days for melena, which revealed diffuse ulcerative esophagitis and gastritis.Repeat endoscopy after another 7 days for recurrent bleeding revealed alarge gastric clot and resolving gastric injury. He did well until approxi-mately one month post-ingestion when he developed symptoms of gastricoutlet obstruction. Endoscopic exam revealed gastric scarring with markedpyloric stenosis. Endoscopic balloon dilation was performed with tempo-rary improvement. Recurrent symptoms of gastric outlet obstruction 4months later led to a gastrojejunostomy for relief of symptoms. A gastrec-tomy was considered, but at the time of surgery the stomach was tooscarred to make this a viable procedure. After his surgery he has beenasymptomatic for 2 months of follow-up.Conclusions: Caustic acid ingestion can lead to severe sequelae includingesophageal and pyloric stenosis in a relatively short time. Endoscopyallows assessment and DPEJ placement for nutritional support. Continuedevolution of pyloric stricturing following concentrated acid ingestion mayoccur over several months following caustic ingestion.

792

Pseudomyxoma peritonei presenting as a rectal massJorge Sotelo, M.D.1, Mitchell Chorost, M.D.1, Gerald Fruchter, M.D.1

and Ayse Aytaman, M.D.1*. 1Gastroenterology, VA NY Harbor HCSBrooklyn Campus, Brooklyn, New York, United States.

Purpose: Pseudomyxoma peritonei (PMP) is characterized by gelatinousintraperitoneal fluid collections and mucinous implants on the peritonealsurfaces and omentum which usually is derived from an underlying ap-pendiceal or intestinal mucin secreting adenoma or adenocarcinoma. Typ-ical presentations are increasing abdominal girth, ovarian mass, new onsetinguinal hernia or rarely acute appendicitis. We describe a case of PMPpresenting with a rectal mass simulating a rectal carcinoma.Case History: The patient is a 69 year old male, who was evaluated 4 yearsearlier for right lower quadrant pain and constipation. A computed tomog-raphy (CT) scan of the abdomen revealed at that time a right lower quadrantmass and multiple hepatic lesions suspicious for metastasis. Two CTguided biopsies of the liver lesions revealed cavernous hemangioma.Colonoscopy was unremarkable except for a small ulceration at the appen-diceal orifice with biopsy showing nonspecific inflammation.

He re-presented with a 3 month history of weight loss, constipation,increasing abdominal girth and was found to have massive ascites and apainful, hard and fixed rectal mass. Repeat colonoscopy revealed a sub-mucosal, 5cm rectal mass encroaching upon 50% of the lumen, biopsy wasnon-diagnostic; in addition there was a 4mm nodule overlying the appen-diceal orifice, biopsy revealing acute and chronic inflammation and villo-tubular changes. CT scan showed extensive ascites with multiple areas ofenhancement, and an extrinsic rectal mass. Paracentesis revealed welldifferentiated, bland and tall columnar cells noted in the background ofmucus lakes, consistent with PMP.

Patient underwent surgery for debulking and to relieve obstructive symp-toms. Findings revealed bulky gelatinous masses throughout the perito-neum with omental, pelvic, bilateral subdiaphragmatic caking and neartotal extrinsic compression of the recto-sigmoid. Patient underwent trans-verse loop colostomy and limited debulking. Pathology was consistent withwell differentiated mucinous adenocarcinoma consistent also with PMP.Conclusions: The treatment of PMP is aggressive debulking via laparot-omy and possible use of chemotherapy. Except in patients with high-grademalignant process where only palliative therapy may be indicated, themedian survival can be increased significantly with early diagnosis andtreatment before large volume of disease leads to bowel entrapment bytumor.

Conclusion: In the differential diagnosis of rectal obstructing lesions thisrare entity has to be considered. It is important to pay special attention tolesions found at the level of the appendix.

