• Machine learning
• Mortality prediction
• SHAP
• Severe acute pancreatitis
• XGBoost

• Humans
• Machine Learning
• Pancreatitis/mortality
• Male
• Female
• Middle Aged
• Aged
• Adult
• Prognosis

• 81070125 National Natural Science Foundation of China
• 2010B031600032 Science and Technology Foundation in Guangdong Province
• 2017A030313503 National Natural Science Foundation of Guangdong Province
• 201806020084 Science and Technology Foundation in Guangzhou City
• FTWS2019001 Futian District Health and Public Welfare Research Project of Shenzhen City
• FTWS2021016 Futian District Health and Public Welfare Research Project of Shenzhen Cit
• JCYJ20190808101405466 Shenzhen Fundamental Research Program
• 13ykzd16 Fundamental Research Funds for the Central Universities

• Acute pancreatitis
• clinical decision support
• intensive care unit
• risk score
• supervised machine learning

Gastrointestinal (GI) complications frequently necessitate intensive care unit (ICU) admission. Additionally, critically ill patients also develop GI complications requiring further diagnostic and therapeutic interventions. However, these patients form a vulnerable group, who are at risk for developing side effects and complications. Every effort must be made to reduce invasiveness and ensure safety of interventions in ICU patients. Artificial intelligence (AI) is a rapidly evolving technology with several potential applications in healthcare settings. ICUs produce a large amount of data, which may be employed for creation of AI algorithms, and provide a lucrative opportunity for application of AI. However, the current role of AI in these patients remains limited due to lack of large-scale trials comparing the efficacy of AI with the accepted standards of care.

• Artificial intelligence
• Critical care
• Gastroenterology
• Hepatology
• Intensive care unit
• Machine learning

• Acute kidney injury
• Acute pancreatitis
• Cys C

• Humans
• Retrospective Studies
• Cystatin C
• Acute Disease
• Pancreatitis/complications
• Pancreatitis/diagnosis
• Acute Kidney Injury/diagnosis
• Acute Kidney Injury/etiology
• Biomarkers
• ROC Curve

• Acute biliary pancreatitis
• asymptomatic cholelithiasis
• silent gallstones

• Acute pancreatitis
• Intensive care unit
• Machine learning
• Xgboost

• Humans
• Retrospective Studies
• Pancreatitis/diagnostic imaging
• Critical Illness
• Acute Disease
• Machine Learning

Acute kidney injury (AKI) is one of the most common acute pancreatitis (AP)-associated complications that has a significant effect on AP, but the factors affecting the AP patients’ survival rate remains unclear.

To assess the influences of AKI on the survival rate in AP patients.

A total of 139 AP patients were included in this retrospective study. Patients were divided into AKI group (n = 72) and non-AKI group (n = 67) according to the occurrence of AKI. Data were collected from medical records of hospitalized patients. Then, these data were compared between the two groups and further analysis was performed.

AKI is more likely to occur in male AP patients (P = 0.009). AP patients in AKI group exhibited a significantly higher acute physiologic assessment and chronic health evaluation II score, higher Sequential Organ Failure Assessment score, lower Glasgow Coma Scale score, and higher demand for mechanical ventilation, infusion of vasopressors, and renal replacement therapy than AP patients in non-AKI group (P < 0.01, P < 0.01, P = 0.01, P = 0.001, P < 0.01, P < 0.01, respectively). Significant differences were noted in dose of norepinephrine and adrenaline, duration of mechanical ventilation, maximum and mean values of intra-peritoneal pressure (IPP), maximum and mean values of procalcitonin, maximum and mean serum levels of creatinine, minimum platelet count, and length of hospitalization. Among AP patients with AKI, the survival rate of surgical intensive care unit and in-hospital were only 23% and 21% of the corresponding rates in AP patients without AKI, respectively. The factors that influenced the AP patients’ survival rate included body mass index (BMI), mean values of IPP, minimum platelet count, and hospital day, of which mean values of IPP showed the greatest impact.

AP patients with AKI had a lower survival rate and worse relevant clinical outcomes than AP patients without AKI, which necessitates further attention to AP patients with AKI in surgical intensive care unit.

