INTRODUCTION:We previously reported the results of tofacitinib induction therapy in the prospective multisite US real-world Tofacitinib Response in Ulcerative Colitis registry. We now assessed patient-reported outcomes (PROs) and predictors of success during tofacitinib maintenance therapy. METHODS:Tofacitinib Response in Ulcerative Colitis included 103 patients with refractory ulcerative colitis (UC); 67% had failed ≥ 2 biologics. Patients reported the Simple Clinical Colitis Activity Index (SCCAI), Patient-Reported Outcome Measurement Information System measures for anxiety, depression, social satisfaction, and adverse events between weeks 8 and 52 using a web-based system. Paired t test and P for trend were used to compare changes in PRO measures over time. Bivariate analyses and logistic regression models were used to determine factors associated with response (SCCAI <5) or remission (SCCAI <2) at week 52. RESULTS:Of 103 patients, 82.5% entered the maintenance phase and 43.7% remained on tofacitinib at week 52. Tofacitinib de-escalation to 5 mg BID occurred in 15% of patients. At week 52, 42.7% and 31.1% of all patients reported an SCCAI <5 and SCCAI ≤2, respectively. Normalization of bowel frequency, rectal bleeding, and urgency occurred in 79%, 61%, and 48% of patients remaining on maintenance therapy. Social satisfaction improved significantly ( P < 0.001), while anxiety and depression scores only numerically improved. No consistent predictors for tofacitinib long-term treatment efficacy were identified, and safety findings were consistent with the known safety profile of tofacitinib. DISCUSSION:Tofacitinib is an effective maintenance therapy in patients with refractory UC. Dose reductions infrequently occurred during maintenance. Unmet needs in UC maintenance include improvement of urgency and psychosocial factors (NCT03772145).

Abstract Background Tofacitinib is an oral, small-molecule JAK inhibitor for the treatment of ulcerative colitis (UC). Using a novel electronic reporting tool, we aimed to prospectively describe the onset of tofacitinib efficacy during induction therapy in a real-world study. Methods Patient-reported outcome data (PROs) including the simple clinical colitis activity index (SCCAI), PRO Measurement Identification Systems (PROMIS) measures, and adverse events were collected daily for the first 14 days and at day 28 and 56. Paired t tests and P for trend were utilized to compare changes in SCCAI over time. Bivariate analyses and logistic regression models were performed to describe response (SCCAI <5) and remission (SCCAI ≤2) by clinical factors. Results Of all included patients (n = 96), 67% had failed ≥2 biologics, and 61.5% were on concomitant steroids. Starting at day 3, PROs showed significant and persistent decline of the mean SCCAI (−1.1, P < 000.1) including significantly lower SCCAI subscores for stool frequency (−0.3; P < .003), bleeding (−0.3; P < .0002) and urgency (−0.2; P < .001). Steroid-free remission at day 14, 28, and 56 was achieved in 25%, 30.2%, and 29.2% of patients, respectively. Neither prior biologics nor endoscopic severity were independently predictive of response or remission in multivariate models. Numeric improvements in all PROMIS measures (anxiety, depression, social satisfaction) were seen through day 56. Rates of discontinuation due to adverse events were low. Conclusions In this prospective real-world study, tofacitinib resulted in a rapid and persistent improvement in UC disease activity PROs. The safety findings were consistent with the established safety profile of tofacitinib.

A 35-year-old woman with a history of lung transplantation presented with diarrhea and postprandial abdominal pain. Her immunosuppressive medications included tacrolimus, prednisone, and mycophenolate mofetil. Mycophenolate mofetil was empirically changed to azathioprine without leading to improvement. Stool pathogen panel was negative, and blood cytomegalovirus level was undetectable using polymerase chain reaction. The patient underwent esophagogastroduodenoscopy, which showed numerous raised white plaques scattered throughout the duodenum (Figure 1). Colonoscopy showed similar plaques and nodules throughout the colon and terminal ileum (Figure 2). Pathology of the lesions revealed Histoplasma infection, characterized by marked expansion of the lamina propria by histiocytes in fi ltrated with Histoplasma capsulatum organisms visible by periodic acid-Schiff stain (Figure 3). Immunostains for cytomegalovirus, herpes simplex virus, and adenovirus were negative. Urine and serum Histoplasma antigen tests were positive. The patient was treated with isavuconazole and had resolution of symptoms within 1 month. H. capsulatum , the causative agent of histoplasmosis, is

