Risk Factor For Acute Pancreatitis Research Articles

IL27 and IL1RN are causally associated with acute pancreatitis: a Mendelian randomization study.

The interleukin (IL) plays a role in the development of acute pancreatitis (AP). However, the specific IL in AP has not been fully revealed. Therefore, the association between prospective IL and AP was studied via Mendelian randomization (MR). The HUGO Gene nomenclature committee (HGNC) database provided 47 interleukin related genes (ILRGs). ILRGs and differentially expressed genes (DEGs) from GSE194331 were overlapped to create differently expressed ILRGs (DE-ILRGs). The integrative epidemiology unit (IEU) open genome-wide association study (GWAS) database provided exposure and outcome datasets. Univariate MR (UVMR) analysis using MR-Egger, IVW, simple mode, and weighted mode was done. UVMR results were verified using sensitivity analysis. Drug prediction, MVMR analysis, and PPI network development were also performed. Six DE-ILRGs were obtained. IL27 and IL1RN were substantially causally linked with AP by UVMR analysis (OR = 0.926, P < 0.001 and OR = 1.031, P = 0.023). Our sensitivity analysis showed the dependability of our results. Direct effect of IL27 was suggested by MVMR analysis. In the cytokine receptor binding pathway, IL27 and IL1RN interacted with IL36G and IL1R2. TAE-684, ARQ-680, and 12 other IL1RN and 14 IL27 medications were predicted. IL1RN was identified as a risk factor for acute pancreatitis (AP), but IL27 was found to be a protective factor for AP.

Acute Pancreatitis in Pregnancy: A Propensity Score Matching Analysis and Dynamic Nomogram for Risk Assessment.

Acute pancreatitis is easily confused with abdominal pain symptoms, and it could lead to serious complications for pregnant women and fetus, the mortality was as high as 3.3% and 11.6-18.7%, respectively. However, there is still lack of sensitive laboratory markers for early diagnosis of APIP and authoritative guidelines to guide treatment. The purpose of this study was to explore the risk factors of acute pancreatitis in pregnancy, establish, and evaluate the dynamic prediction model of risk factors in acute pancreatitis in pregnancy patients. Clinical data of APIP patients and non-pregnant acute pancreases patients who underwent regular antenatal check-ups during the same period were collected. The dataset after propensity matching was randomly divided into training set and verification set at a ratio of 7:3. The model was constructed using Logistic regression, least absolute shrinkage and selection operator regression, R language and other methods. The training set model was used to construct the diagnostic nomogram model and the validation set was used to validate the model. Finally, the accuracy and clinical practicability of the model were evaluated. A total of 111 APIP were included. In all APIP patients, hyperlipidemic pancreatitis was the most important reason. The levels of serum amylase, creatinine, albumin, triglyceride, high-density lipoprotein cholesterol, and apolipoprotein A1 were significantly different between the two groups. The propensity matching method was used to match pregnant pancreatitis patients and pregnant non-pancreatic patients 1:1 according to age and gestational age, and the matching tolerance was 0.02. The multivariate logistic regression analysis of training set showed that diabetes, triglyceride, Body Mass Index, white blood cell, and C-reactive protein were identified and entered the dynamic nomogram. The area under the ROC curve of the training set was 0.942 and in validation set was 0.842. The calibration curve showed good predictive in training set, and the calibration performance in the validation set was acceptable. The calibration curve showed the consistency between the nomogram model and the actual probability. The dynamic nomogram model we constructed to predict the risk factors of acute pancreatitis in pregnancy has high accuracy, discrimination, and clinical practicability.

Assessing the causal link between liver function and acute pancreatitis: A Mendelian randomisation study.

