Clean-based Ulcers Research Articles

HEMOLYTIC ANEMIA IN ALCOHOL USE DISORDER: A CASE OF ZIEVE SYNDROME

HEMOLYTIC ANEMIA IN ALCOHOL USE DISORDER: A CASE OF ZIEVE SYNDROME

S3582 Disguised as Post-Operative Ileus: A Case of a Giant Gastric Ulcer Causing Outlet Obstruction and Gastric Pneumatosis

Introduction: Giant gastric ulcers (GGU), defined as ulcers larger than 2-3cm, are relatively rare in the setting of widespread proton pump inhibitor (PPI) use. Though usually located in the lesser curvature, GGU may occur in any part of the stomach. Typical symptoms are similar to that of peptic ulcer disease (PUD), i.e. epigastric pain and gastrointestinal bleeding, however GGU are highly prone to perforation and are more likely to be malignant in the elderly. Overall, gastric outlet obstruction is the least common complication of PUD. Case Description/Methods: A 74-year-old obese male with history diabetes, sleep apnea, and prior laparoscopic gastric banding surgery was admitted for elective surgery for Charcot arthropathy. Post-operatively, he developed nausea, vomiting and abdominal bloating. Abdominal x-ray showed distention of the small bowel concerning for ileus. Exam showed a non-tender abdomen with distention and tympany on percussion. His emesis resolved with antiemetics, however distention persisted despite passing gas and stool. Three days after surgery, he developed acute anemia without overt bleeding requiring blood transfusions. Abdominal X-ray and CT was performed which showed marked gaseous distention of the stomach and gastric wall pneumatosis. Nasogastric tube was placed for decompression with subsequent resolution of his distention. Due to concern for gastric band erosion, Gastroenterology was consulted. Upper endoscopy was performed which revealed a 4cm clean-based ulcer with overlaying eschar along the greater curvature with surrounding erythema and edema. Biopsies of the ulcer border showed acute erosive gastropathy with focal clustering of eosinophils without evidence of dysplasia. He was started on PPI and sucralfate, and remained clinically stable without further gastrointestinal symptoms. (Figure) Discussion: Gastric pneumatosis due to gastric emphysema is caused by disruption of mucosa leading to air migrating into the gastric wall. Etiologies vary, including injury from instrumentation, severe vomiting, pulmonary pathology, penetrating gastric ulcers, or gastric outlet obstruction. Few cases reports have described gastric emphysema resulting from gastric band erosion, however there are no reports describing this occurring in the absence of full erosion. Overall, gastric emphysema is relatively rare, as is development of GGU. To our knowledge, this is the first reported case of unperforated giant gastric ulcer resulting in outlet obstruction with gastric pneumatosis.Figure 1.: CT abdomen showing marked gaseous distention of the stomach and gastric wall pneumatosis (Figure 1a). Upper endoscopy findings of a friable, erythematous giant ulcer with clean-base overlaying the greater curvature with significant surrounding erythema and edema in the fundus/cardia (Figure 1b and 1c), as well as multiple surrounding small ulcerations, some with clean-base and some with flat pigmented spots, throughout (not pictured). No evidence of active bleeding, visible vessel, or high-risk features for bleeding.

P-140 Simple endoscopic scoring of patients with rectal cancer after concurrent chemoradiation therapy

Neoadjuvant concurrent chemoradiotherapy (CCRT) is an effective treatment option for patients with rectal cancer. In this study, we investigated the clinical efficacy of simple endoscopic scoring of patients with rectal cancer after CCRT. Between July 2008 and October 2015, medical records including endoscopic imaging from 41 patients with rectal cancer who received CCRT were retrospectively reviewed. Two expert gastroenterologists reviewed the endoscopic images and assigned scores from 0–3 according to post-CCRT findings. The scoring criteria were as follows: 0=no ulcer; 1=clean-based ulcer without marginal elevation; 2=clean-based ulcer with marginal elevation; 3=non-clean-based ulcer. We evaluated image scores to predict long-term outcomes using Kaplan-Meier curves and Cox regression models. The median follow-up duration was 55 months (interquartile range: 35–76). Patients with a low score (≤2) had a 17.2% recurrence rate, whereas patients with a high score (3) had a 50.0% recurrence rate. Patients with a low score had longer disease-free survival (DFS) than those with a high score in log-rank test (p=0.026). In multivariate Cox regression analysis, a high score was a significant predictor of poor DFS in patients with rectal cancer after CCRT treatment (hazard ratio=4.89, 95% confidence interval: 1.11–21.50, p=0.036). This simple endoscopic scoring approach is helpful for predicting prognosis of patients with rectal cancer after treatment with CCRT.

