bluuebunny/crossref_metadata_2025_split huggingface dataset:
2692 Dunbar Syndrome: A Rare Cause of Abdominal Pain
Authors: Ali Farhan , Steimle Cassandra , Reddy Dayakar , Kelts Andrew , Jeng Jennifer , Kochik Michael , Golikov Edwin , Raborn Eric 
Published: October 2019

INTRODUCTION:
Dunbar Syndrome, also known as median arcuate ligament syndrome (MALS), is a rare condition with a reported incidence of 2 per 100,000. It is characterized by an extrinsic compression of the celiac trunk, and should be considered when evaluating patients with abdominal pain of unknown etiology.

CASE DESCRIPTION/METHODS:
A 78 year old female presented with a complaint of epigastric discomfort that was post-prandial in nature, with associated weakness and early satiety. Her symptoms had been persistent for one year. Workup prior to her presentation included a normal nuclear medicine (NM) gastric emptying scan and normal NM hepatobiliary scan with CCK. A detailed history revealed that her pain was particularly worse after eating and was associated with early satiety. Laboratory results on admission were unremarkable. Contrast-enhanced CT scan of the abdomen and pelvis showed external compression and indentation of the superior aspect of the proximal celiac axis with post-stenotic dilation. Further diagnostic evaluation utilized end-inspiratory phase CT angiography of the abdomen, which showed an approximately 1 cm length segment of proximal celiac arterial narrowing, measuring 70% maximally at its origin. She was diagnosed with MALS after review of the CTA reconstructive images which showed moderate external compression of the celiac artery.

DISCUSSION:
MALS predominantly affects women between the ages of 30 and 50 and is marked by the hallmark feature of postprandial abdominal pain. Other signs and symptoms may include nausea, vomiting, and consequent weight loss from an inability to tolerate oral intake. Symptoms are thought to have both a vascular (mesenteric ischemia) as well as neurogenic component (somatic pain thought to originate from the splanchnic plexus). CT angiography and conventional angiography are considered to be gold standard imaging modalities for Dunbar syndrome. They demonstrate focal stenosis that has a characteristic hooked appearance due to the indentation of the celiac trunk on its superior surface. Imaging for an accurate diagnosis should ideally be performed during the end-inspiratory phase, as indentation of the celiac trunk may be seen normally during expiration. Additional imaging features may include post-stenotic dilation, prominent collateral vessels, and thickening of the median arcuate ligament. Treatment includes endovascular transluminal angioplasty and stent placement, as well as laparoscopic division of the arcuate ligament and resection of the celiac plexus.
2695 Pedunculated Polyp at the Pyloric Channel Causing Intermittent Gastric Outlet Obstruction
Authors: Rezaie Aida , Ahmed Shifat , Mann Saba , Abidali Hussein 
Published: October 2019

INTRODUCTION:
Gastric outlet obstruction (GOO) is the intrinsic or extrinsic obstruction of the pyloric channel or duodenum. The most common cause remains to be peptic ulcer disease which results in inflammation, edema or fibrosis. GOO typically presents with epigastric abdominal pain and postprandial vomiting. While the incidence of GOO is unclear, it has declined since the identification of Helicobacter pylori, H2-receptor antagonists and endoscopic therapy. We present a case of a benign polyp obstructing the pyloric channel.

CASE DESCRIPTION/METHODS:
39 year-old female with a history of pulmonary embolism on Eliquis, Diabetes mellitus type 2 who presents for several months of epigastric pain, nausea and intractable vomiting. Prior to arrival, she had endoscopic evaluation at an outside hospital showing evidence of 1.5 cm gastric polyp in the pyloric channel. At the time, the polyp was not excised due to the patient being on anticoagulation. On admission, she underwent CT angiography showing no evidence of clot. She subsequently underwent repeat endoscopic evaluation demonstrating a 15 mm non-bleeding, pedunculated polyp at the pyloric channel obstructing the pyloric opening. The polyp was resected with hot snare. Biopsy showed a hyperplastic gastric polyp negative for malignancy. To prevent bleeding post-intervention, two hemostatic clips were placed. The patients abdominal pain, nausea and vomiting nearly resolved one day after her procedure.