A correlation has been reported to exist between exposure factors (e.g. liver function) and acute pancreatitis. However, the specific causal relationship remains unclear. This study aimed to infer the causal relationship between liver function and acute pancreatitis using the Mendelian randomisation method. We employed summary data from a genome-wide association study involving individuals of European ancestry from the UK Biobank and FinnGen. Single-nucleotide polymorphisms (SCNPs), closely associated with liver function, served as instrumental variables. We used five regression models for causality assessment: MR-Egger regression, the random-effect inverse variance weighting method (IVW), the weighted median method (WME), the weighted model, and the simple model. We assessed the heterogeneity of the SNPs using Cochran's Q test. Multi-effect analysis was performed using the intercept term of the MR-Egger method and leave-one-out detection. Odds ratios (ORs) were used to evaluate the causal relationship between liver function and acute pancreatitis risk. A total of 641 SNPs were incorporated as instrumental variables. The MR-IVW method indicated a causal effect of gamma-glutamyltransferase (GGT) on acute pancreatitis (OR = 1.180, 95%CI [confidence interval]: 1.021-1.365, P = 0.025), suggesting that GGT may influence the incidence of acute pancreatitis. Conversely, the results for alkaline phosphatase (ALP) (OR = 0.997, 95%CI: 0.992-1.002, P = 0.197) and aspartate aminotransferase (AST) (OR = 0.939, 95%CI: 0.794-1.111, P = 0.464) did not show a causal effect on acute pancreatitis. Additionally, neither the intercept term nor the zero difference in the MR-Egger regression attained statistical significance (P = 0.257), and there were no observable gene effects. This study suggests that GGT levels are a potential risk factor for acute pancreatitis and may increase the associated risk. In contrast, ALP and AST levels did not affect the risk of acute pancreatitis.

Analysis of risk factors for acute pancreatitis complicated with pancreatic sinistral portal hypertension and construction of predictive model.

Objective: Pancreatic sinistral portal hypertension (PSPH) is a common complication of acute pancreatitis (AP) and can cause massive gastrointestinal bleeding, which is one of the causes of AP-related mortality. However, there is currently no predictive model for AP concurrent with PSPH. This study aimed to identify the risk factors for AP concurrent with PSPH and use these factors to build a related predictive model. Materials and methods: We collected clinical data from 282 patients with AP. 192 patients were used as a training group and 90 patients as a validation group. Univariate and multivariate analyses were used to identify independent risk factors for AP complicated with PSPH, and then a nomogram was established. The models are cross verification and Internal verification. The predictive ability and accuracy of the model were evaluated based on the working curve of the subjects and the calibration curve, respectively. The clinical value of the model was evaluated using decision curve analysis (DCA). Results: The univariate analysis revealed significant differences in the occurrence of PSPH with respect to sex, recurrent AP, history of hypertension, smoking history, patency of the splenic vein, pancreatic necrosis or pancreatic pseudocyst formation, the most significant site of pancreatic swelling, presence of a Dmure D polymer, MCTSI, and involvement of lipase and amylase. The logistic multivariate regression analysis showed that male sex, splenic-vein stenosis or occlusion and swelling were located in the body-tail, and MCTSI was an independent risk factor for PSPH. The nomogram and ROC curve were constructed. The area under the working curve of the subjects was 0.91, and the sensitivity and specificity were 82.5% and 89.1%, respectively. In the validation group, the C-index is 0.826. The nomogram was internally validated using 1,000 bootstrap samples, and the c-index was 0.898. The calibration curve demonstrated that the predicted probability was concordant with the observed probability, and the DCA confirmed that the model had robust clinical utility. Conclusion: Male sex, splenic-vein stenosis or occlusion, recurrent AP, and swelling are located in the body-tail, and MCTSI is an independent risk factor for the occurrence of PSPH. The predictive model developed for AP complicated with PSPH may serve toward developing preventive and therapeutic approaches for PSPH.

Adverse events of self-expandable metal stent placement for malignant distal biliary obstruction: a large multicenter study

