raphy revealed hepatomegaly without any signs of primary sclerosing cholangitis (PSC). Liver biopsy showed portal inflammation without signs of bile duct involvement. Corticosteroids and sulfasalazine were started and the clinical condition of the patient improved. Progressive normalization of her liver function tests and inflammatory parameters were observed. One year after beginning treatment a follow-up biopsy confirmed complete remission. The patient is presently under maintenance therapy with aza- thioprine. Hepatobiliary complications associated with Crohn’s disease (CD) in- clude cholelithiasis, hepatitis (granulomatous and autoimmune), amyloid- osis, PSC, small-duct PSC, cholangiocarcinoma, liver abscess and toxic hepatopathy (mesalazine). PSC is the most common hepatobiliary disease seen in association with IBD but is less frequent in CD than in ulcerative colitis. PSC may also be indistinguishable from autoimmune hepatitis (AIH). Histologically, AIH is characterized by portal and periportal mono- nuclearcell infiltrates while in PSC, biliary lesions predominate. These biliary changes are the best discriminatory factor between PSC and AIH. Using Johnson’s score, which has been validated for the diagnosis of AIH, we obtained a score of 11 before therapy and 13 after, which is compatible with AIH. The strongest argument for the diagnosis is the striking im- provement under corticotherapy. Indeed AIH is responsive to steroids, while PSC is not. This case is exceptional because of the development of a cholestatic AIH mimicking PSC in a patient with previously undiagnosed CD. 673 Eosinophilic esophagitis: atypical presentation of a rare disease Sylvie Evrard, Michel Kahaleh, Hubert Louis, Issam El Nakadi and Jacques Deviere*. 1 Gastroenterology, Easme Hospital, Brussels, Belgium. A previously healthy 72-yr-old man consults for dysphagia and regurgita- tion of recent onset, his past medical history is relevant for pulmonary tuberculosis treated successfully with triple therapy. Initial EGD was nor- mal except for a functional spasm at the lower third of the esophagus. Three months later he came back with worsening symptoms and weight loss of 7 pounds. Manometry disclosed aperistaltism in the lower half of the esoph- agus and high lower sphincter pressure with uncomplete relaxation sug- gesting pseudoachalasia. Barium meal showed narrowing and dysmotility in the inferior third of the esophagus. CT-Scan demonstrated circular thickening of this portion without mediastinal adenopathies; EUS con- firmed an infiltrating process extending beyond the muscularis mucosa and effracting the serosa and the muscular layer. EGD was repeated to obtain macro-biopsies but pathology only revealed rare eosinophils and polyneu- trophils in the submucosa. Laboratory findings showed hypergammaglobu- linemia at 1.6 g/dl and eosinophilia up to 1700/mm3. No parasitic infection was demonstrated. The dramatic presentation of the patient and the inabil- ity to exclude an esophageal cancer lead us to offer him surgery. A superior esogastrectomy with intrathoracic anastomosis was performed. The re- sected segment revealed a diffuse infiltration of all layers by eosinophils compatible with Idiopathic Eosinophilic Esophagitis (IEE). IEE is a variant of an uncommon disease: Idiopathic Eosinophilic Gastroenteritis which can affect any part of the digestive tract, but most frequently the antrum or the small bowel. Esophageal involvement occurs rarely, less than 1.5% of IEG. Only 43 cases have been published. Typically it occurs in young adult, mainly male. They present with intermittent dysphagia without weight loss. Manometry shows motility disorders in 20 to 40% of cases. Allergic conditions are presumed to be the causal factor for inducing initial mast cell degranulation and then eosinophils activation. Infiltration may extend be- yond the mucosa to all layers, histological demonstration of submucosal involvement requires large biopsy specimens with macro-biopsy forceps, but muscularis or serosal invasion need surgical sampling. The prevalence of deep involvement is unknown since diagnosis is based on routine superficial biopsies; only 3 patients in our review required surgical thera- peutic sanction allowing complete examination of the esophageal wall. Conclusion: We report an unusual presentation of IEE which underlines the need for surgical sampling to rule out a neoplastic process. 