Alcohol-induced Acute Pancreatitis Research Articles

Causal link between gut microbiota and four types of pancreatitis: a genetic association and bidirectional Mendelian randomization study

BackgroundA number of recent observational studies have indicated a correlation between the constitution of gut microbiota and the incidence of pancreatitis. Notwithstanding, observational studies are unreliable for inferring causality because of their susceptibility to confounding, bias, and reverse causality, the causal relationship between specific gut microbiota and pancreatitis is still unclear. Therefore, our study aimed to investigate the causal relationship between gut microbiota and four types of pancreatitis.MethodsAn investigative undertaking encompassing a genome-wide association study (GWAS) comprising 18,340 participants was undertaken with the aim of discerning genetic instrumental variables that exhibit associations with gut microbiota, The aggregated statistical data pertaining to acute pancreatitis (AP), alcohol-induced AP (AAP), chronic pancreatitis (CP), and alcohol-induced CP (ACP) were acquired from the FinnGen Consortium. The two-sample bidirectional Mendelian randomization (MR) approach was utilized. Utilizing the Inverse-Variance Weighted (IVW) technique as the cornerstone of our primary analysis. The Bonferroni analysis was used to correct for multiple testing, In addition, a number of sensitivity analysis methodologies, comprising the MR-Egger intercept test, the Cochran’s Q test, MR polymorphism residual and outlier (MR-PRESSO) test, and the leave-one-out test, were performed to evaluate the robustness of our findings.ResultsA total of 28 intestinal microflora were ascertained to exhibit significant associations with diverse outcomes of pancreatitis. Among them, Class Melainabacteria (OR = 1.801, 95% CI: 1.288–2.519, p = 0.008) has a strong causality with ACP after the Bonferroni-corrected test, in order to assess potential reverse causation effects, we used four types of pancreatitis as the exposure variable and scrutinized its impact on gut microbiota as the outcome variable, this analysis revealed associations between pancreatitis and 30 distinct types of gut microflora. The implementation of Cochran’s Q test revealed a lack of substantial heterogeneity among the various single nucleotide polymorphisms (SNP).ConclusionOur first systematic Mendelian randomization analysis provides evidence that multiple gut microbiota taxa may be causally associated with four types of pancreatitis disease. This discovery may contribute significant biomarkers conducive to the preliminary, non-invasive identification of Pancreatitis. Additionally, it could present viable targets for potential therapeutic interventions in the disease’s treatment.

Causal associations between modifiable risk factors and pancreatitis: A comprehensive Mendelian randomization study.

The pathogenesis of pancreatitis involves diverse environmental risk factors, some of which have not yet been clearly elucidated. This study systematically investigated the causal effects of genetically predicted modifiable risk factors on pancreatitis using the Mendelian randomization (MR) approach. Genetic variants associated with 30 exposure factors were obtained from genome-wide association studies. Summary-level statistical data for acute pancreatitis (AP), chronic pancreatitis (CP), alcohol-induced AP (AAP) and alcohol-induced CP (ACP) were obtained from FinnGen consortia. Univariable and multivariable MR analyses were performed to identify causal risk factors for pancreatitis. Genetic predisposition to smoking (OR = 1.314, P = 0.021), cholelithiasis (OR = 1.365, P = 1.307E-19) and inflammatory bowel disease (IBD) (OR = 1.063, P = 0.008) as well as higher triglycerides (OR = 1.189, P = 0.016), body mass index (BMI) (OR = 1.335, P = 3.077E-04), whole body fat mass (OR = 1.291, P = 0.004) and waist circumference (OR = 1.466, P = 0.011) were associated with increased risk of AP. The effect of obesity traits on AP was attenuated after correcting for cholelithiasis. Genetically-driven smoking (OR = 1.595, P = 0.005), alcohol consumption (OR = 3.142, P = 0.020), cholelithiasis (OR = 1.180, P = 0.001), autoimmune diseases (OR = 1.123, P = 0.008), IBD (OR = 1.066, P = 0.042), type 2 diabetes (OR = 1.121, P = 0.029), and higher serum calcium (OR = 1.933, P = 0.018), triglycerides (OR = 1.222, P = 0.021) and waist-to-hip ratio (OR = 1.632, P = 0.023) increased the risk of CP. Cholelithiasis, triglycerides and the waist-to-hip ratio remained significant predictors in the multivariable MR. Genetically predicted alcohol drinking was associated with increased risk of AAP (OR = 15.045, P = 0.001) and ACP (OR = 6.042, P = 0.014). After adjustment of alcohol drinking, genetic liability to IBD had a similar significant causal effect on AAP (OR = 1.137, P = 0.049), while testosterone (OR = 0.270, P = 0.002) a triglyceride (OR = 1.610, P = 0.001) and hip circumference (OR = 0.648, P = 0.040) were significantly associated with ACP. Genetically predicted higher education and household income levels could lower the risk of pancreatitis. This MR study provides evidence of complex causal associations between modifiable risk factors and pancreatitis. These findings provide new insights into potential therapeutic and prevention strategies.

