History Of NSAID Use Research Articles

Profile of gastroduodenal perforation patients admitted in a rural tertiary care hospital: An observational cross-sectional study.

Gastro-duodenal perforation is a common surgical emergency that remains a formidable health burden worldwide with significant morbidity and mortality. Ulcer disease remains the most common cause of gastro-duodenal perforation. Diagnosing the presence of H. pylori can help eradicate the infection from the community at large and thereby reduce the chances of gastro-duodenal perforation. To assess the clinical presentation of gastro-duodenal perforation patients and to evaluate the detection of Helicobacter pylori infection by available investigations. A descriptive observational study was conducted among 80 patients presenting with clinical features suggestive of gastro-duodenal perforation and confirmed by clinical, radiological basis and operative findings admitted at a rural tertiary care hospital during 2019-2020. Detailed history was taken from the patient/party, clinically examined, and blood/tissue samples were investigated. The patients were managed with standard treatment modality in the studied institute. Data were collected, compiled, and entered MS Excel and analyzed using appropriate software. Descriptive analysis was done in the form of proportion for categorical variables, mean or median for continuous variables. Cases of gastro-duodenal perforations were more among middle to later age of life, mostly affecting married male patients hailed from rural area and unskilled workers. History of intake of spicy food, prolonged starvation, history of NSAID use were common among them. Majority of the patients had history of pain abdomen in the past suggesting of PUD and history of taking variety group of acid reducing agents. Most of them presented with epigastric pain, vomiting, abdominal distension along with other signs of peritonitis. Obliteration of liver dullness and free gas under right dome of diaphragm was also noted in large proportion among them. Majority of cases were found positive for H. pylori on Histology (85%), followed by rapid urease test (RUT) (80%) and a positivity of 72.5% and 68.8% on serum IgG and IgA antibody respectively. Rapid Urease Test was more sensitive as well as specific in diagnosing of H. pylori than antibody detection test. Early detection of H. pylori infection and treatment with potent anti H. pylori therapy postoperatively has been found to be adequate.

The Effects of COVID-19 on Clinical Outcomes of Non-COVID-19 Patients Hospitalized for Upper Gastrointestinal Bleeding during the Pandemic.

This study aims to investigate the effects of COVID-19 on clinical outcomes of non-COVID-19 patients hospitalized for upper gastrointestinal bleeding (UGIB) during the pandemic. A retrospective review is conducted. We recruited patients with UGIB admitted during the pandemic’s first wave (April 2020 to June 2020), and the year before the pandemic. The outcomes between the two groups were compared using propensity score matching (PSM). In total, 60 patients (pandemic group) and 460 patients (prepandemic group) are included. Patients admitted during the pandemic (mean age of 67 ± 14 years) had a mean Glasgow–Blatchford score of 10.8 ± 3.9. They were older (p = 0.045) with more underlying malignancies (p = 0.028), had less history of NSAID use (p = 0.010), had a lower platelet count (p = 0.007), and had lower serum albumin levels (p = 0.047) compared to those admitted before the pandemic. Esophagogastroduodenoscopy (EGD) was performed less frequently during the pandemic (43.3% vs. 95.4%, p < 0.001). Furthermore, the procedure was less likely to be performed within 24 h after admission (p < 0.001). After PSM, admissions during the pandemic were significantly associated with decreased chances of receiving an endoscopy (adjusted odds Ratio (OR), 0.02; 95% CI, 0.003–0.06, p < 0.001) and longer hospital stay (adjusted OR, 2.17; 95% CI, 1.13–3.20, p < 0.001). Additionally, there was a slight increase in 30-day mortality without statistical significance (adjusted OR, 1.92; 95% CI, 0.71–5.19, p = 0.199) and a marginally higher rebleeding rate (adjusted OR, 1.34; 95% CI, 0.44–4.03, p = 0.605). During the pandemic, the number of EGDs performed in non-COVID-19 patients with UGIB decreased with a subsequent prolonged hospitalization and potentially increased 30-day mortality and rebleeding rate.

Weil syndrome coincident with upper gastrointestinal bleeding.