• Acute kidney injury
• Acute pancreatitis
• Surgical intensive care unit
• Survival rate
• Risk factors
• Intra-peritoneal pressure

• Acute Disease
• Acute Kidney Injury/diagnosis
• Acute Kidney Injury/etiology
• Acute Kidney Injury/therapy
• Humans
• Intensive Care Units
• Male
• Pancreatitis/complications
• Pancreatitis/diagnosis
• Prognosis
• Retrospective Studies
• Risk Factors
• Survival Rate

Glucose metabolism and systemic inflammation have been associated with prognosis in acute pancreatitis (AP) patients. However, the possible value as a prognostic marker of the glucose-to-lymphocyte ratio (GLR) has not been evaluated in critically ill patients with AP.

This study included 1,133 critically ill patients with AP from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database, who were randomly divided into the training cohort (n=806) and the validation cohort (n=327) at a ratio of 7:3. X-tile software was used to determine the optimal cut-off values for GLR. Area under the curve (AUC) analysis was performed to compare the performance between GLR and other blood-based inflammatory biomarkers. Univariate and multivariate Cox regression analyses were applied to select prognostic factors associated with in-hospital mortality. A nomogram model was developed based on the identified prognostic factors and the validation cohort was used to further validate the nomogram.

The optimal cut-off value for GLR was 0.9. The ROC analyses showed that the discrimination abilities of GLR were better than other blood-based inflammatory biomarkers. Multivariate Cox regression analysis demonstrated that age, platelet, albumin, bilirubin, Sequential Organ Failure Assessment (SOFA) score, and GLR are independent predictors of poor overall survival in the training cohort and were incorporated into the nomogram for in-hospital mortality as independent factors. The nomogram exhibited better discrimination with C-indexes in the training cohort and the validation cohort of 0.886 (95% CI=0.849–0.922) and 0.841 (95% CI=0.767–0.915), respectively. The calibration plot revealed an adequate fit of the nomogram for predicting the risk of in-hospital mortality in both sets.

As an easily available biomarker, GLR can independently predict the in-hospital mortality of critically ill patients with AP. The nomogram combining GLR with other significant features exerted favorable predictive performance for in-hospital mortality.

• acute pancreatitis
• critically ill
• glucose-to-lymphocyte ratio
• predict

• adult intensive & critical care
• gastroenterology
• pancreatic disease

• Acute Disease
• Cohort Studies
• Critical Care
• Female
• Hospital Mortality
• Humans
• Male
• Nomograms
• Pancreatitis
• Prognosis
• Retrospective Studies

• gastrointestinal diseases
• pancreas

• Alcohol Drinking/adverse effects
• Azocines
• Biliary Tract Diseases/complications
• Cholangiopancreatography, Endoscopic Retrograde/adverse effects
• Female
• Humans
• Hypertriglyceridemia/complications
• Male
• Pancreatitis/epidemiology
• Pancreatitis/etiology
• Pancreatitis/mortality
• Pancreatitis, Acute Necrotizing/epidemiology
• Pancreatitis, Acute Necrotizing/etiology
• Recurrence
• Severity of Illness Index

• Emberi Erőforrás Fejlesztési Operatív Program
• Nemzeti Kutatási, Fejlesztési és Innovaciós Alap
• Economic Development and Innovation Operational Programme
• Magyar Tudományos Akadémia

• Acute pancreatitis
• Extrapancreatic infection
• Infectious complications
• Mortality

• APACHE
• Adult
• Female
• Humans
• Infections/etiology
• Infections/physiopathology
• Male
• Middle Aged
• Morbidity
• Pancreatitis, Acute Necrotizing/complications
• Pancreatitis, Acute Necrotizing/physiopathology
• Prognosis
• Retrospective Studies

