from the anastomosis of patients with Billroth II (BII) were cut from tissueblocks fixed in formalin and embedded in parafin. Biopsies were immu-nostained for CK7 (DAKO OV-TL 12/30, 1/100) and CK20 (Dako Ks20.8,1/200). The pattern of CK7/CK20 immunostaining in the surface epithe-lium(S) and the deep glandular(G) areas was rated as diffuse(D), patchy(P)or absent(A) by 2 independent examiners. The characteristic reportedstaining pattern for BE is strong SD and GD for CK7 and strong SD andGP for CK20. The gastric CK7/CK20 pattern depicts a CK7 stain, whichis patchy and weak in the deep glands, and CK20 which stains SP and GP.Tissue from adenocarcinoma of the lung and colon served as positivecontrols for CK7 and CK20, respectively.Results: Specimens from 11 patients with LSBE, 30 with SSBE and 6 withBII were processed and analyzed. All specimens from LSBE patientsdemonstrated the characteristic CK7 strong SD/GD and CK20 strongSD/GP staining pattern. Specimens from 19 of 30 (63%) SSBE patientsstained with the esophageal CK7/CK20 pattern. In 11 of 30 patients (37%)the charcateristic gastric IM pattern (CK7 GP and CK20 SP/GP) wasconsistent with IM of the gastric cardia. CK7 staining was absent in thesurface epithelium (SA) and glands (GA) of the IM tissue in all of thepatients with a BII. CK20 stained patchy in the surface epithelium (SP) andabsent in the deep glands (GA) in the IM tissue of the gastric remnant inall of these patients.Conclusions: LSBE demonstrates a distinct and reproducible CK7/CK20staining pattern that differs from staining in the gastric cardia and remnant.More than one-third of patients with endoscopically defined SSBE exhib-ited the characteristic immunohistological gastric cardia pattern. CK stain-ing of IM in the gastric remnant differs from the staining pattern seen in IMof the esophagus and gastric cardia. This suggests that the etiologic causeof IM in the proximal stomach (cardia) is different from that of the moredistal gastric remnant. These results may help to understand the malignanttransformation of IM in these three sites.

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The clinical significance of thickened gastric folds found on uppergastrointestinal seriesThomas Tran, MD, Patrick Hung, MD, Rodolfo Laucirica, MD, RaoufHilal, MD and Richard Goodgame, MD*. 1Department of Medicine,Baylor College of Medicine, Houston, TX, United States; and2Department of Pathology, Baylor College of Medicine, Houston, TX,United States.

Purpose: Barium upper gastrointestinal series (UGIS) is commonly per-formed on patients suspected to have disease in the esophagus, stomach, orduodenum. A finding of thickened gastric folds on UGIS frequently leadsto recommendation by the radiologist to perform an esophagogastroduo-denoscopy (EGD). We assessed the impact of EGD and biopsy on theoutcome of patients with isolated thickened gastric folds found on UGIS.Methods: A total of 8325 consecutive UGIS reports from January 1997 toDecember 2000 were reviewed to identify 182 patients who had isolatedthickened gastric folds. Patients with other serious radiologic abnormalitieswere excluded. The included patients were studied by a systematic reviewof the EGD findings, gastric biopsy results, and clinical outcome.Results: The study included 96 males (52.7%) and 86 females (47.3) whowere found to have isolated thickened gastric folds on the UGIS. EGD wasspecifically recommended in 76 (41.8%) of the 182 reports. A total of 74patients underwent the EGD and 108 patients did not. The EGD group andthe no-EGD group were similar in demographic and clinical features. TheEGD results were: normal 18 (24.3%), thickened gastric folds 12 (16.2%),hiatal hernia 12 (16.2%), mucosal inflammation 11 (14.9%), erosions 8(10.8%), portal gastropathy 3 (4.1%), and gastric ulcer 1 (1.4%). None hadobvious malignancy on EGD. Forty-eight of the 74 EGD patients had agastric biopsy. The findings were chronic active gastritis 39 (81.3%),chronic antral gastritis 5 (10.4%), and others 4 (8.3%). Evidence forHelicobacter pylori gastritis was present in 91.7% of the gastric biopsies.No malignancies were diagnosed by biopsy. Clinical outcome (mean fol-low-up 28.5 months) was assessed in 49 patients in the EGD group and 55