DISCUSSION:
While the incidence of GOO has declined, it should continue to be considered in patient’s presenting with recurrent epigastric abdominal pain. Recent reviews estimate that, contrary to earlier years, 50 to 80% of cases have been attributable to malignancy such as pancreatic adenocarcinoma and distal gastric cancer. CT scan may show gastric distension or retained material within the gastric lumen. However, identifying the obstruction with upper endoscopy establishes the diagnosis. Treatment should be aimed at the underlying cause.
2697 Gastrointestinal Stromal Tumor Mimicking a Small Lymphocytic Lymphoma
Authors: Garcia-Rodriguez Victor , Coronel Emmanuel 
Published: October 2019

INTRODUCTION:
Gastrointestinal stromal tumors (GIST) have been associated with synchronous or metachronous secondary malignancies in up to 43% cases. The occurrence between GIST and hematological malignancies is approximately 7%. Here, we present a case of a GIST mimicking Small Lymphocytic Lymphoma (SLL).

CASE DESCRIPTION/METHODS:
A 70-year-old male presented with a one-month history of bilateral axillary lymphadenopathy. Physical exam revealed a conglomerate of lymph nodes of both axillary regions. CT of the chest-abdomen-pelvis showed diffuse axillary, mesenteric, retroperitoneal and inguinal lymphadenopathy. In addition, it showed a 40 mm mass in the lesser curvature of the stomach (Figure 1). FNA of the axillary region showed findings consistent with SLL. Upper endoscopy showed a large subepithelial mass in the stomach (Figure 2). Biopsies were taken with cold forceps showing reactive white blood cells, this was suspected to be lymphoma. The patient was diagnosed with Stage IV SLL and started on Ibrutinib. Three months after therapy was started, CT revealed significantly improved on adenopathy but an increase in the size of the gastric mass. A repeat upper endoscopy with endoscopic ultrasound (EUS) showed a hypoechoic, heterogeneous round mass with well-defined borders, originating from muscularis propria layer (Figure 3). Fine needle biopsy (FNB) was performed and showed clusters of neoplastic cells, positive for CD117 and DOG1, negative for CK7, CK20, and CDX2, consistent with a GIST.

DISCUSSION:
Little is known about the coexistence of GIST and other metachronous tumors of different anatomic location. Several theories have been proposed to explain this link. These theories include pro-oncogenic changes in the tissue microenvironment, carcinogenic effect by chemotherapy and desmoid-type fibromatosis after trauma or surgery. When located in the stomach, GISTs most commonly present as subepithelial lesions. Since mucosal biopsies have a false negative rate of almost 50%, additional evaluation with EUS and EUS guided tissue acquisition is of essential importance. Obtaining core samples by FNB is useful for tissue architecture evaluation and immunohistochemistry assessment of the sample. In this particular case, EUS was not performed initially; instead, mucosal biopsies were obtained leading to a false negative result. This case highlights the rare association between GISTs and other malignancies, as well as, the importance of EUS for the evaluation and accurate diagnosis of different subepithelial lesions.
2702 Tumor Lysis Syndrome in a Patient With Gastric Adenocarcinoma
Authors: Lingamaneni Prasanth , Desai Parth M. , Mathew Madhu , Moturi Krishna Rekha , Gupta Shweta 
Published: October 2019

INTRODUCTION:
Tumor lysis syndrome (TLS), considered a hematologic emergency, is uncommonly seen with solid tumors. TLS is most often seen in the context of aggressive lymphomas, where cell turnover is high. We present a case of tumor lysis syndrome in a patient with gastric adenocarcinoma, as a complication of FOLFOX (5-fluorouracil, leucovorin, oxaliplatin) chemotherapy.

CASE DESCRIPTION/METHODS:
48-year-old male with metastatic gastric adenocarcinoma (Figure 1), who received his first cycle of FOLFOX 4 days prior, presented to the emergency department with slurred speech and altered mental status. Vitals at presentation were normal. Systemic examination was remarkable for agitation and disorientation to time, place and person. He had no focal neurologic deficits and rest of the exam was unremarkable. CT scan of the head and EEG were unrevealing. Laboratory analysis was significant for an elevated creatinine, phosphorus and uric acid (Table 1 day 5). The pattern of electrolyte abnormalities and their development after recent chemotherapy was consistent with a diagnosis of chemotherapy-induced laboratory and clinical TLS. Patient was managed with aggressive IV fluids and rasburicase, following which, the electrolyte abnormalities resolved, and he improved clinically back to baseline.

