Family History Of Pancreatitis Research Articles

ExoLuminate: An observational registry study for detection of pancreatic adenocarcinoma (PDAC) in high-risk or clinically suspicious patients.

TPS4203 Background: The detection of pancreatic ductal adenocarcinoma (PDAC) at early-stages is critical to improving patient survival. However, the lack of a clinically useful biomarker assay poses a challenge for earlier detection. A liquid biopsy test (ExoVita Pancreas) which uses extracellular vesicles (EV) protein biomarkers has been developed for detection of PDAC. In a previous case-control study of n=715 (75 cases of PDAC Stage I and II, 640 controls), the EV-protein biomarker assay yielded a sensitivity of 96.0% and specificity of 91.1%. By optimizing the assay for high sensitivity, we aim to generate evidence for earlier detection of PDAC in high-risk and clinically suspicious patients in the hope of impacting PDAC patient diagnostic journeys. Methods: ExoLuminate is a prospective, multi-center, observational registry study to demonstrate that early detection of PDAC using ExoVita is non-inferior to current standard of care methods of surveillance. The study duration will be 36 months (24-month accrual, 12-month follow-up), with a minimum of 1000 subjects to be enrolled between two cohorts as described below. The first cohort enriches for “high-risk” individuals without a cancer suspicion or diagnosis including those with intraductal papillary mucinous neoplasms (IPMNs), personal or family history of pancreatitis, family member(s) who have at least one first-degree relative affected by pancreatic cancer, patients over 50 years of age with new-onset diabetes (NOD), and germline mutations known to be associated with PDAC. The second cohort includes patients with clinical findings suspicious for early-stage PDAC or those with biopsy-proven PDAC. Patients enrolled in the study will have their blood obtained at six-month intervals. The performance of ExoVita liquid biopsy will be compared to standard-of-care imaging and biomarkers such as CA19-9. Through this registry, which began enrollment in December 2022 and is open for accrual (NCT0562552), we aim to demonstrate the clinical utility of a novel liquid biopsy based on detection of EV-derived biomarkers for early diagnosis of PDAC which can provide credence to a new paradigm in early detection to improve patient outcomes. Clinical trial information: NCT0562552 .

PSUN236 Previously Undiagnosed Hereditary Pancreatitis Presenting as New Onset Type 3c Diabetes Mellitus

Abstract Background Type 3c Diabetes Mellitus (DM3c) or Pancreatogenic Diabetes is defined as diabetes secondary to pancreatic disease. The most common cause of Type 3c Diabetes is chronic pancreatitis, accounting for 80% of cases.1 Hereditary pancreatitis, with mutations such as SPINK1, CFTR, CTRC, is an underdiagnosed cause of chronic pancreatitis leading to Type 3c Diabetes Mellitus.1 The typical disease course for hereditary pancreatitis is recurrent episodes of acute pancreatitis that leads to chronic pancreatitis.1 The average time between hereditary pancreatitis diagnosis and development of DM3c has been shown to be 80 +/- 24 months.1 We present a case of previously undiagnosed hereditary pancreatitis presenting as new onset Type 3c Diabetes Mellitus. Clinical Case A 33-year-old male presents with a two month history of diarrhea, epigastric pain, and weight loss. Vital signs on presentation were blood pressure 105/74, heart rate 59, BMI 13. Physical exam revealed a cachectic appearing male with epigastric tenderness. Lab-work showed blood glucose 819 mg/dL, SOsm 313 mOsm/kg, lipase 21 U/L, bicarbonate 33 mmol/L. A computed tomography (CT) of the abdomen revealed punctate pancreatic parenchymal calcifications, suggestive of chronic pancreatitis. He was admitted to general medicine for management of HHS, where he was treated with IV hydration and insulin therapy. Workup for new onset diabetes revealed a negative anti-GAD Ab <5.0 U/mL, and C peptide level 0.5 ng/mL which suggested β cell dysfunction and decreased endogenous insulin secretion. With these lab values, along with radiographic findings consistent with chronic pancreatitis, the likely driving factor for his diabetes was pancreatic disease and he was diagnosed with DM3c. Severe pancreatic disease was further shown by a reduced fecal elastase level of <50, suggesting exocrine pancreatic insufficiency. Investigating the etiology of his chronic pancreatitis, history revealed no prior episodes of acute pancreatitis or abdominal pain, and no family history of pancreatitis. Workup for common causes of pancreatitis, including alcohol use, hypertriglyceridemia, and gallstones was negative, and genetic workup was pursued. The patient was found to be heterozygous for a SPINK1 mutation, which is a known mutation in hereditary pancreatitis.1 Therefore, hereditary pancreatitis was determined to be the likely cause of his chronic pancreatitis which led to Type 3c Diabetes Mellitus. He was started on daily insulin therapy and pancreatic enzymes for his endocrine and exocrine pancreatic dysfunction respectively, with improvement in symptoms. Conclusion This is a unique case of hereditary pancreatitis presenting as new onset Type 3c Diabetes Mellitus with no prior episodes of acute pancreatitis or established diagnosis of chronic pancreatitis. References Ramalho, G. X., & Dytz, M. G. (2020). Diabetes of the exocrine pancreas related to hereditary pancreatitis, an update. Current Diabetes Reports, 20(6). Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Pancreatitis in the Complex Care Population: Presentation, Incidence, and Severity.