Background and aimEndoscopic placement of self-expandable metal stents (SEMSs) for malignant distal biliary obstruction (MDBO) may be accompanied by several types of adverse events. The present study analyzed the adverse events occurring after SEMS placement for MDBO. MethodsThe present study retrospectively investigated the incidence and types of adverse events in patients who underwent SEMS placement for MDBO between April 2018 and March 2021 at 26 hospitals. Risk factors for acute pancreatitis, cholecystitis, and recurrent biliary obstruction (RBO) were evaluated by univariate and multivariate analyses. ResultsOf the 1425 patients implanted with SEMS for MDBO, 228 (16.0%) and 393 (27.6%) experienced early adverse events and RBO, respectively. Pancreatic duct without tumor involvement (p = 0.023), intact papilla (p = 0.025), and SEMS placement across the papilla (p = 0.037) were independent risk factors for acute pancreatitis. Tumor involvement in the orifice of the cystic duct (OCD) was an independent risk factor for cholecystitis (p < 0.001). Fully and partially covered SEMSs were independent risk factors for food impaction and/or sludge. Fully covered SEMS was an independent risk factor for stent migration. Uncovered SEMS and laser-cut SEMS were independent risk factors for tumor ingrowth. ConclusionsPancreatic duct without tumor involvement, intact papilla, and SEMS placement across the papilla were independent risk factors for acute pancreatitis, and tumor involvement to the OCD was an independent risk factor for cholecystitis. The risk factors for food impaction and/or sludge, stent migration, and tumor ingrowth differed among types of SEMS.

Clinical impact of pancreatic steatosis measured by CT on the risk of post-ERCP pancreatitis: a multicenter prospective trial

Pancreatic steatosis (PS) may be a risk factor for acute pancreatitis. Whether it is also a risk factor for post-ERCP pancreatitis (PEP) has not been evaluated. This study aimed to determine the impact of PS on PEP development. This multicenter prospective trial enrolled 786 consecutive patients who underwent contrast-enhanced abdominal CT and subsequent first-time ERCP. PS was evaluated based on pancreatic attenuation on unenhanced CT images. The risk of PS for the development of PEP was evaluated using a logistic regression model. Of 527 patients included in the study, 157 (29.8%) had PS and 370 (70.2%) did not. At 24 hours after ERCP, there was a significant difference in the PEP identified in 22 patients (14.0%) in the PS group and 23 patients (6.2%) in the "no PS" (NPS) group (P= .017). Diabetes and hypertension were more common in the PS group than in the NPS group; no differences in dyslipidemia were found. Patients with PS had a higher risk for the development of PEP than those with NPS (odds ratio, 2.09; 95% confidence interval, 1.08-4.03). No other variables were identified as risk factors for PEP. PS is a significant risk factor for PEP for which preventive measures should be considered. Standardized measurement protocols to assess PS by CT are needed. (Clinical trial registration number: KCT0006068.).

Incidence, clinical features, and risk factors for acute pancreatitis following posterior instrumented fusion surgery for lumbar degenerative disease: a single-center, retrospective analysis of 20,929 patients.

The aim of this study is to identify the incidence, clinical features, and risk factors for postoperative acute pancreatitis (PAP) after lumbar surgery. We retrospectively analyzed patients who developed PAP after posterior lumbar fusion surgery. For each PAP patient, data were collected for four controls who underwent procedures in the same period and did not develop PAP. Statistical methods included univariate and multivariate analyses. Totally, 21 out of 20,929 patients were diagnosed with PAP (0.10%) after posterior lumbar fusion surgery. Patients with degenerative lumbar scoliosis were at higher risk of developing PAP (P < 0.05). With atypical clinical features, PAP occurred within 3days (0-5) after surgery. PAP patients had significantly higher incidence of osteoporosis (47.6 vs. 22.6%, P = 0.030) and fusion of L1/2(42.9 vs. 4.3%, P = 0.010), lower albumin (42.2 ± 4.1 vs. 44.3 ± 3.2g/L, P = 0.010), more fusion segments (median 4 vs. 3, P = 0.022), larger surgical invasiveness index (median 9 vs. 8, P = 0.007), longer operation duration (232 ± 109 vs. 185 ± 90min, P = 0.041), greater estimated blood loss (median 600 vs. 400mL, P = 0.025), lower intraoperative mean arterial pressure (87.2 ± 9.9 vs. 92.1 ± 8.8mmHg, P = 0.024). Multivariate logistic regression analysis found three independent risk factors: fusion of L1/2, surgical invasiveness index > 8, and intraoperative mean arterial pressure < 90mmHg. All patients were treated with conservative therapy and fully recovered after 8.1 (4-22) days. The incidence of PAP following posterior surgery for degenerative lumbar disease was 0.10%, and its clinical features were not typical. The fusion of L1/2, high surgical invasiveness index, and low intraoperative mean arterial pressure were independent risk factors for PAP after surgery for lumbar degenerative disease.

