709

A cecal polyp concealed within the appendiceal orificeCarol E. Mallette, M.D.1 and David Schreiber, M.D.2*. 1Dept. ofMedicine, Brown University School of Medicine, Providence, RI, UnitedStates; and 2Gastroenterology, Miriam Hospital, Providence, RI, UnitedStates.

Purpose: The purpose is to describe an interesting presentation of a cecalpolyp completely concealed within the appendiceal orifice identified duringa routine screening colonoscopy.Methods: The patient is a 67 year old Caucasian female who presented tothe GI clinic with several years of constipation and a recent 10 lb weightloss. She was scheduled for a routine colonoscopy for colon cancer screen-ing. During colonoscopy, several small, adenomatous appearing polypswere found throughout the large bowel. At initial evaluation, the iliocecalarea looked completely benign with a normal appendiceal orifice and nopolyps noted. As this area was explored further, a small 1 cm polyp wasfound within the appendix itself. This intermittantly prolapsed out of theorifice and into the cecal lumen. The polyp was completely excised withsnare and cautery.Results: The pathology results revealed an adenomatous polyp.Conclusions: Colonic polypectomy is performed in order to decrease theincidence of colorectal cancer. Despite the ability to directly visualize thewall, some polyps can be hidden by mucosal folds or other normal colonicanatomy. We present a case in which an adenomatous polyp was com-pletely concealed within the appendiceal orifice.

710

Liver hematoma: an unusual complication of ERCPShahid Mehboob, M.D., Mohammad M Alsolaiman, M.D., RichardMacDowell, M.D. and Howard S Malamood, M.D.*. 1InternalMedicine, Division of Gastroenterology, Albany Medical Center, Albany,New York, United States.

Purpose: Hematoma of the liver has not been previously described as acomplication of ERCP. We report the case of a 28 year old woman, whounderwent ERCP for choledocholithiasis. She had a precut needle-knifesphincterotomy for deep cannulation followed by an occlusive ballooncholangiogram and stone extraction. Within 24 hours, she presented withepigastric pain and a significant drop in hematocrit. CT-scan of abdomenshowed left subcapsular hematoma & free intraperitoneal fluid. Laparo-scopic examination confirmed the above findings. The peritoneal blood wasremoved but the hepatic hematoma was left in-situ without manipulationbecause there was no active bleeding at the time of laparoscopy. Herabdominal pain resolved and hematocrit remained stable along with nor-malizing liver function tests, thereafter.

We postulated two mechanisms that could have caused this complicationin absence of abdominal trauma or coagulopathy in a patient with previ-ously normal liver: (a). Guide-wire used (0.025 inch/480 cm), might havecaused perforation of the liver capsule, if it was advanced too far into theproximal hepatic duct. It could have happened while inserting the balloonover the guide-wire, which pushed the wire further if the assistant had notsecured the wire during the exchange of catherters. (b). Alternatively,Pressure used for the occlusive cholangiogram, might have caused ruptureor “blow out” of a superficial hepatic ductule associated with pericapsularvascular injury, leading to hematoma.Conclusions: Based upon our unusual experience, we recommend advanc-ing the guide-wire cautiously during the deep biliary cannulation to avoidthis potential complication. Care should also be taken during contrastinjection to avoid excessive hydrostatic pressure and to use a 10 cc syringe(or smaller) to assure proper pressure.

711

A case of multiple myeloma associated light chain disease:presenting with severe intrahepatic cholestasis and renal failureMeyer D. M.D., Gotian A. M.D., Edelman M. M.D., Reiunus J. M.D.Montefiore Medical Center, Bronx N.Y.

A 49-y/o man presented with a 6-week history of fever, RUQ abdominalpain, jaundice, pruritus and weight loss. He had no risk factors for, orhistory of, chronic hepatobiliary disease. On physical examination thepatient was noted to have jaundice, hepatomegaly, ascites and lowerextremity edema. Admission laboratory results were: Hct.–34%, MCV–82fL, Na–131 mEq/1, K–5.3 mEq/l, HCO3–14 mEq/l, BUN–74 mg/dl andCr.–15.1 mg/dl. Liver tests shown Total Protein–6.0 g/dl, Albumin–3.1g/dl, Total Bili-11.2 mg/dl, Direct Bili–8.2 mg/dl, Alk Phos–401 U/L,AST–41U/L and ALT–43 U/L. Viral hepatitis serologies were negative.Cross-sectional imaging demonstrated nephro- and hepatomegaly withoutabnormality of the biliary tract, mass or adenopathy.

In our hospital, the patient was begun on hemodialysis, and developedUGI bleeding from esophageal varices, loose watery stools and encepha-lopathy with hallucinations. His ascites was refractory to dialysis andparacentesis. SPEP and UPEP demonstrated monoclonal kappa lightchains; bone marrow biopsy was consistent with multiple myeloma withmonoclonal IgA kappa protein. Microscopic examination of a transjugularliver-biopsy specimen revealed marked cholestasis with ductular prolifer-ation, moderate interface hepatitis and large areas of centrilobular hepato-cyte dropout. The patient expired prior to beginning chemotherapy. EMexamination of autopsy tissues showed renal peritubular and hepatic peri-sinusoidal kappa light chain deposits leading to a final diagnosis of rapidlyprogressing multiple myeloma with associated light chain deposition dis-ease (LCDD), secondary renal failure, and cholestatic hepatitis.