To describe the incidence and presentation of pancreatitis in Children with Medical Complexity (CMC) while evaluating severity of disease and outlining risk factors. This was a retrospective chart review between January 2010 and December 2019 of patients seen in the complex care clinic at Nationwide Children's Hospital (NCH) and Cincinnati Children's Hospital Medical Center (CCHMC). Data collected included sex, underlying diagnosis, family history of pancreatitis, type of pancreatitis, signs/symptoms, abdominal imaging, severity of attack, and presence of various risk factors associated with pancreatitis. Severity and diagnosis of pancreatitis was determined based on North American Society for Pediatric Gastroenterology, Hepatology and Nutrition criteria. One hundred and twelve patients from both institutions were included, 62% from NCH, median age 11.5 [interquartile range (IQR): 5-16 years], 50% male. Most patients were less than 18 years of age with a median age of 8 years (IQR: 4-13 years). Underlying diagnoses included seizures (67%), cerebral palsy/spastic quadriplegia (65%), diabetes (3.6%), and mitochondrial disease (3%). Majority of patients were found to have multiple underlying diagnoses (88%). Incidence of pancreatitis for both institutions was 336 of 100,000 patients/year which is significantly higher than the general pediatric population ( P < 0.0001). Majority of first episodes of pancreatitis were mild (82%) with abdominal pain as the predominant symptom (50%). Adult patients were more likely to have pancreatitis related to medication use than pediatric patients (70% vs 38%, respectively P = 0.007). Individuals in the CMC population at our institutions have a high incidence of pancreatitis with unique risk factors compared to the general pediatric/young adult populations.

Estrogen-induced gallstone pancreatitis in a transgender female.

The case of a transgender female who developed gallstone pancreatitis in the context of estrogen use for gender-affirming hormone therapy is reported. A 24-year-old Caucasian transgender female presented to the emergency department for abdominal pain and vomiting after referral from urgent care for suspected pancreatitis. Her home medications included estradiol, medroxyprogesterone, and spironolactone for gender-affirming hormone therapy and omeprazole for reflux. The patient reported minimal alcohol intake, presented with mildly elevated triglyceride levels, and did not have a family history of pancreatitis or gallstone disease. She underwent a laparoscopic cholecystectomy on hospital day 4 and was given a postoperative diagnosis of chronic cholecystitis, cholelithiasis, and pancreatitis. Given her history and the present illness, the use of estrogen therapy is a likely risk factor for the development of gallstone pancreatitis. Estrogen is a cornerstone of gender-affirming hormone therapy used by transgender women; however, in addition to its role in gender identity confirmation, estrogen can result in drug-induced pancreatitis.

Necrotizing Pancreatitis Secondary to Dulaglutide Use

Introduction/ Background: GLP-1 agonists are an essential component of the anti-diabetes armamentarium. Common side effects include mild gastrointestinal distress and headaches. Uncommon side effects include acute pancreatitis and can limit use. We report a case of acute severe necrotizing pancreatitis most likely attributed to dulaglutide.Clinical Case: A 69-year-old man presented lethargic with diffuse abdominal pain associated with nausea and vomiting of 1-day duration. His past medical history consisted of type 2 diabetes, hyperlipidemia, hypertension, and hypothyroidism. His diabetes regimen included metformin, glipizide, and empagliflozin. Dulaglutide was added three months prior at 0.75 mg weekly, and the dose was increased to 1.5 mg weekly three days before presentation, the patient having received one such dose. Initial workup showed lipase 2800 units/mL, amylase 1185 units/mL, lactate 12.6 mmol/L, white blood cells 20 x 109/L, glucose 348 mg/dL, AST 30 unit/L, hematocrit 51.5%, blood urea nitrogen 24 mg/dL, and serum creatinine 1.57 mg/dL, calcium 8.1 mg/dL. No stones or CBD dilation were noted on ultrasound. Initial CT showed an enlarged pancreas with peripancreatic stranding and slightly diminished enhancement consistent with early signs of necrotizing pancreatitis. The patient became increasingly hypoxic and hypotensive and required intubation and triple pressor support to maintain adequate perfusion. On the second day of hospitalization, his hematocrit was 35.7%, blood urea nitrogen 37 mg/dL, calcium 6.8 mg/dL, and bicarbonate 21 mmol/L. AST and ALT peaked at 209 and 398 unit/L respectively. Calculated 48 hours Ranson’s score was 7. He completed 7 days of meropenem for necrotizing pancreatitis. He developed cholecystitis secondary to inflammatory damage of the biliary tract and received a cholecystostomy tube. A follow-up CT scan 7 days after the initial scan showed a prominent pancreas with extensive inflammation and without cysts, with several areas of nonenhancement/poor perfusion in the pancreatic head consistent with pancreatic necrosis. The patient made a full recovery and was discharged to a rehabilitation unit. Investigation into other causes of pancreatitis revealed triglycerides 104 mg/dL, a normal distribution of IgG subclasses (IgG4 36 mg/dL), no significant alcohol use, and no family history of pancreatitis.Conclusion: Pancreatic safety studies of dulaglutide have shown a good safety profile1. However, FDA safety warning exists on GLP-1 agonist prescriptions. Necrotizing pancreatitis with GLP-1a is rarely reported. We present a case of severe necrotizing pancreatitis due to dulaglutide use with the existence of temporality, after ruling out other causes of pancreatitis.Reference: 1. Nauck MA et al. Assessment of Pancreas Safety in the Development Program of Once-Weekly GLP-1 Receptor Agonist Dulaglutide. Diabetes Care 2017;40:647–54.