DISCUSSION:
Tumor lysis syndrome occurs when tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy, leading to hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Complications include renal insufficiency, cardiac arrhythmias, seizures and death. Rapidly proliferating tumors like high-grade lymphomas and acute leukemias are predisposed to TLS. TLS occurs infrequently with solid tumors. TLS-associated mortality rate, with solid tumors, is around 35%; higher than that with hematologic malignancies. This is likely explained because prophylactic measures are implemented more often in hematological malignancies and less often in solid tumors. Our patient fulfilled the Cairo-Bishop criteria for grade II TLS. To our knowledge, there have been only nine cases of TLS secondary to gastric adenocarcinoma published in the literature. We present the first case of FOLFOX-induced TLS in a patient with gastric adenocarcinoma. This case highlights the importance of early recognition of TLS in patients with gastric cancer. Initiation of early treatment can reduce the high morbidity and mortality associated with this condition.
2711 A Rare Cause of Hematemesis: Metastatic Prostate Cancer to the Stomach
Authors: Then Eric O. , Lopez Michell , Ofosu Andrew , Chaudhri Ali , Culliford Andrea , Gaduputi Vinaya 
Published: October 2019

INTRODUCTION:
Prostate cancer is a malignancy that constitutes the third most common type of cancer in males. Present day its mortality rate is decreasing with better screening in the form of prostate specific antigen (PSA). The most common site of metastasis is the bone. Rarely will this form of malignancy metastasize to the gastrointestinal tract. Here we present a rare case of advanced prostate cancer with gastric metastasis.

CASE DESCRIPTION/METHODS:
Patient is an 81 year old male with a medical history of hypertension and prostate cancer (on anti-androgen therapy) who presented to our emergency department with altered mental status, aphasia, and left sided hemiparesis. Given his poor neurologic status and inability to maintain oxygenation the patient was intubated. Notable imaging included a computed tomography (CT) scan of the brain showing findings consistent with acute infarct of the left middle cerebral artery. Notable laboratory workup included a hemoglobin 7.8 gm/dL. Physical exam was notable for a cachectic male with left sided weakness in the left upper extremity and left lower extremity. He was then admitted to the intensive care unit (ICU) where he was noted to have an acute drop in hemoglobin to 5.0 gm/dL with coffee ground emesis. An esophagogastroduodenoscopy (EGD) was then performed which showed a large infiltrative, ulcerated, friable mass lesion with contact oozing in the gastric body along the greater curvature which was biopsied. The pathology results of the biopsy specimen returned with positive staining to prostate specific antigen (PSA) consistent with metastatic prostatic adenocarcinoma in the gastric mucosa. During his hospital course at our facility, the patient's condition worsened and his family decided to withdraw care. The patient then underwent palliative extubation and expired peacefully.

DISCUSSION:
There are multiple primary malignancies that have the potential for metastasis to the stomach. Of these, the most common cancers include those of the lung, breast, kidney, esophagus and finally, cancers of the head and neck. Rarely will prostate cancer present with gastric metastasis. Symptoms of metastatic lesions to the stomach mimic those of primary gastric cancers and include abdominal pain, nausea, vomiting and hematemesis. Treatment of metastatic prostate cancer is best managed with androgen deprivation therapy. If this fails, alternate treatment options include chemotherapy or immunotherapy with androgen receptor antagonists or androgen synthesis inhibitors.
2712 Pyloric Crohn's Disease: A Rare Presentation of Gastric Outlet Obstruction
Authors: Then Eric O. , Are Vijay S. , Ofosu Andrew , Chaudhri Ali , Culliford Andrea , Gaduputi Vinaya 
Published: October 2019

INTRODUCTION:
Crohn’s disease is an inflammatory bowel disease that may present anywhere along the gastrointestinal tract, spanning from the esophagus to the large intestine. The majority of cases of Crohn’s disease are located in the colon and small intestine, constituting approximately 70% of cases. Rarely will Crohns disease present in the stomach. Here we present a rare case of gastric outlet obstruction secondary to Crohn’s disease of the stomach.

