated cytokines (IL-1a, IL-5, IL-12, MIP-1a, and Rantes) and dysfunction of the intestinal barrier both in control and AP groups. The bloom of Lachnospirales and Erysipelotrichales was observed as a specific profile of gut microbiota in KD-fed mice with AP, along with downregulation of carbohydrate metabolism and depletion of short-chain fatty acids (SCFAs). Antibiotic decontamination reduced the cytokine storm and tissue necrosis but did not significantly improve the integrity of the intestinal barrier in KD-fed mice with AP. The overgrowth of Mycoplasmatales in feces and Enterobacterales in colonic tissue appears to explain the limitation of antibiotic treatment to aggravate acute pancreatitis. Butyrate supplementation attenuated the depletion of SCFAs, promoted the intestinal barrier, and reduced the necrotic area in AP mice. The bloom of Bacteroidales and the correlated increase in tryptophan metabolism explain the therapeutic potential of butyrate supplements for acute pancreatitis. In conclusion, our findings suggest that the ketogenic diet exacerbates acute pancreatitis through its impact on the gut microbiota and subsequent disruption of the intestinal barrier, while butyrate supplementation reverses this effect.

Maternal and fetal outcomes of acute pancreatitis in pregnancy: a population-based study.

Acute pancreatitis during pregnancy can have negative effects on both the mother and the fetus. The primary aim of this study is to evaluate the trends, maternal and fetal outcomes, and associated comorbidities of acute pancreatitis during pregnancy using data from the USA National Inpatient Sample (NIS) database. This study is a retrospective analysis of hospital discharge records from the NIS database from 2009 to 2019. Delivery patients with acute pancreatitis faced a higher risk of maternal mortality (AOR 91.02, 95% CI 28.47-291.06), postpartum hemorrhage (AOR 1.59, 95% CI 1.02-2.49), and hypertensive complications (defined as preeclampsia, eclampsia, or HELLP syndrome) (AOR 3.42, 95% CI 2.56-4.56) compared to those without acute pancreatitis. Moreover, we saw an increased incidence of preterm labor (AOR 3.94, 95% CI 3.02-5.12) and fetal death (AOR 3.12, 95% CI 1.76-5.53). Rates of fetal restriction and large fetal size were comparable. Additionally, the acute pancreatitis group showed higher rates of acute kidney injury (4.2% vs. 0.06%; AOR, 31.02, 95% CI 12.50-76.98), severe sepsis (0.8% vs. 0.01%; AOR, 34.49, 95% CI 7.67-155.14), and respiratory failure (2.4% vs. 0.06%; AOR, 20.77, 95% CI (8.55-50.41). There were no significant differences in maternal and perinatal outcomes in biliary pancreatitis after the intervention compared to conservative treatment. Acute pancreatitis during pregnancy can have negative effects on both the mother and fetus. Treatment for biliary pancreatitis does not affect maternal and fetal outcomes. An interdisciplinary approach is essential to ensure optimal outcomes for mothers and their offspring in these cases.

GlycA: Evaluation of a New Biomarker of Acute Pancreatitis.

Acute pancreatitis (AP) is a leading cause of gastrointestinal hospital admissions, with up to 40% mortality in patients with moderate-severe AP. Glycoprotein acetylation (GlycA) is measured as a nuclear magnetic resonance signal (NMR) of the post-translational modification of glycosylated acute-phase proteins released during inflammation. We aimed to investigate the role of GlycA as an inflammatory biomarker of AP. We prospectively enrolled 20 AP patients and 22 healthy controls and collected EDTA plasma samples at admission and discharge. NMR spectra were acquired from these samples using a 400 MHz Vantera® Clinical Analyzer, and GlycA concentrations were calculated (normal = 400 μmol/L). The GlycA NMR signal, at 2.00 ± 0.01 ppm in the NMR spectrum, is derived from the N-acetyl methyl group protons within the carbohydrate side chains of circulating glycoproteins such as α1-acid glycoprotein, haptoglobin, α1-antitrypsin, α1-antichymotrypsin, and transferrin. GlycA levels were then compared between AP patients and controls, as well as within the AP group, based on etiology and severity. Demographic comparisons were similar, except for a higher BMI in AP patients compared to healthy controls (29.9 vs. 24.8 kg/m2; p < 0.001). AP was mild in 10 patients, moderate in 7, and severe in 3. GlycA levels were higher in AP patients than healthy controls on admission (578 vs. 376 μmol/L, p < 0.001) and at discharge (655 vs. 376 μmol/L, p < 0.001). GlycA levels were significantly higher in patients with moderate-severe AP than in those with mild AP at discharge (533 vs. 757 μmol/L, p = 0.023) but not at admission. After adjusting for BMI, multivariable regression indicated that patients with GlycA levels > 400 μmol/L had significantly higher odds of having AP of any severity (OR = 6.88; 95% CI, 2.07-32.2; p = 0.004) and mild AP (OR = 6.12; 95% CI, 1.48-42.0; p = 0.025) than controls. Our pilot study highlights the use of GlycA as a novel diagnostic biomarker of inflammation in patients with AP. Our study shows that GlycA levels were significantly higher in hospitalized AP patients compared to healthy controls. Patients with moderate-to-severe AP had higher GlycA levels compared to patients with mild AP at the time of their hospital discharge, suggesting persistent inflammation in patients with severe disease.