patients were NPO during the first 24 hr of treatment and received therapyfor at least 2 days and up to 7 days. Gastric aspirates were obtained every2 hr for determination of gastric pH. Enteral feedings were to be giventhrough the jejunum via a NJ tube or jejunostomy; patients receivingenteral feeding through a NG tube were fed QID and pH readings taken lessoften.Results: A total of 202 patients were randomized, but only 192 had enoughpH measurements for evaluation. 50 P and 4 C patients actually receivedenteral feedings. As shown in Table 1, all pantoprazole treatments in-creased in mean pH at 8 hrs post initiation of feeding and remained abovepH 5 at 16 hrs. Cimetidine treated patients had a marked decline in pH at8 hours post feeding and continued to decrease at 16 hrs.

Mean Gastric Aspirates pH Pre & Post-enteral Feed

Pantoprazole Cimetidine

P40 mgQD

P40 mgBID

P80 mgQD

P80 mgBID

P80 mgTID

300 mg bolus� 50 mg/hr

n�5 n�14 n�8 n�8 n�15 n�4

Pre Feeding(�8 hr)

4.5 (�2.5) 4.9 (�1.9) 5.4 (�1.7) 5.8 (�1.8) 6.5 (�1.0) 5.5 (�1.6)

Post Feeding(�8 hr)

5.7 (�1.6) 5.6 (�1.3) 5.5 (�1.7) 5.6 (�1.5) 6.6 (�0.8) 4.7 (�1.7)

Post Feeding(�16 hr)

6.2 (�0.3) 5.1 (�1.6) 5.5 (�1.7) 5.7 (�1.6) 6.2 (�1.1) 4.3 (�2.5)

Conclusions: All dosing regimens of IV P were higher than C in theenterally fed patient within hours of starting the feed. C pH values con-tinued to drop while IVP values continued to rise to pH of 5 and 6. Lossof pH control occurred rapidly in the C high risk ICU patients. The currentrecommended dosing regimen of C may not be as effective in raisinggastric pH in enterally fed high risk ICU patients as compared with IV P.

120

GASTRIC pH ABOVE 2.5 IS OF LIMITED USE AS A MEASUREOF ACID INHIBITIONVijaya S. Pratha, M.D., Richard B. Lynn, M.D.,Robyn G. Karlstadt, M.D.*, Michael S. Burton, B.S.,Daniel L. Hogan, M.D. Clinical Applications Laboratories, San Diego,CA and Wyeth Pharmaceuticals, Radnor, PA.

Purpose: Acid in the gastric refluxate is a key contributor to mucosal injuryin GERD. Hence, quantification of gastric acid secretion is a logicalmeasure of efficacy of medical therapy for GERD. Gastric acid output(GAO � [H�] gastric volume) measures actual gastric acid secretion.However, intragastric pH is frequently used to assess the efficacy of protonpump inhibitor therapy. The purpose of this study was to assess theaccuracy of intragastric pH as a measure of gastric acid secretion andpotential esophageal acid load.Methods: 155 healthy subjects (49 female, 106 male) were dosed (singledose, double-blind) with either placebo or a proton pump inhibitor. At thetime of dosing, gastric acid secretion was stimulated with a continuousinfusion of pentagastrin (1 mcg/kg/h IV) for 24 hours. Beginning 2 hoursafter dosing and continuing for 22 hours, gastric acid was continuouslyaspirated in 30-minute periods via nasogastric tube. For each 30 minsample, the volume of the gastric aspirate was recorded, pH was measuredusing a pH meter, [H�] determined by titration to pH 7.0, and GAO wasthen calculated.Results: Over 6,500 samples of gastric aspirate were analyzed. All sampleswith gastric pH greater than 2.5 had scant GAO (�2mEq/30min). Whereas,samples with pH between 1.0 and 2.0 had a wide range of GAO (up to 45mEq/30min). Overall, GAO correlated well with volume of gastric aspirate(r�0.89; p�0.001).

Conclusions: Intragastric pH above 2.5 is associated with scant gastric acidoutput and therefore differences in gastric pH above 2.5 are not meaningfulfor comparison of acid inhibition or risk of esophageal acid exposure. Thisis explained at least in part by the fact that pH is a logarithmic scale, whilevolume (like hydrogen ion concentration) is a linear measure. These resultsconfirm similar findings in a previous smaller study that used this model(Pratha, V. et. al. Am. J. Gastro. 2001;96:S66). In conclusion, measurementof gastric pH alone may not be a useful predictor of gastric acidity andpotential esophageal acid load.

121

PROTON PUMP INHIBITORS HEAL, BUT MAY CONCEAL: ACASE OF MALIGNANT GASTRIC ULCER RE-EPITHELISEDBY OMEPRAZOLEShailender Singh, M.D., Christopher Buckley, D.O.,Steven Lichtenstein, D.O.*. Mercy Catholic Medical Center, Darby, PAand Lehigh Valley Hospital, Lehigh Valley, PA.

Purpose: An 87-year-old male presented with weight loss and epigastricpain. General physical examination was unremarkable. Upper endoscopywas performed and a large 2.5 cm white based ulcer was visualized justproximal to the angularis. Multiple biopsies were taken along the borderand the patient was started on omeprazole 20 mg daily. Biopsy wasreported as “strongly suspicious for poorly differentiated carcinoma withulceration”. The patient underwent follow-up endoscopy 3 weeks later anda 9 mm healing gastric ulcer was observed. Multiple brushings and biopsieswere again taken. The pathology report stated “gastric segments of unre-markable gastric mucosa and granulation tissue with acute and chronicinflammation compatible with benign ulcer bed. Negative for malignancy”.About 3 months later, the patient underwent endoscopy which showed theinitial ulcer be to be completely healed and re-epithelised. Surprisingly,biopsy of the healed ulcer bed revealed, “poorly differentiated invasiveadenocarcinoma with signet ring cells”. Patient opted for comfort care andexpired a year later.Discussion: Today, proton pump inhibitors (PPI’s) are considered veryeffective medications for dyspeptic symptoms and ulcer healing. Currently,it is well accepted that the first-line drug therapy for patients diagnosedwith gastric ulcer should be a proton pump inhibitor. They provide fasteronset of action, greater relief of symptoms and increased healing rates. Toexclude malignancy, it is widely recommended that gastric ulcers befollowed up with repeat gastroscopies until their complete healing. Im-provement in the survival of patients with gastric cancer relies largely onearlier diagnosis. Our case is one of the few in the literature, whichillustrates that mucosal healing by PPI’s can obscure the endoscopic signsof malignant gastric ulcer. It has been noted that there may be pressure frompatients to have their dyspeptic symptoms quelled prior to having outpa-tient endoscopies performed. This can lead to delay and in some cases maskthe diagnosis of gastric cancer making the prognosis unfavorable.

S42 Abstracts AJG – Vol. 98, No. 9, Suppl., 2003