CASE DESCRIPTION/METHODS:
Patient is a 53 year old female with a medical history of Crohn’s disease who presented to the emergency department complaining of epigastric abdominal pain, nausea and yellow vomiting for three days. Notable laboratory workup included a complete blood count and comprehensive metabolic panel within normal limits. Notable imaging included a computed tomography of the abdomen with contrast which showed a dilated stomach suggestive of gastric outlet obstruction. This was followed by a barium swallow which showed a dilated stomach, delayed gastric emptying, and inflammatory changes in the pyloric channel. An upper esophagogastroduodenoscopy was then done which showed diffuse edematous, ulcerated mucosa in the antrum with pyloric narrowing. Biopsies were taken of this area which showed extensive surface erosion and fresh granulation tissue with transmural chronic inflammation. The option for repeat EGD with balloon dilation or surgical intervention were discussed with the patient, but she opted for conservative measures. This consisted of total parenteral nutrition and treatment with intravenous high dose steroids (Solumedrol 60 mg IV). During her course the patient slowly improved was able to tolerate oral intake. She was then discharged with oral steroids and follow up appointments.

DISCUSSION:
Crohn’s disease of the stomach is rare occurrence. The first case of gastric crohns disease was reported in 1949. Since then current data suggests that a mere 0.5 to 4% of all Crohns disease cases present with gastric involvement. Diagnosis of gastric crohns disease can be accomplished through biopsy. This would show classic transmural inflammation, which was consistent with the biopsy findings in our patient. Symptoms of gastric Crohn’s disease are varied and can include symptoms of gastric outlet obstruction if the pylorus is involved. This includes nausea, post-prandial vomiting, abdominal pain and bloating. These cases have been successfully treated with endoscopic balloon dilation, Adalimumab, and surgical resection in more severe cases.
2713 Ulcerated Gastric Leiomyoma: A Rare Cause of Gastric Outlet Obstruction
Authors: Then Eric O. , Deda Xheni , Ofosu Andrew , Maddika Srikanth , Chaudhri Ali , Gaduputi Vinaya 
Published: October 2019

INTRODUCTION:
True leiomyomas are rare tumors that can be found anywhere along the gastrointestinal tract, more commonly in the esophagus, stomach and colon. These tumors are usually asymptomatic but may present with abdominal pain and gastrointestinal bleeding. Here, we present a rare case of a gastric leiomyoma resulting in gastric outlet obstruction.

CASE DESCRIPTION/METHODS:
The patient is a 52-year-old male with a past medical history of Asthma, Heroin abuse, and Peptic ulcer disease who presented to the emergency department complaining of epigastric abdominal pain accompanied by non-bloody vomiting. Notable laboratory workup included a Hemoglobin of 10.3 gm/dL. Notable imaging included a computed tomography (CT) scan of the abdomen without contrast which showed large volume gastric debris suggestive of gastric outlet obstruction. This was followed by small bowel series which showed loculated barium within the stomach with no barium seen within the pylorus. Gastroenterology service was then consulted to perform an upper esophagogastroduodenoscopy. This was done and showed severe luminal distortion of the pylorus making intubation of the duodenum difficult. This was accompanied by a large, unhealed 3 cm deep cratered ulcer just beneath the incisura. Biopsies were taken which returned showing histology consistent with gastric leiomyoma. This diagnosis was supported by diffuse positive staining with SMA and desmin and negative staining with c-kit and DOG1 immunostaining. During his admission a nasogastric tube was unable to be placed due to the level of obstruction in the pylorus. He was then started on total parenteral nutrition to meet her dietary needs. The patient was then discharged home on TPN but was lost to follow up thereafter.

DISCUSSION:
Gastric leiomyomas represent approximately 2.5% of all gastric neoplasms and are mostly encountered in patients aged 50-70 years with no gender predilection. Most gastric leiomyomas are slow-growing and asymptomatic; therefore, they are usually found incidentally on EGD, surgical exploration, or at autopsy. Rarely will gastric leiomyomas result in gastric outlet obstruction. The gold standard for diagnosis is biopsy which will show spindle cells that display smooth muscle differentiation and stain positively to desmin and actin. Submucosal leiomyomas less than 3 cm may be followed up by periodic EGD or endoscopic ultrasound. Lesions greated than 3 cm however may require surgical or endoscopic excision to rule out malignancy.
2714 Famotidine-Induced Hypomagnesemia Leading to Hypocalcemia
Authors: Essrani Rajesh , Mehmood Asif , Kirshan Ravi Shri Jai 
Published: October 2019

INTRODUCTION:
Famotidine is a long-acting histamine H2 receptor antagonist that is indicated for the treatment of gastroesophageal reflux disease (GERD), peptic ulcer disease and Zollinger- Ellison syndrome. It is considered to have an excellent safety profile with only a few side effects like constipation, diarrhea, and headache. We present a case of famotidine induced hypomagnesemia and functional hypoparathyroidism causing hypocalcemia.