In 1976, LCDD was first described by Randall et al.. Most case reportsof LCDD describe renal failure preceding or in conjunction with asymp-tomatic hepatic involvement. The most common clinical presentation ofliver disease is hepatomegaly with a modest elevation in the serum AlkPhos level. Symptomatic liver disease due to light chain deposition isextremely rare, although jaundice is seen occasionally with hepatic amyloiddeposition. This is the first case report in the English-language medicalliterature of which we are aware describing simultaneous renal failure andcholestatic hepatitis due solely to LCDD.

712

Severe abdominal pain, anemia and hepatic dysfunction: an unusualetiologyPrem S. Misra, M.D., FACG, Woo Sup Kim, M.D. Wyckoff HeightsMedical Center, Brooklyn, New York.

A 45-year-old man presented with severe colicky lower abdominal pain,obstipation, nausea and anorexia of two weeks duration. He had lost 20pounds in weight over last three months. His past history included chroniccough, COPD and bronchial asthma. Patient was taking herbal medicine forcough. Pain was only relieved by frequent meperidine injections. A bariumenema (BE) showed multiple areas of spasm and possible annular lesion inright colon.

On physical examination patient was pale and icteric, afebrile, heart rate94/min. His abdomen was soft, non-distended, non-tender with hypoactivebowel sounds.

His serum Na was 121meq, Hemoglobin 9.7gm, Hematocrit 28.7%,Total bilirubin 4.6mg (Direct � 0.7), AST 47u/L, AIP 127. Chest xrayrevealed old healed granulomatous disease. Two attempts at colonoscopycould not enter right colon due to spasm. Repeat BE was normal. HepatitisA, B, C Profile was normal. Alpha-Feto-protein was 30.6(Nl 15ng/L).Peripheral blood smear showed baso-philic stippling.

Urinary delta aminolevulinic acid (Delta ALA) was 4.95 mg (NI 0–0.54)and random quantitative porphobilinogen was 0.27mg (NL 0–0.20). DeltaALA was in a “critical zone” with relationship to lead exposure. Patient’stotal consumption of lead from herbal tea and tablets exceeded 3 grams

S223AJG – September, Suppl., 2001 Abstracts

prior to this encounter. High concentration of arsenic in the tea was alsodocumented. He underwent chelation therapy.

The advent of alternative medicine therapies requires that cliniciansconsider them in the differential diagnosis in puzzling clinical situations,today more than ever before.

713

Combined heart-liver transplant for hemochromatosisBrad R Moore1 and Ira Willner1*. 1Division of Gastroenterology andHepatology, Medical University of South Carolina, Charleston, SC,United States.

Purpose: Hypogonadism and cardiac manifestations are sometimes asso-ciated with hemochromatosis. We present a case in which a patient wasincidentally found to be cirrhotic during transplantation workup for idio-pathic cardiomyopathy.Case Report: A 39-yr. old white male presented with progressive shortnessof breath. His history was significant for recently diagnosed nonischemiccardiomyopathy (ejection fraction �20%) as well as hypogonadism. Hehad required AICD placement due to ventricular tachycardia. He wasreferred for cardiac transplant evaluation. He was found to have a ferritinof 5481 ng/ml (serum Fe 176 mcg/dl and Fe saturation 98%). Albumin was5.5 g/dl and platelet count was 108K/cumm. AST, ALT bilirubin, alkalinephosphatase, and PT/PTT were normal. Abdominal ultrasound was unre-markable. On exam, no hepatosplenomegaly or ascites were appreciated.He was mildly tender in the right upper quadrant. Liver biopsy revealed 4�iron staining (quantitative iron 39097 mcg with iron index 17.5) andcirrhosis. HFE genotype was homozygous for HFE 282Y mutation. Giventhe surprising finding of cirrhosis on liver biopsy, we did not feel the patientwould do well with cardiac transplantation alone, so we recommended acombined heart-liver transplant. The patient’s medical regimen was max-imized, and he was discharged. Several weeks later, the patient underwenta combined orthotopic heart-liver transplant. Four months post-transplant,he is doing well.Conclusions: In patients with hemochromatosis, it is unusual to see hy-pogonadism and cardiomyopathy in the absence of clinical liver disease.However, in a patient who presents with hypogonadism, cardiac arrhyth-mias, or a cardiomyopathy, hemochromatosis should always be in thedifferential diagnosis.

714

Swallowing-induced syncope: sinus arrest successfully treated withshort-acting anticholinergicsMoskovitz M, Fadden R, Malkowski M. Heritage Valley Health System,Beaver, PA and The University of Pittsburgh, Pittsburgh, PA.

