bluuebunny/crossref_metadata_2025_split huggingface dataset:
1388 Dose Increment-Associated Liraglutide-Induced Acute Pancreatitis
Authors: Al-Salameh Nizar , Shah Ruchit N. , Khara Harshit S. 
Published: October 2019

INTRODUCTION:
Diabetes mellitus has been shown to increase the risk of developing acute pancreatitis (AP). Liraglutide is a glucagon-like peptide-1 (GLP-1) agonist used for the treatment of diabetes. Liraglutide has emerged as a preferred agent for the treatment of type II diabetes for its cardiovascular protective features and safety profile. One of the potential adverse effects of liraglutide is acute pancreatitis but we present an intriguing case of dose increment associated liraglutide-induced acute pancreatitis.

CASE DESCRIPTION/METHODS:
A 53-year-old female with a medical history pertinent for type II diabetes mellitus presented to the hospital with 2-days of epigastric abdominal pain, nausea, and non-bilious emesis. Her liraglutide dose had been increased 2 days prior to her symptom onset from 1.2 mg to 1.8 mg. Physical exam revealed epigastric discomfort on palpation without peritoneal signs. Lipase was 240 U/L (normal: 16-63 U/L), CRP 16 mg/L (normal: 0-5 mg/L), normal LFTs, and triglycerides were 148 mg/dL (normal: <200 mg/dL). Abdominal ultrasound and CT of the abdomen showed no evidence of biliary pathology. In the absence of alcohol use, absence of biliary pathology with normal LFTs, or other medical conditions, the patient was diagnosed with acute pancreatitis, likely secondary to liraglutide after a recent dose increment. She was treated with supportive measures and discharged home with cessation of the medication with no symptom reoccurrence.

DISCUSSION:
GLP-1 agonists such as liraglutide, are thought to cause acute pancreatitis by inducing a pro-inflammatory state within the exocrine pancreas. During the clinical phases of liraglutide, there were 8 reported events of acute pancreatitis. Liraglutide was found to have higher incidence of acute pancreatitis of 1.6 cases/1000 patient year exposure (PYE) vs 0.7 cases/1000 PYE which included other oral diabetic agents such as glimepiride, rosiglitazone, insulin glargine, sitagliptin, and exenatide. For diabetic patients on GLP-1 analogs admitted with acute pancreatitis, it is therefore important to consider the medication or its dose adjustment as a possible cause, especially in the absence of other common etiologies. This was a rare presentation of dose adjusted liraglutide induced acute pancreatitis.
1396 Viral Acalculous Cholecystitis: A Rare Extrahepatic Manifestation of Hepatitis A
Authors: Arroyo Yadis M. , Mony Shruti , Agrawal Saurabh , Bertran-Rodriguez Carlos E. , Pagan Andrea 
Published: October 2019

INTRODUCTION:
Hepatitis A (HAV) is the most common form of acute viral hepatitis worldwide with an incidence of 0.6 reported cases per 100,000 population in the United States. Typical clinical symptoms include nonspecific prodromal symptoms such as fever, malaise, weakness, anorexia, nausea, vomiting and abdominal pain. Atypical features of HAV include recurrent hepatitis, prolonged cholestasis and extrahepatic manifestations. Acalculous cholecystitis (ACC) is an extremely rare extrahepatic manifestation of HAV. We present a unique case of acute hepatitis A presenting as ACC in an adult male with IV drug use.