A 48 year old male was referred to our center due to a gastrointestinal bleeding with melena secondary to a Forrest IIb gastric ulcer treated endoscopically. Physical examination revealed bilateral conjunctival suffusion, bradypsychia, and asterixis. Epidemiological history included a trip to Dominican Republic two weeks before, presenting later a flu-like syndrome. He had no history of NSAID use. Laboratory tests showed a normocytic anemia, leukocytosis with neutrophilia, acute renal failure, severe hyponatremia, a predominant direct hyperbilirubinemia, hyperamylasemia, and mild coagulopathy (Table 1). An abdominal ultrasound was performed, with no pathological findings, and a chest-abdominal computed tomography (CT), bilateral diffuse ground glass pulmonary opacities and pleural effusion, mild hepatomegaly, and peritoneal and gastrohepatic ligament lymphadenopathy, with no signs of acute pancreatitis. A second look upper endoscopy revealed a Forrest III gastric ulcer. Gastric biopsies results ruled out malignancy and Helicobacter pylori infection. Due to his recent travel history combined with his characteristic signs and symptoms a clinical diagnosis of leptospirosis was made and empirical antibiotic therapy with meropenem was started. The serology for Leptospira was positive (IgG 1/1600) and antibiotic therapy was de-escalated to ceftriaxone with clinical and analytical remission on day five of his hospital stay with complete radiological resolution at 6 months.

Sarcina ventriculi: A Rare Case of Life-Threatening Perforated Gastric Ulcer and Review of Literature

Sarcina ventriculi is a gram-positive anaerobic bacterium reported rarely in patients with a history of gastrointestinal surgery and delayed gastric emptying. Sarcina has been implicated in the development of gastric ulcers, emphysematous gastritis, and gastric perforation. So far, less than 30 cases of Sarcina isolated from gastric specimens have been reported, including 3 cases associated with life-threatening illness: emphysematous gastritis and gastric perforation. Herein, we report a case of a 58-yearold woman with history of gastric surgery who presented for evaluation of persistent gastric pain and incurable ulcer. She underwent total gastrectomy, and the resected stomach demonstrated a perforated ulcer with the presence of Sarcina microorganisms. We also report a second case of a 56-year-old woman with history of NSAID use who presented with gastric outlet obstruction. The gastric biopsy identifi ed concurrent Helicobacter pylori and Sarcina. Given Sarcina‘s association with emphysematous gastritis and gastric perforation, its identifi cation on gastric biopsies should be clearly stated in pathology reports and, depending on the clinical scenario, prompt clinicians to add adjunctive antimicrobials to anti-ulcer therapeutic regimens.

1844 A Case of Idiopathic Esophageal Ulceration as Initial Presentation of Acquired Immune Deficiency Syndrome

INTRODUCTION: Esophageal ulceration (EU) is most frequently caused by gastroesophageal reflux disease. However, immunocompromised individuals are particularly susceptible to EU caused by infections including herpes simplex virus (HSV), cytomegalovirus (CMV), and candida species. Furthermore, patients with acquired immunodeficiency syndrome (AIDS) can also develop idiopathic EU even in the absence of infection. CASE DESCRIPTION/METHODS: A 30-year-old male with no significant past medical history presented with 6 months of profound weight loss, odynophagia, dysphagia, and chest pain. He had no history of NSAID use. Symptoms had persisted despite trials of proton pump inhibitors, H2 antagonists, and sucralfate. His physical exam was notable for cachexia and bi-temporal wasting. Esophagogastroduodenoscopy revealed two large hemi-circumferential cratered distal esophageal ulcers separated by a mucosal bridge. Endoscopic ultrasound demonstrated an isoechoic mass in the lower third of the esophagus measuring 1.2 cm in thickness, obliterating the wall layer architecture, along with three enlarged gastro-hepatic lymph nodes. Pathology demonstrated granulation tissue with fibro-inflammatory debris and was negative for malignancy, HSV, and CMV. Fine needle aspiration of one of the enlarged lymph nodes was also negative for malignancy. A contrasted computed tomography scan of the chest, abdomen, and pelvis did not reveal any additional findings. Laboratory evaluation was most notable for worsening leukopenia (WBC count: 3000 cells/μL) and anemia (Hgb: 9.9 g/dL). Further history revealed unprotected sexual encounters with multiple females in the last 10 years. Subsequent workup demonstrated a positive human immunodeficiency virus (HIV) antibody screen with a CD4 count of 44 cells/µL. Patient was ultimately diagnosed with idiopathic EU from AIDS and was initiated on highly active antiretroviral therapy. DISCUSSION: While EU is a common complication in patients with AIDS, it is normally associated with infections such as CMV and HSV. Idiopathic EU in these patients are rarer and typically found in those with CD4 cell counts less than 100 cells/µL. Our case was unique in that the patient's development of large EU was his initial presentation of AIDS. In these cases, establishing the correct diagnosis and ruling out malignancy is important as misdiagnosis can significantly alter treatment plan and prognosis. This case further highlights the necessity for HIV testing in patients who present with idiopathic EU.