Association between Dietary Habits and Pancreatitis among Individuals of European Ancestry: A Two-Sample Mendelian Randomization Study

Dietary factors are believed to potentially influence the risk of pancreatitis. Here, we systematically investigated the causal relationships between dietary habits and pancreatitis by using two-sample Mendelian randomization (MR). Large-scale genome-wide association study (GWAS) summary statistics for dietary habits were obtained from the UK Biobank. GWAS data for acute pancreatitis (AP), chronic pancreatitis (CP), alcohol-induced AP (AAP) and alcohol-induced CP (ACP) were from the FinnGen consortium. We performed univariable and multivariable MR analyses to evaluate the causal association between dietary habits and pancreatitis. Genetically driven alcohol drinking was associated with increased odds of AP, CP, AAP and ACP (all with p < 0.05). Genetic predisposition to higher dried fruit intake was associated with reduced risk of AP (OR = 0.280, p = 1.909 × 10-5) and CP (OR = 0.361, p = 0.009), while genetic predisposition to fresh fruit intake was associated with reduced risk of AP (OR = 0.448, p = 0.034) and ACP (OR = 0.262, p = 0.045). Genetically predicted higher consumption of pork (OR = 5.618, p = 0.022) or processed meat (OR = 2.771, p = 0.007) had a significant causal association with AP, and genetically predicted higher processed meat intake increased the risk of CP (OR = 2.463, p = 0.043). Our MR study showed that fruit intake may be protective against pancreatitis, whereas dietary intake of processed meat has potential adverse impacts. These findings may inform prevention strategies and interventions directed toward dietary habits and pancreatitis.

In-hospital patient education markedly reduces alcohol consumption after alcohol-induced acute pancreatitis

In-hospital patient education markedly reduces alcohol consumption after alcohol-induced acute pancreatitis

Readmission in acute pancreatitis: Etiology, risk factors, and opportunities for improvement

Acute pancreatitis is associated with a readmission rate ranging from 7 to 34%. Readmission rates are highest among biliary (4–37%) and alcohol-induced (2–60%) acute pancreatitis. Severe acute pancreatitis and necrotizing pancreatitis have readmission rates ranging from 20 to 75%. The most common causes of readmission include recurrent acute pancreatitis (17–45% of readmissions) and smoldering symptoms/local complications (17–38%). A number of risk scores reliably estimate risk of readmission in acute pancreatitis. Decreased rates of readmission were reported in patients that underwent same-admission cholecystectomy in biliary pancreatitis and alcohol cessation interventions in alcohol-induced pancreatitis. This review article discusses readmission in acute pancreatitis, including etiology, risk factors, and opportunities for improved patient care.

COMPARATIVE STUDY OF DISEASE SEVERITY, COURSE, COMPLICATIONS, AND CLINICAL OUTCOME BETWEEN ALCOHOL-INDUCED PANCREATITIS AND GALL STONE-INDUCED PANCREATITIS