793

Successful treatment of hepatitis B-associated vasculitis withlamivudineVeslav Stecevic1, Martin M. Pevzner2 and Stuart C. Gordon1*.1Gastroenterology/Hepatology, William Beaumont Hospital, Royal Oak,Michigan, United States; and 2Rheumatology, William BeaumontHospital, Royal Oak, Michigan, United States.

Purpose: Vasculitis is a potentially serious extrahepatic manifestation ofhepatitis B virus (HBV) infection. The treatment of HBV-associated vas-culitis with corticosteroids and immunosuppressive agents may worsen thehepatic disease. We report a case of HBV-associated leukocytoclasticvasculitis that responded to oral lamivudine as monotherapy.Case report: A 59-year-old Caucasian woman with chronic HBV devel-oped biopsy-confirmed leukocytoclastic vasculitis in 1978. She had recur-rent flares of vasculitis over 20 years, treated continuously with prednisone,up to 30 mg/d. On initial evaluation in 1998 she had purpuric skin lesionsabout her upper and lower extremities and was on prednisone, 30 mg/d. Shehad no hepatosplenomegaly or stigmata of chronic liver disease. Labora-tory studies showed normal AST and ALT. HBsAg and anti-HBc werepositive, anti-HBs negative, HBeAg negative, anti-HBe positive, HBVDNA level of 9.3 pg/mL, anti-HCV negative. She was started on lamivu-dine 150 mg/d. One month later, quantitative HBV DNA was undetectable,and her vasculitis flares were less intense. Over the next seven months, theprednisone was tapered and eventually stopped. Twenty-one months later,her vasculitic lesions had completely resolved. She remains on oral lami-vudine. Her HBV DNA is undetectable. She is still HBsAg and anti-HBepositive and anti-HBs negative. She has not taken any immunosuppressiveagents for over 3 years.Conclusions: This case illustrates successful treatment of HBV-associatedvasculitis with lamivudine that allowed the patient to stop high doseprednisone therapy. Acecdotal case reports suggest that lamivudine may beused in the treatment of HBV-related polyarteritis nodosa in combinationwith immunosuppressive agents, but there are no previous reports oflamivudine as a single agent in the treatment of vasculitis.

794

Pancreatic stenting as a treatment for pancreatic pseudocystDeborah A Streletz, Fernando Ramos, Eric M Osgard and Darren SBaroni*. 1Medicine, Tripler Army Medical Center, Honolulu, HI,United States.

Purpose: Often pancreatic duct strictures can be a cause of recurrentpancreatitis and lead to pseudocyst formation. We present a case of apatient with a high-grade stricture in the pancreatic head and secondarypseudocyst, both of which responded to endoscopic dilation and stenting ofthe pancreatic duct.Methods: Our patient is a 40-year-old African American female whopresented in November 2000 with her first documented episode of alcoholicpancreatitis. A CT scan done at the time revealed diffuse pancreaticinflammation, a dilated pancreatic duct and a 3 to 4 cm peripancreaticpseudocyst. Her pancreatitis improved with medical management and shewas eventually discharged. As an outpatient, however, even with discon-tinuation of alcohol, the patient continued to require daily narcotics for paincontrol for several months. She presented with recurrent pancreatitis re-quiring admission in both December 2000 and January 2001. Repeat CTscans done during both hospital admissions showed persistent dilation ofthe pancreatic duct and continued presence of the pseudocyst. In December2000 the patient was also diagnosed with a right-sided pancreatic pleuraleffusion. Eventually, in January 2001 an ERCP was performed and re-vealed a single marked stricture in the pancreatic head with upstreamdilation in the uncinate, body and tail of the pancreas. Also noted, justproximal (upstream) to the pancreatic head stricture, was a side branch thatdirectly communicated with peripancreatic pseudocyst. Dilation of thestricture was performed with catheter dilators and a 5 Fr 7cm pancreaticstent was placed which transversed the stricture.

S248 Abstracts AJG – Vol. 96, No. 9, Suppl., 2001