Diabetic Ketoacidosis and Acute Pancreatitis in Covid-19 Setting

Introduction: Respiratory, kidney and gastrointestinal are some of the systems affected by COVID-19. Although COVID-19 has been studied as a lung pathogen, endocrine system involvement has rarely been studied. In this case report, we present a case of diabetic ketoacidosis (DKA) and acute pancreatitis in the setting of COVID-19. Case Description: A 52-year-old female with a PMH of type 1 diabetes mellitus and hypothyroidism, presented to the ED with nausea, vomiting, fatigue and diffuse abdominal pain. She reports cosmetic surgery a few weeks prior and she started feeling these symptoms at the beginning of admission day of admission. On admission, WBC was 34.9, blood glucose was 496, lactic acid of 3.1. Arterial blood gas revealed pH of 6.96, PCO2 of 17 mEq/L, PO2 of 143, HCO3 of 5 and anion gap of 23. DKA protocol was initiated and was upgraded to ICU. She was found to be RT-PCR positive for SARS-CoV-2. She denied other symptoms, including melena, jaundice, hematochezia, hematemesis, cough, SOB or diarrhea. She also denied use of alcohol, tobacco or illicit drugs, prior hospitalizations, or family history of pancreatitis. The physical exam was significant for tenderness to palpation in epigastric region without guarding or rebound. Laboratory studies revealed lipase: > 4000U/L, AST: 64 U/L, ALT: 57 U/L, ALKPHOS: 152 U/L, and total bilirubin: 1.1 mg/dL. Serum triglycerides and calcium levels were within normal limits. CT abdomen showed a severe peripancreatic inflammation and edema, moderate non-organized fluid surrounds pancreas. An abdominal ultrasound showed no calcified gallstone or gallbladder wall thickening. The common bile duct was 3 mm, normal size. Over the course of 24 hours, anion gap was 7, pH was 7.28, blood glucose was 158. For sepsis, lactic acid was 0.7 after initiation of azithromycin. For acute pancreatitis, she was treated conservatively with intravenous fluids, bowel rest and analgesia. Patient denied any upper respiratory symptoms and did not require oxygen so steroids were not started for COVID PNA. Her symptoms improved and she was discharged home. Discussion: Here we report a case of a patient who presented with DKA, found to have severe acute pancreatitis as well as SARS-CoV2 PCR positive. Few case reports have reported an association of DKA and acute pancreatitis. Although the exact mechanism by which SARS-CoV-2 is evolving, it is thought to be mediated by the Angiotensin-Converting Enzyme-2 which is present in intestine, and on islet cells of the pancreas. This injury may be due to cytopathic effect of viral replication or indirectly caused by the inflammatory response induced by the virus. Further studies are needed to better understand the pathophysiology behind AP in the setting of COVID-19. Conclusion: This case highlights DKA and AP as a possible initiating presenting manifestation of COVID-19 infection

Genetic Evaluation of Children with Idiopathic Recurrent Acute Pancreatitis.

Several genetic risk factors have been identified in adults with idiopathic acute recurrent pancreatitis (IARP). However, the literature regarding the genetics of IARP is sparse in children. In this study, we aimed to analyze the genetic risk factors in children with IARP. All children (< 18years) with ARP from January 2015 to May 2018 were prospectively enrolled in the study. Children with a known cause of ARP like obstructive, toxic/metabolic, and autoimmune were excluded from the final analysis. Children with IARP underwent genetic testing for mutations/polymorphisms in genes known to predispose to pancreatitis including cationic trypsinogen protease serine 1 (PRSS1), serine protease inhibitor Kazal type 1 (SPINK1), cystic fibrosis transmembrane conductance regulator gene (CFTR), chymotrypsin C (CTRC), claudin-2 (CLDN2) and cathepsin B (CTSB). A total of 239 children (116 boys, 10.3 ± 3.7years) were enrolled during the study period. Of these, 204 (85.35%) children were identified as IARP. The mean age of symptom onset and the number of pancreatitis episodes were 8.3 ± 3.7years and 3.3 ± 1.8, respectively. A family history of pancreatitis was noted in 4.6% children. Mutations/polymorphisms in at least 1 gene were identified in 89.5% (129/144) children including SPINK1 in 41.9%, PRSS1 (rs10273639) in 58.2%, CTRC in 25.6%, CTSB in 54.9%, CLDN2 in 72.9%, and CFTR in 2.3%. There was no significant incidence of genetic mutations/polymorphisms in IARP with or without pancreas divisum (95.7 vs 88.4%; p = 0.467). Genetic alterations are present in the majority of the children with IARP. The incidence of genetic mutations is similar in children with or without pancreas divisum.