Objective:To assess whether the etiological factors of alcohol and gall stones affect the disease severity, course, disease-associated complications, and clinical outcome in terms of length of hospital stay, infection/organ failure rates, intervention rates, and mortality. Materials and Method: We conducted a hospital-based prospective study in the Department of Radio-Diagnosis, Assam Medical College, where 75 cases with acute pancreatitis were screened and subdivided into three etiological groups: (i) alcoholism (33 cases), (ii) cholelithiasis (23 cases), and (iii) other causes (19 cases), out of which 56 cases with etiology of alcoholism and gall stones were included in our study. The severity was scored using the Modified CT Severity Index. Clinical follow-up was done for both alcohol-induced Pancreatitis and Gall stone-induced pancreatitis groups to assess the disease course, disease-associated complications&amp; clinical outcome. Statistical analysis: We analyzed data using the computer program Statistical Package for Social Sciences (SPSS for Windows, version 21.0. Chicago, SPSS Inc.) and Microsoft Excel 2010. Results: In a total of 75 cases screened for our study, alcohol-induced pancreatitis was the leading cause of acute pancreatitis (33 cases), followed by gall stone-induced pancreatitis (23 cases). Together, they accounted for 56 cases and constituted our study population. The majority of cases in our study were categorized under Moderate acute Pancreatitis in both alcohol-induced acute pancreatitis and gall stone-induced Pancreatitis as per the Modified CT Severity Index. The occurrence of ascites was more in alcohol-induced A.P. No significant difference was noted between the two groups in parameters such as peripancreatic or pancreatic fluid collection, necrosis, pleural effusion, extrapancreatic parenchymal abnormality, vascular complications &amp; G.I. complications. There was no statistically significant difference in clinical outcome between the two groups regarding the length of hospital stay, infection/organ failure evidence, need for intervention, and mortality. Conclusion: Our study found no significant difference between the two etiological groups regarding disease severity, course &amp; complications, and clinical outcome except for the increased occurrence of ascites in alcohol-induced pancreatitis.

The Quick Sepsis-Related Organ Failure Assessment Score Is Prognostic of Pancreatitis Severity in Patients With Alcohol-Induced Pancreatitis.

The aim of this study was to determine if the quick Sepsis-Related Organ Failure Assessment (qSOFA) score assessed at and 48 hours after admission is prognostic for alcohol-induced acute pancreatitis (AAP) severity. This is a retrospective cohort review study of 161 patients admitted to a single academic hospital in Houston, TX, with the diagnosis of AAP. Receiver operator characteristics analysis and logistic regression were used to assess the diagnostic accuracy and prognostic ability of the qSOFA score. A qSOFA score of 2 or higher at and 48 hours after admission had a specificity of 94% or greater and sensitivity of 33% or higher for pancreatitis severity and need for intensive care admission, intubation, or vasopressors. The qSOFA score at and 48 hours after admission was prognostic of intensive care unit admission by an adjusted odds ratio of 48.5 (95% confidence interval [CI], 6.4-1013.3; P &lt; 0.001) and 18.8 (95% CI, 2.2-467.3; P &lt; 0.05), respectively. The qSOFA score at admission was prognostic of severe pancreatitis by an adjusted odds ratio of 35.3 (95% CI, 7.2-224.3; P &lt; 0.001). A qSOFA score of 2 or higher is highly specific and prognostic of multiple clinical outcomes both at and 48 hours after admission in patients with AAP.

Transcriptomics and Network Pharmacology Reveal the Protective Effect of Chaiqin Chengqi Decoction on Obesity-Related Alcohol-Induced Acute Pancreatitis via Oxidative Stress and PI3K/Akt Signaling Pathway.

Obesity-related acute pancreatitis (AP) is characterized by increasing prevalence worldwide and worse clinical outcomes compared to AP of other etiologies. Chaiqin chengqi decoction (CQCQD), a Chinese herbal formula, has long been used for the clinical management of AP but its therapeutic actions and the underlying mechanisms have not been fully elucidated. This study has investigated the pharmacological mechanisms of CQCQD in a novel mouse model of obesity-related alcohol-induced AP (OA-AP). The mouse OA-AP model was induced by a high-fat diet for 12 weeks and subsequently two intraperitoneal injections of ethanol, CQCQD was administered 2 h after the first injection of ethanol. The severity of OA-AP was assessed and correlated with changes in transcriptomic profiles and network pharmacology in the pancreatic and adipose tissues, and further docking analysis modeled the interactions between compounds of CQCQD and their key targets. The results showed that CQCQD significantly reduced pancreatic necrosis, alleviated systemic inflammation, and decreased the parameters associated with multi-organ dysfunction. Transcriptomics and network pharmacology analysis, as well as further experimental validation, have shown that CQCQD induced Nrf2/HO-1 antioxidant protein response and decreased Akt phosphorylation in the pancreatic and adipose tissues. In vitro, CQCQD protected freshly isolated pancreatic acinar cells from H2O2-elicited oxidative stress and necrotic cell death. The docking results of AKT1 and the active compounds related to AKT1 in CQCQD showed high binding affinity. In conclusion, CQCQD ameliorates the severity of OA-AP by activating of the antioxidant protein response and down-regulating of the PI3K/Akt signaling pathway in the pancreas and visceral adipose tissue.