ACUTE PANCREATITIS REVEALING MAJOR HYPERTRIGLYCERIDEMIA

Objective: Severe hypertriglyceridemia is a common risk factor for acute pancreatitis and atherosclerotic vascular disease. Our aim was to report a rare case of acute pancreatitis due to major hypertriglyceridemia. Design and method: We report a case of acute pancreatitis revealing major hypertriglyceridemia. Results: A 53-year-old man, was hospitalized in May 2022 in endocrinology departement with abdominal pain, nausea,vomiting and alteration of general condition. History: high blood pressure, type 2 diabetes, alcohol consumption and family history of high blood pressure, type 2 diabetes, dyslipidemia. Clinical examination showed defense on palapation in epigastrium and right flank. Biochemical analyses were as follows: hypertriglyceridemia at 76.42 mmol/L associated with hypercholesterolemia at 17.58 mmol/L, LDL-C = 2.25 mmol/L, HDL-C = 2.12 mmol/L, hyperglycemia = 10.62 mmol/L, HBA1C = 8.1%, Lipasemia = 281 UI/L. Abdominal ultrasound did not show lithiasis, abdominal CT scan revealed pancreatitis. The diagnosis of acute pancreatitis due to major hypertriglyceridemia was made. The patient was treated by plasmapheresis and triglyceride level was reduced to 2.5 mmol/L. The lipidogram showed an isolated elevation of VLDL and defined hypertriglyceridemia as Familial hyperlipoproteinemia type 4. Conclusions: Familial hyperlipoproteinemia type 4 syndrome is an uncommon condition. Acute pancreatitis secondary to severe hypertriglyceridemia is a condition with a high risk of mortality which requires prompt clinical suspicion and treatment.

Metabolic-associated fatty liver disease is associated with acute pancreatitis with more severe course: Post hoc analysis of a prospectively collected international registry.

Non-alcoholic fatty liver disease (NAFLD) is a proven risk factor foracute pancreatitis (AP). However, NAFLD has recently been redefined as metabolic-associated fatty liver disease (MAFLD). In this post hoc analysis, we quantified the effect of MAFLD on the outcomes of AP. We identified our patients from the multicentric, prospective International Acute Pancreatitis Registry of the Hungarian Pancreatic Study Group. Next, we compared AP patients with and without MAFLD and the individual components of MAFLD regarding in-hospital mortality and AP severity based on the revised Atlanta classification. Lastly, we calculated odds ratios (ORs) with 95% confidence intervals (CIs) using multivariate logistic regression analysis. MAFLD had a high prevalence in AP, 39% (801/2053). MAFLD increased the odds of moderate-to-severe AP (OR=1.43, CI: 1.09-1.89). However, the odds of in-hospital mortality (OR=0.89, CI: 0.42-1.89) and severe AP (OR=1.70, CI: 0.97-3.01) were not higher in the MAFLD group. Out of the three diagnostic criteria of MAFLD, the highest odds of severe AP was in the group based on metabolic risk abnormalities (OR=2.68, CI: 1.39-5.09). In addition, the presence of one, two, and three diagnostic criteria dose-dependently increased the odds of moderate-to-severe AP (OR=1.23, CI: 0.88-1.70, OR=1.38, CI: 0.93-2.04, and OR=3.04, CI: 1.63-5.70, respectively) and severe AP (OR=1.13, CI: 0.54-2.27, OR=2.08, CI: 0.97-4.35, and OR=4.76, CI: 1.50-15.4, respectively). Furthermore, in patients with alcohol abuse and aged ≥60years, the effect of MAFLD became insignificant. MAFLD is associated with AP severity, which varies based on the components of its diagnostic criteria. Furthermore, MAFLD shows a dose-dependent effect on the outcomes of AP.