S3192 Doxycycline: An Unlikely Culprit for Gastric Mucosal Injury

Introduction: Tetracyclines, such as doxycycline, are well-described in literature as a culprit for pill-induced esophagitis. Although rare, there may be a connection to gastric mucosal injury. Given the ubiquitous use of doxycycline, it is worthwhile to investigate the association. Case Description/Methods: A 61 year-old man presented with syncope, melena and acute anemia. Esophagogastroduodenoscopy (EGD) showed erosions and two clean-based ulcers (5 mm and 8 mm) in the antrum (Figure 1A and 1B). Retroflexed view of the incisura revealed fibrinous deposition on the cardia and fundus that was unable to be washed off despite irrigation and suctioning (Figure 1C). Biopsies demonstrated idiosyncratic features consistent with doxycycline-induced injury, with reactive erosions and superficial fibrinoid vascular degeneration. The patient had been taking doxycycline 100 mg daily for three years for chronic dermatomyositis. He was started on pantoprazole twice daily to facilitate mucosal healing and an alternative agent in place of doxycycline was recommended. Follow-up EGD ten weeks later showed normal gastric mucosa without evidence of prior injury. Biopsies were not obtained given healed appearance of the tissue (Figure 1D). Discussion: While doxycycline is widely recognized as an etiology of pill esophagitis, its effect on the gastric mucosa has been highlighted in very few cases. Doxycycline-induced gastric injury is described endoscopically as a superficial, erythematous mucosal erosion with occasional deep ulceration in the antrum or body. It presents with an adherent, light-colored and fibrinous plaque. Histologically, there are reactive changes in the foveolar cells with mucin loss and serrated gastric pits. There is also a distinct pattern of superficial eosinophilic capillary vascular degeneration, which is associated with superficial mucosal necrosis and scattered fibrinous microthrombi (Figure 1E). Clinically, patients present with nonspecific symptoms of epigastric pain or substernal burning. If history reveals doxycycline use, an EGD can be helpful. In most cases, once the offending agent is removed, the symptoms do resolve. It is unclear why only a small subset with doxycycline ingestion develops gastric injury, although we postulate that the incidence is likely under-recognized. It remains unknown how long-term or repeated usage affects the gastric mucosa, as patients on this medication do not routinely undergo endoscopic evaluation in the absence of overt upper gastrointestinal symptoms.Figure 1.: Endoscopic images showing diffuse necrosis of stomach.

Behcet's Disease Unmasked after Heart Transplantation

<h3>Introduction</h3> Behcet's disease (BD) is an autoinflammatory, multisystem vasculitis. Cardiac involvement is rare and clinical diagnosis is challenging. We present a case of Behcet's disease diagnosed after heart transplantation (HTx). <h3>Case Report</h3> A 24 year-old female with a history of morbid obesity, unprovoked venous thrombus and nonischemic cardiomyopathy with biventricular systolic dysfunction who presented in cardiogenic shock. Echocardiogram revealed an EF of 10-15%, LVEDD of 4.9cm, LV apical thrombus and severe RV dysfunction. Right heart catheterization showed RA 14 PA 38/23 (29) and wedge of 24 with calculated cardiac index of 1.6 and PAPi of 1.07. She required VA-ECMO and IABP followed by HM3 BiVAD as bridge to HTx. The explanted heart revealed myocyte hypertrophy and severe interstitial fibrosis, no evidence of vasculitis or inflammation. At 10 months post-transplant she presented with new painful oral and genital ulcers. Prednisone at this time was 2.5 mg daily. Complete infectious and viral work-up was negative and there was no resolution with empiric valganciclovir and antibiotics. Pathergy test was positive and treatment for BD was initiated with dapsone 150 mg twice daily and steroids. Two months, later after tapering steroids, she presented with hematochezia. Colonoscopy revealed multiple, deep, clean-based ulcers in the terminal ileum, a classic finding in BD (Figure 1). <h3>Summary</h3> BD presents a diagnostic challenge in the absence of classic clinical findings. Initial presentation is often thrombosis, which was the case in this patient years preceding her severe heart failure. Cardiac involvement is rare and to our knowledge has only been described in case reports with predominantly LV dysfunction. Long term morbidity and outcomes in BD and HTX is not well known. This is the first case reported of BD unmasked after HTx and describing biventricular failure as a possible manifestation of BD.