In-Hospital Patient Education Markedly Reduces Alcohol Consumption after Alcohol-Induced Acute Pancreatitis.

Although excessive alcohol consumption is by far the most frequent cause of recurrent acute pancreatitis (AP) cases, specific therapy is still not well established to prevent recurrence. Generally, psychological therapy (e.g., brief intervention (BI)) is the cornerstone of cessation programs; however, it is not yet widely used in everyday practice. We conducted a post-hoc analysis of a prospectively collected database. Patients suffering from alcohol-induced AP between 2016 and 2021 received 30 min BI by a physician. Patient-reported alcohol consumption, serum gamma-glutamyl-transferase (GGT) level, and mean corpuscular volume (MCV) of red blood cells were collected on admission and at the 1-month follow-up visit to monitor patients’ drinking habits. Ninety-nine patients with alcohol-induced AP were enrolled in the study (mean age: 50 ± 11, 89% male). A significant decrease was detected both in mean GGT value (294 ± 251 U/L vs. 103 ± 113 U/L, p < 0.001) and in MCV level (93.7 ± 5.3 U/L vs. 92.1 ± 5.1 U/L, p < 0.001) in patients with elevated on-admission GGT levels. Notably, 79% of the patients (78/99) reported alcohol abstinence at the 1-month control visit. Brief intervention is an effective tool to reduce alcohol consumption and to prevent recurrent AP. Longitudinal randomized clinical studies are needed to identify the adequate structure and frequency of BIs in alcohol-induced AP.

CRAC channel inhibitors in pancreatic pathologies.

CRAC channel inhibitors in pancreatic pathologies.

Bile acid- and ethanol-mediated activation of Orai1 damages pancreatic ductal secretion in acute pancreatitis.

Regardless of its aetiology, sustained intracellular Ca2+ overload is a well-known hallmark of acute pancreatitis (AP). Toxic Ca2+ elevation induces pancreatic ductal cell damage characterized by impaired ion and fluid secretion - essential to wash out the protein-rich fluid secreted by acinar cells while maintaining the alkaline intra-ductal pH under physiological conditions - and mitochondrial dysfunction. While prevention of ductal cell injury decreases the severity of AP, no specific drug target has yet been identified in the ductal cells. Although Orai1, a store-operated Ca2+ influx channel, is known to contribute to sustained Ca2+ overload in acinar cells, details concerning its expression and function in ductal cells are currently lacking. In this study, we demonstrate that functionally active Orai1 channels reside predominantly in the apical plasma membrane of pancreatic ductal cells. Selective CM5480-mediated Orai1 inhibition impairs Stim1-dependent extracellular Ca2+ influx evoked by bile acids or ethanol combined with non-oxidative ethanol metabolites. Furthermore, prevention of sustained extracellular Ca2+ influx protects ductal cell secretory function in vitro and decreases pancreatic ductal cell death. Finally, Orai1 inhibition partially restores and maintains proper exocrine pancreatic secretion in in vivo AP models. In conclusion, our results indicate that Orai1 inhibition prevents AP-related ductal cell function impairment and holds the potential of improving disease outcome. KEY POINTS: Sustained intracellular Ca2+ overload in pancreatic acinar and ductal cells is a hallmark of biliary and alcohol-induced acute pancreatitis, which leads to impaired ductal ion and fluid secretion. Orai1 is a plasma membrane Ca2+ channel that mediates extracellular Ca2+ influx upon endoplasmic reticulum Ca2+ depletion. Results showed that Orai1 is expressed on the luminal plasma membrane of the ductal cells and selective Orai1 inhibition impaired Stim1-dependent extracellular Ca2+ influx evoked by bile acids or ethanol combined with non-oxidative ethanol metabolites. The prevention of sustained extracellular Ca2+ influx protected ductal cell secretory functions in in vitro models and maintained exocrine pancreatic secretion in in vivo acute pancreatitis models. Orai1 inhibition prevents the bile acid- and alcohol-induced damage of the pancreatic ductal secretion and holds the potential of improving the outcome of acute pancreatitis.