2019 Lower Gastrointestinal Bleeding Due to Sevelamer-Induced Colitis

INTRODUCTION: Acute lower gastrointestinal (GI) bleeding is uncommonly due to medication induced-colitis, reported in less than 6% of all lower GI bleeds. Identifying medications that may cause GI bleeding is particularly important in chronically ill patients at high risk for morbidity and mortality. A commonly used medication in patients with advanced renal disease is sevelamer, a phosphate binder in renal failure patients. CASE DESCRIPTION/METHODS: A 53-year-old female with end-stage renal disease presented with hematochezia for 2 days. She notes dark black stools for two weeks followed by rectal bleeding. Her past history is notable for a renal transplantation in 2008 with graft failure requiring hemodialysis. She has no history of NSAID use and her prior screening colonoscopy showed no evidence of colitis. Her medication list was extensive and included sevelamer and cinacalcet. The patient was hemodynamically stable. Initial labs showed a hemoglobin of 6.0 g/dl, baseline was 8.0-9.0 g/dl. She was resuscitated with intravenous fluids and received 2 units of blood. Next, the patient’s upper endoscopy showed gastric erythema only with no stigmata of recent bleeding. Her colonoscopy showed a macroscopically normal appearing colon however random biopsies revealed expansion of the lamina propria with significant population of increased eosinophils. Several crystals were embedded within the colonic mucosa and submucosa resembling sevelamer crystals. Based on the pathology, she was diagnosed with sevelamer-induced colitis and this medication was discontinued. Follow-up at 3 months showed the patient remained asymptomatic without further GI bleeding. DISCUSSION: Sevelamer is a common medication used in renal failure patients. It is a resin that binds and prevents absorption of phosphate within the GI tract and has been shown to cause GI issues such as nausea, vomiting and diarrhea. Rarely it can crystalize, become embedded in the GI tract and ulcerate and cause bleeding. A few case reports have described rectosigmoid ulceration and pseudotumor presentation of sevelamer induced colitis.1,2 Understanding and recognizing the potential for sevelamer-induced colitis is important with such a widely used medication.

1918 A Case of Recurrent Pneumatosis Intestinalis and Portal Venous Gas

INTRODUCTION: Mesenteric ischemia (MI) is caused by inadequate blood flow through the mesenteric vessels resulting in ischemic bowel. The most serious cases cause gangrenous bowel, leading to pneumatosis intestinalis (PI) and portal venous gas (PVG), often an ominous sign. CASE DESCRIPTION/METHODS: This is a case of a 63-year-old male who presented to the hospital with hematemesis and severe anemia. After massive transfusion, an EGD revealed actively bleeding gastric ulcers, requiring serial EGDs for successful control of bleeding. A CT revealed gastric distention with thickening of the duodenum and bilateral femoral vein opacities, later confirmed as deep vein thromboses. An IVC filter was subsequently placed, as he was not a candidate for anticoagulation. The patient was subsequently discharged on oral pantoprazole. Of note, there was no history of NSAID use or evidence of H. pylori. Repeat EGD 2 months later noted mild gastritis, but no ulcers were seen. A screening colonoscopy at the time noted only diverticulosis. He was continued on pantoprazole. 3 months later he presented to the hospital with acute onset nausea, vomiting, and diarrhea. A CT revealed PI at the gastric fundus, as well as PVG. An infectious work-up was negative, lactate was normal, and his symptoms resolved quickly. A subsequent repeat CT noted resolution of the PVG and reduction in PI. He represented to the hospital 1 month later again with nausea, vomiting, and diarrhea. A CT noted small bowel dilatation with air fluid levels, PI at the esophagus, stomach, and jejunum, and significant PVG. The initial lactate level was mildly elevated and his symptoms resolved quickly after bowel decompression. A subsequent CTA noted a significant reduction in PVG without evidence of vascular occlusion. A follow up EGD showed diffuse subepithelial hemorrhages without any evidence of recurrent ulcers. A subsequent CTE noted a thrombus above the IVC filter and an evolving hepatic infarction. He was asymptomatic at the time, however, he was admitted to the hospital for anticoagulation. He has since remained on warfarin without any recurrence of symptoms, PI, or PVG. A follow-up CTA showed a full resolution of venous thromboses. DISCUSSION: Previous case reports have described the development of PI and PVG secondary to underlying MI. This case highlights an example of MI secondary to an increase in the resistance of mesenteric blood flow due to venous thromboses. When investigating IP and PVG, underlying venous thromboses should always be considered.

