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EFFECTIVENESS OF ENDOSCOPIC DILATION FORDYSPHAGIA FROM CRICOPHARYNGEAL BARSAndy Wang, M.D., Peter J. Kahrilas, M.D., Ikuo Hirano, M.D.*Northwestern University Feinberg School of Medicine, Chicago, IL.

The cricopharyngeal (CP) bar is a common radiographic finding that cancause oropharyngeal dysphagia (OPD). Treatment options include CPmyotomy, which is problematic given that CP bars primarily affect elderlypatients with comorbidities who are at higher risk for peri-operative com-plications. The aim of this study was to examine the effectiveness ofendoscopic dilation in the management of dysphagia attributed to a CP bar.Review of upper endoscopic (EGD) and videofluoroscopic swallowingstudies from 1999-2002 identified 32 patients with CP bars. CP bar wasdefined by radiology as a distinct posterior impression in the cervicalesophagus inferior to the vocal cords. Six of these patients had dysphagiawithout any other identifiable cause aside from the CP bar. Each of thesesix patients underwent EGD with Savary (5) or balloon dilation (1) of theupper esophageal sphincter to a diameter of 51–60 Fr. Short- and long-termfollow-up was conducted post-dilation at 1–4 weeks and 10–27 months,respectively. The median age of the 32 patients with CP bars was 63 yrs.The 6 symptomatic patients who underwent endoscopic therapy werewomen with median age of 62 yrs. Each of the 6 patients experiencedimmediate improvement in dysphagia. None of the patients developedcomplications of post-dilation pain, bleeding or perforation. Five patientshad continued improvement of their OPD at short-term follow-up. Onepatient who was dilated to 51 Fr using a Savary dilator experienced returnof globus sensation after 48 hours, although dysphagia and regurgitationhad resolved. A second Savary dilation, one month after the initial proce-dure, resulted in complete elimination of symptoms at subsequent short-term follow-up. Four patients had continued complete resolution of OPD atlong-term follow-up. The remaining two patients reported the recurrence ofsignificant dysphagia after 6 and 8 months, which they stated was lesssevere than at initial presentation. None of the patients required surgical orendoscopic myotomy for residual or refractory dysphagia. Every patientwas satisfied with the results and stated they would recommend endoscopicdilation to others with the same problem.(1) CP bar is an important causeof dysphagia that affects elderly patients. (2) Endoscopic dilation of symp-tomatic CP bars can produce long-term relief of dysphagia. (3) Furthercontrolled studies are warranted to better define the efficacy and safety ofendoscopic CP bar dilation as an alternative to surgical myotomy insymptomatic patients.

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IS RENAL FAILURE A CONTRAINDICATION FOR STEROIDUSE IN ACUTE ALCOHOLIC HEPATITIS?Gonzalo Pandolfi, M.D., Sanjay Nayyar, M.D., Franjo Vladic, M.D.,Gijo Vettiankal, M.D., Melchor Demetria, M.D.,Bashar M. Attar, M.D., FACG* John H. Stroger Hospital of CookCounty, Rush Medical College, Chicago, IL.

There is limited data on the benefit of steroids in patients with severealcoholic hepatitis who have concomitant renal failure, previous studieshave shown that patients with renal failure due to hepatorenal syndrome donot benefit from steroids. We present a case of a 42 year-old Caucasianmale, a heavy alcohol user who presented with a 2 weeks history ofjaundice and increasing abdominal girth. Physical exam was significant forpresence of icterus, smooth hepatomegaly and ascites. There was nohepatic encephalopathy. Initial laboratory analysis performed showed BUN33, Cr 2.5, total protein 6.8, albumin 3.4, total bilirubin 37.2, directbilirubin 31.4, Alk Phos 279, GGT 365 and AST 207, ALT 74, PT 19.9,PTT 44.3, INR 2.56, Hgb 12, WBC 22,000, with 80% PMN’s and platelets388,000. In the absence of other causes of liver disease a diagnosis ofsevere alcoholic hepatitis (DF score 74) was made. CT with contrast wasdone in the emergency department which showed ascites with hepatomeg-aly, no biliary dilatation or liver mass lesion. The alcoholic hepatitis did not