3025 Losartan-Induced Pancreatitis: A Rare Cause

INTRODUCTION: Acute pancreatitis (AP) is an acute inflammatory state caused by multiple etiologies, the most common being gallstones, alcohol and hypertriglyceridemia. Less than &lt;5% of pancreatitis is caused by medications and have excellent prognosis. Multiple medications have been associated with developing pancreatitis, and among these, one is losartan. So far there has been 3 case reports of losartan induced pancreatitis. Losartan is a class 1b medication associated with pancreatitis. Medications are classified into group based on number of cases reported, recurrence with re-challenge. Class 1 medications have the highest association with pancreatitis. CASE DESCRIPTION/METHODS: 49 year old male with a past medical history of substance abuse, schizoaffective disorder, hepatitis C and hypertension presented to the hospital with epigastric abdominal pain radiating to the back for 2 days and was found to have elevated lipase of 1600 U/L with computed tomography suggestive of AP. He had no family history of pancreatitis. There was no recent alcohol use. Serum triglycerides, blood alcohol level and urine toxicology screen were negative. There was elevation in liver enzyme, Aspartate aminotransferase 148 U/L, Alanine aminotransferase 92 U/L, Alkaline phosphatase 149 U/L, total bilirubin 1.7 mg/dl. Magnetic resonance cholangiopancreatography revealed normal caliber common bile duct without filling defects. The elevated enzyme likely were due to underlying hepatitis C. Upon medication review, patient was found to be taking losartan for his hypertension since 2018. He was treated with intravenous fluids and pain control. His blood pressure medication was switched to amlodipine and was discharged after 4 days, uneventfully. Patient had a prior admission two months ago for AP while he was on losartan which was not discontinued and workup for gallstone, alcohol, hypertriglyceridemia, hypercalcemia or illicit substance use was negative. DISCUSSION: There have been only few case reports of losartan-induced AP. The exact mechanism of losartan causing pancreatitis is not understood. Drug induced pancreatitis is not well studied due to limited number of cases. Establishing diagnosis involves ruling out other common etiology as challenging with medication in ethically difficult. This case emphasizes the importance of reviewing the medication of patients with an unclear etiology of pancreatitis.

1411 A Rare Cause of Acute Pancreatitis in a Transgender Female

INTRODUCTION: While hypertriglyceridemia and certain medications are known causes of acute pancreatitis, estrogen resulting in secondary hypertriglyceridemic acute pancreatitis (HTG-AP) is rare. To our knowledge, this is only the third case of a transgender female presenting with acute pancreatitis secondary to estrogen-induced hypertriglyceridemia. CASE DESCRIPTION/METHODS: A 31-year-old transgender female presented to the hospital with epigastric pain, fever, chills and decreased appetite. Laboratory work-up was significant for lipase &gt;7,500 u/L, triglycerides &gt;7,000 mg/dL and calcium of &lt;4 mg/dL. The patient denied alcohol use, diabetes, hypothyroidism or family history of pancreatitis. Initial management included aggressive intravenous fluid resuscitation. CT scan of the abdomen was performed and was notable for a large peripancreatic fluid collection most consistent with walled off necrosis (Figures 1 and 2). Three retroperitoneal drains were placed into the fluid collections with clinical improvement. Upon further questioning, it was discovered that several months prior to admission, the patient had started taking oral estrogen therapy obtained via an online store to transition from male to female, which was ultimately felt to be the most likely cause of her very severe hypertriglyceridemia. Two weeks after discharge, patient had IR drain exchange and repeat CT scan showed almost complete resolution of the fluid collections and her drains were removed. DISCUSSION: Medications are often described as the etiology for why people develop pancreatitis. However, to clearly prove a medication as the inciting factor, reinitiation of that medication needs to occur in order to establish a temporal relationship. Estrogen is a rare cause of drug-induced pancreatitis with approximately 40 cases reported worldwide. It is one of the few medications that has a described mechanism, hypertriglyceridemia, for the development of pancreatitis. Of the 40 cases described only 2 published case reports involve transgender females (7) (Table 1). The number of transgender patients presenting to the healthcare system for care is growing (9.2 per 100 000). Importantly, transgender females require supraphysiologic doses of estrogen therapy to maintain secondary sexual characteristics. Accounting for these factors, it is important for healthcare providers to understand their risk for and ways to prevent acute pancreatitis from occurring in their transgender patient population (8).