patients in the no-EGD group. There were no cases of serious or new uppergastrointestinal problems in either group. Two patients in the EGD groupdied of acute myocardial infarction and chronic liver cirrhosis. One patientin the no-EGD group died of liver cirrhosis.Conclusions: The finding of isolated thickened gastric folds on UGIS isfrequently associated with Helicobacter pylori gastritis and is not associ-ated with gastric malignancy or other serious gastric disease. Performingendoscopy and biopsy did not appear to alter the outcome of patients withisolated thickened gastric folds found on UGIS. (Supported by the LanzaResearch Fund)

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Pantoprazole IV dramatically suppresses gastric secretion in a shortbowel patient uncontrolled by H2RAsAnthony Troitino, MD1, Elaine Soffer2 and Wieslaw J. Bochenek, MD2*.1Upstate Medical Associates, P.C., Troy, NY, United States; and 2WyethAyerst Research, Radnor, PA, United States.

Purpose: Gastric hypersecretion is a frequent finding in patients with shortbowel syndrome that often contributes to excessive diarrhea. Following isa case presentation of successful use of Pantoprazole IV in a short bowelpatient.Methods: A 72-year-old female with functional short bowel was admittedto the hospital with dehydration and metabolic alkalosis. She had almostcomplete obstruction at the mid-duodenum from adhesions and was main-tained on home total parenteral nutrition (TPN). Because of excessiveregurgitation, a gastric fistula had been created to allow for drainage ofgastric contents. Upon admission, the patient was stabilized with correctionof volume status and acid/base balance. To decrease volume of gastricdrainage, Ranitidine IV was increased from 125 to 250 mg/24 h with noimprovement. Gastric contents remained at a pH level of 2.0 to 3.0 with avolume in excess of 500 mL/24 h. Ranitidine was discontinued and, aftera 24 h washout, she was started on Pantoprazole IV.Results: Pantoprazole IV 40 mg was administered intravenously over 15min. twice daily, at the beginning and end of TPN infusion. Following arethe data on volume and pH of gastric drainage while on the differenttreatment regimens. The patient remained fasting on the measurement days.

Table. 24h Volume and pH of Gastric Drainage

Day Treatment Volume (ml) pH

�1 Ranitidine 655 2.90 Washout 415 1.81 Pantoprazole 205 3.9

2–5 Pantoprazole Negligible 6–7

The patient was discharged from the hospital and continued to take PantoprazoleIV as part of her routine home TPN regimen. She tolerated Pantoprazole withoutany adverse effects.

Conclusions: The dramatic response observed in this patient indicates thatPantoprazole IV may suppress gastric secretion in short bowel syndromewhen H2RAs are ineffective. Such patients may respond with markedreduction of the volume of gastric secretion and change in pH to nearneutral.

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Relationship among homocysteine, Helicobacter pylori infection andcoronary artery diseaseChung-Jyi Tsai* and Tsuei-Yuen Huang. 1Department of Medicine, ChiMei Foundation Hospital, Yung Kang City, Taiwan.

Purpose: H. pylori infection is suggested to be associated with coronaryartery disease (CAD). Yet the mechanism is obscure. Reports indicatehyperhomocysteinemia is toxic to endothelial cells and increases risk ofCAD. These two factors could be linked by a deficiency of vitamins andfolate caused by chronic gastritis in H. pylori infection. This nutritionaldefect could lead to failure of methylation by 5-methyltetrahydrofolic acid

S76 Abstracts AJG – Vol. 96, No. 9, Suppl., 2001