A population-based cohort study on risk factors for acute pancreatitis: A comparison by age group

Background/objectives: Acute pancreatitis (AP) is an acute inflammatory disorder that can occur in all age groups. The risk of AP has been shown to increase with age. However, no study has compared risk factors for AP according to age group yet. Thus, the aim of this study was to perform such comparison. MethodsClinical data from individuals 20 years of age and older who received a health examination arranged by the Korean national health insurance program in 2009 (n = 4,238,822) were used. First-attack AP was identified using claims data from baseline to December 2018. Incidence and risk factors of AP were analyzed for young (20–39 years old), middle-aged (40–64 years old), and old (over 65 years old) groups. ResultsIncidences of AP in young, middle-aged, and old groups were 16.30, 27.85, and 57.19 per 100,000 person-years, respectively. Smoking, alcohol drinking, diabetes, gallstone, and chronic pancreatitis were associated with increased risk of AP in all age groups. Meanwhile, male, older age, and higher waist circumference were associated with increased risk of AP in middle-aged and old groups. In young and middle-aged groups, risk of AP was increased in the presence of hypertension and dyslipidemia. However, high income was associated with decreased risk of AP in these groups. ConclusionsIn this population-based cohort study, incidences and risk factors for AP differed according to age group. Thus, a tailored strategy might be needed to prevent AP according to age group.

Evinacumab in severe hypertriglyceridemia with or without lipoprotein lipase pathway mutations: a phase 2 randomized trial

Severe hypertriglyceridemia (sHTG) is an established risk factor for acute pancreatitis. Current therapeutic approaches for sHTG are often insufficient to reduce triglycerides and prevent acute pancreatitis. This phase 2 trial (NCT03452228) evaluated evinacumab (angiopoietin-like 3 inhibitor) in three cohorts of patients with sHTG: cohort 1, familial chylomicronemia syndrome with bi-allelic loss-of-function lipoprotein lipase (LPL) pathway mutations (n = 17); cohort 2, multifactorial chylomicronemia syndrome with heterozygous loss-of-function LPL pathway mutations (n = 15); and cohort 3, multifactorial chylomicronemia syndrome without LPL pathway mutations (n = 19). Fifty-one patients (males, n = 27; females, n = 24) with a history of hospitalization for acute pancreatitis were randomized 2:1 to intravenous evinacumab 15 mg kg−1 or placebo every 4 weeks over a 12-week double-blind treatment period, followed by a 12-week single-blind treatment period. The primary end point was the mean percent reduction in triglycerides from baseline after 12 weeks of evinacumab exposure in cohort 3. Evinacumab reduced triglycerides in cohort 3 by a mean (s.e.m.) of −27.1% (37.4) (95% confidence interval −71.2 to 84.6), but the prespecified primary end point was not met. No notable differences in adverse events between evinacumab and placebo treatment groups were seen during the double-blind treatment period. Although the primary end point of a reduction in triglycerides did not meet the prespecified significance level, the observed safety and changes in lipid and lipoprotein levels support the further evaluation of evinacumab in larger trials of patients with sHTG. Trial registration number: ClinicalTrials.gov NCT03452228.

Risk Factors Associated with Acute Pancreatitis after Percutaneous Biliary Intervention: We Do Not Know Nearly Enough.

Percutaneous transhepatic cholangiodrainage (PTCD) and percutaneous transhepatic biliary stenting (PTBS) may be used as a palliative treatment for inoperable patients with malignant biliary obstruction (MBO) to improve the prognosis and their quality of life. However, acute pancreatitis is a common and severe complication that cannot be ignored after PTCD and PTBS in patients with MBO. A few cases may develop severe pancreatitis with a higher mortality rate. In this study, we summarize the known risk factors for acute pancreatitis after percutaneous biliary interventional procedures and investigate possible risk factors to reduce its occurrence by early identifying high-risk patients and taking appropriate measures.

Risk factors for acute pancreatitis in children

Risk factors for acute pancreatitis in children

Long-term follow-up of endoscopic papillectomy and the value of preventive pancreatic stent placement (with videos).