1324 Recurrent Pancreatitis Associated With Pancreas Divisum and Rare Solid Pseudopapillary Neoplasm of the Pancreas

INTRODUCTION: Pancreas Divisum (PD) is a benign congenital anomaly found in approximately 4-10% of general population. Rare cases of acute pancreatitis associated with PD and pancreatic tumors have been described. While most common causes of pancreatitis are gallstones and alcohol use, uncommon causes such as anatomic/genetic variants and malignancies of the pancreaticobiliary system should be investigated especially in case of recurrent cryptogenic pancreatitis. We present a case of recurrent pancreatitis in a patient with pancreas divisum and rare solid pseudopapillary neoplasm of the pancreas. CASE DESCRIPTION/METHODS: A 65-year old woman with past medical history of psoriatic arthritis on methotrexate therapy and no family history of pancreatitis was evaluated for recurrent pancreatitis. Patient had at least eight episodes of acute pancreatitis from 2011 to 2019. Patient denied any alcohol/tobacco history. Serum triglycerides/calcium were not elevated. Genetic causes were excluded. Imaging ruled out gallstones but showed presence of pancreas divisum. Endoscopic ultrasound (EUS)/Endoscopic retrograde cholangiopancreatography (ERCP) in 2016 was negative for stricture, focal mass or lesions. In April 2017, patient underwent repeat EUS/ERCP with stent placement into the minor papilla for presumed stenosis. However, that resulted in an exacerbation of her symptoms and the stent was subsequently removed. Patient continued to have recurrent acute pancreatitis and underwent repeat EUS in August 2018 which showed an 8 × 8 mm pancreatic genu mass adjacent to the Santorini duct. Biopsy was consistent with rare, slow growing solid pseudopapillary neoplasm (SPN) of the pancreas. Patient underwent pancreaticoduodenectomy in 2019. Pathology confirmed SPN. Patient has had no further episodes of pancreatitis. DISCUSSION: Pancreas Divisum (PD) results from failure of fusion of ventral and dorsal pancreatic ducts during embryogenesis. It has been controversial whether PD by itself causes recurrent pancreatitis. Clearly, in our patient, addressing the PD alone did not resolve her symptoms of recurrent pancreatitis. Sporadic hemorrhage within the SPN and intermittent compression of the Santorini duct was the likely cause of recurrent pancreatitis in our patient. Patients with cryptogenic recurrent pancreatitis should be evaluated periodically for the presence of slow growing tumors that may not be evident on initial imaging and may be the cause of recurrent pancreatitis in such patients.

Pancreas Divisum in Pediatric Acute Recurrent and Chronic Pancreatitis: Report From INSPPIRE.

The significance of pancreas divisum (PD) as a risk factor for pancreatitis is controversial. We analyzed the characteristics of children with PD associated with acute recurrent or chronic pancreatitis to better understand its impact. We compared children with or without PD in the well-phenotyped INSPPIRE (INternational Study group of Pediatric Pancreatitis: In search for a cuRE) cohort. Differences were analyzed using 2-sample t test or Wilcoxon rank sum test for continuous variables, Pearson χ or Fisher exact test for categorical variables. PD was found in 52 of 359 (14.5%) subjects, a higher prevalence than the general population (∼7%). Females more commonly had PD (71% vs. 55%; P=0.02). Children with PD did not have a higher incidence of mutations in SPINK1, CFTR, CTRC compared with children with no PD. Children with PD were less likely to have PRSS1 mutations (10% vs. 34%; P<0.01) or a family history of pancreatitis (P<0.05), and more likely to have hypertriglyceridemia (11% vs. 3%; P=0.03). Children with PD underwent significantly more endoscopic procedures and pancreatic sphincterotomy. Patients with PD had fewer attacks of acute pancreatitis (P=0.03) and were less likely to develop exocrine pancreatic insufficiency (P=0.01). Therapeutic endoscopic retrograde cholangiopancreatography was considered most helpful if pancreatic duct was impacted with stones (83% helpful). PD is likely a risk factor for acute recurrent pancreatitis and chronic pancreatitis in children that appears to act independently of genetic risk factors. Patients with PD and stones obstructing the pancreatic duct benefit most from therapeutic endoscopic retrograde cholangiopancreatography.

Prevalence of abnormal glucose metabolism in pediatric acute, acute recurrent and chronic pancreatitis.

Type 3C Diabetes, or diseases of the exocrine pancreas has been reported to occur in approximately 30% of adult patient with pancreatitis. The incidence of glucose abnormalities or risk factors that may predict the development of abnormal glucose in the pediatric pancreatitis population is not known. We performed a retrospective chart review from 1998–2016 for patients who carry the diagnosis of acute pancreatitis (AP), acute recurrent pancreatitis (ARP), and chronic pancreatitis (CP). We extracted glucose values, HbA1c%, and data from oral glucose tolerance and mixed meal testing with timing in relation to pancreatic exacerbations. Patient characteristic data such as age, gender, body proportions, family history of pancreatitis, exocrine function and genetic mutations were also assessed. Abnormal glucose was based on definitions put forth by the American Diabetes Society for pre-diabetes and diabetes. Fifty-two patients had AP and met criteria. Of those, 15 (29%) had glucose testing on or after the first attack, 21 (40%) were tested on or after the second attack (in ARP patients) and 16 (31%) were tested after a diagnosis of CP. Of the patients tested for glucose abnormalities, 25% (13/52) had abnormal glucose testing (testing indicating pre-DM or DM as defined by ADA guidelines. A significantly higher proportion of the abnormal glucose testing was seen in patients (85%, 11/13) with a BMI at or greater than the 85th percentile compared to the normal glucose patients (28%, 11/39) (p = 0.0007). A significantly higher proportion of the abnormal glucose patients (77%, 10/13) had SAP during the prior AP episode to testing compared to the 10% (4/39) of the normal glucose patients (p<0.0001). Older age at DM testing was associated with a higher prevalence of abnormal glucose testing (p = 0.04). In our patient population, a higher proportion of glucose abnormalities were after the second episode of pancreatitis, however 62% (8/13) with abnormalities was their first time tested. We identified obesity and having severe acute pancreatitis (SAP) during the prior AP episode to testing could be associated with abnormal glucose. We propose that systematic screening for abnormal glucose after the first episode of acute pancreatitis in order to better establish the timing of diabetes progression.