Acute lung injury (ALI) is a critical event involved in the pathophysiological process of acute pancreatitis (AP). Many methods have been widely used for the treatment of AP-ALI, but few are useful during early inflammation. Lipoxin A4 (LXA4), a potent available anti-inflammatory and novel antioxidant mediator, has been extensively studied in AP-ALI, but its underlying mechanism as a protective mediator is not clear. This research was conducted to identify the possible targets and mechanisms involved in the anti-AP-ALI effect of LXA4. First, we confirmed that LXA4 strongly inhibited AP-ALI in mice. Next, using ELISA, PCR, and fluorescence detection to evaluate different parameters, LXA4 was shown to reduce the inflammatory cytokine production induced by AP and block reactive oxygen species (ROS) generation in vivo and in vitro. In addition, TNF-α treatment activated the nuclear factor E2-related factor 2 (Nrf2) signaling pathway and its downstream gene heme oxygenase-1 (HO-1) in human pulmonary microvascular endothelial cells (HPMECs), and LXA4 further promoted their expression. This study also provided evidence that LXA4 phosphorylates Ser40 and triggers its nuclear translocation to activate Nrf2. Moreover, when Nrf2-knockout (Nrf2^−/−) mice and cells were used to further assess the effect of the Nrf2/HO-1 pathway, we found that Nrf2 expression knockdown partially eliminated the effect of LXA4 on the reductions in inflammatory factor levels while abrogating the inhibitory effect of LXA4 on the ROS generation stimulated by AP-ALI. Overall, LXA4 attenuated the resolution of AP-induced inflammation and ROS generation to mitigate ALI, perhaps by modulating the Nrf2/HO-1 pathway. These findings have laid a foundation for the treatment of AP-ALI.

• Severe acute pancreatitis (SAP); Acute kidney injury (AKI); Glycocalyx; Dexamethasone; Tumor necrosis factor-α (TNF-α)

• acute kidney injury
• acute pancreatitis
• biomarkers
• diagnostic accuracy
• inflammation

• Acute Kidney Injury/blood
• Acute Kidney Injury/etiology
• Acute Kidney Injury/urine
• Biomarkers/blood
• Biomarkers/urine
• Cystatin C/blood
• Humans
• Leukocyte L1 Antigen Complex/blood
• Lipocalin-2/blood
• Lipocalin-2/urine
• Pancreatitis/blood
• Pancreatitis/complications
• Pancreatitis/urine
• Tissue Inhibitor of Metalloproteinase-2/blood

The aim of this study was to evaluate the effect of a simple visceral obesity phenotype, known as the hypertriglyceridemic waist phenotype and its quantitative indicator waist circumference index on the severity of acute pancreatitis.

Diagnosis and severity analysis of acute pancreatitis were determined according to the Atlanta classification guidelines, revised in 2012. We considered the hypertriglyceridemic waist phenotype as characterized by increased waist circumference and elevated triglyceride concentrations. We investigated the association between the acute pancreatitis severity and hypertriglyceridemic waist phenotype, including waist circumference index.

The hypertriglyceridemic waist phenotype was significantly associated with systemic inflammatory response syndrome, organ failure, and severe acute pancreatitis. The median waist circumference index and demonstration of hypertriglyceridemic waist phenotype were positively correlated with acute pancreatitis severity. In addition, multivariate logistic analysis showed that patients with the hypertriglyceridemic waist phenotype had 1.664 times the risk of organ failure and 1.891 times the risk of systemic inflammatory response syndrome, compared with the other groups.

Upon admission, the hypertriglyceridemic waist phenotype was strongly associated with acute pancreatitis in patients. This phenotype, including waist circumference index, might be a simple method for evaluating individuals at high risk of severe acute pancreatitis.

The online version of this article (10.1186/s12944-019-1019-2) contains supplementary material, which is available to authorized users.

• Acute pancreatitis
• Hypertriglyceridemic waist phenotype
• Retrospective study
• Waist circumference index

• Bedside Index of Severity in Acute Pancreatitis
• Goal-directed fluid resuscitation
• Pain management
• Prophylactic antibiotics
• Systemic inflammatory response syndrome

• Critical care
• Outcome
• Pancreatitis
• Retrospective
• Tertiary

Lipoprotein lipase deficiency (LPLD) is an autosomal recessive inherited disorder caused by loss-of-function mutations in genes involved in the lipoprotein lipase pathway. It is characterised by chylomicronaemia, severe hypertriglyceridaemia and an increased risk of recurrent pancreatitis that often requires hospitalisation. This research aimed to improve our understanding of the debilitating impact that LPLD has on the daily lives of patients and their families.

The research comprised a 2-h interview with the patient and, where possible, a 1-h interview with a family member; a 1-week pre- and post-interview task (written and/or video diary); and a 30–45-min follow-up telephone interview. Feelings and thoughts at each stage of the disease journey were captured on a 0–10 rating scale, while the impact of disease on overall health status was measured via the EuroQoL 5 domains, 3 levels (EQ-5D-3L) questionnaire (descriptive and visual analogue scale).