Frequency of Celiac Disease in Children with Peptic Ulcers.

The aim of the present study is to investigate the frequency of celiac disease in children with peptic ulcers and to compare it with that of non-celiac peptic ulcers in terms of clinical and laboratory values. Upper gastrointestinal endoscopy was performed in 1769 patients at the Department of Pediatric Gastroenterology, The Faculty of Medicine, Cukurova University, Turkey, between January 2012 and January 2017. These cases consisted of subjects presenting with various GIS symptoms and indicated for endoscopy (with chronic diarrhea, delayed growth and development, abdominal pains, GIS bleeding, etc.). The levels of immunoglobulin A (IgA) serum anti-tissue transglutaminase antibodies, IgA anti-endomysial antibodies (EMA), and IgA serum were estimated in the patients with peptic ulcers. Celiac disease was diagnosed with serology, endoscopy, and histopathology in 250 (14%) of all cases undergoing endoscopy. Peptic ulcers were diagnosed in 74 patients (4.2%) of all cases undergoing endoscopy. tTGA and EMA (+) levels were determined in 22 (29%) of the 74 patients with peptic ulcers, and then the presence of peptic ulcers was investigated in the upper gastrointestinal system using gastrointestinal endoscopy, followed by histopathological confirmation of celiac disease. HP infection was present in 14 (63%) of the patients with celiac disease and in 23 (44%) of non-celiac peptic ulcers; the difference was not statistically significant (p = 0.12). In the total ulcer group, 10.8% (8/74) of patients with celiac peptic ulcers were negative for HP infection, whereas 21% (8/37) of HP-negative patients with ulcers had celiac disease. There exists a high risk of celiac disease in children with peptic ulcers. We thus recommend celiac disease to be investigated, particularly in HP-negative patients with peptic ulcers but with no history of NSAID use.

Posterior Gastric Perforation in Liberia: A Case Report and Review of the Literature

Background: The incidence of posterior gastric perforation worldwide is low; the literature has no previous record of its occurrence in Liberia. The diffuse symptoms of a perforated posterior gastric ulcer, delay by patients before they present to hospital, and the lack of skilled personnel and facilities in Liberia to diagnose and treat this condition increase the mortality associated with posterior gastric perforation. Objective: To report the first case of posterior gastric perforation encountered in Liberia. Materials and Method: Case report. Case Presentation/Report: A 44 year old male was referred to John F. Kennedy Memorial Hospital (Liberia’s principal teaching hospital) with a diagnosis of gastritis after six days of worsening epigastric pain. He had a history of NSAID use for a chronic leg and foot ulcer. Physical examination revealed a moderately distended, markedly tender abdomen characterized by guarding, rigidity and low-pitched bowel sounds. Patient was resuscitated with intravenous fluids, antibiotics and analgesics. An emergency exploratory laparotomy subsequently performed revealed a large collection of purulent peritoneal fluid, a 3 × 4 cm perforation on the posterior wall of the stomach and a 3 × 2.5 cm perforation of the transverse mesocolon. The perforations were repaired and the patient recovered satisfactorily. Conclusion: Though relatively rare and associated with a high morbidity and mortality, this case report shows that the paucity of reported cases of posterior gastric perforation may also be attributable to lack of specialist staff with capacity for clinical diagnosis and surgical intervention in a resource poor setting. Identifying patients with gastric perforation and having the skill to repair the perforations significantly enhance the clinical outcome.

Risk Factors of Peptic Ulcer Disease in Khorramabad city, Southwest of Iran : A Case Control Study