Early-stage ampullary adenomas have only been reported in a small case series on endoscopic management. Hence, this study aimed to evaluate the long-term outcomes of early ampullary adenoma with endoscopic management and identify the risk factors for acute pancreatitis after endoscopic papillectomy (EP). In this study, 115 patients who underwent EP at Changhai Hospital (Shanghai, China) between January 2012 and December 2018 were retrospectively analysed. Endoscopy was performed at 1, 3, 6, and 12 months after EP. Data were statistically analysed using the t-test or the Mann-Whitney U test. A total of 107 patients were included in this study and the follow-up period was 75 ± 43 months. The average age of the 107 patients was 54.6 years and the average tumor size was 17 mm. The average age of the patients (53.7 ± 10.7 years vs 55.2 ± 10.5 years, P = 0.482), minimum tumor size (13 vs 19 mm, P = 0.063), and complete resection rate (84.78% vs 85.25%, P = 0.947) did not differ significantly between the stent placement and non-stent placement groups. Post-EP acute pancreatitis rates in the non-stent placement and stent placement groups were 11.48% and 4.35%, respectively. The risk of post-EP acute pancreatitis was significantly associated with the preoperative carcinoembryonic antigen level in univariate analysis, but not in multivariate analysis. The risk of post-EP acute pancreatitis was not significantly associated with the placement of the pancreatic stent in either univariate or multivariate analysis. Moreover, delayed proximal pancreatic duct stenosis was not noted in either group during long-term follow-up. EP is a satisfactory option for treating adenomas of the ampulla of the duodenum.

Tendency and risk factors of acute pancreatitis in children with severe motor and intellectual disabilities: A single-center study

ObjectiveAcute pancreatitis (AP) is a life-threatening disease in children with severe motor and intellectual disabilities (SMID). This study aimed to determine the clinical characteristics and causes of AP in children with SMID. MethodsWe enrolled 29 children with AP admitted to our hospital. Patients were divided into children with SMID (AP with SMID group) and the remaining patients (AP without SMID group). All patients in the AP without SMID group had no pre-existing neurological disabilities. We obtained data on the clinical background of patients, severity of AP, treatments, and outcomes. We enrolled 34 children with SMID without a history of AP (SMID control group) to compare their clinical characteristics with the AP with SMID group. We statistically compared the data between the AP with SMID and AP without SMID groups and between the AP with SMID and SMID control groups. ResultCompared to the AP without SMID group, the AP with SMID group showed significantly more severe pancreatitis (50% vs 12%) and recurrent pancreatitis (58% vs 18%). Moreover, compared with the SMID control group, the AP with SMID group showed significantly more frequent absence of voluntary movement (83% vs 26%), requirement of respiratory devices (75% vs 35%), panhypopituitarism (33% vs 6%), thermoregulatory dysfunction (58% vs 18%), and low serum albumin levels (3.6 vs 4.1 g/dL). ConclusionAP in children with SMID tended to be associated with severe and recurrent pancreatitis. Children with SMID who had a history of AP had more severe neurological impairment among children with SMID. Hypothalamic-pituitary system dysfunction caused by severe cerebral damage may contribute to the development of AP.

PSUN241 A Case of Dulaglutide-Induced Acute Pancreatitis in a Diabetic Patient – A Case Report

