Introduction: MII-pH was performed on 8 patients who failed PPI therapy before and after Endolumenal “barrier” treatment and characterized for esophageal pH exposure, clearance time, total and supine reflux and proximal migrations (>15 cm). Methods: Eight GERD patients unresponsive to PPI therapy underwent 24 hour MII-pH testing. The MII-pH catheter was placed transnasally and manometrically located. All reflux events were measured by impedance and simultaneous pH-metry to characterize them into number and type (acid/nonacid) of events, as well as extent of proximal migration. Upright and supine positions could also be subcategorized. All eight patients underwent endoluminal therapy with Plicator (6) or Enteryx (2). Post-procedural MII-pH testing was performed. Results: Following endoluminal therapy, 5 patient were asymptomatic and not on PPI therapy. Two patients had symptomatic improvement, but remained on PPI therapy. Post-endoluminal therapy MII-pH measurements show improvements in Johnson-DeMeester scores, total pH exposure time, proximal migration height, and number of impedance reflux episodes, however bolus clearance time was not changed (see Table I for patient results). Conclusion: Patients with symptomatic GERD are dramatically helped by endoluminal therapy as evidenced by improvements in objective parameters as measured by MII-pH. Traditional pH only testing has been shown to miss the subgroups of patients with nonacid reflux as the cause of symptoms, especially patients tested on PPI therapy. Although subjective patient improvement was observed post Endoluminal therapy, addition of combined impedance and pH testing also showed improvements in objective paramenters of reflux. Treatment of properly selected symptomatic GERD patients with a “barrier” therapy such as endoluminal therapy appears effective. Tabled 1Pre and Post Endolumenal Therapy MII-pH Characteristics Patient Total pH Exposure (%) PRE/POST MeanBolus Clearance (sec) PRE/POST Johnson Demeester PRE/POST Reflux Episodes (total) PRE/POST Reflux Episodes (upright) PRE/POST Reflux Episodes (supine) PRE/POST Proximal Migration PRE/POST A ∗ NDO plicator 5.2 / 0.7 13 / 12 23.2 / 2.3 48 / 43 25 / 42 0 / 1 21 / 20 B Enteryx 9.0 / 4.5 8 / 13 37 / 19.5 49 / 39 42 / 29 7 / 10 12 / 19 C Enteryx 0.2 / 2.0 16 / 20 1.8 / 12 161 / 81 136 / 48 25 / 33 42 / 40 D ∗ NDO plicator 0.1 / 0 4 / 5 0.9 / 0.9 75 / 28 4 / 0 71 / 28 32 / 8 E ∗ NDO plicator 17 / 9.2 15 / 21 152 / 60.9 45 / 15 38 / 10 7 / 5 17 / 5 F ∗ NDO plicator 6.7 / 0.6 10 / 17 30 / 2.9 37 / 22 29 / 18 8 / 4 9 / 12 G ∗ NDO plicator 4.8 / 0.5 14 / 12 14.7 / 3.9 83 / 44 58 / 13 25 / 31 48 / 18 H ∗ NDO plicator 8.7 / 3.4 22 / 11 28 / 18 72 / 50 50 / 38 22 / 18 55 / 18 ∗ NDO plicator ∗∗ Enteryx Open table in a new tab

Introduction: MII-pH was used to detect nonacid reflux in patients who failed PPI therapy and might be helped by a “barrier” therapy such as endoluminal therapy. Methods: Six GERD patients unresponsive to PPI therapy underwent 24 hour MII-pH testing. The MII-pH catheter was placed transnasally and manometrically located. Symptom Index (SI) & Symptom Association Probability (SAP) were calculated to show symptoms associations with all reflux events as measured by impedance and characterized as acid or nonacid by pH-metry. SI is positive at ≧50% and SAP is positive at ≧95%. The proximal height of reflux migration was also measured. All six patients underwent endoluminal therapy with Plicator or Enteryx. Post-procedural MII-pH testing was performed. Results: Following endoluminal therapy, 5 patient were asymptomatic and not on PPI therapy. One patient had symptomatic improvement, but remained on PPI therapy. Mean and (median) values for pre-procedural symptom-reflux association include: SI + nonacid 21.69% (21.55%), SAP + nonacid 67.1% (80.2%), SI + acid 17.66% (22.97%), SAP + acid 59.2% (80.2%). Symptom association for nonacid reflux was more prevalent than that for acid reflux. Post-endoluminal therapy MII-pH measurements show improvements in symptom association analysis, proximal migration height of reflux, acid exposure, and impedance reflux episodes. (see Table I). Conclusion: Patients with symptomatic GERD who have more nonacid than acid exposure are dramatically helped by endoluminal therapy as evidenced by improvements in objective parameters as measured by MII-pH. In this group failing acid suppressive therapy, nonacid reflux was likely to be the major cause of their persistent symptoms. Traditional pH only testing would have missed this subgroup of patients. Impedance and pH testing improved the diagnostic yield of reflux monitoring and provides more accurate symptom association analysis. Furthermore, for those patients with normal or physiologic acid exposure, better symptom association analysis can be accomplished with combined pH and impedance reflux testing. Treatment of nonacid reflux with a “barrier” therapy such as endoluminal therapy appears effective in properly selected patients. Tabled 1MII-pH results: pre/post symptom association analysis Pre % mean Post % mean SI + acid 17.66 16.7 SI + nonacid 21.69 3.75 SAP + acid 59.2 29.0 SAP + nonacid 67.1 5.78 Proximal events 28.50 17.50 %

Purpose: Painless jaundice and CA 19–9 levels in the tens of thousands has been suggested to equate to malignancy with nearly 100% probability. Here we report a case of a 55 yr-old alcoholic male presenting with painless jaundice and a CA 19–9 of 62,000 IU/L which normalizes after removal of a large CBD stone. Methods: A 55-yr-old hispanic male with an admitted history of heavy alcohol use presented with jaundice that was recognized by friends over a 2 week period with no complaint of abdominal pain or fever. He stated he had a decreased appetite for several days and a subjective history of weight loss, but other than the jaundice had no other symptoms. The results of the physical examination were unremarkable except for icteric skin and sclera. Laboratory data on showed a leukocytosis of 23 UL; normal Hgb and Plt. The bilirubin level was 22.6 mg/dL with a direct of 21.4 mg/dL. Alkaline phospatase 293 IU/L; AST 62 mg/dL; ALT 166 mg/dL. Amylase and Lipase were normal. His CA 19–9 was found to be 62,500 IU/L with a CEA and CA 125 within normal limits. CT scan of the abdomen showed intra/extra hepatic ductal dilatation with CBD to 1.6 cm near the pancreatic head. Normal pancreatic duct and no appreciable mass. An ERCP was performed which showed a large mobile filling defect in the mid CBD. An extraction of a 2 cm stone was performed. Results: Follow up studies 3 weeks post extraction showed a normalization of all liver function tests, negative ANA, ASMA, and AMA; as well as a normailization of the CA 19–9 to 18 IU/L. All biliary pathology specimens were negative for malignancy. Conclusion: CA 19–9 is a glycoprotein synthesized by normal pancreatic, biliary, gastric, colonic, endometrial, and salivary epithelial cells. It has “tumor association” but is not a specific tumor marker. Reports estimate that CA 19–9 has a sensitivity of 80–90% for pancreatic cancer and 60–70% for biliary cancer. Non-cancerous lesions such as cholangitis, cholestasis, and pancreatitis can be associated with elevated CA 19–9 levels, but are thought to be uncommon higher than 1000 IU/L. Thus, an elevated CA 19–9, even with high clinical suspicion for malignancy is not always malignancy.[figure1]Figure