Background & Aims: The aim of this study is to determine the demographic characteristics, endoscopic findings, morphological and pathological characteristics of the ulcer in patients with peptic ulcer disease, and also to compare the odds ratio of exposure to possible risk factors of disease in patients with peptic ulcer disease and a healthy control group in Khorramabad city. Materials & Methods: In the present case-control research, all the patients who had referred to a digestive tract sub-specialist's office in Khorramabad in 2015 and had been diagnosed with peptic ulcer disease via endoscopy and pathological studies were enrolled in the study. The control group were selected from among those referring to the ophthalmological and dermatological clinics of the Shahid Rahimi Hospital. The data collection instrument used in this study was a questionnaire that included items related to the demographic information of the patients, and also questions regarding the patient's background as to smoking, alcohol consumption, NSAIDs or corticosteroids usage, and peptic ulcer disease among first-degree relatives. The same data were collected from the members of the control group. All patients signed written consent forms regarding their participation in the study. The data were analyzed using SPSS software. Findings: In the present study, 60 patients with PU and 60 subjects as the control group were examined. Most patients were between 30 and 44 years old (60%). In the present study, the mean age of patients with PUD was 35 +/- 10.6 years. Among all patients with PUD, three (5%) had gastric ulcer and 57 (95%) had duodenal ulcer. Anatomical location of all ulcers (3 cases) was in the small curvature of stomach and 47.4% of duodenal ulcers were in the anterior wall. In multivariate analysis, which was performed using logistic regression, there was a statistically significant relationship among history of NSAID use (PV = 0.047) and smoking history (PV = 0.042) with occurrence of PUD. Conclusion: In general, peptic ulcer is considered as a common and serious problem all around the world and 5 to 10% of the population are affected by PU during their life. Therefore, the incidence and complications of this disease can be significantly prevented by correcting risk factors and lifestyle, as well as by improving the health conditions of the community.

Modelling the Development of Precancerous Polyps: Utility of Social History, Comorbidities, FOBT/FIT Testing, and NSAID Use

Introduction: Studies have attempted to ascertain the risk factors (RF) for developing colorectal cancer (CRC), but few have attempted to elucidate the causes of precancerous (PC) polyposis. Early detection of PC polyps is essential to prevent progression to CRC. Evaluation of RF such as family history (FH), tobacco and alcohol abuse, and glycemic control may be useful in determining which patients may be more likely to have PC polyps. Methods: Data were collected on 4200 patients at the Robley Rex VAMC in Louisville, Ky. 2758 were excluded based on exclusion criteria: diagnosis of IBD and pre-existing malignancies, birth prior to 1948, poor bowel preparation, and lack of pathologic/histologic data from first colonoscopy. Of the 1442 patients included in the study, a subset had: FOBT or FIT testing, positive family history of CRC, positive smoking history, COPD, history of NSAID use, and hemoglobin A1c within 6 months of colonoscopy. A Poisson regression was used for analysis of relative risk (RR). P<0.05, was deemed statistically significant. Results: Delaying colonoscopy had a RR of 1.03 (P<0.001) per year and males had an increased RR of 1.32 (P=0.011) when compared to females. Family history of CRC (first degree relative) had a RR of 1.179 (P=0.016). Hemoglobin A1c >6.5% had a RR of 1.147 (P=0.031). A positive FOBT/FIT also demonstrated an increase in RR of 1.677 (P<0.001). Current smokers had a RR of 1.215 (P=0.003) when compared to those who never smoked. Patients with COPD had a RR of 1.348 (P<0.001). NSAID users had a decreased RR of 0.688 (P<0.001), if NSAIDs were used within 6 months preceding initial colonoscopy. Conclusion: Development of PC polyps is multifactorial. Increased risk occurs in those with a positive family history, smoking, history of COPD and suboptimal glycemic control. Results indicate that positive FOBT and FIT are also associated with an increased relative risk for PC polyps. This may illustrate a greater ability of these testing modalities to detect PC polyps. Interestingly, the use of NSAIDs appears to have a protective effect, thereby decreasing the RR. The major limitation of this study is the primarily male VA population. In the future, utilization of the factors identified in this study may allow for further risk stratification, resulting in specific target years for initial screening colonoscopies.Table: Table. Model for precancerous colonic polyp risk

This Aimless Cobra Spits Blood: A Dieulafoyʼs Lesion as the Cause of Massive Hematemesis