CASE DESCRIPTION/METHODS:
A 55-year-old female with a past medical history of GERD was admitted to hospital due to increased lethargy, confusion, and muscle cramps for last 15 days. These muscle cramps affected functions of her hands and legs, causing multiple falls. She was taking famotidine 20 mg twice a day for the last two years. Her vital signs were stable. On exam, alert and oriented 2x, dry skin, positive Chvostek’s and Trousseau's sign. Initial blood work showed sodium 141 mmol/L, BUN 13 mg/dL, creatinine 0.7 mg/dL, calcium 5.7 mg/dL, magnesium 0.55 mg/dL, phosphorus 3.4 mg/dL. She was treated with multiple doses of intravenous (IV) 2 g magnesium sulfate and 1 g of calcium gluconate. Further work showed low PTH but normal PTHrP, vitamin D (25) and vitamin D (1,25). Her calcium and magnesium level normalized with IV therapy, so she was discharged home on oral electrolyte supplements. She followed up with her family doctor with a repeat blood work and noted to have very low calcium and magnesium so admitted to hospital. Extensive workup including 24 hours urine calcium and magnesium was unimpressive. She was treated with IV therapy and discharged to follow up with nephrology in the clinic with a repeat blood work. Her famotidine was discontinued on discharge. Her calcium and magnesium level remained normal, and few weeks later, oral electrolyte supplements were discontinued.

DISCUSSION:
This is the first reported case of famotidine induced hypomagnesemia and functional hypoparathyroidism causing hypocalcemia. Famotidine might cause impaired absorption of magnesium, leading to hypomagnesemia and functional hypoparathyroidism. Patients being started on a H2 receptor antagonist for the long-term course should have a baseline serum calcium and magnesium level and periodic monitoring as well. The optimal timing for monitoring levels is unknown, but annual monitoring (sooner if the patient develops symptoms) may be reasonable. Long-term use of famotidine should be considered in the differential diagnosis for hypomagnesemia and hypocalcemia.
2715 A Hiatal Hernia Causing Atrial Fibrillation Through Direct Mechanical Irritation
Authors: Sourial Kirolus , Yaqoob Zaid , Chahin Anthony , Borgan Saif , Gonzaga Ernesto Robalino , Javaid Aamir 
Published: October 2019

INTRODUCTION:
Hiatal hernia (HH) is anatomically classified into four types according to herniated structures. Giant HH refers to a herniation of >50% of the stomach. Atrial fibrillation (AF) is a common arrhythmia, frequently seen in association with cardiovascular diseases. We report a case of AF caused by a giant HH compressing the left atrium.

CASE DESCRIPTION/METHODS:
A 90+ year-old female with a past medical history of gastroesophageal reflux disease (GERD), was admitted for surgical evaluation of symptomatic HH. During hospital stay the patient developed AF with rapid ventricular response, became hypotensive and lightheaded. EKG (Figure 1) confirmed new onset AF with non-specific ST-T wave changes. Sinus rhythm conversion was achieved by amiodarone drip. Metabolic and endocrine causes of the AF were ruled out. Ischemic etiology of the AF was ruled out by a normal myocardial perfusion imaging study. Computed tomography Angiography of the chest (Figure 2) was only remarkable for persistent giant hiatal hernia. Echocardiogram (Figure 3) showed external material compressing against the heart and the left atrium. At that point, the patient and the surgical team have decided on conservative management for her HH due to her high surgical risk. Patient was discharged home in sinus rhythm on oral anticoagulant and beta blocking agent.

DISCUSSION:
Gastroesophageal reflux disease (GERD), HH and AF are often seen in association. AF in GERD patients is likely due to local cytokine release from esophageal injury or vagal overstimulation. Such association is supported by reduced AF recurrences by reflux suppression with PPI use or fundoplication. However, the underlying mechanism of AF in HH patients has not been fully understood. In our case, left atrial compression and impingement were seen, which indicates direct left atrial irritation causing atrial arrhythmia. Surgical reconstitution of HH to relieve the cardiac compression would be the definitive treatment. Unfortunately, our patient was not a candidate for such invasive thoracic surgery due to her age. A similar case scenario was previously reported, in which AF was suppressed after laparoscopic surgical repair of a giant paraesophageal hernia. More cases need to be studied to confirm the hypothesized etiology of AF in patients with giant HH.