Abstract Introduction Dulaglutide is a glucagon-like peptide-1 (GLP-1 RA) receptor agonist that was approved by the FDA as a pharmacological treatment of diabetes management over the last decade. It is available in an injectable form that is dosed weekly which increases patients’ adherence and improves outcomes. The mechanism of action of GLP-1 RA is through regulation of blood glucose levels through glucose-dependent stimulation of insulin secretion and inhibition of glucagon release. Also, their effect on GLP-1 receptors in the CNS and the gastrointestinal tract leads to delay in gastric emptying and induces satiety. Such mechanism of action decreases the risk of hypoglycemia and facilitates weight loss. All these features make GLP-1 RA of great interest among new diabetes pharmacological options.The most frequently reported adverse effects from GLP-1 RA are gastrointestinal symptoms and injection-site pruritus. Acute pancreatitis is a rare but serious complication of GLP-1 RA use. We present a case of Dulaglutide-induced acute pancreatitis in a diabetic patient. Case presentation 77-year-old type II diabetic male on Dulaglutide 1.5 mg weekly which was increased to 3 mg weekly 2 weeks prior to a presentation presented with epigastric pain, nausea, and vomiting for 2 days. The patient denied any previous episodes, history of gallstones or alcohol use or recent endoscopic retrograde cholangiogram. An abdominal exam revealed epigastric tenderness. Laboratory workup was remarkable for Lipase of 953, otherwise, Calcium, triglycerides, liver enzymes were within normal limit. Computed tomography scan of the abdomen confirmed pancreatitis. Right upper quadrant ultrasound showed no evidence of gallstones or biliary system dilation. Holding Dulaglutide with standard treatment for pancreatitis resulted in symptom resolution. Discussion GLP-1 RA-induced pancreatitis is a very serious adverse event, yet this association has not been well established in humans, especially that baseline rate of pancreatitis in diabetic patients (most population studied using GLP-1 agonist) is higher compared to the general population. Until now most available data are driven from studies on animals, case reports, and a few observed cases on studies.Pathophysiologyis not well understood. One theory is thought to be due to GLP-1 RA effect on decreasing gut motility including biliary and gallbladder, which increases the risk of gallstone formation. However, not all reported cases had history of gallstones. This leads us to the other suggested mechanism through effect of GLP-1 RA on exocrine pancreas through ductal proliferation and metaplasia which if severe, can lead to hemorrhagic pancreatitis.Hence, the GLP-1 RA use should be judicious in patients with high risk of pancreatitis, such as severe hypertriglyceridemia, alcohol intake, or prior pancreatitis history. Conclusion Diabetes and hypertriglyceridemia are independent risk factors of acute pancreatitis. Future studies are warranted to assess GLP-1 RA-induced pancreatitis in non-diabetic patients and to investigate its dose-dependence relationship. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

S1933 Acute Pancreatitis Attributed to COVID-19: An Unusual Infectious Etiology

Introduction: COVID-19 can affect multiple organs and has various presentations, including respiratory symptoms and fever being the most common. Gastrointestinal symptoms can be reported in up to 25% of patients, with diarrhea, nausea, and emesis the usual presentation. However, abdominal pain is less than 6.8% of cases, and of those, only 27% presented with Acute Pancreatitis (AP). Here we present a case of severe AP with multiorgan involvement as the initial presentation of COVID19. Case Description/Methods: Case of a 19 y/o Female with a medical history of Obesity class I arrived at the ED with recurrent emesis and altered mental status. Symptoms began around four days prior with 6-7 episodes of non-bloody, non-bilious emesis, fatigue, subjective fever, and decreased oral intake, followed by acute onset of diffuse abdominal pain. Upon arrival, the patient was found encephalopathic with dry oral mucosa, tachycardic and tachypneic. Laboratories were remarkable for lipase 2483, amylase 382, LDH 315, ALP 219 U/L, sodium 155 mEq/L, creatinine 1.33 mg/dL, bicarbonate < 9 mmol/L, pH 7.0, pO2Sat 96%, hematocrit 51.8%, WBC 14.9 cells/L, glucose 774 mg/dL, and COVID 19 PCR positive. Abdominal US and CT with no findings suggestive of gallstones or intraabdominal pathology. Aggressive intravenous fluid, insulin, broad-spectrum antibiotics, bicarbonate replacement, analgesia, and antiemetics were implemented. Hospitalization was complicated as the patient did not tolerate PO intake, and the high anion gap metabolic acidosis was difficult to close for several days. After almost two weeks in the ICU, the patient was discharged home without apparent pancreatitis or COVID-19 repercussions. Discussion: Our case did not have any risk factors for AP, and extensive investigations did not reveal a clear etiology. Viral, bacterial, fungal, and parasitic infections are less common causes of AP. There are limited data on COVID-19 and pancreatitis; however, recent studies suggest a higher mortality rate with a 20% increased chance of dying and worse clinical outcomes. The mechanism of pancreatic injury is not well understood, but there is a link between COVID-19 and the precipitation of autoimmune and systemic diseases. Our case is an example of severe pancreatic injury with multiorgan involvement in mild symptomatic COVID 19.

Underweight Is Associated with a Higher Risk of Acute Pancreatitis in Type 2 Diabetes: A Nationwide Cohort Study.