CASE DESCRIPTION/METHODS:
A 50 year old male with a history of active IV heroin use and treated hepatitis C presented with nausea and RUQ abdominal pain for 3 days. On admission, laboratory findings were remarkable for AST of 2574 U/L, ALT of 3214 U/L, ALP 321 U/L and total bilirubin of 4.0 mg/dl. On physical examination patient was afebrile and hemodynamically stable with normal bowel sounds, soft abdomen, mild RUQ tenderness to deep palpation and Murphy's sign negative. CT abdomen demonstrated an edematous gallbladder wall with mild pericholecystic fluid and fat stranding, CBD diameter 4.0 mm (Figures 1 and 2). General Surgery believed his overall clinical picture to be due to acalculous cholecystitis and recommended non-operative management. Patients IgM Hepatitis A returned positive, Hepatitis B and C non-reactive. Thus, his findings were attributed to an active hepatitis A viral infection. He was treated conservatively with intravenous fluids and pain control. On discharge the patient remained afebrile, abdominal pain had resolved and liver function tests had normalized.

DISCUSSION:
Acute Hepatitis A with gallbladder involvement has been described in approximately 50 to 98% of adults. Although the etiology remains unclear, the invasion of the gallbladder by HAV and cell-mediated immunologic response have been proposed in the pathogenesis of HAV induced cholecystitis. The treatment is mainly conservative, as ACC due to HAV is transient and improves with resolution of viremia. Thus, patients do not require surgical interventions, unless they develop severe complications from ACC including gangrene and empyema. Our case demonstrates the importance of having a high clinical suspicion for HAV, especially in patients with known risk factors. Physicians should be cognizant of Hepatitis A and its rare extra hepatic manifestation, such as acalculous cholecystitis in order to avoid unnecessary surgical interventions.
1401 The Pancreatic and Pancytopenic Predicament
Authors: Ahmed Bilawal , Chaudhary Omar , Shah Shil , Mustafa Mazhar , Sonpal Niket , Okwesili Byron 
Published: October 2019

INTRODUCTION:
Systemic lupus erythematosus (SLE) is a multisystem disease, that may affect multiple organ systems in the body.

CASE DESCRIPTION/METHODS:
15 yo female patient presented with chief complaints of abdominal pain, nausea, vomiting & nonbloody diarrhea. Onset of abdominal pain started 4 days prior to admission, localizing to the RUQ on day 2. Associated symptoms of nonbloody diarrhea & nonbloody/nonbilious vomit for 4 days. No contributory past medical history or past surgical history. Patient denies any drug allergies. On general physical examination, a fine lacy rash noted on all 4 extremities. Vitals T 37.9, HR 104, RR 18, BP 99/58. No guarding/rigidity & no masses/organomegaly were appreciated. CBC revealed pancytopenia with a platelet count of 115 (150-400 × 103/uL), Hb 8.5 (12-15 g/dL) & WBC 1.5 (4.5-13 × 10^3/uL). Lipase was 489 u/L and LDH was 2392 u/L. Other laboratories, including CMP, lipid panel, CRP, and pregnancy test, were all within normal limits. Patient was admitted with diagnosis of pancreatitis with pancytopenia and supportive treatment with investigative studies was initiated. Bone marrow biopsy was unequivocal. New laboratory test results indicated positive IgG and IgM antibodies to Brucella, Rickettsia, Ebstein Barr Virus and Parvovirus, complicating the diagnosis. Patient started on doxycycline empirically. Rheumatology consulted most likely etiology to be SLE and await Lupus Panel Results. ESR was 74 mm/hr, positive antinuclear antibody (ANA) 1/640, positive anti doublestranded DNA Antibody 1/320, positive anti Smith antibody, negative rheumatoid factor, C3 < 40 mg/dL, Lipase 2784 u/L, fecal occult bkood test positive. Following lab results and clinical course, the diagnosis of Systemic Lupus Erythematosus was made on day 4 of admission. Steroids were initiated, and the patient's status was observed closely. Lipase continued to rise to 8,136 u/L which prompted MRCP. MRCP showed extensive changes of pancreatitis with upper abdominal fluid, no organized collection or dilation of ducts. Also noted was extensive wall edema of the gallbladder with no filling defect. Lipase began trending down on day 2 of steroids. CBC corrected to within normal limits. Patient reported feeling better and continued improving.