A197 COLONIC AMYLOIDOSIS: A CAUSE OF RECURRENT HYPOVOLEMIA

Abstract Background Systemic amyloidosis is a multi-organ disease characterized by abnormal extracellular protein deposition. The most common type is primary (AL) amyloid relating to underlying plasma cell dyscrasias. Other major variants include secondary (AA) amyloid from chronic inflammation, dialysis related amyloid (DRA) with β2-microglobulin, and heritable protein mutations. Management of the underlying disorder can limit further organ damage; however, no definitive treatment exists for familial causes. While uncommon, gastrointestinal involvement is variable and can cause asymptomatic infiltration, liver impairment, bleeding, or chronic diarrhea. Aims To discuss an unusual case of gastrointestinal amyloidosis as a cause of recurrent diarrhea and hypovolemic shock. Methods The patient records were examined, and a review of the literature was performed. Results An 87-year-old male with dementia, coronary artery disease and end stage renal disease from PCKD presented in hypovolemic shock. He had a two-week history of gradual onset, non-bloody, watery diarrhea with up to 20 bowel movements daily. He denied fever, sick contacts, travel, or recent antibiotic use. He had previously foregone endoscopy for a remote history of self-resolved hematochezia. Examination was notable for an uncomplicated inguinal hernia. Labs showed an anion-gap metabolic acidosis but no leukocytosis. He initially received iv hydration, vasopressors, and empiric antibiotics. CT showed diffuse wall thickening of the terminal ileum, colon and rectum with relative sigmoid sparing concerning for enterocolitis. Stool culture grew C. albicans, but C. difficile toxin and Ova and Parasite PCR were negative. He clinically improved with loperamide and was discharged only to be readmitted four days later with recurrent diarrhea and hypovolemia. Repeat cultures were negative. Endoscopy showed diffuse well-demarcated clean-based ulcers and colonic edema. Biopsies excluded viral causes but showed a classic appearance of apple-green birefringence on Congo red staining suggesting amyloid deposition. Raised light chain immunoglobulins and lysozyme on proteomic analysis indicated either AL or a heritable amyloid but excluded AA and DRA. Full diagnostic criteria for AL were not met as free light chain ratio was preserved without clear monoclonality. While his diarrhea again improved, next-of-kin opted for palliative care due to repeated admissions for delirium and generalized deterioration. Conclusions This case was indicative of atypical AL amyloidosis versus a rare lysozyme mutation involving renal and GI systems. AL amyloid has a classic appearance on special stains and mass spectrometry that distinguishes it from most subtypes, however, given elevated lysozyme levels further genetic analysis is needed to guide management. In the appropriate clinical context, gastrointestinal amyloidosis can be considered as a rare cause of recurrent unexplained diarrhea. Funding Agencies None

S3573 Duodenal Diverticulum Masquerading as a Perforated Abdominal Viscus

INTRODUCTION: Diverticula are defined as sac-like protrusions that may occur anywhere along the gastrointestinal tract, from the esophagus to the large intestine. Small bowel diverticula are less common than their counterparts in the large intestine, and are usually diagnosed incidentally. Here we present a case of a duodenal diverticulum that was incidentally found after abdominal imaging suggested a bowel perforation. CASE DESCRIPTION/METHODS: The patient is a 50-year-old male with a medical history of Diabetes Mellitus, Gastroesophageal reflux disease, and Hepatitis C Virus who presented to the emergency department (ED) complaining of upper abdominal pain for one day that was associated with nausea and one episode of non-bloody vomiting. On physical examination the abdomen was soft with mild epigastric tenderness and regular bowels sounds. Notable workup in the ED included a computed tomography (CT) scan of the abdomen, which showed pneumoperitoneum in the right upper quadrant with a possible focal irregularity of the duodenal wall concerning for perforation (Figure 1). The patient was then admitted under impression of perforated abdominal viscus. The patient was started on empiric intravenous antibiotics and morphine for pain control. On his first day the patient’s symptoms improved and were out of proportion with the imaging findings. The gastroenterology service was then called to perform an endoscopy for further evaluation. This was done and showed a large non-bleeding diverticulum in the duodenal bulb (Figure 2). Additionally there was a large clean-based ulcer distal to the diverticulum with no evidence of active bleeding. The patient was then started on intravenous proton pump inhibitor twice daily. On the next day the patient reported resolution of symptoms, was tolerating per oral feeding and was discharge home vitally stable. DISCUSSION: Duodenal diverticula were first described by Chomel in 1710. Since then their true prevalence has been difficult to calculate due to most cases causing little to any symptoms. Regarding diagnosis, most cases are found incidentally. It is estimated that they are found in 6% of upper gastrointestinal series, 9–23% of endoscopically, and in 22% of autopsies. Considering most of these diverticula are incidental findings with no clinical symptoms, they are managed conservatively. Interventions are only indicated if the patient develops sequela, such as infection, small bowel obstruction or small intestinal bacterial overgrowth (SIBO).Figure 1.: CT of the abdomen showing free air in the right upper quadrant (blue arrow).Figure 2.: Endoscopy showing large duodenal diverticulum.

The clinical significance of simple endoscopic scoring of patients with rectal cancer after concurrent chemoradiotherapy.

109 Background: Neoadjuvant concurrent chemoradiotherapy (CCRT) is an effective treatment option for patients with rectal cancer. In this study, we investigated the clinical efficacy of simple endoscopic scoring of patients with rectal cancer after CCRT. Methods: Between July 2008 and October 2015, medical records including endoscopic imaging from 41 patients with rectal cancer who received CCRT were retrospectively reviewed. Two expert gastroenterologists reviewed the endoscopic images and assigned scores from 0–3 according to post-CCRT findings. The scoring criteria were as follows: 0 = scar without marginal elevation; 1 = clean-based ulcer without marginal elevation; 2 = clean-based ulcer with marginal elevation; 3 = non-clean-based ulcer. We evaluated image scores to predict long-term outcomes using Kaplan-Meier curves and Cox regression models. Results: The median follow-up duration was 55 months (interquartile range: 35–76). Patients with a low score (≤2) had a 17.2% recurrence rate, whereas patients with a high score (3) had a 50.0% recurrence rate. Patients with a low score had longer disease-free survival (DFS) than those with a high score in log-rank test (p = 0.026). In multivariate Cox regression analysis, a high score was a significant predictor of poor DFS in patients with rectal cancer after CCRT treatment (hazard ratio = 4.89, 95% confidence interval: 1.11–21.50, p = 0.036). Conclusions: This simple endoscopic scoring approach is helpful for predicting prognosis of patients with rectal cancer after treatment with CCRT.