Background: Specialty infusion and self-injectable biologic drugs for the treatment of inflammatory bowel disease (IBD) are high-cost medications. When administered to hospital-admitted patients, these medications are not reimbursed on an individual basis but rolled into a per diem payment by most payers in the United States (US). Therefore, choosing to administer these medications in the inpatient setting may reveal negative financial implications for some health care institutions. Selecting an alternative site of care to administer these medications during the clinical management process may lead to cost savings. Objective: Review the clinical necessity of inpatient specialty biologic administrations for the treatment of IBD to identify and quantify potential cost saving opportunities. Methods: Using patient medical records at a US academic medical center, we retrospectively identified inpatient administrations of specialty infusion and self-injectable biologic medications for IBD treatment from June 1, 2016 to May 31, 2017. Guided by a standardized form, an evaluation team consisting of 3 of the investigators determined the clinical necessity of each specialty biologic medication administration within the inpatient setting. Costs and reimbursement rates for administration in both the inpatient and outpatient settings were procured and tabulated. Results: Seventeen inpatient specialty biologic administrations for IBD during the 12 month study period were identified. Of these, 11 administrations were given for the treatment of Crohn's disease (CD) and 6 for ulcerative colitis (UC). The evaluation team determined that 65% of these administrations were clinically necessary as inpatient administrations, and that 35% were not. The sum of the wholesale acquisition costs (WAC) for clinically necessary inpatient biologic administrations totaled $54 737, and the WAC for those administrations deemed not clinically necessary totaled $43 702. Further analysis of administration events revealed that the institution could have realized an estimated $13817 in additional revenue above the cost of the drug if eligible inpatient biologic administrations had been received in the institution's outpatient clinic setting instead. Conclusion: Administering specialty biologic drugs for the treatment of IBD in the care setting best aligned with existing reimbursement structures may lead to institutional cost savings.

Introduction: Inflammatory bowel disease (IBD) dysplasia surveillance protocols call for a representative number of untargeted or 'random' biopsies to increase the odds of detection of 'invisible' or flat dysplasia. In current practice, the benefit of untargeted surveillance biopsies over a targeted surveillance approach with or without adjunctive chromoendoscopy is unclear. Our study retrospectively examines outcomes of endoscopic dysplasia surveillance at a single institution and compares yields of targeted and untargeted biopsies for the detection of dysplasia from both chromoendoscopy (CE) and traditional high definition white light (HD-WLE) examinations. Methods: A retrospective chart review of all IBD patients (ulcerative colitis, Crohns, and indeterminate colitis) undergoing dysplasia surveillance at a single center between 1/2015 and 10/2021 was performed. Patients younger than 18 and those with a pre-existing diagnosis of dysplasia or cancer were excluded. All surveillance exams done for each patient during the study period were reviewed. Presence or absence of endoscopic and microscopic inflammation, use of targeted biopsies or polypectomy, number of untargeted biopsies, and presence or absence of dysplasia from both targeted and untargeted biopsies were noted for both HD-WLE and CE exams. All instances of ‘invisible’ dysplasia were confirmed by a second reviewer following manual review of endoscopy and pathology reports. Results: 200 IBD patients (96 UC, 94 Crohns, 10 indeterminate) underwent 492 endoscopic surveillance procedures (199 CE, 293 WLE). 11,094 untargeted biopsies and 242 targeted biopsies or polypectomies were performed. Invisible dysplasia was detected 9 times for a yield of 0.06% per untargeted biopsy. 37.2% of endoscopically targeted biopsies or polypectomies were positive for dysplasia (39.6% CE, 33.9% WLE) and accounted for 90.9% of dysplasia detected during the study period. Conclusion: Random biopsies are a low yield means for detection of dysplasia, accounting for < 10% of dysplastic lesions observed during the study period. No patients with ‘invisible’ dysplasia had PSC, opted for colectomy, or had evidence of progression on follow up examination. Given the high yield of targeted biopsy and polypectomy, and low likelihood of missed high risk lesions if untargeted biopsies are not performed, it may be reasonable to emphasize high quality endoscopic examination and targeted biopsies/polypectomies and to de-emphasize the role of untargeted random biopsies.

