described in the esophagus, fundus, and antrum. Etiologies of colonicmasses in immunocompromised patients include lymphoma, Kaposi’s sar-coma, Mycobacterium tuberculosis, histoplasmosis, and toxoplasmosis.This case illustrates that CMV colitis should also be considered when acolonic mass is found in a patient who is imunosuppressed after solid organtransplantation.

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HEPATOCELLULAR CARCINOMA IN HIV PATIENTCO–INFECTED WITH HEPATITIS B VIRUS: AN EMERGINGPROBLEM?Chris B. Hyun, M.D. and Walter J. Coyle, M.D.*. GastroenterologyDivision, Naval Medical Center, San Diego, CA.

Purpose: There are 400 million people worldwide who are hepatitis Bvirus (HBV) carriers and 1.25 million people are estimated to have chronicHBV infection in the United States. Infections with HBV and humanimmunodeficiency virus (HIV) have similar risk factors and routes oftransmission. The interaction between HBV and HIV is complex and itsclinical implications are unclear. This report describes a 44–year–old malewith HBV/HIV infections who developed metastatic hepatocellular carci-noma (HCC) despite quiescent HBV and HIV disease courses. He has hadundetectable HBV–DNA levels, with positive HBsAg, for as far back asseven years, consistent with an inactive carrier state. HIV viral loadremained undetectable for over four years on highly active antiretroviraltherapy (HAART). CD4 count had been consistently over 300 /�l (normal237–1130), and hepatitis C virus (HCV) antibody was negative. Liverfunction tests remained unremarkable as well. He presented with abdom-inal pain, low–grade fever, and weight loss. An enlarged and palpable liverwas noted on physical examination and CT scan revealed a large hetero-geneous mass that appeared to be originating from the duodenal posteriorwall. Additionally, a diffuse foci of decreased attenuation was noted withinthe liver. Endoscopic ultrasound subsequently showed that the extrahepaticmass was a large, well–circumscribed lesion located outside the duodenum.HBV–DNA was now 4.76 pg/mL (�0.01) and HCV antibody remainednegative. CD4 was 343 /�l and PCR HIV–RNA again demonstratedundetectable level. Alpha–fetoprotein tumor marker was elevated at 3175ng/mL (0–15). Cytologic, histologic, and immunohistochemical findings ofthe fine needle aspiration specimen were consistent with metastatic HCC.During 3 months of follow–up, his metastatic HCC has aggressivelyprogressed and his prognosis is extremely poor.

Hepatocellular carcinoma will likely be an emerging problem facingincreasing number of HBV/HIV co–infected individuals. HAART hasrevolutionized HIV disease and consequently, HIV–infected patients willcontinue to experience increases in morbidity and mortality from non–HIV– related diseases and tumors such as the HCC reported here. Routineserologic monitoring to detect active HBV replication and an aggressiveHCC screening practice, even in inactive carrier–state patients, may bewarranted in HBV/HIV co–infected individuals.

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EVEN A VERY HIGH CONCENTRATION OF CA19–9 IS NOT ARELIABLE MARKER OF PANCREATOBILIARYMALIGNANCYCuruchi Anand, M.D. and Vivek Raj, M.D.*. Gastroenterology andHepatology, University of Arkansas for Medical Sciences, Little Rock,AR.

Purpose: At high concentrations CA 19–9 has been suggested as a reliablemarker for the presence of pancreatobiliary tumors. It is appreciated thatCA 19–9 can be elevated in a wide range of benign conditions such as liverdisease, cholangitis, obstructive jaundice and pancreatitis. In the past,efforts have been made to establish a cut off value to increase the specificityof CA 19–9 for tumor diagnosis. At levels greater than 1000u/ml thespecificity has been stated to approach 100%.

We report a patient with an exceptionally high CA 19–9 due to amp-

ullary stenosis. A 74–year–old gentleman was referred for evaluation ofjaundice and a significantly elevated CA 19–9 level of 1670 u/ml. He hada cholecystectomy 6 months ago and had recurrence of abdominal pain andjaundice. An ERCP with sphincterotomy was performed for a distal CBDstricture 3 months prior to presentation to our hospital. Following ERCP hisbilirubin improved but did not normalize. Liver function tests showed abilirubin of 3.3 mg/dl, ALT 59 IU/L, AST 40 IU/L, Alk Phos 153 IU/L andGGT 77 IU/L. CA 19–9 was highly elevated at 1670 u/ml (reference range:0–37 u/ml). CEA was normal. CT scan of abdomen, EGD and colonoscopywere all normal. Endoscopic ultrasound examination of pancreas and CBDwas normal. ERCP was repeated and showed an ampullary stenosis whichwas treated with an extension of sphincterotomy. Biopsy of the ampulla andbrushings from distal CBD were negative for malignancy. The CA 19–9and liver function tests gradually decreased to normal levels. Patient hasbeen asymptomatic on follow up for 1 year and repeat MRI of abdomen at1 year was normal.

We conclude that it is not possible to reliably distinguish between benignand malignant pancreatobiliary disease based on a significantly elevatedCA 19–9 level. Serial measurements of CA 19–9 after biliary decompres-sion may be more reliable in this context; a steady or rising level of CA19–9 after improvement of jaundice could suggest malignant disease.