Introduction: Dieulafoy's lesion is a tortuous, dilated aberrant submucosal artery that can erode through the mucosa and rupture spontaneously to cause severe gastrointestional bleeding. The lesion is most commonly found in the proximal stomach along the lesser curvature within 6 cm of gastroesophageal junction. It has up to 80% mortality rate because of its tendency to cause intermittent but severe bleeding and diagnostic challenges.Table 1: Neuroendocrine Tumor Characteristics on Surgical PathologyFigure 1Figure 2Case: A 39-year-old Hispanic male presented with sudden onset of melena and painless massive hematemesis. He was a nonsmoker and nonalcoholic with no history of NSAID use. His past medical history was significant for GERD and similar complaints of melena and hematemesis 8 years previously. Extensive prior investigations including CT abdomen and pelvis, esophagogastroduodenoscopy (EGD) and nuclear medicine scan failed to reveal the source of bleeding. He was hemodynamically stable at the time of presentation but his hemoglobin dropped from a baseline of 13 to 8. EGD showed mild reflux esophagitis, acute duodenitis, and gastric varices in the fundus of the stomach. CTA showed a small tangle of abnormally enlarged tortuous bleeding vessels along the posterior cardia of stomach with the absence of early venous return, suggestive of multiple Dieulafoy's lesions. IR-guided mesenteric angiogram was subsequently performed with successful embolization of multiple Dieulafoy's lesions arising from the proximal splenic artery and coursing through the region of the gastric cardia and fundus. The patient had an uneventful recovery and he was discharged home. He did not have recurrence of bleeding and his hemoglobin was within the normal limits at a 3 month follow-up visit.Figure 3Discussion: Diagnosis of Dieulafoy's lesion presents a formidable challenge for physicians and radiologists. Endoscopy is the diagnostic modality of choice but it is often unrevealing due to small size of the Dieulafoy's lesion, normal appearance of surrounding mucosa and intermittent bleeding patterns. These lesions have been known to be mistaken for other entities such as arteriovenous malformations, aneurysms, Mallory-Weiss tears and gastric varices, such as in our case. Contrast-enhanced CT and angiography can be helpful in cases where initial endoscopy fails to reveal the diagnosis of Dieulafoy's lesion and can offer minimally invasive therapeutic alternatives to surgical resection through selective arterial embolization.

Factors associated with gastro-duodenal disease in patients undergoing upper GI endoscopy at the Korle-Bu Teaching Hospital, Accra, Ghana.

There is a high prevalence of gastro-duodenal disease in sub-Saharan Africa. Peptic ulcer disease in dyspeptic patients, 24.5%, was comparable to prevalence of gastro-duodenal disease among symptomatic individuals in developed countries (12 - 25%). Limited data exists regarding its associated risk factors despite accumulating evidence indicating that gastroduodenal disease is common in Ghana. This study investigates risk factors associated with gastro-duodenal disease at the Korle-Bu Teaching Hospital, Accra, Ghana. This study utilized a cross-sectional design to consecutively recruit patients referred with upper gastro-intestinal symptoms for endoscopy. The study questionnaire was administered to study participants. Helicobacter pylori infection was confirmed by rapid-urease examination at endoscopy. Of 242 patients sampled; 64 had duodenal ulcer, 66 gastric ulcer, 27gastric cancer and 64 non-ulcer dyspepsia. Nineteen (19) had duodenal and gastric ulcer while 2 had gastric ulcer and cancer. A third (32.6%) of patients had history of NSAID-use. H. pyloriwas associated with gastric ulcer (p=0.033) and duodenal ulcer (p=0.001). There was an increased prevalence of duodenal ulcer in H. pylori-infected patients taking NSAIDs, P=0.003. H. pylori was a major risk factor for peptic ulcer disease. However, NSAID-related gastro-duodenal injury has been shown to be common in H. pylori infected patients. It highlights the need for awareness of the adverse gastro-intestinal effects in a H. pylori endemic area.

A Rare Case of Hypoplastic Pancreas Presenting as Normal Lipase Pancreatitis

Partial agenesis of the dorsal pancreas is a rare condition resulting in varying degrees of pancreatic body and tail hypoplasia. This embryologic underdevelopment is usually associated with reduced endocrine function and diabetes mellitus; in this case, however, we examine how this anomaly impacts pancreatic exocrine function, known to be concentrated in the affected area. We discuss the case of a 47 year old woman with history of diabetes who was seen in the ED complaining of two days of epigastric pain radiating to her left back, nausea, and vomiting. She denied history of NSAID use, alcohol ingestion, or gallstones. Initial vitals were normal, and examination was remarkable for left upper quadrant tenderness without rebound. The patient's presentation was suspicious for acute pancreatitis (AP), yet amylase and lipase levels were normal at 40 U/L (25-150 U/L) and 251 U/L (73-393 U/L), respectively. Serum calcium was also normal, however triglycerides (TG) were elevated at 537 mg / dL. Clinical suspicion for AP remained, and while abdominopelvic computed tomography (CT) did confirm marked inflammatory changes in the peripancreatic mesentery consistent with the diagnosis, it was also noteworthy for congenital absence of the pancreatic tail. Gallbladder ultrasound demonstrated no evidence of cholelithiasis, and cholescintigraphy confirmed patency of the common bile duct and hepatopancreatic ampulla. The patient was managed in the usual fashion without issue, and lipase remained normal throughout her one-week admission. Repeat CT scan two months later revealed a pancreatic pseudocyst and resolution of the previously noted inflammation. This is a rare case of clinical and radiographic normal-lipase pancreatitis (NLP). The estimated negative predictive value of this enzyme in diagnosing AP is 94-100%; in fact, less than ten cases of NLP are described in the English literature, none of which occur in the setting of partial agenesis of the dorsal pancreas. We propose that reduction in exocrine pancreatic mass due to this defect decreases measurable serum lipase. In fact, this abnormality may even predispose the patient to hypertriglyceride-associated pancreatitis (HTGP); while HTGP is generally involves TG levels over 1000 mg / dL, we theorize that TG levels in this case were sufficient to induce AP because of decreased available enzymatic activity. Thus, we believe this case establishes a link between total exocrine mass and the somewhat uncertain mechanism of HTGP.Figure 1

