hepatic ducts (Klatskin, type 3). Balloon dilatation of the hilar stricture andplacement of a wall stent resulted in prompt drainage of bile with subse-quent improvement in appetite and reduction of her fatigue and anorexia.Conclusion: Carcinoid tumors typically originate in the appendix, rectum,ileum, lungs, or bronchi, and may cause carcinoid syndrome with livermetastasis. While most tumors are indolent, midgut carcinoid tumors oftenpresent with bowel obstruction, abdominal pain, or carcinoid syndrome.Carcinoid tumors are a rare cause of biliary obstruction. Jaundice mostcommonly results from metastatic liver disease, but may also be due tobiliary obstruction from tumor extension. Primary bile duct carcinoid isvery rare. Symptomatic palliation by biliary stents is possible in selectedcases. Because biliary obstruction is potentially amenable to palliativeendoscopic drainage, differentiation of obstruction from metastatic liverdisease is important in selected jaundiced patients with carcinoid tumor.

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GASTRIC OUTLET OBSTRUCTION IN AN ELDERLY MALEWITH CELIAC SPRUCE: AN UNDESCRIBED ASSOCIATIONOF PANCREATIC CANCER WITH CELIAC SPRUCERitu Khurana, M.D., Raza Anees, M.D., Vikas Khurana, M.D.*Louisiana State University Health Sciences Center and Overton BrooksVA Medical Center, Shreveport, LA.

Introduction: Celiac spruce is a malabsorption disease that carries anincreased but underestimated risk of gastrointestinal malignancy. Wepresent a rare combination of unusual presentations, which made this casefrustrating and intellectually stimulating at the same time.Case Report: A 77 year-old white man with a history of Non Hodgkin’sLymphoma 10 years ago and constipation since childhood presented witha 2 year history of progressive intermittent abdominal pain, bloating,vomiting, severe reflux and 20 lb wt loss without diarrhea. His physicalexam was significant for cachexia. An upper endoscopy revealed dilatedstomach and significant edema with narrowing of the duodenum, but noobstruction. Duodenal Biopsies reveled focal villous atrophy. Serum anti-endomysial antibodies were strongly positive. CT of the abdomen revealedonly a dilated stomach. After 3-week trial of gastric decompression, repeatendoscopies and barium studies revealed persistent narrowing of the duo-denum. Surgery was consulted and at laparotomy a hard and induratedsegment encasing second portion of duodenum was noted. Whipple’sresection was performed. Pathology revealed well-differentiated infiltratingadenocarcinoma of the pancreas.Discussion: Our case is exceptional as celiac disease was diagnosed in the8th decade and was complicated by adenocarcinoma of the pancreas on abackground of untreated active celiac disease. Ten to 15% of the patientswith celiac sprue will develop a gastrointestinal malignancy. Immunologicperturbations, premalignant changes in the damaged regenerating epithe-lium, increased permeability to oncogenic substances and malabsorption ofprotective substances have been implicated in the pathophysiology. Diag-nosis of celiac disease in the elderly may be difficult because older patientshave multiple illnesses, a high prevalence of nutritional deficiencies,chronic diarrhea and constipation and bone diseases. It is likely thattreatment is given without full investigations as compared to youngerpatients.Conclusion: Early treatment on strict gluten free diet decreases the risk ofmalignancies. It has major health care and financial implications, especiallyin the elderly. A disease missed in childhood evolved into a disease ofelderly with sinister complications signifying changing epidemiology ofthe disease, which is under diagnosed and under recognized.

586

GASTRIC ISCHEMIA: AN UNDESCRIBED MANIFESTATIONOF NSAID ABUSERambabu Chalasani, M.D., Vikas Khurana, M.D.* Louisiana StateUniversity Health Sciences Center, Shreveport, LA and Louisiana StateUniversity Health Sciences Center and Overton Brooks VA MedicalCenter, Shreveport, LA.