improve on conservative management. The renal function progressivelyworsened despite hydration and the BUN and creatinine increased to 133and 8 respectively. The work-up was consistent with ATN, possibly due toradiocontrast. At this point, the patient was started on prednisone 40mg POdaily. Subsequently the liver and renal function improved and returned tobaseline over a period of 2 weeks. The patient was discharged with a2-week course of corticosteroids.The efficacy of steroids has not been wellstudied in patients with severe alcoholic hepatitis and renal failure. Successof steroid use in this subgroup probably depend on the etiology of renalfailure. This case indicates that corticosteroids may be beneficial in thesetting of severe alcoholic hepatitis and acute renal failure not due tohepatorenal syndrome.

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HAMARTOMA AS A CAUSE OF HIGH INTESTINALOBSTRUCTIONSanjay Nayyar, M.D., Gonzalo Pandolfi, M.D., Melchor Demetria, M.D.,Benjamin T. Go, M.D., Katherine Liu, M.D.,Bashar M. Attar, M.D., FACG* John H. Stroger Hospital of CookCounty, Rush Medical College, Chicago, IL.

Mechanical outlet obstruction in the upper GI tract can often times becaused by obstructive peptic ulcer disease or gastric carcinoma. We presenta case of a hamartoma causing a mechanical outlet obstruction. The patientpresented with 2–3 weeks of abdominal pain accompanied by occasionalbouts of vomiting which had progressively gotten worse over the last 2–3weeks. An upper endoscopy was performed which showed a large friablemalignant looking mass in the second and third part of the duodenum withsignificant amount of food residue in the stomach. Biopsies obtained fromthis lesion showed it to be an adenocarcinoma. CT scan of the abdomenrevealed a 9 cm mass lesion in the third part of the duodenum without anymetastasis. A curative (Whipple) surgery was performed and pathologyshowed two separate lesions.There was a hamartoma with tubular adeno-matous change proximally and an adenocarcinoma distally. Based on theintraoperative impression the hamartoma was the cause of patient’s ob-structive symptoms. Subequently the patient was discharged from thehospital with a normal post operative course.Benign hyperplasia of Brun-ner’s gland and hamartomas leading to adenocarcinoma in the setting ofPeutz-Jeghers syndrome have been well reported. There have been veryfew case reports where a hamartoma lead to an adenocarcinoma in theabsence of Peutz-Jegher’s syndrome. This case illustrates a separate butsynchronous occurrence of a hamartoma and an adenocarcinoma

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CUTANEOUS TUBERCULOSIS ASSOCIATED WITHINFLIXIMAB TREATMENTSumir Patel, M.D., Abhijit Kulkarni, M.D.*, Rad Agrawal, M.D.,Arezo Shahwali, M.D. Allegheny General, Pittsburgh, PA.

Introduction: A 56 year white old male with a history of Crohn’s diseasepresented with right lower quadrant abdominal pain and fever. He alsoreported episodes of diarrhea four days prior to admission. He deniednausea, vomiting, cough, sputum production or headache. The patient hadbeen treated with infliximab in the recent past. He had tested PPD positivein the distant past and received INH for one year. Physical exam wasremarkable for a temperature of 39.9 and right lower quadrant tendernesson palpation. The CBC with differential, basic metabolic panel and liverfunction tests were unremarkable. Patient was admitted for presumedexacerbation of Crohn’s disease. He continued to have fevers (Tmax: 39.2),chills and rigors. Blood and urine cultures were sent and empiric antibiotictreatment was started. A 3x1 cm painful, firm, erythematous nodule withirregular borders was noted on the right upper extremity. The nodule wasbiopsied. A flexible sigmoidoscopy was performed which did not show anyabnormalities. Blood cultures, urine and stool studies were all unremark-able. He continued to have fevers and night sweats. A new lesion was notedon the right thigh which was also biopsied. On further questioning the

S185AJG – September, Suppl., 2003 Abstracts