Recurrent Pancreatitis in a Patient With Abnormal Pancreaticobiliary Junction: Case Report

Introduction: 22-year-old female being followed for idiopathic recurrent pancreatitis with negative genetic testing, HIDA scan, and image findings status post elective cholecystectomy was found to have pancreaticobiliary junction anomaly with pancreatic duct emanating from common bile duct. Case Description: Patient was seen in July 2017 for chronic abdominal pain and idiopathic pancreatitis with negative HIDA scan and equivocal CT and MRI findings. Genetic workup of PRSSI, CFTR, and SPINK were negative. No family history of pancreatitis. No alcohol consumption. EUS done in July 2017 showed hyperechoic material consistent with sludge in the gallbladder along with thickened gall bladder walls. Pancreatic duct had an irregular contour along with parenchymal abnormalities consistent of hyperechoic foci and the pancreatic duct appeared to disappear into the common bile dict. Patient underwent cholecystectomy in December 2017 without much relief. Patient was again seen in May 2018 at which EUS was again performed along with ERCP. ERCP showed a filling defect on the pancreatogram that consisted of a common channel whereby the pancreatic duct emanates from the common bile duct approximately 2 cm proximal to the sphincter of Oddi (figure 1). A biliary sphincterotomy was performed and temporary stent was placed into the common bile duct. This has so far controlled the patients' symptoms. Discussion: Abnormal pancreaticobiliary junction (APBJ) is a rare disorder that has been associated with high incidence of gallbladder cancer especially in Asian population. This congenital disorder causes the junction of biliary and pancreatic duct to be located outside the duodenal wall forming a common channel. Since the junction doesn't involve the duodenal wall, it's functions is not under the influence of sphincter of Oddi causing pancreatic biliary reflux (PBR). This reflux is associated with likely hyperplasia and carcinoma of the biliary system. APBJ is almost always seen in patients with choledochal cyst. There have been studies that have shown acute and chronic pancreatitis in setting of choledochal cyst but to our knowledge pancreatitis without choledochal cyst in a setting of APBJ has not been described. Clinician and researchers should be aware of APBJ with pancreatic duct emanating from common bile duct as a cause of recurrent pancreatitis.1430.tif Figure 1: A filling defect as seen on the pancreatogram that consist of a common channel whereby the pancreatic duct emanates from the common bile duct approximately 2 cm proximal to the sphincter of Oddi.

Escitalopram Induced Pancreatitis: An Unusual Culprit

Drug-induced pancreatitis accounts for 3-5% of all cases of acute pancreatitis. Over 12% of US adolescents and adults use antidepressants. We hereby report a case of acute Escitalopram-induced non-necrotizing pancreatitis in a 27-year-old male complaining of epigastric pain. He had no family history of pancreatitis or pancreatic cancer, and reported drinking less than 2 alcoholic drinks weekly. His only medication was Escitalopram, which he started 2 weeks prior for panic disorder and denied any supplement use. His diagnostic evaluation revealed (a)A normal CBC and kidney function (b)Serum lipase of 1746 U/L (c) Abdomen CT-scan with no pancreatic masses and evidence of acute pancreatitis(d) Absence of gallstones, biliary sludge or CBD dilation on ultrasound (e)Normal serum glucose,calcium and triglyceride levels (f)Normal IgG and IgG subclass levels. Intravenous hydration was initiated, and Escitalopram was discontinued with complete symptom resolution in 4 days. No re-challenge was performed. A Naranjo adverse drug reaction score was 6 suggesting a probable reaction given no previous reports on Escitalopram. Three cases of sertraline-induced pancreatitis have been reported in the literature with a latency period of a few days to 4 weeks reported [1,2]. A population study in Taiwan suggest a class effect given an association between recent SSRI use and risk of acute pancreatitis [3]. This wasn't re-demonstrated in a different population cohort in Sweden, however, a much longer latency period was studied which is inconsistent with the reported cases [4]. Further research and population studies are required to better characterize the risk of drug-induced acute pancreatitis with SSRI use, given the high prevalence of use of these agents and the significant morbidity with this adverse effect.