DISCUSSION:
This case aims to facilitate diagnosticians in the evaluation of patients presenting with rare manifestations of SLE. SLE should be considered in cases of pancreatitis when common etiologies have been ruled out & symptoms are not residing despite appropriate treatment.
1405 Bevacizumab-Linked Acute Pancreatitis: A Case Report
Authors: Albagoush SARA , McGuire Shannon , Buaisha Haitam M. , Mukherjee Sandeep 
Published: October 2019

INTRODUCTION:
Bevacizumab is a recombinant humanized monoclonal antibody which inhibits vascular endothelial growth factor. It has been added to chemotherapy for the treatment of various solid tumors including cervical cancer, ovarian cancer, renal cell cancer, colon cancer, and glioblastoma. Several side effects have been attributed to bevacizumab of which the most common are hypertension, bleeding, infection, fatigue. However, one case of bevacizumab- linked acute pancreatitis has been reported in the literature in combination with cisplatin and gemcitabine for metastatic ovarian cancer as reported by Onder et al.

CASE DESCRIPTION/METHODS:
We herein present the case of a 78-year-old man with metastatic colon cancer treated with Leucovorin, 5- fluorouracil and irinotecan plus bevacizumab. After seven days of treatment, he suffered nausea, vomiting, and loss of appetite followed by epigastric and right upper quadrant pain. Imaging studies demonstrated evidence of acute pancreatitis and a pancreatic pseudocyst. As hypertriglyceridemia, hypercalcemia, alcohol and biliary etiologies and trauma were excluded, the most likely etiology of the patient's pancreatitis was felt to be an adverse reaction to bevacizumab.

DISCUSSION:
To date, this is the second bevacizumab-linked acute pancreatitis reported in the literature and the first in a patient with metastatic colon cancer. Due to the widespread use of bevacizumab in patients with a variety of malignancies, it is important that health care providers be aware of acute pancreatitis as a possible side effect of bevacizumab. Our aim is to raise awareness among gastroenterologists and other medical professionals to consider acute pancreatitis as a possible side effect of bevacizumab.
1408 A Tail of Acute Diarrhea
Authors: Mohamed Abdalla , Abboud Rachel , Estifan Elias , Cavanagh Yana , Adib Sami , Barham Shaker , Botros Youssef , Grossman Matthew , Baddoura Walid , Christian Derick 
Published: October 2019

INTRODUCTION:
VIPomas are neuroendocrine neoplasms arising from the pancreas in 90% of the cases reported, while the remaining 10% occur in other tissues of neural crest origin. The symptoms found are secondary to an excessive secretion of vasoactive intestinal peptide (VIP) including profuse watery diarrhea, dehydration, hypokalemia and hypoclorhydria. VIPomas are classically slow-growing, and previously reported cases consistently describe chronic diarrhea and a slowly progressing constellation of associated symptoms. We present a case of acute onset of secretory diarrhea secondary to a VIPoma.

CASE DESCRIPTION/METHODS:
The patient is a 62 y/o F with PMHx of HTN who presented to the ED w/complaints of abdominal pain, diarrhea, nausea and vomiting for approximately 3 days. Patient reported she was having 5-6 episodes of large volume, pale colored diarrhea. She denied any weight loss, change in diet, recent travel, blood in the stool, foul smell or bulky stool. She was initially found to be hypotensive BP 85/45, MAP 58, HR 88. Labs revealed K+ 3.1 meq/L, HCO3 was 16 meq/L, she had an AGMA measured at 15, and AKI with BUN: Cr 52:3.60 mg/dl respectively. On exam of the stool she was noted to have a stool osmolar gap of -14. Given no obvious underlying cause for these findings she underwent CT A/P which revealed a 7.8 × 6 cm mass contiguous w/both body/tail of the pancreas and posterior wall of the stomach, with no other sites of metastasis. EUS/FNA was done and pathology returned as NET type 1. VIP levels were subsequently sent and were elevated at 1385.8 pg/mL. She was started on octreotide 50 mcg TID with significant improvement in her diarrhea. She underwent surgery with distal pancreatectomy and splenectomy. Pathology confirmed the presence of a grade 2, stage T3 well differentiated NET. She had an uneventful recovery and was discharged home. She continues to be asymptomatic several weeks after surgery.