Of four patients identified, three (two female, one male) were recruited to participate in the study; the male patient did not complete the pre-interview task or consent to a family member interview. Demographics and medical history differed among patients in terms of age at symptom onset, their journey to LPLD diagnosis, treatments, the number of attacks of pancreatitis and lengths of hospitalisations. Health-related quality of life, assessed by the EQ-5D-3L, was poor during acute attacks of pancreatitis but was minimally impacted by their condition at interview. Patients described feeling apprehensive, frightened, anxious, depressed or frustrated during and after hospitalisations; spouses of the two female patients also reported being worried or afraid. LPLD affected many aspects of daily living, including diet; socialising and building relationships; state of mind (fear of another attack of pancreatitis or lack of disease control); college and working life (through absenteeism and consequent financial implications); and being reliant on family and friends for support.

The interviews of the three patients with LPLD highlighted several concerns and emphasised the need for improved education, support, dietary advice and appropriate disease management. Additional support services would ease the fear and uncertainty surrounding attacks of pancreatitis, and would allow for improved treatment during hospitalisations.

The online version of this article (10.1186/s13023-017-0706-1) contains supplementary material, which is available to authorized users.

• Burden of disease
• Chylomicronaemia
• Health-related quality of life
• Hypertriglyceridaemia
• Lipoprotein lipase deficiency
• Pancreatitis

Necrotising pancreatitis, and particularly infected necrosis, are still associated with high morbidity and mortality. Since 2011, a step-up approach with lower morbidity rates compared to initial open necrosectomy has been established. However, mortality and complication rates of this complex treatment are hardly studied thereafter.

The German Pancreatitis Study Group performed a multicenter, retrospective study including 220 patients with necrotising pancreatitis requiring intervention, treated at 10 hospitals in Germany between January 2008 and June 2014. Data were analysed for the primary endpoints "severe complications" and "mortality" as well as secondary endpoints including "length of hospital stay", "follow up", and predisposing or prognostic factors.

Of all patients 13.6% were treated primarily with surgery and 86.4% underwent a step-up approach. More men (71.8%) required intervention for necrotising pancreatitis. The most frequent etiology was biliary (41.4%) followed by alcohol (29.1%). Compared to open necrosectomy, the step-up approach was associated with a lower number of severe complications (primary composite endpoint including sepsis, persistent multiorgan dysfunction syndrome (MODS) and erosion bleeding: 44.7% vs. 73.3%), lower mortality (10.5% vs. 33.3%) and lower rates of diabetes mellitus type 3c (4.7% vs. 33.3%). Low hematocrit and low blood urea nitrogen at admission as well as a history of acute pancreatitis were prognostic for less complications in necrotising pancreatitis. A combination of drainage with endoscopic necrosectomy resulted in the lowest rate of severe complications.

A step-up approach starting with minimal invasive drainage techniques and endoscopic necrosectomy results in a significant reduction of morbidity and mortality in necrotising pancreatitis compared to a primarily surgical intervention.

• Acute necrotizing
• Mycoplasma pneumoniae
• Pancreatitis

• Amylases/blood
• Animals
• Arginine/adverse effects
• Ceruletide/adverse effects
• Disease Models, Animal
• Epoxide Hydrolases/antagonists & inhibitors
• Gene Expression Regulation/drug effects
• Interleukin-1beta/genetics
• Interleukin-6/genetics
• Lipase/blood
• MAP Kinase Signaling System/drug effects
• Mice
• Pancreatitis/chemically induced
• Pancreatitis/drug therapy
• Pancreatitis/genetics
• Phenylurea Compounds/administration & dosage
• Phenylurea Compounds/pharmacology
• Piperidines/administration & dosage
• Piperidines/pharmacology
• Tumor Necrosis Factor-alpha/genetics