The clinical significance of simple endoscopic scoring of patients with rectal cancer after concurrent chemoradiotherapy.

Neoadjuvant concurrent chemoradiotherapy (CCRT) is an effective treatment option for patients with rectal cancer. In this study, we investigated the clinical efficacy of simple endoscopic scoring of patients with rectal cancer after CCRT. Between July 2008 and October 2015, medical records including endoscopic imaging from 41 patients with rectal cancer who received CCRT were retrospectively reviewed. Two expert gastroenterologists reviewed the endoscopic images and assigned scores from 0-3 according to post-CCRT findings. The scoring criteria were as follows: 0= scar without marginal elevation; 1= clean-based ulcer without marginal elevation; 2= clean-based ulcer with marginal elevation; 3= non-clean-based ulcer. We evaluated image scores to predict long-term outcomes using Kaplan-Meier curves and Cox regression models. The median follow-up duration was 55 months (interquartile range: 35-76 months). Patients with a low score (≤2) had a 17.2% recurrence rate, whereas patients with a high score [3] had a 50.0% recurrence rate. Patients with a low score had longer disease-free survival (DFS) than those with a high score in log-rank test (P=0.026). In multivariate Cox regression analysis, a high score was a significant predictor of poor DFS in patients with rectal cancer after CCRT treatment (hazard ratio =4.89, 95% confidence interval: 1.11-21.50, P=0.036). This simple endoscopic scoring approach is helpful for predicting prognosis of patients with rectal cancer after treatment with CCRT.

3142 Atypical Presentation of an Upper Gastrointestinal (GI) Bleed Manifesting as Extranodal Involvement of Diffuse Large B-Cell Lymphoma (DLBCL) Diagnosed in a Community Setting

INTRODUCTION: Diffuse large B-cell lymphoma (DLBCL) is the most common type of Non-Hodgkin's Lymphoma (NHL), with 5.4 new cases diagnosed per 100,000 persons as of 2016. There is a male predominance, with an average age of 64.2. One extranodal site involves the GI tract, predominantly the stomach. Commonly seen are mucosa associated lymphoid tissue lymphomas and DLBCL. The majority of cases present at stage III/IV, with 40% presenting as local involvement. Here we present an unusual case of extranodal DLBCL in a patient presenting with dysphagia and an upper GI bleed. CASE DESCRIPTION/METHODS: An 85 year-old female presented for evaluation of dysphonia, ongoing for several months. The patient complained of bilateral submandibular adenopathy, dysphagia, trouble breathing, and a 15 pound weight loss over two weeks. Computed tomography of the neck revealed a nasopharyngeal mass in the left (L) nasopharynx extending into the nasal cavity, right (R) nasopharynx, and eroding into the skull. Additionally, bilateral necrotic cervical lymph nodes and L supraclavicular adenopathy were also seen. Histologic sample was consistent with DLBCL, non-germinal center type. Fluorescence in-situ hybridization was negative for MYC rearrangement, t(8:14), t(4:18), and Epstein Barr Virus, but indeterminate for BCL6 rearrangement. She was staged IIA and underwent radiation therapy without chemotherapy. During treatment, the patient was admitted for evaluation of an upper GI bleed associated with dysphagia, fatigue, and progressive weakness. She underwent an esophagogastroduodenoscopy with findings showing Los Angeles class A esophagitis, large, inflammatory nodular tissue within the lesser curvature of the stomach with associated linear ulcerations, multiple punctate ulcers throughout the gastric body and antrum, duodenitis, and a small, clean-based ulcer in the duodenal sweep. Histology of the gastric mass revealed an atypical clonal lymphoid infiltrate involving the gastric mucosa, suggestive of DLBCL, with clonal immunoglobulin heavy chain gene rearrangement. DISCUSSION: This case represents an atypical presentation of an upper GI bleed that is the result of extranodal involvement of DLBCL. An atypical presentation like this should have lymphoma in the differential for those with a history. Treatment is dependent upon the extent of disease, usually starting with the regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone therapy. If left untreated, this disease can progress rapidly and prove fatal.

