The incidence of new mental health disorders after acute pancreatitis: A large, propensity-matched, observational study.

INTRODUCTION: The prevalence of acute pancreatitis (AP) and mental health disorders (MHDs) are rising. While the association between chronic pancreatitis (CP) and MHDs is established, it is unknown whether there is a risk of MHDs after an index episode of AP. The aim of this study was to evaluate the incidence of MHDs and pharmacotherapy use after an episode of AP. METHODS: This was a large observational study using the TriNetX research network, an electronic health record dataset containing inpatient and outpatient data from more than 50 healthcare organizations. Patients with AP from 2015-2020 were identified. Four cohorts were created: acute necrotizing pancreatitis (ANP), acute pancreatitis without necrosis (AP-WON), acute appendicitis, and healthy controls without pancreatitis. The cohorts were matched by age, sex, race, ethnicity, and nicotine and alcohol use. The primary outcome was new composite MHDs at one-year. Secondary outcomes included stratified MHDs, psychiatric medication use, opioid analgesic use, and all-cause mortality. RESULTS: The ANP, AP-WON, appendicitis, and healthy control cohorts contained 11,806, 177,266, 27,187, and 561,833 patients, respectively. Patients with AP-WON had significantly higher rates of composite MHDs compared with those hospitalized for appendicitis (9.7% vs 4.7%, HR 1.9, 95% CI 1.7-1.9). This association was augmented when comparing ANP to appendicitis (12.8% vs 5.2%, HR 2.4, 95% CI 2.1-2.7). All secondary outcomes were observed at significantly higher rates in the AP-WON cohort when compared to appendicitis. Again, these associations were augmented comparing ANP to appendicitis. CONCLUSION: Compared with controls, patients with AP had significantly higher rates of new MHDs and their associated pharmacotherapies at one-year, suggesting that a single episode of AP may independently place patients at risk for developing MHDs irrespective of whether they go on to develop CP.

Preoperative predictors of choledocholithiasis in patients presenting with acute calculous cholecystitis.

BACKGROUND AND AIMS: Markedly increased liver chemistries in patients presenting with acute calculous cholecystitis (AC) often prompt an evaluation for concomitant choledocholithiasis (CDL). However, current guidelines directing the workup for CDL fail to address this unique population. The aims of this study are to define the range of presenting laboratory values and imaging findings in AC, develop a model to predict the presence of concurrent CDL, and develop a management algorithm that can be easily applied on presentation. METHODS: We conducted a retrospective review of patients presenting with AC to a large tertiary hospital over a 3.5-year period. CDL was defined as common bile duct (CBD) stone(s), sludge, or debris seen on any of the following studies: US, CT, magnetic resonance imaging/MRCP, EUS, ERCP, or intraoperative cholangiogram. A multivariable model to predict CDL was developed on 70% of the patients and validated on the remaining 30%. RESULTS: A total of 366 patients were identified and 65 (17.8%) had concurrent CDL. Univariable analysis was used to predict CDL and demonstrated statistically significant odds ratios for transaminases >3 times the upper limit of normal, alkaline phosphatase (AlkPhos) above normal, lipase >3 times the upper limit of normal, total bilirubin ≥1.8 mg/dL, and CBD diameter >6 mm. In the validation cohort, an optimal model containing alanine transaminase (ALT) >3 times the upper limit of normal, abnormal AlkPhos, and CBD diameter >6 mm was found to have an area under the receiver operating curve of 0.91. When 0 or 1 risk factors were present, 98.6% of patients did not have CDL. When all 3 risk factors were present, 77.8% were found to have CDL. CONCLUSIONS: The prevalence of CDL is high among patients with AC. When a validated model is used, application of cutoffs for ALT, AlkPhos, and CBD diameter can effectively triage patients with low and high likelihood for CDL to surgery or ERCP, respectively.

Differential regulation of MMP-2 in the gastrohepatic ligament of the gastroesophageal junction.

INTRODUCTION: Ligamentous attachments maintain the normal anatomic position of the gastroesophageal (GE) junction. Failure of these elastic ligaments through an alteration in collagen synthesis, deposition, and metabolism may be a primary etiology of hiatal hernia formation. Differential expression of zinc-dependent matrix metalloproteinases (MMPs) is largely responsible for collagen remodeling. The purpose of this study was to survey baseline levels of MMPs in supporting ligaments of the GE junction from patients without hiatal hernia. METHODS: Following an institutional review board-approved protocol, plasma and tissue biopsies of the gastrohepatic ligament (GHL), gastrophrenic ligament (GPL), and phrenoesophageal ligament (PEL) were obtained in six patients without a hiatal hernia during laparoscopic anterior esophageal myotomy for achalasia. Total protein extracts from tissue biopsies were analyzed for elastases MMP-2, -9, and -12 and collagenases MMP-1, -3, -7, -8, and -13 using a multiplex profiling kit (R&D Systems, Minneapolis, MN). Data are reported as mean +/- standard deviation. Statistical significance (p < 0.05) was determined using Tukey's test and analysis of variance. RESULTS: In control patients without hiatal hernias, increased levels of MMP-2 (p < 0.02) were detected in the GHL compared with the GPL and PEL, respectively. Tissue levels of MMP-1, -12, and -13 were not detectable. CONCLUSIONS: Gelatinase-A (MMP-2) is present in the GHL and plasma of control patients. The GHL may provide the primary GE junction supporting ligament to compare tissue from patients with type I (sliding) and type III (paraesophageal) hiatal hernias to examine the role of altered collagen metabolism in hiatal hernia formation.