Inpatient Alcohol Cessation Counseling Is Associated With a Lower 30-Day Hospital Readmission in Acute Alcoholic Pancreatitis.

Alcohol use is a common cause of recurrent acute pancreatitis. Thus, guidelines recommend providing alcohol prevention resources during hospitalization. There is limited data on the real-world implementation of this recommendation. We aimed to assess how often inpatients admitted with alcohol-induced acute pancreatitis (AAP) receive counseling and to determine the impact of counseling on readmissions for AAP. We retrospectively studied patients admitted with AAP at a tertiary care center from 2008 to 2018. We compared demographics, clinical features, and outcomes in patients who did and did not receive counseling. Outcomes studied were the proportion of patients with AAP receiving counseling, and readmission rates for AAP at 30 days and 1 year. A total of 243 patients with AAP were identified, of which 115 had inpatient alcohol counseling (47%). Demographic data were comparable between the 2 groups. Fewer patients receiving alcohol counseling were readmitted at 30 days compared with patients not receiving counseling (19.3% vs. 31.2%, P =0.048). At 1 year, the 2 groups had similar readmission rates. On multivariate analysis, patients who received counseling were half as likely to be readmitted in 30 days compared with those who did not receive counseling [odds ratio=0.52 (0.27, 0.98), P =0.046]. We note that <50% of patients receive alcohol counseling. Patients receiving alcohol counseling were less likely to be readmitted at 30 days, inferring possible value in the intervention provided. Similar readmission rates at 1 year suggest that the single intervention may not have a durable effect on alcohol prevention.

Recurrent acute pancreatitis prevention by the elimination of alcohol and cigarette smoking (REAPPEAR): protocol of a randomised controlled trial and a cohort study

Background/objectivesAcute recurrent pancreatitis (ARP) due to alcohol and/or tobacco abuse is a preventable disease which lowers quality of life and can lead to chronic pancreatitis. The REAPPEAR study aims to...

Relationship of Arterial Changes in Acute Pancreatitis on CT Angiography with Modified CT Severity Index

Abstract Purpose To evaluate the prevalence of arterial changes in patients with acute pancreatitis (AP) on computed tomography angiography (CTA) and determine their association with etiology of AP, presence of necrosis, collections and severity of AP. Materials and Methods A total of 50 patients (20 women, 30 men; mean age: 43.04 ± 13.98; age range: 18–77 years) with AP underwent contrast-enhanced computed tomography (CECT) scan and CTA of abdomen, which was evaluated for necrosis and fluid collection (s). On CTA, splanchnic arterial structures were assessed for vascular complications. Association between vascular changes and presence of necrosis, fluid collections, etiology of AP and severity of AP (as assessed by modified computed tomography severity index CTSI) was determined. Results Arterial complications were seen in 28 percent (14/50). The most frequently involved artery was superior pancreaticoduodenal artery (12 percent), followed by splenic artery (8 percent) and right gastric artery (8 percent; Fig. 1). No significant association was seen between arterial changes and gallstone or alcohol-induced AP. Arterial changes showed a significant association with presence of acute necrotizing pancreatitis (ANP), presence of collections and severe AP (CTSI 8–10) (p &lt; 0.05 for each). Conclusion Arterial changes on CTA are frequently seen in patients of AP having ANP. There is a significant association between arterial changes and presence of necrosis, collections and severe AP.

Impacts of body composition parameters and liver cirrhosis on the severity of alcoholic acute pancreatitis.