Transhiatal Herniation of the Pancreas as a Cause of Acute Pancreatitis

Introduction The two most frequent causes of pancreatitis are gallstones and alcohol, accounting for 80% of cases. Other less common causes include hypertriglyceridemia, trauma, toxins, drugs and other causes. Our case highlights a patient presenting with pancreatitis due to a large hiatal hernia. Case report A 95-year-old woman with history of prior cholecystectomy and known large hiatal hernia presented with severe epigastric pain that radiates to the back. She denied alcohol use, family history of pancreatitis, new medications or trauma. Vital signs were within normal limit. Physical exam was notable for abdominal wall hernia and moderate epigastric tenderness. Lab data revealed normal LFTs, but an elevated serum lipase of 9736 U/L and amylase of 1597U/L. Computed tomography of the abdomen with contrast large hiatus hernia containing most of stomach, portions of pancreas and omentum.1423_A.tif Figure 1: CT abdomen - Coronal view Pancreas indicated by red arrow Pancreatic duct indicated by white arrow Stomach indicated by blue arrowThe patient was managed conservatively with IV fluid and parenteral analgesia. Surgical repair of the herniation was discussed, due to advanced age and resolution of symptoms, a decision to avoid operative management was made. Discussion Transhiatal herniation of the pancreas is rare due to its retroperitoneal location and fixation by the ligament of Treitz. Acute pancreatitis as a complication of this phenomenon is uncommon. Symptoms consist of pain localized to the chest and epigastrium, dyspepsia, nausea, vomiting, and dyspnea. The diagnosis is confirmed by significant serum lipase elevation and imaging evidence of pancreatic herniation with inflammatory changes suggestive of pancreatitis A variety of mechanisms have been proposed to explain hernia-associated pancreatitis. The parenchymal trauma from repetitive transhiatal sliding may itself induce pancreatitis, or it may cause intermittent ischemia. Other possibilities include volvulus formation or intermittent folding of the pancreatic duct leading to pancreatic secretion against a fixed obstruction. Historically, patients were managed with immediate hiatal hernia repair, however recent cases have demonstrated successful supportive management. Severe cases involving incarceration, perforation, or unresponsiveness to medical therapy should be managed surgically Conclusion Pancreatic herniation is a rare entity which may lead rare complications, including pancreatitis. Our case report highlights the importance of maintaining a broad differential diagnosis when approaching patients to include uncommon causes of disease entities1423_B.tif Figure 2: CT Abdomen - Sagittal View Pancreas indicated by red arrow Stomach indicated by blue arrow1423_C.tif Figure 3: CT Abdomen - Coronal View Pancreas indicated by red arrow Pancreatic duct indicated by white Stomach indicated by blue arrow

Acute Epstein-Barr Virus-Induced Acute Pancreatitis and Cholestatic Hepatitis

Epstein-Barr virus (EBV) is a herpesvirus that is spread through saliva between susceptible individuals and asymptomatic EBV shedders. A majority of EBV infections are subclinical and approximately 90% of adults are eventually EBV-seropositive. Infectious mononucleosis is a common clinical manifestation of EBV. Besides fever, adenopathy, fatigue, pharyngitis, and atypical lymphocytosis, other manifestations include splenomegaly, splenic rupture, generalized maculopapular rash, and a variety of neurologic syndromes. EBV can effect any organ system and has reportedly been associated with myocarditis, pneumonia, hepatitis, pancreatitis, acute renal failure, and glomerulonephritis. A 17-year-old female with no significant history presented with non-radiating, dull, epigastric pain with associated decreased appetite, nausea and vomiting. On physical examination, her abdomen was non-distended with mild epigastric tenderness on palpation, without guarding or rebound tenderness, Murphy sign was not present. Initial laboratory data revealed a normal white blood cell count with elevated lymphocytes, alkaline phosphatase 205 IU/L, AST 270 IU/L, ALT 281 IU/L, total bilirubin 2.7 mg/dL, direct bilirubin 1.8, and a lipase of 937 u/L which elevated to 2839 u/L the following day. Right upper quadrant ultrasound was unremarkable. MRCP was negative for choledocholithiasis, but did reveal hepatosplenomegaly. Patient did not endorse a history of alcohol consumption, medications known to cause pancreatitis, trauma, surgery, or family history of pancreatitis. Workup for hypertriglyceridemia, autoimmune pancreatitis, and viral hepatitis was negative. A heterophile antibody test was positive and virology revealed acute infection of Epstein-Barr virus. Acute pancreatitis is not a common complication of acute EBV infection. A recent review of literature revealed acute pancreatitis in 14 patients with acute EBV infection, with five cases being acute pancreatitis with cholestatic hepatitis. In contrast to the review, this patient presented with abdominal pain and vomiting, and did not present with classic infectious mononucleosis symptoms. Mechanism of acute pancreatitis and hepatitis due to infectious mononucleosis are likely due to an inflammatory reaction to the virus, but the underlying mechanism needs further investigation. Although it is rare, EBV infection should be considered in the differential diagnosis if the patient has acute cholestatic hepatitis with acute pancreatitis.

A Rare Cause of Acute Pancreatitis

Energy Drinks (EDs) have become increasingly popular in recent years, but their safety profile is less well known. Case reports about the adverse effects of EDs are emerging Some known gastrointestinal adverse effects are dyspepsia, diarrhea and heart burn, all of which have been linked to excessive caffeine content. We report a rare case of acute pancreatitis from consumption of ED. A 27-year-old male with history of cholecystitis s/p cholecystectomy presented to Emergency department with epigastric abdominal pain, nausea and vomiting for one day. Of note patient had presented with acute pancreatitis (AP) 1 month prior when no clear etiology was found. History was negative for alcohol, recreational drug use, trauma or family history of pancreatitis but positive for excessive consumption of EDs up to 6 cans per day. Physical examination was unremarkable except for epigastric tenderness. Labs were significant for lipase 2,375 U/L, aspartate aminotransferase 121 U/L, alanine aminotransferase 180 U/L and alkaline phosphatase 51 U/L. BMP, Lipid panel, Immunoglobulin G4 and urine toxicology were unremarkable. Computed tomography abdomen revealed common bile duct dilation of 10 mm but no choledocolithiasis (figure 1 and 2). Further work up with magnetic resonance cholangiopancreatography revealed no obstruction, microlithiasis or ampullary abnormality (figure 3). Genetic mutations CFTR and PRSS were also negative. At this point etiology was thought to be excessive consumption of EDs. Use of EDs to improve stamina, performance and alertness has increased significantly in past two decades. To our knowledge there is only one more case report of EDs induced AP. This is a rare case showing association between acute pancreatitis and consumption of EDs. The mechanism how EDs cause pancreatitis is unclear and further research is warranted.