DISCUSSION:
Pancreatic VIPoma was first described in 1958 by Verner and Morrison in a patient with chronic refractory diarrhea and hypokalemia. VIPoma is very rare with an estimated incidence of 0.05-0.2 cases per million people. Acute diarrhea resulting from a VIPoma is rare event in an already rare malignancy. Our patient presented with acute secretory diarrhea proven by a stool osmolar gap less than 50, which resulted in acute kidney injury. Her diarrhea, secondary to VIPoma responded well to octreotide. VIPomas are classically rare tumors, but our specific case presents an even more rare presentation.
1409 Casting a Wide Net to Find a Rare NET: A Case of Gallbladder Large Cell Neuroendocrine Carcinoma
Authors: Law Jade , Zhornitskiy Alex , Tabibian James H. , Baltayan Armine 
Published: October 2019

INTRODUCTION:
Primary neuroendocrine tumors (NETs) of the gallbladder account for <0.5% of all NETs.
1
Large-cell neuroendocrine carcinoma (LCNEC) represents an extremely rare subtype of this uncommon malignancy, and as such, clinical features, optimal treatment, and overall prognosis remains largely unknown.

CASE DESCRIPTION/METHODS:
A 58-year-old women presented to the emergency department with food intolerance due to nausea and pain at her cholecystostomy drain site. Two weeks prior, she had been admitted to an outside hospital for severe right upper quadrant (RUQ) pain without nausea, vomiting, or fever. Work-up included computed tomography (CT) of the abdomen and a RUQ ultrasound, which appeared to reveal changes of cholecystitis and cholelithiasis. Cholecystectomy was attempted, but due to an intraoperative finding of a hardened gallbladder mass, the procedure was aborted, and a surgical cholecystostomy tube was placed instead. Upon admission to our hospital, the patient had normal vital signs. Physical examination was notable for mild RUQ tenderness and a cholecystostomy drain with small amounts of dark bilious fluid. Laboratory testing was significant for total bilirubin of 3.6 mg/dL, alkaline phosphatase of 557 U/L, and AST of 57 U/L. Repeat CT of the abdomen revealed a mass in the hepatic lobe and circumferential soft tissue spanning the tract of the cholecystostomy tube. Endoscopic retrograde cholangiopancreatography (ERCP) showed an extrinsically narrowed proximal duodenum and a 1.5 cm intracholedochal tumor thrombus. Histopathology revealed high grade LCNEC with 80% Ki67 proliferative activity. Oncology was consulted, and although chemotherapy was initiated during the hospitalization, the patient expired from cardiac arrest days after discharge.

DISCUSSION:
Patients with LCNEC present with non-specific symptoms such as abdominal pain or weight loss, and imaging cannot reliably differentiate gallbladder NETs from adenocarcinoma or other pathology. Thus, many are identified incidentally peri-cholecystectomy. Treatment options include resection if distant metastases are not present; if unresectable, palliative chemotherapy and radiation may be administered. The overall prognosis of gallbladder NETs is poor, even worse than gallbladder adenocarcinoma. Early detection with aggressive surgical resection is believed to be the only potential for cure.
1410 A Rare Case of Extrahepatic Cholestasis Secondary to Acquired Immunodeficiency Syndrome (AIDS)—Related Kaposi Sarcoma
Authors: Flores Estefania , Mathew Madhu , Oramas Diana M. , Mbachi Chimezie , Desai Parth M. , Noboa Danilo , Sarda Vanessa 
Published: October 2019

INTRODUCTION:
Kaposi sarcoma is an aggressive cancer seen in immunocompromised patients caused by Human Herpesvirus-8 (HHV-8) infection. Cutaneous and pulmonary complications are the most frequent, biliary tract involvement is rarely reported, typically asymptomatic but may present as cholangitis or progress to liver failure.