Introduction: Sarcina ventriculi is an anaerobic, gram-positive coccus that grows in acidic environments including the stomach. Case reports have implicated its role in causing gastric ulcers, emphysematous gastritis, and gastric perforation. There has been only one case report in the literature on S. ventriculi causing gastric mass lesion to our knowledge.1 Here we report a rare case of S. ventriculi infection causing a pyloric mass leading to gastric outlet obstruction (GOO). Case Description/Methods: A 65-year-old male with a past medical history of Barrett’s esophagus and tobacco use presented to the emergency department with progressive worsening of abdominal pain, nausea, and vomiting. Esophagogastroduodenoscopy (EGD) performed locally showed a small pyloric channel ulcer with traversable pyloric narrowing. Gastric biopsies showed no significant pathology and were negative for H. pylori. Abdominal computed tomography showed circumferential nodular wall thickening of the pylorus and a dilated, fluid-filled stomach consistent with GOO (Figure 1A). No pneumatosis or perforation of the stomach was noted. EGD was repeated one month later at our institution due to worsening symptoms and revealed near complete obstruction of the pyloric channel by a protruding friable pyloric mass (Figure 1B). Biopsies of the mass revealed S.ventriculi organisms in the background of reactive gastropathy, with no evidence of malignancy (Figure 1C, D). A nasojejunal feeding tube was placed and the patient was treated with ciprofloxacin and metronidazole for 7 days along with pantoprazole twice daily. Repeat EGD performed two weeks later showed near complete resolution of the mass lesion. Discussion: S. ventriculi infections are associated with delayed gastric emptying.1 It is unclear if the infection is a result of the poor gastric emptying or the cause of it. In our case the patient presented with an obstructing pyloric mass due to reactive gastropathy in the setting of S. ventriculi infection, and repeat EGD after treatment with antibiotics and a proton pump inhibitor showed near complete healing of the mass and ulcer but persistent poor gastric emptying in the absence of obstruction. We report this case to expand on the paucity of literature regarding S. ventriculi gastrointestinal infections and to raise awareness of it presenting as a gastric mass lesion.Figure 1.: A: Abdominal CT axial section showed circumferential nodular wall thickening of the pylorus (yellow arrows) and distended fluid-filled stomach. B: EGD showed circumferential, protruding, friable mass at the pylorus causing near obstruction of the pyloric channel. C: Low-power view (50×) of the pyloric mass revealed polypoid reactive gastropathy with S. ventriculi organisms present on the mucosal surface. D: High-power view (300×) of the green frame area in (C) demonstrating S. ventriculi organisms with characteristic thick cell walls and arrangement in tetrads.

Introduction: Autoimmune enteropathy (AIE) is a rare cause of small intestinal villous atrophy. This condition is more frequently diagnosed in children, with only a handful of case series describing its presentation in adults. We present a case of adult-onset AIE in which diagnosis was made based on its unique endoscopic and histologic findings. Case Description/Methods: A 54 year-old previously healthy woman was hospitalized with profuse watery diarrhea, abdominal pain, and weight loss of six months duration. Stool testing was negative for infection. Inflammatory markers were mildly elevated. Computer tomography imaging showed hyperenhancement of the small bowel consistent with enteritis, without evidence of stricture or abscess. She underwent esophagogastroduodenoscopy which revealed diffuse edema of the duodenal mucosa with villous blunting and cracked-earth appearance (Figure A, B). She had normal appearing mucosa of the distal small bowel and colon on video capsule endoscopy and colonoscopy, respectively. Pathology from duodenal biopsies showed chronic active duodenitis characterized by marked villous blunting, reduced goblet and Paneth cells, neutrophilic and lymphocytic infiltration of deep crypts, and basal layer apoptosis (Figure C). Similar findings were seen in random ileal biopsies, while random colon biopsies were normal. Anti-enterocyte antibodies and anti-transglutaminase antibodies were negative. Patient was treated for AIE with intravenous methylprednisolone and she required supplemental parental nutrition. Within days of initiating steroids, her diarrhea had improved and she was transitioned to oral prednisone. Several days later she was weaned off parenteral nutrition and stable for discharge with plans to introduce a thiopurine at follow-up. Discussion: AIE should be suspected in a patient with chronic diarrhea, signs of severe malabsorption, and characteristic histologic features in absence of other causes of villous atrophy such as Celiac disease. Specific histologic features of AIE include absence of goblet cells and Paneth cells and presence of crypt apoptotic bodies in intestinal biopsies. Development of autoantibodies against enterocytes are associated with this condition, but not required for diagnosis. Steroids are the mainstay of therapy and have variable effect. We aim to raise awareness of AIE, as the rarity of this condition can make its diagnosis elusive.Figure 1.: 1A. EGD shows villous blunting and edema of duodenal mucosa. Figure 1B. EGD shows cracked-earth appearance of duodenal mucosa. Figure 1C. Duodenal biopsy reveals chronic active duodenitis characterized by marked villous blunting, reduced goblet and Paneth cells, neutrophilic and lymphocytic infiltration of deep crypts, and basal layer apoptosis.