3235 Black Stomach: A Rare Clinical Entity in a Patient With Recurrent Primary Sclerosing Cholangitis With Cirrhosis

INTRODUCTION: Acute gastric necrosis is rarely encountered given the stomach's rich vascular distribution and collateral circulation. Reported causes of gastric necrosis include gastric outlet obstruction, intrathoracic herniation, ingestion of caustic substances, anorexia nervosa and bulimia, and systemic hypotension. We present a case of “black stomach” secondary to persistent shock in the setting of end-stage liver disease. CASE DESCRIPTION/METHODS: A 33-year-old female with a history of primary sclerosing cholangitis status post orthotopic liver transplant in 2017 was initially hospitalized for pneumonia complicated by worsening graft function (MELD 38). Liver biopsy confirmed recurrent PSC with cirrhosis. Her course deteriorated after developing multiple episodes of coffee-ground emesis and melena requiring pressors. Initial EGD showed mild portal hypertensive gastropathy and two, 5 mm clean-based ulcers in the gastric antrum. No esophageal varices were visualized. Despite medical therapy, her melena and hypotension continued, leading to acute renal failure requiring CVVH. Repeat EGD two days later showed an adherent clot in the gastric fundus and severe portal hypertensive gastropathy with spontaneous oozing. Despite supportive measures, she continued to have melena. A third EGD showed a large blood clot in the fundus that was unable to be removed. Friable mucosa was noted throughout, as well as a non-healing, clean-based antral ulcer. Two days later, a fourth EGD revealed mucosa in the fundus and proximal body that appeared black and diffusely necrotic with sloughing of mucosa, with normal mucosa distally. The patient was not a candidate for IR embolization, TIPS procedure or surgery. One week later, she decompensated and died of septic shock from VRE bacteremia. DISCUSSION: Our case demonstrates that persistent gastric ischemia in the setting of shock and underlying end-stage liver disease results in gastric necrosis noted endoscopically over the course of a week. It is possible that the patient's underlying decompensated graft cirrhosis predisposed her to developing segmental gastric necrosis and “black stomach” in the area supplied and drained by the left gastric vessels, which can be affected by shock and portal congestion. Despite aggressive measures and supportive care, gastric necrosis carries a high morbidity and mortality. Therefore, a high index of clinical suspicion is required to make an early diagnosis in order to guide potential therapeutic interventions in such critically ill patients.

2541 Cryptosporidial Colonization of a Peptic Ulcer in a Healthy Patient—Random Occurrence or a Risk Factor?

INTRODUCTION: The incidence of Cryptosporidial enteritis (CE) has recently risen in the USA due to water and foodborne outbreaks. It has a self-limited course in healthy hosts. We describe a case of a healthy female with history of gastric bypass surgery who presented with a one-month history of voluminous watery diarrhea and vomiting. This was a rare case of CE diagnosed by endoscopic biopsies of two anastomotic peptic ulcers that were colonized by Cryptosporidium spp. CASE DESCRIPTION/METHODS: 57-year-old female with a history of GERD, iron deficiency anemia, and Roux-en-y gastric bypass complicated by jejunal strictures with revision of the gastro-jejunal anastomosis, presented with a 7-day history of vomiting and crampy epigastric abdominal pain. She recently returned from a two-week vacation to Latin America. Upon arrival, she experienced progressively worsening voluminous watery diarrhea associated with intermittent melanotic stools followed by frequent episodes of non-bilious, non-bloody vomiting along with reduced oral intake. Abdominal exam revealed hyperactive bowel sounds with tenderness to deep palpation of the epigastrium. Her hemoglobin dropped from a baseline of 11.2 g/dL to 9.1 g/dL. CT scan of the abdomen with contrast showed inflammation around the gastro-jejunostomy site. Blood and stool cultures were negative. Upper endoscopy revealed a 1 cm and 2 cm clean-based ulcers with a deep crater at the anastomotic site. Biopsy demonstrated spherical bluish-purple organisms, 2-5 µm in diameter on hematoxylin and eosin, Gomori Methanamine Silver Nitrate and Masson's trichrome stains. They were suggestive of Cryptosporidium, and the patient was diagnosed with CE. Patient's immunodeficiency workup was unremarkable. Patient's symptoms resolved with a three-day course of Nitazoxanide 500 mg twice per day. DISCUSSION: CE is a significant cause of chronic diarrhea in both healthy and immune-compromised individuals, thus stands as a key differential in those presenting with persistent voluminous diarrhea. The modified acid-fast stain carries only 50% sensitivity to this protozoan, and diagnosis is often missed on routine stool ova and parasite tests. Novel diagnostic modalities have proven useful in identifying this protozoan in stool samples. We report the first case documenting Cryptosporidium colonization of anastomotic site peptic ulcers with complete resolution of symptoms following a short course of Nitazoxanide.