CASE DESCRIPTION/METHODS:
35-year-old male with HIV and CD4 count of 35 cells/uL, not on antiretroviral therapy for the past year, presented with fever, fatigue, diffuse lymphadenopathies, unintentional weight loss, generalized abdominal pain and scleral icterus for the last 2 weeks. Physical exam showed icterus, small hyperpigmented lesions throughout his trunk, a violaceous nodular enlargement of the hard palate, generalized lymphadenopathy, diffusely tender abdomen and hepatomegaly. Laboratory studies were significant for total bilirubin 23 mg/dL, direct bilirubin 16 mg/dL, ALP 288 U/L, GGT 193 U/L, AST 66 U/L, ALT 40 U/L, INR 1.3. CT of the abdomen showed hepatomegaly and an infiltrative process in the portal hepatis to the celiac area with obstruction of the biliary tract with intrahepatic biliary dilation. Endoscopic retrograde cholangiopancreatography demonstrated 3 cm stricture in the common hepatic duct, a biopsy was taken, and 2 stents were placed. Endoscopic ultrasound with biopsies taken from a stomach nodule and porta hepatis were performed as well. Pathology from porta hepatis mass showed blood clot however, HHV-8 stain from the common hepatic duct and stomach nodule biopsies was positive for Kaposi sarcoma. Doxorubicin and antiretroviral therapy were started, and patient was discharged in view of symptomatic improvement. Liver function tests normalized 8 weeks after presentation.

DISCUSSION:
Kaposi sarcoma involving the biliary tract has been associated with cholangitis and jaundice and may also be caused from extensive disease of the porta hepatis with compression of the extrahepatic biliary tree. Current first-line treatment for advanced Kaposi sarcoma is lipososomal anthracyclines (doxorubicin, daunorubicin). HHV-8 infection cannot be eradicated, but long-term remission is possible. Treatment is indicated in patients with progressive hepatic and biliary disease. Kaposi sarcoma has also been associated with AIDS (acquired immunodeficiency syndrome) cholangiopathy, a form of biliary tract inflammation with stricture formation in severely immunosuppressed HIV patients and management consists of endoscopic sphincterotomy for papillary stenosis and stenting.
1416 Rare Presentation of Large Pancreatic Mass With Chylous Ascites
Authors: Badrinath Madhuri , Mandru Rachana , Saleem Sheikh A. , Heisig David 
Published: October 2019

INTRODUCTION:
Primary pancreatic lymphomas (PPL) are very rare and mimic pancreatic head cancer. We present a case of a man who presented with a pancreatic mass and chylous ascites, and was found to have PPL.

CASE DESCRIPTION/METHODS:
A 69-year-old man presented with 2 months of anorexia, abdominal pain and distension. He denied fever, chills or weight loss. Abdomen was distended, soft, non-tender with shifting dullness and fluid thrill. Laboratory tests were noncontributory except for mildly elevated LDH 254 U/L. Abdominal computed tomography (CT) showed a 20 × 10 × 17 cm soft tissue mass impinging the distal duodenum, replacing the proximal pancreatic parenchyma, encasing the celiac and superior mesenteric arteries; ascites, lymphadenopathy and multiple omental nodules were seen. No cirrhosis or hepatomegaly noted. 2.5 L of grossly chylous fluid was drained with lymphocytic predominance, high triglycerides 980 mg/dL and negative cytology. Endoscopic ultrasound (EUS) showed an irregular hypoechoic mass. Fine needle aspiration (FNA) showed lymphoid cells with irregular nuclear membrane contours strongly positive for CD20, consistent with B cell lymphoma. PET-CT scan confirmed a metabolically active pancreatic mass with inguinal, aortocaval, juxtadiaphrgamatic and inframammary lymphadenopathy. Diagnostic laparoscopic biopsy confirmed diffuse B-cell lymphoma of germinal center origin positive for CD10, BCL6, BCL2 and CD45. Patient received 6 cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) which he tolerated well. Follow-up PET CT scan showed reduction in size of pancreatic mass and lymph nodes without areas of new/worsening lymphoma.

