Su1957 Granulomatous Gastritis–Sarcoidosis or Idiopathic? A Diagnostic Dilemma

AGA Abstracts

a lumen 2-3mm in diameter. Next an ultra thin scope was used to pass a guidewire into the stomach and a Hurricane biliary balloon was used to sequentially dilate the stricture from 6-8 mm. An 18mm X 170mm- FCSEMS (HANAROSTENT-ESOPHAGUS CCC) was advanced via guide wire and deployed with fluoroscopic guidance (image 2). Post-stent placement the patient was able to tolerate a full fluid diet. Subsequent EGDs at 2 week intervals have identified 5 cm of distal stent migration for which proximal esophageal dilation and lasso repositioning have been required. He will be followed biweekly. CONCLUSION: Our case is unique as it describes a severe esophageal stricture from Mg citrate, prescribed by the patient's naturopath, which is previously unreported.

diagnosis of isolated gastric sarcoidosis is extremely challenging due to its variability in presentation and clinical course. Endoscopic evaluation and mucosal biopsy are paramount in identifying GG. Only time and close follow up with frequent re-evaluations will determine if our patient has gastric sarcoidosis or idiopathic GG.

Figure 1: Hemorrhagic ulcerative gastritis of the body of the stomach

A tapered narrowing of the proximal esophagus begins 3 cm below the cricopharyngeus. The narrowing persists over 13 cm demonstrating long segment stenosis of the esophagus.

Figure 2: Mucosal biopsy depicting gastric mucosa with a large area of non-caseating granulomatous inflammation (left half) associated with active inflammation (right half) Su1958 Probiotic Preparation "Biofermin Powder" Prevents NSAID-Induced Small Intestinal Lesions in Rats Kikuko Amagase, Toshiko Murakami, Riho Tanaka, Koji Takeuchi, Shinichi Kato Background & Aim: Probiotics are known to be live bacteria that have a beneficial effect on human health. Some probiotics, such as lactic acid bacteria, have been used to improve symptoms resulting from changes in the intestinal flora. Furthermore, several reports have revealed that these probiotics can protect intestinal disorders. BIOFERMIN POWDER is a lactic acid bacterium originally isolated from humans and useful for gastrointestinal protection as probiotics. The enterobacteria play a major role in the pathogenesis of non-steroidal antiinflammatory drugs (NSAID)-induced intestinal lesions. In this study, we investigated the effect of probiotic preparations on the development of small intestinal lesions induced by loxoprofen, a NSAID frequently used in Asian countries, in rats. Methods: Male SD rats without fasting were administered loxoprofen (60 mg/kg, PO) and killed 24 h later to examine hemorrhagic lesions developed in the small intestine. Probiotic preparations (BIOFERMIN POWDER, BIOFERMIN TABLETS, MIYA-BM FINE GRANULES, BIOLACTIS POWDER) and Streptococcus faecalis (a main compounded viable bacteria of BIOFERMIN POWDER) were given p.o. once daily for 7 days before loxoprofen treatment. Mucus secretion was examined by PAS staining, while enterobacterial count in the mucosa was determined by a culture method. The mucosal mRNA expression of iNOS and various inflammatory cytokines was determined by RT-PCR. Results: Loxoprofen induced hemorrhagic lesions in the small intestine accompanied by the decrease in mucus secretion, the increase in bacterial invasion, MPO activity, and the up-regulation of iNOS expression. Pretreatment of the animals with probiotic preparations such as BIOFERMIN POWDER, BIOFERMIN TABLETS and BIOLACTIS POWDER but not MIYA-BM FINE GRANULES for 7 days significantly prevented loxoprofen-induced intestinal lesions, together with suppression of bacterial invasion, as well as iNOS up-regulation and MPO activity. In addition, BIOFERMIN POWDER treatment increased mucus secretion and reverted the decrease in mucus secretion following loxoprofen treatment. Repeated treatment for 7days with Streptococcus faecalis, a gram positive bacteria belonging to lactic acid bacteria group, also significantly inhibited the loxoprofen-induced intestinal lesions. Conclusion: These results suggest that BIOFERMIN POWDER protect the loxoprofen-induced small intestinal lesions. This protective action may be associated with the increase in mucus secretion and suppression of bacterial invasion, inflammatory cytokine expressions by lactic acid bacteria but not butyric acid bacteria. It is assumed that lactic acid bacteria, as probiotics would be useful for NSAID-induced small intestinal lesions via the improvement of imbalance of bacterial flora.

Expandable metallic stent is demonstrated in satisfactory position after EGD and antegrade instrumentation of the midthoracic esophageal stricture including balloon dilatation. Su1957 Granulomatous Gastritis--Sarcoidosis or Idiopathic? A Diagnostic Dilemma Caitlin Sullivan, Kishore Vipperla, Dayakar Kancherla, Lia C. Kaufman, Adam Slivka Introduction: Granulomatous gastritis (GG) is an extremely rare (0.08% to 0.31%) form of chronic gastritis. It is categorized into infectious (e.g. H. pylori, Tuberculosis, fungal, and parasitic infections), non-infectious (e.g. Crohn's disease, tumors, drugs, reaction to foreign bodies, and vasculitides) and idiopathic (~25%) types. Sarcoidosis and Crohn's disease are the most common causes of GG in the Western nations. Case: A 38-year old Caucasian female with a longstanding history of dyspepsia presented with worsening epigastric abdominal pain of a 3-week duration, associated with nausea and several episodes of non-bloody emeses. She had moderate epigastric tenderness on abdominal examination. Blood tests were notable for normal cell counts, renal and liver functions, but an elevated lipase level at 835 units/ L (normal range 15-70 units/L). However, abdominal computed tomography (CT) did not reveal evidence of pancreatic inflammation. Her symptoms progressed despite nasojejunal feeding with normalization of her pancreatic enzymes, analgesia, intravenous fluids and proton-pump inhibitor infusion. Esophagogastroduodenoscopy (EGD) revealed hemorrhagic ulcerative gastritis of the body of the stomach with sparing of the fundus and antrum (Figure 1). The mucosa was firm and somewhat cyanotic and the ulcers were large and deep. Mucosal biopsies revealed non-caseating granulomatous inflammation (Figure 2). A comprehensive workup for GG ruled out inflammatory bowel disease (anti-saccharomyces cerevisiae antibody, IBD-7 serology panel, colonoscopy with ileoscopy and small bowel imaging); connective tissue disease (anti-neutrophil cytoplasmic, anti-nuclear, anti-Ro, anti-La, anti- SCL70 antibodies, and angiotensin converting enzyme level), autoimmune gastroenteritis (IgG-4 level); and tuberculosis (Quantiferon gold TB test). CT of the chest did not show pulmonary or hilar abnormalities and abdominal CT angiography did not reveal any evidence of mesenteric ischemia or vasculitis. Histopathology did not have any features of malignancy; staining for cytomegalovirus, H. pylori, fungus, amyloid, and tuberculosis were negative. Prednisone (40mg/day) therapy improved her symptoms within a few days and a repeat EGD showed resolution of the gastric cyanosis, hyperemia, and healing ulcers. Discussion: We suspect this patient has idiopathic GG. In gastrointestinal sarcoidosis, sub-clinical gastric involvement is common, but symptomatic manifestations are extremely rare (