The Impact of Risk Factors of Chronic Pancreatitis on Secretin Pancreatic Function Testing: Results of a 20-Year Study.

The aim of this study was to determine the effect of established risk factors on the outcome of secretin pancreatic function testing (sPFT) in patients undergoing work-up for suspected chronic pancreatitis. We completed a retrospective review of patients who underwent sPFT for suspected chronic pancreatitis over 20 years. We compared peak bicarbonate concentrations between groups and completed univariate and multivariate analyses to determine associations between risk factors and positive sPFT results (peak bicarbonate <80 mEq/L). Forty-three of 162 patients had positive sPFT results. There were significant differences in peak bicarbonate concentrations in patients with and without recurrent acute pancreatitis (RAP) and with local complications from acute pancreatitis (AP) (P ≤ 0.05). The bicarbonate concentration in patients with and without other risk factors such as tobacco use, alcohol use, and family history of pancreatitis was not significantly different. Female sex, a history of AP, and a history of RAP were associated with positive sPFT results on univariate analysis (P ≤ 0.05). On multivariate analysis, sex and RAP remained significant. Our study demonstrates that female sex, history of AP and RAP, and AP with local complications are associated with positive sPFT results or lower peak bicarbonate concentration. However, other risk factors do not impact the results of sPFT.

Early-Onset Acute Recurrent and Chronic Pancreatitis Is Associated with PRSS1 or CTRC Gene Mutations

To assess whether the age of onset was associated with unique features or disease course in pediatric acute recurrent pancreatitis (ARP) or chronic pancreatitis (CP). Demographic and clinical information on children with ARP or CP was collected at INSPPIRE (INternational Study Group of Pediatric Pancreatitis: In Search for a CuRE) centers. The Cochran-Armitage trend test and Jonckheere-Terpstra test were used to examine for differences between pediatric age groups (<6, 6-11, and ≥12 years). Between September 2012 and March 2016, 342 children with ARP or CP were enrolled; 129 (38%) were <6 years of age at the time of first diagnosis of acute pancreatitis, 111 (32%) were 6-11 years of age, and 102 (30%) were ≥12 years of age. Early-onset disease was associated with mutations in cationic trypsinogen (PRSS1) (P < .01), chymotrypsin C (CTRC) (P = .01), family history of acute pancreatitis (P = .02), family history of CP (P < .01), biliary cysts (P = .04), or chronic renal failure (P = .02). Later-onset disease was more commonly present with hypertriglyceridemia (P = .04), ulcerative colitis (P = .02), autoimmune diseases (P < .0001), or medication use (P < .01). Children with later-onset disease also were more likely to visit the emergency department (P < .05) or have diabetes (P < .01). Early-onset pancreatitis is associated strongly with PRSS1 or CTRC mutations and family history of pancreatitis. Children with later-onset disease are more likely to have nongenetic risk factors. Future studies are needed to investigate whether the disease course, response to therapy, or clinical outcomes differ relative to the timing of disease onset.

An Evaluation of Factors Associated With Pathogenic PRSS1, SPINK1, CTFR, and/or CTRC Genetic Variants in Patients With Idiopathic Pancreatitis.

We evaluated factors associated with pathogenic genetic variants in patients with idiopathic pancreatitis. Genetic testing (PRSS1, CFTR, SPINK1, and CTRC) was performed in all eligible patients with idiopathic pancreatitis between 2010 to 2015. Patients were classified into the following groups based on a review of medical records: (1) acute recurrent idiopathic pancreatitis (ARIP) with or without underlying chronic pancreatitis; (2) idiopathic chronic pancreatitis (ICP) without a history of ARP; (3) an unexplained first episode of acute pancreatitis (AP)<35 years of age; and (4) family history of pancreatitis. Logistic regression analysis was used to determine the factors associated with pathogenic genetic variants. Among 197 ARIP and/or ICP patients evaluated from 2010 to 2015, 134 underwent genetic testing. A total of 88 pathogenic genetic variants were found in 64 (47.8%) patients. Pathogenic genetic variants were identified in 58, 63, and 27% of patients with ARIP, an unexplained first episode of AP <35 years of age, and ICP without ARP, respectively. ARIP (OR: 18.12; 95% CI: 2.16-151.87; P=0.008) and an unexplained first episode of AP<35 years of age (OR: 2.46; 95% CI: 1.18-5.15; P=0.017), but not ICP, were independently associated with pathogenic genetic variants in the adjusted analysis. Pathogenic genetic variants are most likely to be identified in patients with ARIP and an unexplained first episode of AP<35 years of age. Genetic testing in these patient populations may delineate an etiology and prevent unnecessary diagnostic testing and procedures.