DISCUSSION:
PPLs comprise 0.5% of all pancreatic masses. Diagnostic criteria include dominant pancreatic mass, without superficial or mediastinal lymphadenopathy, absent hepatosplenic involvement and a normal blood leukocyte count. Clinical presentation is non-specific without classic symptoms of nodal lymphoma. Abdominal pain is the most common symptom (83%), followed by abdominal mass and weight loss. High tumor burden, β2-microglobulin levels >2 mg/l and high LDH levels are poor prognostic markers. Definitive diagnosis requires histologic confirmation, EUS-guided sampling is highly accurate. Treatment options include surgery, chemotherapy, radiation, alone or in combination. Cure rates upto 30% have been reported. Long term remission can be obtained with CHOP chemotherapy alone in majority of patients. Addition of rituximab results in overall improvement in patient survival.
1417 Gastric Outlet Obstruction Caused by Infiltrative Pancreatic Cancer Mimicking Benign Peptic Ulcer Disease
Authors: Bhardwaj Gaurav , Nawaz Waqas , Hertan Hilary 
Published: October 2019

INTRODUCTION:
Gastric outlet obstruction (GOO) is a known complication of peptic ulcer disease (PUD) and pancreatic cancer. Pancreatic cancer causing GOO can sometimes be missed on endoscopic ultrasound (EUS) due to limited access, thus presenting a diagnostic challenge. We report a case of pancreatic cancer causing GOO which was missed on EUS and GOO was attributed to the duodenal ulcers.

CASE DESCRIPTION/METHODS:
A 59-year-old man with medical history of diabetes and PUD presented with epigastric pain and persistent vomiting for last 2 months associated with weight loss. He had upper endoscopy 4 weeks prior that revealed multiple ulcers in second part of the duodenum. Exam was remarkable for epigastric tenderness. Laboratory data showed hypokalemic metabolic alkalosis and acute kidney injury. Liver function tests were normal. Considering patient's clinical presentation an underlying malignancy was high on differential. CT abdomen showed GOO with duodenal narrowing and a normal pancreas. Endoscopy showed duodenal bulb stricture which could not be traversed. Biopsy showed inflamed duodenal mucosa. EUS showed no pancreatic pathology. GOO was attributed to the duodenal ulcers noted on prior endoscopy and a Roux-en-Y gastrojejunostomy was performed. He returned 12 weeks later with painless jaundice and elevated liver enzymes. MRI abdomen revealed a 2.5 cm infiltrative pancreatic head tumor extending to the pancreaticoduodenal groove resulting in dilatation of the duodenal stump and bile duct. The patient underwent Whipple's pancreaticoduodenectomy. The histopathology showed pancreatic adenocarcinoma with distal involvement of the duodenal margin.

DISCUSSION:
Pancreatic cancer is the second most common malignancy causing GOO. EUS is the most sensitive diagnostic modality for pancreatic cancer with a sensitivity of 94%. However, its accuracy can be limited in setting of duodenal stricture and infiltrating type of the pancreatic lesion. The best station to evaluate the head and genu of the pancreas is second part of the duodenum. In case of duodenal stricture, EUS cannot be stationed properly and can miss an infiltrating pancreatic head lesion causing the GOO, which can be attributed to some other co-existent etiology like PUD, especially in the setting of normal liver tests and CT abdomen. This case also highlights the utility of MRI which is more sensitive than CT in diagnosing small pancreatic lesions and sometimes might be the only revealing modality in instances where EUS is limited by duodenal stricture.