An 82-year-old woman was admitted with a sensation of low substernaldysphagia after food ingestion followed by syncope resulting in a fall. Shehad similar symptoms for over 2 years. She has had ulcerative esophagitisin the past and despite PPI therapy was still symptomatic with pyrosis andtherefore was referred for a laparoscopic Nissen fundoplication 4 monthsprior. This improved all of her symptoms dramatically, but one monthsubsequent to the operation, the syncopal spells reoccurred. These alwaysfollowed a sensation of food sticking in the low substernal region followingswallowing solids. Physical examination was unremarkable. A burger wasingested while she was being monitored and syncope reoccurred. Simul-taneous cardiac monitoring showed a 6 second sinus arrest with AV block.Her medications consisted of simvastain, salmeterol, albuterol, andzafirlukast. A temporary pacemaker was placed but didn’t capture. Apermanent pacemaker was an inserted but was complicated by right ven-tricular perforation treated with pericardiocentesis. The pacemaker was stillnot uniformly functional. Upper endoscopy showed a distal esophagealbenign ulcer unassociated with a stricture. She was treated with lansopra-zole, and hyoscyamine 0.125 mg. 30 min. AC sublingually. She becameasymptomatic and has not developed any further symptoms of swallowinginduced syncope in four months of follow-up.

Deglutition syncope is rare, usually associated with esophageal disordersincluding strictures, carcinoma, and rarely without underlying disease.Cardiac etiologies have been associated on occasion in including certaincardiac drugs, or in an acute M.I. setting. The cardiac mechanism usuallyhas been heart block or sinus arrest, and felt to be mediated vagally.Treatments and past have usually consisted of pacemaker insertion, treat-ment of the stricture with dilation, long-acting anticholinergic drugs in onecase, or beta-adrenergic blockade.

This case shows that short-acting anticholinergic therapy given 30 min-utes prior to eating, along with PPI therapy were successful treatment inthis case of deglution syncope, where cardiac pacing was technicallyunsuccessful.

715

Bloody diarrhea in a patient with Behcet’s diseaseRossana Moura, MD, and Arvey I. Rogers, MD. Jackson MemorialHospital, University of Miami School of Medicine, Miami, FL.

We describe a patient with Behcet’s disease with the unusual presentationof an ulcerative colitis-like picture.

A 35 year old white female presented with 7 days of bloody diarrheaassociated with lower abdominal cramps. She was experiencing worseningof arthralgias of knees, hands and feet, and for the 8 days precedingadmission, oral aphthous ulcers had recurred. Two years earlier she wasdiagnosed as having Behcet’s disease following recurrent episodes oforogenital ulcerations, arthritis, uveitis and pericarditis. At that time shewas started on colchicine and tapering doses of steroids, which inducedremission of her disease. On admission her oral mucosa revealed two smallaphthous ulcers. Her abdomen was diffusely tender with no guarding orrebound. Laboratory values included normal CBC, amylase, lipase, elec-trolytes and transaminases. The stools were negative for WBC, ova, par-asites and C. difficile, and no organisms were cultured. Fecal occult bloodwas positive. Abdominal series was suggestive of thickening of large bowelat the level of the descending colon and splenic flexure. A flexible sig-moidoscopy revealed diminished vascular pattern and edema from the analverge to 25 cm, proximal to which multiple clean based ulcers with areasof erythema and edema and subepithelial hemorrhages were visualized foran additional 20 cm. Biopsies from ulcer bases revealed acute and chroniccolitis with hemorrhage. The patient was treated with hydrocortisone 300mg/day IV continuous infusion. After 72 hours, steroid therapy waschanged to prednisone orally 40 mg/day. The patient did not show anysignificant clinical improvement during her hospitalization, and a weekafter her admission a colonoscopy revealed normal mucosa in the terminalileum, cecum and ascending colon, but diffuse erythema, edema, friabilityand superficial ulcerations from the mid transverse colon to the rectum.Biopsies revealed chronic active inflammation, focal crypt destruction withno dysplasia and no granulomas. She was then started on 6-mercaptopurine100 mg daily, and discharged home also on colchicine 0.6 mg BID,mesalamine 3.6 g/day and slow taper of prednisone. She remains asymp-tomatic one year later with healed colonic lesions on a recent colonoscopy.

This case illustrates that findings of inflammatory bowel disease shouldbe considered secondary to Behcet’s disease in patients who meet thecriteria for this syndrome.

716

A case of intraductal papillary cholangiocarcinomaPavani Muddasani1, Howard M Dubner1 and Lee K Kenneth2*. 1 Dept.of Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA;and 2 Dept. of Gastroenterology, UPMC Shadyside, Pittsburgh, PA,United States.

Purpose: A 55 y female with past history of thyroidectomy and cholecys-tectomy, presented with intermittent RUQ and epigastric pain of 6–7month duration. Pain was described as pressure and bloating with noradiation or association with meals. Occasional nausea and vomiting but noweight loss. Physical exam was only significant for moderate obesity,

S224 Abstracts AJG – Vol. 96, No. 9, Suppl., 2001