A Rare Case of Hemorrhagic Gastritis Caused By Sevelamer-Induced Necrosis

Case Report: A 64 year-old-male with history of ESRD, currently on hemodialysis presented with chief complain of nausea, bloody emesis and diffuse abdominal pain. His home medications were aspirin, hydralazine, gabapentin and sevelamer (4000 mg TID). He denied any history of NSAID use. On presentation, he was febrile, tachycardic and hypotensive. His labs were remarkable for Hb of 7.8, WBC of 10.3 and Cr of 7.7. The patient was resuscitated with normal saline and 1 unit of PRBC. CT abdomen showed pneumatosis with intramural air in the gastric fundus (Figure 1) Upper endoscopy revealed diffuse, severely friable mucosa in the gastric body, biopsy of which revealed pale yellow sevelamer crystals (Figure 2) deposited in the lamina propria of the body of the stomach. Sevelamer was discontinued and he was started on a low phosphate diet and a proton pump inhibitor. He was also advised to obtain a repeat EGD in 1 month.Figure 1: Pneumatosis with intramural air in posterior wall of the fundus of the stomach.Figure 2: Hematoxylin and eosin stain of ulcer bed with sevelamer crystals.Discussion: Sevelamer is anion exchange resin used to treat hyperphosphatemia in patients with ESRD. On hematoxylin and eosin stain, the crystals are 2-toned in appearance with bright pink accentuations on a rusty yellow background. There is very little literature on the mechanism of sevelamer mediated gastric mucosal injury. Sodium polysyterene sulfonate, a cation exchange resin used to treat hyperkalemia, is known to cause mucosal ischemia and ulceration by direct toxicity. Being an exchange resin, it is likely that sevelamer crystals cause mucosal injury by a similar mechanism of direct toxicity. To our knowledge, this is the first reported case of hemorrhagic gastritis due to sevelamer induced necrosis in the literature.

AB0712 Level of Awareness of Inflammatory Back Pain and Axial Spondyloarthritis among Medical Specialties Who Frequently SEE Patients with Low Back Pain

BackgroundRecognition of inflammatory back pain (IBP) is central to early diagnosis of ankylosing spondylitis (AS), as well as to that of axial spondyloarthritis (AxSpA), which has been introduced as a...

Novel Use of Endoscopic Ultrasound and Injection of Sclerosant for the Treatment of Bleeding Stomal Varices

Purpose: An 82-year-old male presented to the ED with large volume red blood from his ileostomy. His PMH was significant for a total proctocolectomy with end-ileostomy 8 years prior due to diverticulitis. He had similar presentations multiple times over the past few years with numerous ileoscopies and EGDs. No definite source had been identified. At presentation, hemoglobin was 5 gm/dL with symptoms of weakness and fatigue. Chemistry and coagulation panel were unremarkable. Physical exam was remarkable for red blood in the ostomy bag. There had been no report of preceding melenic stools,change in ostomy output, history of NSAID use or upper GI complaints. EGD was normal. Ileoscopy revealed no intraluminal bleeding source, but a small oozing area at the inferior margin of the ostomy was seen. Surgical evaluation was obtained and the area was treated with silver nitrate with successful hemostasis. Forty eight hours later, the patient had a repeat episode of clinically significant stomal bleeding. Peristomal Doppler ultrasound revealed prominent vessels in the abdominal wall adjacent to the ostomy opening. With concomitant Stage IV chronic kidney disease, the patient was unable to undergo a contrast enhanced CT or MR. As a result of this and continued, clinically significant bleeding, the patient underwent curvilinear EUS through the stoma. Five cm proximal to the stomal opening, a prominent, dilated vessel was seen. Doppler confirmed venous flow and using a 19G needle the varix was successfully injected with 5% ethanolamine. Repeat doppler post-injection confirmed absence of flow. The patient was discharged 48 hours later and has experienced no further bleeding over the last 9 months. Stomal varices are a rare, but clinically important cause of stomal bleeding. Unlike other ectopic varices throughout the GI tract, stomal varices have traditionally not been amenable to endoscopic treatment due to location exterior to the bowel wall. Historically, treatment included external compression, and percutaneous, blind injection of sclerosant. Percutaneous therapy is limited due to high risk for stomal breakdown/stenosis, ulceration and possible blind injection of a high pressure varix. Currently, the mainstay of therapy for recurrent bleeding includes decompressive procedures such as TIPS or other shunting procedures. These invasive procedures have systemic consequences and risk of their own. We describe a novel approach utilizing therapeutic EUS to treat bleeding stomal varices which appears both safe and efficacious in this challenging clinical situation. Further study is warranted before this modality can be recommended for widespread clinical use.