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SECONDARY AMYLOIDOSIS OF THE LIVER AS THEPRIMARY MANIFESTATION OF CROHNS DISEASEAlex R. Rusynyk, D.O., Martha S. Ghosh, M.D., Vincent J. Varano,M.D.* and Matthew B. Grundfast, D.O. Gastroenterology andNutrition, Geisinger Medical Center, Danville, PA.

Background: Secondary amyloidosis (AA) is a disorder characterized bythe extracellular tissue deposition of fibrils that are composed of fragmentsof serum amyloid A protein, an acute phase reactant. This disorder, alsocalled reactive amyloidosis, can occur in a variety of chronic inflammatoryconditions. We report a case of secondary amyloidosis as the presentingmanifestation of Crohn’s disease.Case Report: A 48–year old female presented to our institution with anelevated alkaline phosphatase (AP) and a three–month history of weightloss. She denied any history of arthralgias, abdominal pain, or history ofinflammatory bowel disease. Her past medical history was significant fornon–insulin dependent diabetes. An ultrasound of her liver revealed mul-tiple hypodense lesions prompting a liver biopsy. The biopsy revealed adiffuse involvement of amorphous material with a sinusoidal pattern.Immunohistochemical staining was positive for an amyloid AA pattern.Hematology and Rheumatology evaluations failed to elucidate the sourceof her secondary amyloidosis. An infrequent history of loose stoolsprompted a colonoscopy, which revealed diffuse erythema and multipleulcerations. Biopsies confirmed Crohn’s disease. She was placed on amesalamine and steroid combination with marked improvement of her APand reversal of her weight loss.Discussion: Secondary amyloidosis may complicate a number of chronicinflammatory conditions. The most common organ system involved is thekidney. The treatment consists of correcting the underlying inflammatorydisorder. This case represents a rare and unusual presentation of inflam-matory bowel disease.

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THE GASTROINTESTINAL ENDOSCOPIC APPEARANCE OFSWEET’S SYNDROMESohail Gagan, M.D., Ramesh Krishnamurthi, M.D., Andrew Libertin,M.D.* and Ronald Crock, M.D. Internal Medicine Department,Affiliated Hospitals at Canton, Canton, OH.

Background: Sweet’s Syndrome was initially described as an acute febrileneutrophilic dermatosis in 1964 by Robert Douglas Sweet. Its most dis-tinguishing characteristics are fever, neutrophilic leukocytosis, abrupt ap-

S161AJG – September, Suppl., 2002 Abstracts

pearance of erythematous, painful cutaneous plaques and a dense dermalinfiltrate consisting of mature neutrophils. Though systemic manifestationsare common, those involving the GI tract are not well described. We areonly the 2nd group to describe and document endoscopically the GI lesionsassociated with Sweet’s Syndrome.Case: Our patient is a 51 year old white male who presented with acuteonset of fever and painful, erythematous, vesiculated lesions scattered overhis face, back and upper extremities. The patient had also been complainingof non–specific abdominal pain. CT examination done prior to admissionrevealed changes consistent with inflammatory bowel disease. Patient’spast medical history was pertinent for myelodysplastic syndrome anddiabetes mellitus with end–stage renal disease. He had leukocytosis with awhite count of 20,000/mm3. Biopsy of the skin lesions was consistent withSweet’s Syndrome. Blood cultures were negative. Patient underwent GIendoscopy for follow up of the abnormal CT scan. Initial endoscopyseemed consistent with pneumatosis cystoides intestinalis. On biopsy of thelesions, however, Sweet’s Syndrome was diagnosed. The patient wasplaced on steroids and skin lesions resolved within a week. Patient refusedfollow up endoscopy.Discussion: The etiology of Sweet’s Syndrome is unknown and in mostcases appears to be idiopathic. Twenty–five % of the cases, however, areassociated with infection, autoimmune disorders, vaccinations or neoplasticdisorders. Systemic symptoms are frequent and have occurred in mostorgan systems. However, as noted by Yuchi, gastrointestinal involvementhas not been well described. In their case, the endoscopic appearance wasthat of multiple, shallow, wide ulcerations. In our case the Sweet’s Syn-drome appeared as described.Conclusion: This case is the 2nd case of Sweet’s Syndrome to be describedendoscopically. Our case greatly adds to the paucity of knowledge forgastroenterologists, surgeons, and others who do endoscopies.

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AN UNUSUAL RECTAL MASS: DIFFERENTIATING MUCOSALPROLAPSE SYNDROME FROM RECTAL CANCERRichard S. Lee, M.D., FACG and Kirk A. Ludwig, M.D.*. NeuseGastroenterology, PA, Smithfield, NC and Department of Surgery, DukeUniversity Medical Center, Durham, NC.