Introduction: Tofacitinib is a Janus kinase inhibitor approved for moderate to severe ulcerative colitis (UC). TOUR is the first real-world registry with prospectively collected data of tofacitinib efficacy in treating UC clinical symptoms in the first 8 week induction period. Methods: A total of 96 patients initiated tofacitinib at 15 academic and community GI practices. Clinical information and Mayo endoscopic scores were obtained. Patient reported outcome (PRO) data were collected using a daily electronic system for the first 14 days and at weeks 4 and 8. NIH PROMIS measures of social satisfaction, anxiety and depression were collected. Disease activity was measured using the simple clinical colitis activity index (SCCAI). A score of ≤2 met criteria for remission; a score of <4 with a decrease by >1.5 points met criteria for response. Specific adverse events were collected. Paired t tests and P for trend compared changes in SCCAI at day 3, 7, 14, week 4 and week 8 to baseline. Outcomes were stratified by number of prior anti-tumor necrosis factor (anti-TNF) agents and Mayo endoscopic score at baseline. Bivariate analyses were performed using chi-squared test statistic. Results: Of the 96 initiating tofacitinib, 95% had failed ≥ 1 anti-TNF and 67% had failed≥ 2 biologics, 61.5% were on steroids and 81.3% had active disease. A total of 96% and 84% of patients remained on tofacitinib through week 4 and 8, respectively. The mean SCCAI of patients at baseline was 5.6, day 3 (4.6), day 7 (3.8), day 14 (3.3), week 4 (3.4), week 8 (3.2), P < 0.001 for each, P for trend < 0.001. Among those active at baseline, response was achieved in 49.3%, 50.8% and 47.4% of patients at week 2, 4 and 8; remission was achieved in 37.3%, 43.1% and 38.6% respectively. At week 8, there were no significant differences in response or remission in patients with <2 vs ≥ 2 previous biologic therapies (P = 0.81) or severe inflammation on endoscopy (Mayo 3 vs Mayo 2 or 1) (P = 0.14). Improvements in all PROMIS measures were seen through week 8. A total of 3.1% of patients developed shingles, 10.4% had an infection requiring antibiotics. Fifteen patients (16%) discontinued tofacitinib in the first 8 weeks. Of these 15 patients, 33% (n = 5) underwent colectomy. Conclusion: In this prospective real-world study of the effectiveness and safety of tofacitinib in a refractory UC population, tofacitinib is associated with rapid response of various PROs within 1 week. No new safety signals were recognized.Figure 1.: Simple Clinical Colitis Activity Index over Induction in the TOUR Real-World CohortTable 1.: Characteristics of Patients in the TOUR Real-World Cohort (n = 96)

INTRODUCTION: Tofacitinib is a Janus kinase inhibitor approved for moderate to severe ulcerative colitis (UC). Prospective real-world data on tofacitinib in UC patients are limited. Using an electronic system to evaluate patient reported outcomes (PROs) in real time, we measured clinical response and PROs during the induction phase of tofacitinib. METHODS: An initial 65 patients initiating tofacitinib were recruited from 13 academic and community gastroenterology practices. Demographic information, disease and medication histories were obtained. Patients completed PRO surveys on days 1–14, and at week 6, 10 and 14. Outcome data included the simple clinical colitis activity index (SCCAI), and PRO measurement information system (PROMIS) measures of depression, anxiety and social satisfaction. A score of < 4 with a decrease by >1.5 points is considered response. PROMIS measures are calibrated using a T score (mean of the US population equal to 50, standard deviation (SD) of 10). A higher PROMIS score equates to more of the measure (higher scores worse for depression, anxiety and better for social satisfaction). RESULTS: A total of 62/65 (95%) completed electronic PRO data through week 6. Mean age was 38.4 (SD 14.9), 61.5% were male, mean disease duration was 9.6 years and 58.5% were on concomitant steroids at baseline. Mean disease activity at baseline (n = 65) was active (SCCAI of 5.6 (SD 3.2)), with reductions in mean disease activity to SCCAI 3.1 on day 14, 2.7 on week 14 (Figure 1). At the time of first in-person clinical visit (week 2–6), only 18.2% remained on steroids. Among patients initiating tofacitinib without concomitant corticosteroid use (n = 27), early reductions in SCCAI were seen (mean SCCAI 5.4 at baseline, reduced to SCCAI 3.8 by day 4). Improvements in all PROMIS measures (anxiety, depression, social satisfaction) were seen through week 14 (Figure 2). A total of 54.2% met criteria for response at day 14, with 52.2% at week 6. CONCLUSION: Real time electronic PRO data capture provided the ability to assess cessation of steroids and time to response to tofacitinib via important PRO outcomes. Tofacitinib was associated with a rapid response in this ongoing prospective multi-center real-world cohort, independent of steroid use. Continued enrollment and long-term data, planned through week 30, will enhance our understanding of UC.Figure 1Figure 2