Introduction: The GI tract is a site for a variety of NSAID-induced injuryincluding erosions, ulcers, strictures and perforation. The mechanism caus-ing the damage is debatable. We report a case of NSAID gastropathymasquerading as ischemia of the GI tract.Case Report: A 72 year-old man with history of peptic ulcer disease,hypertension, arthritis, abdominal aneurysm repair with subsequent smallbowel obstruction presented with complaints of recurrent nausea and ab-dominal distension. He was taking aspirin for more than 20 years andNaproxen for 7 years for chronic knee pain. He recently started increasinghis dose of Naproxen for abdominal pain. On admission his vitals signswere stable. Physical exam was remarkable for an old 3/6 systolic ejectionmurmur, a nontender abdomen with normoactive bowel sounds, withoutany guarding or rigidity. Labs on admission were unremarkable but hishemoglobin dropped 4 grams in the first day. Nasogastric tube lavagereturned dark red fluid. He was transferred to the intensive care unit afterhe became hypotensive, and tachycardic. EGD showed erosive esophagitis,severe diffuse gastric erythema, erosions and subepithelial hemorrhages. Ofnote the antrum was spared and the changes were more pronounced in thefundus and body of the stomach. Biopsies showed mucosal necrosis withepithelial regeneration, inflammatory pseudomembranes and erosions, con-sistent with ischemic damage. CT of the abdomen was normal and ruled outan aorto-enteric fistula. NSAIDs were discontinued and repeat EGDshowed healing of the ulcers and gastric mucosa. The patient’s hemoglobinremained stable and he was discharged home.Discussion: There are a variety of mechanisms suggested to explain themucosal damage caused by the NSAIDs. Prostaglandins mediated mainte-nance of the mucosal blood flow is lost, which is believed to be the majormechanism for NSAID related damage to the GI tract. In our patient theintake of nearly toxic levels of NSAIDs accentuated the decrease of themucosal blood supply to such a level that the ischemic injury ensued.Conclusion: We present a case of suspected gastric ischemia based onendoscopic biopsies, which turned out not to be real but related to theNSAIDs. Our case supports the theory that NSAIDs related GI mucosaldamage is caused by the decreased mucosal blood flow.

587

PNEUMATOSIS INTESTINALIS IN ASSOCIATION WITHACUTE SICKLE CELL CRISISAqib Sultan, M.D., Dhiren Shah, M.D., Nikhil Bhargava, D.O.,Hemant K. Roy, M.D.* Evanston Northwestern Healthcare, Evanston,IL.

Pneumatosis Intestinalis (PI) is characterized by the presence of submu-cosal or subserosal gas-filled cysts in the wall of the GI tract. PI isassociated with a wide variety of diseases, ranging from incidental findingsto being a marker of to life-threatening conditions such as intestinalinfarction or necrotizing enterocolitis. There have been no previous reportsof PI as a manifestation of a sickle cell crisis. A 39 year-old Black malewith a history of sickle cell disease presented with diffuse neck, chest, andback pain consistent with prior sickle cell crisis. He denied any nausea,vomiting, diarrhea, melena, hematochezia or SOB. On admission, physicalexam was remarkable for temp 101.3F and a markedly distended, diffuselytender tympanitic abdomen with moderate involuntary guarding and di-minished bowel sounds. Stool was negative for occult blood. Labs showeda WBC count of 38 109/L, Hb of 7.2 g/dl, ALT of 1530 U/L, AST of1767 U/L, INR of 1.8, total bilirubin of 16.9 mg/dl, serum lytes werenormal. Supportive therapy was instituted including IV antibiotics and NGdecompression. Abdominal X-ray showed moderate colonic distension anda CT scan on the second day revealed dilation and thickening of theascending colon and proximal transverse colon with intramural gas con-sistent with PI . No free air or obstruction was evident. Stool and bloodcultures were negative. Over the following 10 days, the patient improvedclinically and was discharged with a benign abdominal exam and normal-ized transaminases. The exact pathogenesis of PI is unknown with bothbacterial and mechanical etiologies postulated. With regards to potentialinfectious etiologies, sickle cell patients are often functionally asplenic and

S195AJG – September, Suppl., 2003 Abstracts