Prediagnostic non-steroidal anti-inflammatory drug use and survival after diagnosis of colorectal cancer

ObjectiveNon-steroidal anti-inflammatory drug (NSAID) use decreases both the incidence of colorectal cancer and recurrence of adenomas among patients with prior colorectal neoplasia. However, few studies have investigated the association between...

Low-dose aspirin is a prominent cause of bleeding ulcers in patients who underwent emergency endoscopy

This study aimed to clarify the current situation of bleeding peptic ulcers and examined the temporal changes in the pathogenic mechanisms requiring emergency endoscopy. Study subjects were 285 bleeding peptic ulcer patients who received emergency endoscopy in Saga Medical School Hospital between 2000 and 2007. The ratios of H. pylori infection, NSAID use and low-dose aspirin use were analyzed for differences between the two periods by chi-square test. Logistic regression analysis was used to investigate factors such as patient characteristics that influenced the differences between each period. A total of 221 (77.5%) patients were identified as H. pylori-positive. One hundred (35.1%) patients reported a history of NSAID use within 4 weeks. Among NSAID users, 41 patients received daily low-dose aspirin. One hundred forty-one patients had bleeding ulcers in 2000-2003 and 144 patients in 2004-2007. The odds ratio (OR) between the periods was 0.806 (95% CI, 0.461-1.409) for H. pylori infection and 1.590 (95% CI, 0.973-2.598) for NSAID usage. In contrast, the proportion of patients who took low-dose aspirin was 9.9% in the first period and 18.8% in the second period, and the difference was statistically significant (OR 2.093; 95% CI, 1.047-4.185). Logistic regression analysis revealed that cardiovascular disease and cerebral vascular disease were associated with aspirin use. This study indicates that the causes of bleeding ulcers are changing, and the increasing use of low-dose aspirin might become a major cause of bleeding ulcers.

The Effects of Once Daily Versus Twice Daily Proton Pump Inhibitor Therapy on NSAID Induced Gastric Ulcers

Purpose: The effects of once daily versus twice daily PPI therapy administered for an average of 12 weeks on gastric ulcer healing was compared. Methods: A retrospective chart review was preformed on adult patients presenting to a large teaching community hospital over a 5 year period (2001–2006) with melena or hematemesis and a history of NSAID use, who underwent endoscopy revealing gastric ulcers. Patients between the ages of 18 and 95 years, with a non-malignant gastric ulcer who had a history of any NSAID use for at least one week prior to presentation were eligible for enrollment. Patients were divided into two groups according to the anti-secretory therapy received. Group 1 comprised of once daily PPI therapy versus group 2 receiving twice daily PPI therapy. The primary endpoint was evidence of gastric ulcer healing during repeat endoscopy at 8 to 12 weeks. Results: 135 patients met our inclusion criteria, of these, 68 received daily PPI therapy while 67 received twice daily therapy. There was no statistical difference in demographics or co-morbidities in either group. The mean ages of the groups were 73 and 72 respectively. 83.3% of patients with active bleeding (P= 0.015) and 67% of patients with visible vessels on endoscopy (P= .216), were prescribed twice daily therapy. The average time for repeat endoscopy was 12.57 weeks for group 1 and 9.82 weeks for group 2. Healing rates of gastric ulcers at repeat endoscopy were 92.6% and 86.5% respectively with no statistical difference (P= .622) using Pearson Chi-square test. Conclusion: Our retrospective chart review revealed no statistical difference in healing rates of NSAID induced gastric ulcers among patients receiving daily versus twice daily PPI therapy. The lower healing rates in patients receiving twice daily group, maybe related to more severe disease and earlier second endoscopy.