Collagenous duodenitis is an extremely rare disorder of marked subepithelial collagen deposition with associated mucosal inflammation of the duodenum. This rare disease has been reported only four times in English literature and has generally been associated with collagenous colitis (microscopic colitis) which causes chronic intermittent watery diarrhea. The case reported is of a 65 year old male presenting with chronic right upper quadrant abdominal pain, bright red blood per rectum and constipation. Patient was found to have erosive gastritis on endoscopy. Biopsies were done and his pathology report revealed an increased collagen table in the duodenum. Upon diagnostic colonoscopy, multiple tubular adenomas were found. Patient underwent polypectomies which showed no evidence of neoplastic process or microscopic colitis. Some theories postulate that the pathogenesis of the increased collagen deposition may be secondary to inflammatory etiology, an abnormality in collagen sheath or autoimmune injury. Interestingly, the patient presented with evidence of chronic gastritis and Barrett's esophagus, which could have indirectly led to the development of his duodenitis.Figure 1Figure 2

Purpose: A 71-year-old male presented for screening colonoscopy. Last colonoscopy, 10 years ago was negative for polyps, dysplasia or cancer. Past medical history was significant for thromobocytopenia, diagnosed in 2003. Family history was negative for GI cancer and polyps. Physical examination was negative. Colonoscopy from rectum to cecum was negative for any polyps, dysplasia or cancer. In Feb 2011, patient presented for his colonoscopy with no current acute GI symptoms. Colonoscopy revealed numerous 3-6 mm sessile polyps of benign appearance diffusely throughout the colon. Polypectomies showed extensive involvement by a markedly atypical lymphoid infiltrate with a nodular architectural pattern. The cells were monomorphous small to intermediate in size with uniform stippled chromatin, absence of nucleoli and mildly irregular nuclear contours. A panel of immunostains was performed showing atypical lymphoid infiltrate that were overwhelmingly B cell immunophenotype with CD 20 immunostain. There was also co expression of CD 5 and nuclear positivity for cyclin D-1. Based on the morphological findings and immunoprofile, the lymphoid infiltrate represents a neoplastic B cell lymphoproliferative disorder best classified as Mantle Cell lymphoma. In this clinical setting the B cell neoplasm was presenting as lymphomatous polyposis. CT and PET scans revealed metastases involving the jugular chain, supraclavicular, axillary, mediastinal, hilar and subcarinal lymph nodes. The spleen was mildly enlarged. After six cycles of Bendamustine and Rituximab therapy, repeat colonoscopy 9 months later revealed complete resolution of polyposis.Figure 1: Polyp at the transverse colon.Figure 2: Cyclin D immunostain.

Small bowel neoplastic disease is a rare but dreaded occurrence in Crohn's disease (CD) and the diagnosis is often disguised by nonspecific and varied presenting symptoms mimicking active or obstructive CD. As such, the diagnosis is all too often delayed, typically detected at a late stage, and with a poor prognosis. CD has become a well-recognized risk factor for the development of small bowel adenocarcinoma. The data, however, are limited and based on case reports, retrospective studies, and review of the literature.

Purpose: Bravo pH testing is a commonly used procedure to assess gastroesophageal reflux disorders. Accurate placement of the Bravo pH capsule is critical for obtaining reliable results. Failure of attachment of the BRAVO pH capsule to the esophageal mucosa or early detachment may result in an unsuccessful study. The purpose of this study was to determine whether Ultraslim gastroscope compared to regular gastroscope facilitates the placement of Bravo pH capsule and reduces the procedure time. Methods: Records of Bravo pH capsule placement of 30 patients under direct vision by GIF 160 gastroscope (outer diameter, 8.6 mm) (Group 1) and of 30 patients under direct vision by ultraslim XP 160 (outer diameter, 5.9 mm) (Group 2) were reviewed. The mean (ranges) ages were 50 (20–81) and 54 (16–79) years respectively. The male to female ratios were 2.75:1 for both groups. All patients in Group 1 and all but 2 patients in Group 2 received sedation with Propofol. After endoscopic examination was completed, the scope was withdrawn proximal to the selected site of Bravo pH capsule placement (6 cm above the gastroesophageal junction). Bravo delivery catheter was then inserted through the mouth and the deployment was performed following standard protocols. After the deployment was confirmed, delivery system was withdrawn and the esophagus was checked for mucosal injury as scope was withdrawn. Five patients in Group 1 and 4 patients in Group 2 had gastric biopsy. Results: The placement was successful and the data capture was satisfactory for all patients in both groups. Five patients in Group 1 and 4 patients in Group 2 had gastric biopsy. The mean procedure time was decreased from 11.9 (standard deviation [SD], 2.8) minutes for Group 1 to 6.4 (SD, 1.9) minutes for Group 2 (P < 0.0001). No patients had chest pain, dysphagia or other serious procedure-related complications except two patients in Group 1 who had persistent sore throat. Conclusion: Placement of Bravo pH capsule under direct vision can be easily accomplished by Ultraslim gastroscope. The slim scope facilitates the deployment and reduces the procedure time almost in half. It may also cause less frequent sore throat. In selected cases, an Ultraslim gastroscopy may even be performed without sedation.Table: Comparison of regular gastroscopy with Ultraslim gastroscopy