Liver cirrhosis and features of muscle or adipose tissues may affect the severity of acute pancreatitis (AP). We aimed to evaluate the impact of body composition parameters and liver cirrhosis on the severity of AP in patients with alcohol-induced AP (AAP). Patients with presumed AAP who underwent CT within one week after admission were retrospectively enrolled. L3 sectional areas of abdominal fat and muscle, and mean muscle attenuations (MMAs) were quantified. The presence of liver cirrhosis was determined using clinical and CT findings. Factors potentially associated with moderately severe or severe AP were included in the multivariable logistic regression analysis. A total of 242 patients (47.0 ± 12.6 years, 215 males) with presumed AAP were included. The mild and moderately severe/severe (MSS) groups included 137 (56.6%) and 105 patients (43.4%), respectively. Patients in the MSS group had higher rates of liver cirrhosis, organ failure, and local complications. Among body composition parameters, mean MMA (33.4 vs 36.8 HU, P<0.0001) and abdominal muscle mass (126.5 vs 135.1 cm2, P = 0.029) were significantly lower in the MSS group. The presence of liver cirrhosis (OR, 4.192; 95% CI, 1.620-10.848) was found to be a significant risk factor for moderately severe or severe AP by multivariable analysis. The results of this study suggest that liver cirrhosis has a significant impact on the severity of AAP. Of the body composition parameters examined, MMA and abdominal muscle mass showed potential as promising predictors.

Hypophosphatemia Is More Common and Is Prognostic of Poorer Outcomes in Severe Alcoholic Pancreatitis.

The aim of this study was to determine if hypophosphatemia is more common in patients with severe alcohol-induced acute pancreatitis (AAP). This is a retrospective, single institution, cohort study that analyzed 147 patients admitted to the hospital for AAP. Multivariate logistic regression was used to determine if hypophosphatemia would be related to clinical outcomes of disease severity. Hypophosphatemia was more common in patients with severe AAP at admission; in addition, all patients with severe AAP (100%) eventually developed hypophosphatemia during admission, relative to those with mild (43%) and moderately severe (54%) AAP. The magnitude of the lowest phosphate measurement obtained during admission was lower in patients with severe AAP (mean, 1.5 mg/dL, standard deviation [SD], 0.5 mg/dL) relative to those with mild (mean, 2.6 mg/dL; SD, 0.9 mg/dL) and moderately severe (mean, 2.3 mg/dL; SD, 0.9 mg/dL) AAP (P < 0.001). Finally, patients who developed hypophosphatemia during admission were more likely to require intensive care unit admission (P < 0.001), vasopressors (P = 0.01), or intubation (P = 0.003). Hypophosphatemia is more common and of greater magnitude in patients admitted to the hospital with severe AAP. In addition, patients with severe AAP who develop hypophosphatemia during admission are more likely to have poorer clinical outcomes.

Electrocardiographic Changes in a Man With Acute Pancreatitis: A Myocardial Infarction?

A 69-year-old man with a history of heavy alcohol use presented with abdominal pain and was diagnosed with alcohol-induced acute pancreatitis. On admission, he had not reported chest pain, palpitations, or dyspnea. Initial laboratory tests showed a lactic acid level of 8.3 mmol/L (normal, 0.5–2.2 mmol/L), normal renal function, and normal cardiac enzyme levels. An electrocardiogram (ECG) on admission showed sinus tachycardia. His symptoms and lactic acidosis resolved after aggressive fluid resuscitation and bowel rest. Two days later, sudden-onset dyspnea, tachycardia, and hypoxia necessitated the administration of 2 L of supplemental oxygen. A chest radiograph showed acute pulmonary edema. The patient's serum cardiac troponin level peaked at 0.35 ng/mL (normal, &lt;0.03 ng/mL), and his brain natriuretic peptide level was 235 pg/mL (normal, &lt;100 pg/mL). His ECG showed changes (Fig. 1).What is the most likely diagnosis? B) Stress-induced (takotsubo) cardiomyopathyFigure 1 shows sinus tachycardia with premature atrial contractions, new ST-segment elevations (STEs) in the inferior leads and in leads V2 through V6, and T-wave inversions throughout. Figure 2 shows the admission ECG.According to the Mayo Clinic criteria, the most common ECG changes associated with takotsubo cardiomyopathy (TTC) are STE and T-wave inversion. These changes are seen frequently in the precordial leads.1 Clinically, distinguishing TTC from acute coronary syndrome is challenging because of overlapping symptoms, elevated cardiac enzyme levels, and similar ECG changes. Certain ECG patterns indicate TTC rather than acute coronary syndrome, including the absence of ST-segment depression in the reciprocal leads; diffuse STEs extending beyond the territory of a single coronary artery; and STE in lead aVR with STE in the inferior, anterior, or anteroseptal leads.2Patients with suspected TTC may have known coronary artery disease (CAD) or associated risk factors; therefore, STEMI must be ruled out when STE is seen on an ECG.3 If angiograms reveal no fixed obstructive CAD, acetylcholine testing may be considered, because spasm-induced coronary obstruction has been proposed as the mechanism underlying TTC, with atherosclerotic CAD providing a protective “stenting” effect.4 Pulmonary embolism may trigger sinus tachycardia and T-wave inversions, but without STE or pulmonary edema. Wellens syndrome can cause isolated deep T-wave inversions in leads V1 through V3, but it cannot explain inferior-lead STE and T-wave changes.The pathophysiology of TTC involves transient stunning and reversible left ventricular (LV) systolic dysfunction after physiologic or emotional stress. Fewer than 20 cases of TTC have been reported as complications of acute pancreatitis. Of note, pancreatitis itself can cause STE, typically in the inferior leads.5 In our patient's case, an echocardiogram and left ventriculogram revealed severe apical hypokinesis and an LV ejection fraction of 40%; however, a coronary angiogram did not reveal obstructive CAD, so the diagnosis was TTC. Two months later, he had normal LV ejection function, consistent with expected recovery timelines.