1614 Asymptomatic Intestinal Spirochetosis With Colonic Ulcerations

INTRODUCTION: Both the origin and commensal or pathogenic nature of intestinal spirochetes (IS) in humans are poorly understood. Colonization is predominantly found in homosexual males and in HIV patients.1 Homosexual males have shown colonization rates up to 20.6-62.5% leading scientists to hypothesize that IS could be sexually transmitted.2 Colonization can be associated with severe clinical symptoms like persistent diarrhea and rectal bleeding, especially in children.3 Therefore, a greater understanding of clinical presentation and risk factors is needed. CASE DESCRIPTION/METHODS: A 51-year-old asymptomatic male with compensated alcoholic cirrhosis presented for a screening colonoscopy. He denied NSAID use and a personal or family history of inflammatory bowel disease. Colonoscopy revealed multiple clean-based ulcers in the cecum and ascending colon. Histologic examination of the specimens on H&amp;E stain revealed colonic mucosa with focal, acute inflammation and microorganisms consistent with spirochetes. No granulomas, crypt architectural distortion, or dysplasia were identified. The fuzzy, basophilic fringe-like microorganisms were positive for GMS and PAS stains and negative for FITE stain. The findings were consistent with IS and the patient was treated with metronidazole. DISCUSSION: The clinical significance of IS in humans is not well defined. Presentation may vary from asymptomatic to causing chronic diarrhea, rectal bleeding, abdominal pain, and weight loss. IS can be associated with immunodeficiency, alcoholism and drug abuse, poor hygiene, sexual practices, and concomitant bowel content stasis. Pathology reveals presence of spirochetes in the brush border. Transmission electron microscopy reveals spirochetes attached to enterocytes with associated shortened or depleted microvilli. Often endoscopy in IS-infected patients is normal, but in this rare presentation of intestinal spirochetosis, ulcerations of colonic mucosa were noted. Metronidazole is an effective treatment.4-5

1889 Endoscopic Closure of Gastrocolic Fistula Using Hemostatic Clips: A Novel Approach

INTRODUCTION: Traditionally, surgery is the mainstay of treatment for gastrointestinal fistulas; more recently, however, therapeutic endoscopic stent placement is being explored for high-risk patients. Successful endoscopic closure of these fistulas using hemostatic clips offers the possibility of an alternative, viable approach for patients who are nonsurgical candidates and may benefit from noninvasive endoscopic interventions. CASE DESCRIPTION/METHODS: An 82-year-old male with history of peptic ulcer disease, alcohol abuse, and Billroth II gastrojejunostomy &gt;20 years ago was admitted due to bloody diarrhea. Physical examination was unremarkable except for melena. Laboratory testing revealed a hemoglobin level of 4.6g/dL. After resuscitation, upper endoscopy was performed and the patient was found to have a mucosal perforation at the anastomotic site with an adjacent clean-based ulcer (A, B) without active bleeding. The mucosal defect was closed using four hemostatic clips (C). Abdominal CT scan later confirmed a gastrocolic fistula successfully closed with clip placement (D). The patient’s symptoms resolved; his remaining hospital course was uncomplicated. DISCUSSION: Intervention during endoscopy precluded the need for surgical intervention in an elderly patient who would otherwise have been a poor surgical candidate. To the best of our knowledge, this is the first use of hemostatic clip placement for closure of a gastrocolic fistula.

1954 Hyperplastic Polyp: A Rare Case of Recurrent Iron Deficiency Anemia

INTRODUCTION: Hyperplastic polyps are the most common polyps accounting for 17% of all the gastric polyps. Most polyps are asymptomatic but may present with anemia, bleeding or gastric outlet obstruction. Here, we are reporting a case of large benign hyperplastic polyp presenting with iron deficiency anemia. CASE DESCRIPTION/METHODS: A 69-year-old male with a history of chronic back and neck pain and GERD was evaluated for chronic iron-deficiency anemia, treated multiple times with oral and IV iron supplements. The patient had been taking NSAIDs for chronic pain. On labs, patient hemoglobin of 9 with a low iron profile. The patient was scheduled for screening colonoscopy and EGD to further investigate anemia. On EGD patient had a large polypoid lesion about 25 mm in size in the prepyloric antrum extending into the duodenal bulb, likely cause of iron-deficiency anemia. There was also a small superficial clean-based ulcer on the antral lesion. Colonoscopy showed small internal hemorrhoids. Patient was discharged home on PPI and counseled to stop NSAIDs. Pathology report of the biopsies showed fragments of a benign hyperplastic polyp, negative for H pylori. The patient was afterward referred to interventional endoscopist for EUS and polyp excision. DISCUSSION: A hyperplastic gastric polyp is usually an incidental finding on upper endoscopy. With a prevalence of 6.35%, they are seen equally in elderly males and females in their 60s–70s. Hyperplastic polyps are believed to occur as a result of the reactive and inflammatory hyperproliferation of gastric foveolar cells, and Helicobacter pylori are believed to be the precursor. Diagnosis is usually made based on the results of endoscopy and subsequent biopsy of the suspicious area for the histological exam. On endoscopy, they appear as an area of hyperemia with a smooth dome-shaped surface, mostly in the antral area. As the size increases, they become pedunculated and the surface gets eroded resulting in chronic blood loss and anemia. Rarely, gastric outlet obstruction occurs when the large polyps prolapse though the pylorus. Since large polyps (&gt;2 cm) are associated with carcinoma in 0.6%–2% cases, it is important for the pathologist to look carefully for any dysplastic foci and carcinomatous changes in the tissue specimen. Once the diagnosis of hyperplastic polyp is confirmed, treatment consists of endoscopic resection of any polyp measuring &gt;1 cm in size and eradication of H.pylori, when present.