Several techniques for PEG-J tube placement have been described, commonly requiring fluoroscopic guidance and/or fixation of the jejunostomy tube (J-tube) into the small intestine. We describe a modified technique for placing jejunostomy tubes under direct visualization through a PEG with the use of ultra-thin endoscopes and steel guidewire. A retrospective study at a single tertiary academic center evaluating patients who underwent PEG-J placement between 2010 and 2020. All PEG tubes were placed with a pull-through technique. The Olympus GIF-N180 endoscope was advanced through the PEG to the jejunum and a Savary-Gilliard guidewire was used for placement of the J-tube extension. Fifty-eight patients underwent PEG-J placement (median age 61 years; women 52%). Surgically altered gastric anatomy was observed in 11 patients (19%). Median procedure time was 44 min for new PEG-J tube placement (range 26–103) and 20 min for placement of a J-tube extension through an existing PEG tube (range 9–86) or gastrostomy tract. Technical success rate was in 100%. Sixty-two repeat procedures were performed for J-tube exchange in 27 patients (46%, range 1–9 per patient), of which 51 procedures (82%) were done using the same technique. The most common indication for tube replacement was tube dysfunction (63%, n = 39). The median procedure time for tube exchange was 20 min (range 2–62). No major adverse events were encountered. PEG-J tubes can be placed effectively, rapidly, and safely using an ultra-thin caliber endoscope and a stiff steel wire through the PEG tube or mature gastrostomy site, precluding the need for fluoroscopy or oral access. J-tubes can be easily replaced utilizing the same technique.

BACKGROUND: Tofacitinib is a janus kinase (JAK) inhibitor approved for use in ulcerative colitis (UC) in 2018. Prospective real-world data on tofacitinib use in UC patients are limited. We aimed to develop a unique electronic system to obtain patient reported outcomes (PROs) from patients initiating tofacitinib. We aimed to measure response to therapy on days 1-14, anxiety, depression and social satisfaction. METHODS: An initial sample of 23 patients were recruited from 8 academic and community gastroenterology practices. Complete demographic information, disease and medication histories were obtained. Patients completed PRO surveys on days 1-14 after initiation of tofacitinib via a unique electronic self-report system. Outcome data included the simple clinical colitis activity index (SCCAI), and PRO measurement information system (PROMIS) measures of depression, anxiety and social satisfaction. A score of ≤2 on SCCAI was considered to be remission; a score of <4 with a decrease by > 1.5 points was considered to be response. PROMIS measures were calibrated using a T score metric with the mean of the standard US population equal to 50, standard deviation (SD) of 10. A higher PROMIS score equates to more of the measure (higher scores worse for depression, anxiety and higher scores better for social satisfaction). RESULTS: A total of 23/23 (100%) completed electronic PRO data daily in the first 14 days after initiation of tofacitinib. Mean age of the population was 40.7 (SD 18.1), 56.5% were male, mean disease duration was 11.3 years and 73.9% were on concomitant steroids. Mean disease activity at baseline (n = 23) was active (SCCAI of 4.0), with reductions in mean daily disease activity to a nadir of SCCAI 2.2 on day 14. Among patients initiating tofacitinib without concomitant corticosteroid use (n = 6), similar early reductions in SCCAI were seen (mean SCCAI 4.0 at baseline, reduced to 1.8 by day 4). Improvements in all PROMIS measures (anxiety, depression, social satisfaction) were seen in the population by day 7. A total of 8/12 (66.7%) with active disease at baseline met criteria for response at day 14. CONCLUSION(S): Real time electronic PRO data capture directly from UC patients is feasible. This ongoing prospective multi-center real-world cohort demonstrated an excellent patient adherence to the online platform in the first 14 days. Initial data suggest a rapid response to tofacitinib in this sample, with improvements in disease activity, depression, anxiety and social satisfaction. Continued enrollment and long-term follow-up data from this cohort will enhance our knowledge of tofacitinib use in real world UC populations.