• U24 DK092993 NIDDK NIH HHS
• R01-DK095359 NIDDK NIH HHS
• R01 ES002710 NIEHS NIH HHS
• P42-ES04699 NIEHS NIH HHS
• P42 ES004699 NIEHS NIH HHS
• R56-DK084317 NIDDK NIH HHS
• R01 DK090492 NIDDK NIH HHS
• K99 DK100736 NIDDK NIH HHS
• R56 DK084317 NIDDK NIH HHS
• R01 DK095359 NIDDK NIH HHS
• K99-DK100736 NIDDK NIH HHS
• R01-DK090492 NIDDK NIH HHS

Acute pancreatitis (AP) is a potentially life-threatening disease with a wide spectrum of severity. The overall mortality of AP is approximately 5%. According to the revised Atlanta classification system, AP can be classified as mild, moderate, or severe. Severe AP often takes a clinical course with two phases, an early and a late phase, which should both be considered separately. In this review article, we first discuss general aspects of AP, including incidence, pathophysiology, etiology, and grading of severity, then focus on the assessment of patients with suspected AP, including diagnosis and risk stratification, followed by the management of AP during the early phase, with special emphasis on fluid therapy, pain management, nutrition, and antibiotic prophylaxis.

• Acute pancreatitis
• Incidence
• Pathophysiology
• Etiology
• Severity
• Risk stratification
• Fluid therapy
• Pain management
• Nutrition
• Antibiotic prophylaxis

AIM: To examine the effect of PTD-NBD polypeptide on the expression of nuclear factor κB (NF-κB) p65 in inflammatory pancreatic acinar cell injury in rats.

METHODS: Rat pancreatic acinar cells were isolated, cultured, and divided into a normal control group, an acute pancreatitis (AP) group and a PTD-NBD polypeptides group. An in vitro model of AP was induced by treating rat pancreatic acinar cells with lipopolysaccharide (10 mg/L). Cell morphological changes were observed, and the contents of amylase, superoxide dismutase (SOD) and IL-1β in culture medium were tested. Expression of NF-κB p65 mRNA and protein in cells was detected by RT-PCR and Western blot 6 and 12 h after modeling, respectively.

RESULTS: Compared to the control group, pancreatic acinar cell swelling and death were increased (6 h: 8.9 ± 0.34 vs 1.1 ± 0.13; 12 h: 9.4 ± 0.26 vs 1.2 ± 0.15, both P < 0.05), the contents of amylase (6 h: 2135.8 ± 347.2 vs 873.5 ± 91.6; 12 h: 3299.6 ± 217.7 vs 917.7 ± 101.9, both P < 0.05) and IL-1β (6 h: 84.9 ± 15.7 vs 39.3 ± 7.9; 12 h: 95.6 ± 17.1 vs 38.9 ± 5.2, both P < 0.05) were increased and the contents of SOD were decreased in culture medium (6 h: 116.3 ± 30.3 vs 176.2 ± 21.6; 12 h: 101.5 ± 25.6 vs 173.6 ± 27.9, P < 0.05), and the expression of NF-κB p65 in pancreatic acinar cells was increased (P < 0.05) in the AP group at 6 and 12 h after modeling. Compared to the AP group, pancreatic acinar cell swelling and death were lessened (6 h: 6.8 ± 0.23 vs 8.9 ± 0.34; 12 h: 7.5 ± 0.19 vs 9.4 ± 0.26, both P < 0.05), the contents of SOD were raised (6 h: 137.6 ± 27.4 vs 116.3 ± 30.3; 12 h: 144.3 ± 23.6 vs 101.5 ± 25.6, both P < 0.05) and the contents of amylase (6 h: 1951.5 ± 211.7 vs 2135.8 ± 347.2; 12 h: 1761.3 ± 231.5 vs 3299.6 ± 217.7, both P < 0.05) and IL-1β (6 h: 66.8 ± 11.6 vs 84.9 ± 15.7; 12 h: 54.8 ± 21.2 vs 95.6 ± 17.1, both P < 0.05) were decreased in culture medium, and the expression of NF-κB p65 mRNA and protein was down-regulated in the PAT-NBD polypeptide group (P < 0.05).

CONCLUSION: PTD-NBD polypeptide can inhibit LPS-induced activation of NF-κB p65, down-regulate IL-1β expression and up-regulate SOD content, thereby reducing inflammatory pancreatic acinar cell injury.

• Acute pancreatitis
• Pancreatic acinar cells
• Nuclear factor κB
• NBD polypeptide