S105 The Quick Sepsis-Related Organ Failure Assessment Score Is Prognostic of Pancreatitis Severity in Patients With Alcohol-Induced Pancreatitis

Introduction: Multiple models already exist to prognosticate pancreatitis severity and mortality. However, most require invasive measurements and are cumbersome to use. The quick Sequential Organ Failure Assessment (SOFA) score (qSOFA) score is a bedside tool that may be useful in determining prognosis in patients with alcohol-induced acute pancreatitis (AAP). The goal of this study was to determine if the qSOFA and BISAP score assessed at admission is prognostic of severe clinical outcomes in AAP. Methods: This is a retrospective, single center, cohort review study of 147 patients admitted to a community academic hospital in Houston, Texas, USA with the diagnosis of AAP. IRB approval was granted by the University of Texas Health Science Center at Houston, Houston, Texas, USA. Patient records were obtained from an electronic medical record system between December 1st, 2014 to July 1st, 2020. Patients were included if they were >18 years of age, had a history of alcohol consumption and had acute pancreatitis based on the Atlanta criteria. Receiver operator characteristics (ROC) and area under the curve (AUC) analysis was used to assess the diagnostic accuracy of the qSOFA and BISAP score on admission. Logistic regression was used to assess the odds of developing severe pancreatitis based on the Atlanta criteria and need for ICU admission, intubation or vasopressors based on the BISAP and qSOFA scoring systems. Results: The qSOFA score ≥2 at admission to the hospital was found to be ≥94% specific and ≥33% sensitive while a BISAP score ≥3 at admission was found to be ≥96% specific and ≥20% sensitive for multiple clinical outcomes, including severe AAP and need for ICU admission, intubation or vasopressors. A qSOFA score ≥2 was prognostic of need for ICU admission by an adjusted odds ratio (aOR) of 48.5 (95% CI: 6.4-1,013.3; p< 0.001) and of severe AAP by an aOR of 35.3 (95% CI: 7.2-224.3; p< 0.001). A BISAP score ≥3 was prognostic of severe AAP by an aOR 7.1 (95% CI: 1.2-36.0; p< 0.05), need for ICU admission by an aOR 47.7 (95% CI: 6.9-487.1; p< 0.001), need for intubation by an aOR of 25.8 (95% CI: 3.5-238.4; p< 0.01) and need for vasopressors by an aOR of 14.2 (95% CI: 1.1-358.2; p< 0.05). Conclusion: At the time of admission, a BISAP score ≥3 or a qSOFA score ≥ 2 is highly specific and prognostic for multiple severe clinical outcomes of AAP. Since the qSOFA score has fewer variables than the BISAP score, it may be a more useful clinical tool to evaluate prognosis.Figure 1.: ROC-AUC curves showing the diagnostic accuracy of qSOFA score at admission (qSOFAADM) relative to the BISAP score at admission to diagnose clinical outcomes in alcoholic pancreatitis patients. (A) Overlayed ROC curves assessing severe pancreatitis. (B) Overlayed ROC curves assessing need for ICU admission. (C) Overlayed ROC curves assessing need for intubation. (D) Overlayed ROC curves assessing need for vasopressors.