BACKGROUND & AIMSParenteral methotrexate induces clinical remission but not endoscopic improvement of mucosal inflammation in patients with ulcerative colitis (UC). We performed a randomized, placebo-controlled trial to assess the efficacy of parenteral methotrexate in maintaining steroid-free response or remission in patients with UC after induction therapy with methotrexate and steroids.METHODSWe performed a 48-week trial, from February 2012 through May 2016, of 179 patients with active UC (Mayo score of 6-12 with endoscopy subscore ≥ 2) despite previous conventional or biological therapy. The study comprised a 16-week open label methotrexate induction period followed by a 32-week double-blind, placebo-controlled maintenance period. Patients were given subcutaneous methotrexate (25 mg/wk) and a 12-week steroid taper. At week 16, steroid-free responders were randomly assigned to groups that either continued methotrexate (25 mg/wk, n = 44) or were given placebo (n = 40) until week 48. We compared the efficacy of treatment by analyzing the proportion of patients who remained relapse free and were in remission at week 48 without use of steroids or other medications to control disease activity.RESULTSNinety-one patients (51%) achieved response at week 16, and 84 patients were included in the maintenance period study. During this period, 60% of patients in the placebo group (24/40) and 66% in the methotrexate group (29/44) had a relapse of UC (P = .75). At week 48, 30% of patients in the placebo group (12/40) and 27% of patients in the methotrexate group (12/44) were in steroid-free clinical remission without need for additional therapies (P = .86). No new safety signals for methotrexate were detected.CONCLUSIONSParenteral methotrexate (25 mg/wk) was not superior to placebo in preventing relapses of UC in patients who achieved steroid-free response during induction therapy. ClinicalTrials.gov, Number: NCT01393405.

Duodenal diverticula are an rare cause of upper GI bleeding. Endoscopic therapy has been increasing utilized due to its minimally invasive nature. However, it must be used with extreme caution considering high risk of perforation as we depict in our case. An 80-year-old female was admitted to the hospital with melena. EGD showed bleeding angiectasia in fundus that was treated with argon plasma coagulation (APC) to achieve hemostasis. A repeat EGD failed to show any other sites of active bleeding. A Technetium-99m (Tc-99m) bleeding scan showed bleeding from 3rd part of duodenum. Mesenteric angiography with embolization of a branch of gastroduodenal artery was performed. A repeat Tc-99m scan showed active bleeding at the same site. General surgery team was consulted; however, repeat endoscopic intervention was requested. With localization of bleeding likely to a duodenal diverticulum and recent embolization of an artery, the procedure was considered to be of extremely high risk. This was explained to the family and surgical team. EGD showed multiple small bowel diverticula in the duodenum and jejunum. An actively bleeding telengieactasia was localized and treated with APC inside a diverticulum in the 3rd part of duodenum (Fig. 1 A/B). Mild ischemia was also seen in 2nd part of duodenum from the embolization procedure performed earlier. The patient did not develop any further episodes of bleeding. However, she developed retroperitoneal perforation that was successfully managed medically (Fig. 2). Duodenal diverticula are usually found as periampullary lesions in the second portion of the duodenum. They constitute an uncommon cause of upper GI bleeding being responsible for only 0.14% of such cases. Until recently, surgical management with diverticulectomy was utilized to treat such patients. However, endoscopy is being increasing utilized with recent advancements. Localization of bleeding is challenging as seen in our patient. There is no gold standard endoscopic therapy. There is high risk of perforation due to thinner wall of duodenal diverticulum. Even after being extremely careful and utilizing safest option of APC, perforation was witnessed. We managed it medically. We can conclude that endoscopic management for duodenal diverticulum with any modality is a reasonable first option only in patients with high risk for surgery. This case was unique in that the diverticulum was big enough to enter with the scope to treat which is not usually the case.Figure: Active bleeding in duodenum.Figure: Retroperitoneal Perforation.