2684 Gastric Sarcoidosis

INTRODUCTION: Sarcoidosis is a systemic inflammatory disease of unclear etiology. It can involve almost any organ in the body, with pulmonary involvement being the most common. Gastrointestinal (GI) involvement is rare (0.1- 0.9% of all cases) with symptomatic gastric sarcoid, even more rare (with a handful of cases reported in the literature). We present a case of a patient who developed symptomatic gastric sarcoidosis. CASE DESCRIPTION/METHODS: A 48-year old African American male was seen in the GI clinic for a 5-year history of diffuse intermittent abdominal pain. The patient had a known diagnosis of severe sarcoidosis diagnosed 10 years ago. He had multiple organs effected including lungs (Restrictive disease on PFTs), liver (bridging fibrosis with hyalinized nodular sclerosis on the biopsy) and skin involvement (resulting in chronic pruritus treated with Plaquenil). The patient also had a history of H.pylori with multiple small clean-based ulcers in the gastric corpus and erythematous duodenopathy diagnosed on esophagogastroduodenoscopy (EGD) 11 years ago. Following that he completed the triple antibiotic regimen. The patient for the last four months reported severe periumbilical pain with several ED visits. He underwent 3 colonoscopies over the course of the last 5 years, which were unremarkable. EGD was repeated, which showed multiple nonbleeding duodenal ulcers with gastric biopsy showing non-caseating granulomas. His H.Pylori stain was negative on this occasion. At this time a diagnosis of gastric sarcoidosis was made. The patient was placed on a proton pump inhibitor with an escalation in the dose of his systemic steroids resulting in resolution of his symptoms. DISCUSSION: Most cases of gastric sarcoidosis are initially asymptomatic. The most commonly reported symptom is epigastric pain. Other symptoms include nausea, vomiting, hematemesis, melena, and weight loss. Due to the non-specific nature of these reported symptoms, making the diagnosis purely on clinical history is difficult, and a high index of suspicion is needed to make the diagnosis. Endoscopically it can present with ulceration or a diffuse linitis plastica like the involvement of stomach. Pathology is key to diagnosis and shows non- caseating granulomas. Asymptomatic patients do not require treatment though for symptomatic patients recommended treatment is a combination of proton pump inhibitors with systemic steroids. Marvin A. Chinitz et al. reported symptom improvement in 66% of gastric sarcoid patients with systemic steroids.

Prophylactic endoscopic coagulation to prevent delayed post-EMR bleeding in the colorectum: a prospective randomized controlled trial (with videos)

Post-EMR bleeding (PEB) is the most common adverse event after EMR. However, there are no established endoscopic methods for the prevention of PEB. This study aimed to investigate whether prophylactic endoscopic coagulation (PEC) using coagulation probes reduces the incidence of overall delayed PEB. We performed a randomized controlled study of patients undergoing EMR for large (≥10mm) sessile lesions and laterally spreading tumors. Patients were randomized 1:1 to the EMR with coagulation group (n=285) or EMR (control) group (n= 285). Immediate bleeding during colon EMR or clean-based ulcer afterEMR was excluded. Clinically significant PEB was defined as bleeding requiring endoscopic hemostasis, hospitalization, or a decrease in the hemoglobin level >2 g/dL. A total of 569 patients were analyzed. The incidence of overall PEB was significantly lower in the EMR with coagulation group than in the control group (12.6% [36/285] vs 18.7% [53/284], P= .048). However, this waslargely because of a reduction in minor bleeding. There was no difference in clinically significant PEB (1.8% [5/285] vs 3.2% [9/284], P= .276). Rectal location was a risk factor associated with overall PEB (odds ratio, 1.256; 95% confidence interval, 1.12-1.41; P< .001). Although this study found reduced PEB with prophylactic cautery of visible vessels, this was largely because of a reduction in minor bleeding with no benefit observed for clinically significant bleeding. Overall, PEB was more frequent with rectal lesions. (Clinical trial registration number: KCT0000779.).

Disseminated cryptococcosis in Crohn\u2019s disease: a case report

BackgroundGastrointestinal (GI) cryptococcosis is rarely reported. Most cases were diagnosed during evaluation of comorbid conditions, incidental findings, or postmortem. Here, we present a case of Crohn’s disease with gastrointestinal cryptococcosis that resembled exacerbation of Crohn’s disease.Case presentationA 64-year-old woman with Crohn’s disease (CD) was referred to Siriraj Hospital due to worsening of abdominal pain and watery diarrhea for 2 weeks. The dose of immunosuppressive agents was increased for presumed exacerbation of CD. Pathologic examination of tissue obtained from polypoid mass at ileocecal valve and multiple clean-based ulcers at cecum revealed active ileitis and colitis with multiple round shape organisms with capsule, which was compatible with Cryptococcus species. Disseminated cryptococcosis was diagnosed due to gastrointestinal involvement and presumed pulmonary involvement regarding the presence of an oval-shaped cavitary lesion on chest X-ray and computed tomography of the lung. Patient was successfully treated with amphotericin B followed by fluconazole with satisfactory result.ConclusionEarly diagnosis of gastrointestinal cryptococcosis in Crohn’s disease is difficult due to the lack of specific symptoms and sign or mimicking an exacerbation of Crohn’s disease. Seeking for other site of involvement in disseminated cryptococcosis including lung or central nervous system as well as detection of serum cryptococcal antigen would be helpful for early diagnosis and management.