Type 2 diabetes is known as a risk factor for acute pancreatitis, but the risk of acute pancreatitis according to glycemic status and body mass index (BMI) has remained unknown. Therefore, we aim to investigate the risk of acute pancreatitis according to BMI and glycemic status. We included 3,912,496 subjects from the Korean National Health Insurance System cohort who underwent the National Health Screening program in 2009. Each subject’s clinical course was examined through follow-ups until December 2018. BMI and glycemic status were each categorized into five groups. Hazard ratios (HRs) of acute pancreatitis according to BMI and glycemic status were calculated. The adjusted HRs of acute pancreatitis were the highest in the underweight group (BMI < 18.5) in all five glycemic status categories. The HR of acute pancreatitis in the underweight group increased as the glycemic status worsened, excluding the category of diabetes for more than five years (HR 1.381 for normal fasting glucose; 1.805 for impaired fasting glucose; 2.332 for new-onset diabetes; 4.51 for diabetes duration <5 years; 4.135 for diabetes duration ≥5 years). We found that the risk of acute pancreatitis was further increased in the underweight group, depending on the status and duration of type 2 diabetes.

The Pancreas and Known Factors of Acute Pancreatitis.

Pancreatitis is regarded by clinicians as one of the most complicated and clinically challenging of all disorders affecting the abdomen. It is classified on the basis of clinical, morphological, and histological criteria. Causes of acute pancreatitis can easily be identified in 75–85% of patients. The main causes of acute, recurrent acute, and chronic pancreatitis are gallstone migration and alcohol abuse. Other causes are uncommon, controversial, or unexplained. For instance, cofactors of all forms of pancreatitis are pancreas divisum and hypertriglyceridemia. Another factor that should be considered is a complication of endoscopic retrograde cholangiopancreatography: post-endoscopic retrograde cholangiopancreatography acute pancreatitis. The aim of this study is to present the known risk factors for acute pancreatitis, beginning with an account of the morphology, physiology, and development of the pancreas.

Lycopene Induces Expression of NAD(P)H Quinone Oxidoreductase and Heme Oxygenase-1 through Activation of Nrf2 in Ethanol/LPS-stimulated Pancreatic Acinar Cells

ObjectivesHigh alcohol intake is a major risk factor for acute pancreatitis. Alcohol metabolism increases reactive oxygen species (ROS) and lipopolysaccharide (LPS) production, leading to induction of inflammatory cytokines such as IL-6 in pancreatic acinar (AR42J) cells. The nuclear factor erythroid-2-related factor 2 (Nrf2) pathway is activated to induce the expression of antioxidant enzymes such as NAD(P)H: quinone oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) as a cytoprotective response to oxidative stress. Lycopene, a bright-red carotenoid, is a potent antioxidant due to its high number of conjugated double bonds, which exerts anti-inflammatory and antioxidant effects. In this study, we investigated whether lycopene decreases ethanol/LPS-induced increase in ROS levels and IL-6 expression via Nrf2 signaling in AR42J cells.MethodsThe cells were pretreated with or without lycopene for 1 h, and treated with ethanol (250 mM) and LPS (10 mg/l) for 30 min (ROS levels, protein levels of NQO1, HO-1, pNrf2, Nrf2, and Keap1), 6 h (IL-6 mRNA expression), and 24 h (IL-6 protein level).ResultsLycopene increased the expression of NQO1 and HO-1 in ethanol/LPS-stimulated AR42J cells. The phosphorylation and nuclear translocation of Nrf2 were increased by lycopene in ethanol/LPS-stimulated AR42J cells. Lycopene decreased interaction between Keap1 and Nrf2 in AR42J cells, which may induce Nrf2 activation by inhibiting Keap1-mediated sequestration of Nrf2. Lycopene inhibited ethanol/LPS-induced increase in ROS levels and IL-6 expression in AR42J cells.ConclusionsIn conclusion, lycopene inhibits ROS-mediated IL-6 expression by promoting Nrf2-mediated expression of NQO1 and HO-1 in ethanol/LPS stimulated AR42J cells. Therefore, consumption of lycopene-rich foods may be beneficial for preventing the development of alcoholic acute pancreatitis by inhibiting oxidative stress and inflammatory cytokine production by activating Nrf2 signaling in pancreatic acinar cells.Funding SourcesThe Authors declare that there is no conflict of interest.