Purpose: A 52 year old white female presented with blood in her stool,constipation and incomplete evacuation. Review of systems was otherwisenegative. Past medical history was significant for GERD with an esopha-geal stricture and colonic polyps noted at an outside hospital. Colonoscopyrevealed right and left diverticulosis and a 5 x 3 cm rectal mass withmultiple biopsies obtained that were consistent with inflammation. Thisrectal lesion was larger than any lesion noted by report on colonoscopyfrom the outside hospital, 2 years prior to this evaluation. A surgical consultwas obtained and a rigid proctoscopy was performed; grasper biopsiesrevealed mucosal prolapse syndrome, pathology was consistent with aninflammatory cloacogenic polyp. Lower EUS revealed benign inflamma-tory changes. CT of the abdomen and pelvis was negative. Defecographyrevealed a small anterior rectocele and intussusception with incompleteevacuation. A Delorme surgical procedure was performed to remove theinternal rectal prolapse and abnormal inflammatory mass. Surgical pathol-ogy confirmed inflammation consistent with mucosal prolapse syndrome.Follow–up evaluation revealed her bowel function to be much improvedwithout constipation with normal stool consistency.Conclusions: Mucosal prolapse syndrome can be difficult to differentiatefrom a rectal adenomatous lesion or rectal malignancy, even after a detailedhistory and physical, and standard endoscopic and radiographic studies.Surgical intervention for this benign lesion can offer considerable improve-ment in patient’s symptoms and lifestyle.

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CENTRAL NERVOUS SYSTEM AND INTESTINAL VASCULITISASSOCIATED WITH HEPATITIS CCuruchi Anand, M.D., Sandeep Bhargava, M.D., Vivek Raj, M.D. andJean–Pierre Raufman, M.D.*. Gastroenterology, University of Arkansasfor Medical Sciences, Little Rock, AR.

Purpose: Extra hepatic manifestations of hepatitis C infection (HCV) arefrequently its initial presentation and contribute significantly to morbidity.Vasculitis associated with HCV presenting as glomerulonephritis, mono-neuritis multiplex and leukocytoclastic vasculitis of skin has been exten-sively reported. We describe two unusual cases of vasculitis associatedwith HCV.Case 1: A 46–year–old man with isolated central nervous system vascu-litis. He presented with a 2–month history of severe headache. He had righthemiparesis with dysphasia a year ago. He has no history of hypertension,diabetes, hyperlipidemia or drug abuse. MRI/MRA revealed an old isch-emic stroke and beading of arteries suspicious for vasculitis. Cerebralangiogram showed arterial irregularity consistent with vasculitis. CSFshowed an elevated protein of 61mg/dl. CSF VDRL, ANA, ANCA andcomplement levels were normal. RF was positive. Cryoglobulin was neg-ative at 72 hours. HIV was negative. Work up for hypercoagulable statewas negative. Transaminases were elevated and HCV PCR was positive.Liver biopsy showed portal triaditis but no vasculitis involving the liver. Hewas treated with pegylated interferon, ribavarin and prednisone. His head-ache improved after 4 weeks of treatment, and at 6 month follow up heshowed no neurological symptoms.Case 2: A 45 year–old man with cryoglobulinemia and intestinal necrosis.He presented with acute onset of abdominal pain and dysentery. Stoolculture, O&P, C–difficle toxin and Yersinia serology were negative.Colonoscopy showed erythema and friability of mucosa of the terminalileum, cecum and ascending colon. Biopsy showed acute non–specificinflammation. One month later he returned with acute abdominal pain andhad peritoneal signs on examination. Exploratory laparotomy was per-formed and revealed necrotic bowel. His terminal ileum and right colonwere resected. ANA and ANCA were negative. Mesenteric angiogramshowed no obstructing lesion. Work up for a hypercoagulable state re-vealed minor abnormalities secondary to recent thrombosis. A month laterhe developed acute abdominal pain, fever and vomiting. Surgery wasperformed and 50 cm of ischemic small bowel was resected. Cryoglobulinand HCV PCR were positive. We planned to treat him with pegylatedinterferon and ribavarin but the patient failed to follow up. We concludethat testing for HCV should be undertaken in all cases of vasculitis ofuncertain etiology. Pegylated interferon and ribavarin should be consideredfor treating the extra–hepatic manifestations in addition to eradication ofHCV.

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PNEUMOENCEPHALOMENINGITIS COMPLICATINGCROHN’S DISEASEMarie L. Borum, M.D.*, Bruno Petinaux, M.D., Mary A. Camarca,M.D. and Christine Martabano, P.A. Gastroenterology, GeorgeWashington University, Washington, DC; Emergency Medicine, GeorgeWashington University, Washington, DC and Emergency Medicine,INOVA Fairfax Hospital, Falls Church, VA.

Purpose: Fistulas are a common feature of Crohn’s disease that can leadto a variety of complications. We report the first case of pneumoencepha-lomeningitis resulting from an enterospinal fistula in a patient with Crohn’sdisease.Case: A 26 year old woman with a 1–year history of terminal ileal andcolonic Crohn’s disease presented to the ER for evaluation of back dis-comfort and headache. She had been managed with Pentasa and 6–MPwithout difficulty. Occasional Crohn’s exacerbations with diarrhea weretreated with tapering courses of Prednisone.

One month prior to admission the patient reported the onset of back

S162 Abstracts AJG – Vol. 97, No. 9, Suppl., 2002