Rapidly Developing Mixed Acinar-Neuroendocrine Carcinoma of the Stomach

We present a case of a rare, rapidly developing mixed acinar-neuroendocrine carcinoma of the stomach that presented with acute melena and symptomatic iron-deficiency anemia in a patient with history of hepatitis C cirrhosis and lymphoma. A 71-year-old man with history of stage IIIA diffuse large B-cell lymphoma (treated 17 years ago), chronic hepatitis C and compensated cirrhosis (SVR achieved after completing Harvoni therapy 2 years ago) who presented with subacute dyspnea and weakness which began one week after experiencing 8 days of tarry stools associated with epigastric pain. Labs revealed new iron-deficiency anemia with Hgb 8.0 g/dL (previously 12.7) and ferritin of 6 ng/mL. Diagnostic EGD revealed a 3cm clean-based ulcer in the lesser curvature of the gastric body (Image 1 and 2). Notably, 14 months prior to this presentation, an EGD for varices surveillance did not reveal any gastric pathology. Histology of the ulcer edge revealed poorly differentiated neuroendocrine carcinoma, favoring small cell type. Patient underwent distal subtotal gastrectomy with D2 lymphadenectomy and Roux-en-Y reconstruction. Surgical pathology confirmed the diagnosis of poorly-differentiated mixed acinar-neuroendocrine carcinoma (T3N1M0). Immunohistochemistry stained positive for: chromogranin (diffuse); synaptophysin (+ patchy); chymotrypsin (patchy). Ki-67 proliferation index was 70%. Mixed acinar-neuroendocrine carcinomas are rare gastrointestinal tract tumors that typically originate from the pancreas. To our knowledge, this subtype of tumor has been described originating from the stomach in only 5 previous instances. Histologically, both acinar and endocrine components constitute a significant proportion (>25%) of the neoplasm. The progression of this neoplasm was quite rapid as there was no evidence of gastric pathology 14 months prior to diagnosis. Our patient underwent successful gastrectomy and completed 2 [of 4 planned] cycles of platinum-based chemotherapy. He has had no evidence of disease recurrence as of 11 months post-operatively.2671_A Figure 1 No Caption available.2671_B Figure 2 No Caption available.

The Great Masquerader: Syphilis Presenting as Rectal Ulcer in the Setting of Neurosyphilis

Primary and secondary syphilis infections are on the rise. Between 2015 and 2016, cases in persons aged 65 and older increased by 50%. Anorectal infections are uncommon and have a varying clinical and endoscopic presentation, making diagnosis difficult. This is a case of rectal syphilis manifested as gastrointestinal (GI) bleeding, in the setting of neurosyphilis. A 73-year-old male with a history of prostate cancer status post radiation treatment complicated by radiation proctopathy was admitted for hematochezia. Prior to admission, the patient presented to ophthalmology for blurred vision. Based on the ophthalmologic exam and a positive reactive rapid plasma reagin (1:64), he was diagnosed with neurosyphilis. The patient later reported having unprotected receptive anal intercourse with multiple partners. A colonoscopy revealed multiple clean ulcers with surrounding erythema in the rectum, up to 15 cm from the anal verge, deemed to be the source of bleeding. Other notable findings included patchy areas of serpiginous vessels in the distal rectum consistent with radiation proctopathy. Targeted biopsies were collected around the ulcers. The pathology revealed submucosal perivascular cuffing with spirochete-like elements, which in the setting of positive RPR, were consistent with rectal syphilis. He was treated with two weeks of intravenous penicillin and GI bleeding resolved. A repeat flexible sigmoidoscopy two months after treatment showed no evidence of active ulcerations. While the incidence of syphilis is increasing, anorectal syphilis remains an uncommon presentation with a paucity of cases. Presenting symptoms and endoscopic findings of rectal syphilis appear to be variable and non-specific. Prior reports of rectal syphilis included rectal masses, mimicking cancer, or rectal ulcers, concerning for inflammatory bowel disease. In this case, radiation proctopathy was a confounding factor for the etiology of GI bleeding until the diagnosis of rectal syphilis was made. This case highlights a unique GI manifestation of syphilis in the setting of neurosyphilis, manifested as rectal ulcers.1617_A Figure 1. Multiple rectal ulcers.1617_B Figure 2. Clean-based ulcers next to serpiginous vessels.1617_C Figure 3. Surveillance endoscopic image with healed ulcers.