Introduction: ESWL is a relatively noninvasive and effective procedure for the management of nephrolithiasis. Given its widespread use, increased numbers of serious complications are being reported in both the kidney and <1% of the time in surrounding organs. Injuries reported to the gastrointestinal tract include gastric erosions, retroperitoneal hemorrhage, splenic rupture, hepatic hematoma, bile duct injury and bowel perforation. We report the case of a patient who developed acute pancreatitis after undergoing ESWL for left-sided nephrolithiasis. Case Report: A 35-year-old male presented with persistent, severe, diffuse abdominal pain, left flank pain and two episodes of painless hematuria with associated nausea, constipation, and bloating. The patient had undergone ESWL for left-sided nephrolithiasis one day prior to admission with a total of 500 shocks at 22kV. Physical exam was significant for an abdomen that was diffusely tender to palpation, greatest in the left upper quadrant without rebound tenderness or guarding. Urinalysis was significant for hematuria. The patient had an elevated white blood cell (WBC) count of 15000 (mL, and an elevated serum amylase of 251 U/L (normal 25–125 U/L) and lipase of 406 U/L (normal 7–60 U/L) respectively. CT scan with contrast was significant for a small hematoma in the left kidney and small amount of fluid in the tail of the pancreas without evidence of necrosis. A clinical and radiologic diagnosis of acute pancreatitis was made. Gallstones, alcohol abuse, drugs, hypertriglyceridemia and hypocalcaemia were ruled out as etiology of his pancreatitis. Given the patient's history and chronologic clinical course the patient was diagnosed with ESWL induced pancreatitis. He improved clinically with conservative bowel rest. TheWBC count normalized and the amylase and lipase values continued to trend down at the time of his discharge from the hospital. Discussion: Mild elevations of serum and urinary amylase and serum lipase have been noted after ESWL but clinically significant pancreatitis is rare. Shock wave energy at the stone's surface produces mechanical compressive and tensile forces producing stone fragmentation. Shear forces produced by transient cavitation may damage nearby organs. With an increasing number of ESWL procedures being performed these days, consulting gastroenterologists need to be mindful of the collateral damage.

AIDS associated arteriopathy (AAA) of the gastrointestinal tract in adults has not been previously reported. We report the case of a young adult with AIDS and non-infectious recto-colonic ulcerations and postulate that the ulcerations may constitute a complication of AAA. Case Report: A 35 yo male with history of HIV with AIDS, non-Hodgkin's lymphoma, and MAI presented with fever, rectal pain and bleeding. Four months prior to admission, the patient underwent excision of a rectal ulcer, which revealed thick walled vessels with medial hypertrophy and intimal fibrosis within the granulation tissue. A few beaded acid-fast rods, consistent with Nocardia species were noted in adjacent crypts. Follow up colonoscopy revealed multiple ulcerations throughout the colon characterized microscopically as Candida associated colitis. The patient was treated for Nocardia and had complete resolution of his symptoms. 10 weeks later, he presented with diffuse abdominal pain and hematochezia. A repeat colonoscopy revealed a large, irregular fungating, friable cecal mass with biopsy changes similar to those in the rectal ulcer as well as luminal obliteration by organizing thrombi and no inflammation in the adjacent non-ulcerated cecal mucosa. Infectious, inflammatory and neoplastic etiologies were ruled out. The patient underwent a right hemicolectomy with ileo-colonic anastomosis with complete resolution of his pain. Microscopically, the cecal mass had vascular changes similar to those of the biopsy. AAA was the presumed etiology. Discussion: AAA is characterized by intimal fibrosis and fragmentation of the elastic fibers of medium sized arteries as well as fragmentation and calcification of the internal elastic membrane, with luminal narrowing. These changes have been described in children in organs such as the heart, lung, kidney, intestine, brain and spleen. Isolated cases complicated by coronary artery aneurysm, esophageal stricture and colonic perforation have been reported. Increased exposure to endogenous and exogenous elastases resulting from multiple infections secondary to the immunodeficiency in AIDS have been postulated as the pathogenetic mechanism. We report the first case of these vascular changes in the gastrointestinal tract of an adult with AIDS.