Morbid Obesity Is Associated With Worse Outcomes and Increased Inpatient Mortality in Patients With Alcohol Induced Acute Pancreatitis

Introduction: The prevalence of obesity in the United States is rising. Obesity is a known comorbidity with various health impacts. Alcohol is a common etiology for acute pancreatitis. Obesity is known to be associated with liver dysfunction. It is unclear to what extent the degree of obesity affects patients with alcohol induced acute pancreatitis (AAP), as nationally representative data are lacking. This study aimed to ascertain the impact of morbid obesity on outcomes of patients with alcohol induced pancreatitis.Methods: Data was obtained from the Nationwide Inpatient Sample database for 2016 and 2017. Hospital discharges of patients 18 years and over with a principal diagnosis of AAP were included. This cohort was divided based on presence of comorbid obesity into nonobese patients, mild-moderately obese patients (MMO) (BMI: 30.0 - 39.9) and morbidly obese patients (MO) (BMI >/=40.0). Primary outcome was inpatient mortality. Secondary outcomes included length of hospital stay (LOS), total hospital charges (THC), discharge diagnoses of hypocalcemia, sepsis, acute renal failure (AKI) and acute respiratory failure (ARF). Multivariate regression analysis was used to adjust for patients’ sociodemographic factors, Charlson comorbidity index as well as hospital characteristics as confounders.Results: A total of 143650 hospitalizations were principally for AAP, with 5.5% and 2.7% of these patients classified as having MMO and MO, respectively.In MO patients, there was increased odds of mortality (aOR=2.99, 95% CI: 1.509 - 5.917, p=0.002) when compared with patients who were nonobese. There was no difference in mortality in patients with MMO (aOR 0.88 95% CI: 0.383 - 2.026, p=0.765) when compared with the nonobese group. MO patients had increased mean LOS of 1.1 days (95% CI: 0.7 - 1.6, p<0.001) as well as THC of $14481 (95% CI: 7894 - 21068, p<0.001), increased odds of hypocalcemia (aOR=1.77, 95% CI: 1.302 - 2.392, p<0.001), sepsis (aOR=1.84, 95% CI: 1.183 - 2.873, p=0.007), AKI (aOR=1.55, 95% CI: 1.257 - 1.912, p<0.001).Conclusion: Morbid obesity has a negative impact on outcomes of patients with AAP. Efforts should be channeled towards promoting alcohol cessation in at-risk patients as a preventative measure, as well as closer monitoring of hospitalized patients with morbid obesity to mitigated these adverse events.

Trends and seasonality in hospitalizations for acute alcohol-related and biliary pancreatitis in the USA

BackgroundThe incidence of acute pancreatitis (AP) is characterized by circannual and geographical variation. The aim of this study was to describe seasonal variation and trends in hospitalizations for AP in the USA with respect to AP etiology. MethodsThe Nationwide Inpatient Sample data (2000–2016) from the Healthcare Cost and Utilization Project were used. The study population included all primary hospitalizations for AP. Biliary AP (BAP) and alcohol-induced AP (AAP) were distinguished by diagnostic and procedural ICD codes. Seasonal trend decomposition was performed. ResultsThere was a linear increase in annual incidence (per 100 000 population) of AAP in the USA (from 17.0 in 2000 to 22.9 in 2016), while incidence of BAP, equaled 19.9 in 2000, peaked at 22.1 in 2006 and decreased to 17.4 in 2016. AP incidence demonstrated 18% annual incidence amplitude with summer peak and winter trough, more prominent in AAP. In 2016, within AAP, the highest incidence (per 100 000 population) was noted among African-Americans (up to 50.4), followed by males aged 56–70 years (26.5) and Asians of low income (25.5); within BAP, above the average incidence was observed in Hispanic (up to 25.8) and Asian (up to 25.0) population. The most consistent and rapid increase in AP incidence was noted in males aged 56–70 years with an alcoholic etiology (average 6% annual incidence growth). ConclusionsThe incidence and annual trends of AP vary significantly among demographic and socioeconomic groups and this knowledge may be useful for the planning of healthcare resources and identification of at-risk populations.