674 Proctosigmoiditis associated with etodolac Robert C. Kapel, M.D., Iulia Circiumaru, M.D., Joseph Grillo, M.D. Department of Gastroenterology, Danbury Hospital, Danbury, CT. Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are increas- ingly cited as causes of colonic mucosal damage. We describe a case of diarrhea and proctosigmoiditis in a man prescribed etodolac for back pain. Case: A 57 year old man was referred for evaluation of six weeks of diarrhea. The stool was watery brown, without blood, and occurred up to three times a day. He had left lower quadrant cramping relieved with bowel movements. He denied fever and other constitutional symptoms. Two weeks prior to the development of diarrhea and tenesmus, he was started on oral etodolac for exacerbation of his chronic back pain (Lodine XL 500 mg. daily). His only other medication was atorvastatin. He denied recent anti- biotics. Additional medical and social histories were unremarkable. Phys- ical examination was normal and stool was hemoccult negative. CBC and ESR were normal. Stool culture and C. difficile toxin were negative. Abdominal and pelvic CT scan revealed mild diffuse thickening of the wall of the sigmoid colon and rectum. Sigmoidoscopy demonstrated mild loss of the normal vascular pattern in the sigmoid colon. Rectal mucosa appeared normal. Biopsies of the rectum revealed focal crypt injury with neutrophils, and biopsies of the distal sigmoid showed an increased lymphoplasmacytic infiltrate in the lamina propria. There were no hallmarks of chronic inflam- mation, no increase in intraepithelial lymphocytes, and the collagenous plate was not thickened. Descending colon biopsies were normal. Etodolac was stopped and within 48 hours the patient’s tenesmus resolved. Over the next 10 days, his stool returned to normal. Colonoscopy performed three months later revealed normal mucosa and random biopsies did not show any abnormalities. Conclusion: The clinical history and histological findings strongly support the role of etodolac in causing diarrhea and proctosigmoiditis in this patient. Given that biopsies and CT scans are not routinely performed in most cases of medication induced diarrhea, colitis associated with NSAIDs may indeed be more common than we believe. Many diverse presentations of NSAID induced colitis have been reported. The uniqueness of this case of proctosigmoiditis should further heighten our vigilance when encoun- tering patients with diarrhea and a history of NSAIDs. 675 Case of Wilsons disease and PBC overlap Asif Khalid MD 1 , Jawad Ahmad MD 1 , Anthony J Demetris MD 1 , Vijayan Balan MD 1 and Hugo E Vargas MD 1 *. 1 Medicine, Division of Gastroenterology and Hepatology, University of Pittsburgh, Pittsburgh, Pennsylvannia, United States. Purpose: We describe the first reported case of Wilsons disease and Primary biliary cirrhosis (PBC). Results: We recently evaluated a 36 year old white man in referral for elevated liver injury tests (LIT). The patient reported feeling well except recent onset of fatigue. He reported no symptoms suggestive of End stage liver disease (ESLD) or neurologic upset, and denied prior jaundice, high-risk behavior, significant alcohol intake or any medication use. His only other medical problem was hypertriglyceridemia. His brother was diagnosed with Wilsons disease a year ago and was doing well on Trien- tine. He had also manifested liver disease with elevated LITs alone. The physical exam did not reveal stigmata of ESLD or Kayser-Fleischer rings. Blood work revealed a normal blood count and electrolytes. Bilirubin-0.7, AST-76, ALT-117, ALP-151, GGT-251, Albumin-4.3 & INR 1. Anti mitochondrial antibody 400/ M2 subtype, negative Antinuclear and smooth muscle antibody. Ceruloplasmin 2mg/dl, serum copper (Cu) 18mcg/dl, Trig-438. Hepatitis serologies were negative. Urine Cu excre- tion-138mcg/24hrs. Liver biopsy revealed steatohepatitis, bile-ductular in- S212 Abstracts AJG – Vol. 96, No. 9, Suppl., 2001