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Mo1157 Mortality and Rebleeding in Upper Gastrointestinal Bleeding Caused by Idiopathic Ulcers
an endoscopic diagnostic showing the peptic ulcer as the cause of the bleeding and with studies for H. Pylori and other microorganisms. We excluded patients who took NSAIDS in the last 4 weeks. To determinate H. Pylori infection, 2 biopsies of antrum and 2 of gastric body were taken for histologic study, and 1 biopsy of antrum and one of gastric body were taken to do a rapid urease test. H. Pylori was determined with the presence of it in any of the two tests, and was negative when it was not found in neither of two tests. We followed up patients within 30 days after their hospital admission. Rebleeding was considered when a new episode of hematemesis, melena or hematochezia associated with a more than 2 gr/ dl drop in hemoglobin or hemodynamic decompensation. Mortality was considered when the cause of death of the patient was the result of UGIB or other causes. Results: We included 105 patients, 69 of them had a peptic ulcer associated with H. Pylori and 36 had idiopathic ulcers. Patients with idiopathic ulcers, comparing to the ones with H. Pylori, were older (62 years vs 48 years, p<0.001) and with more comorbidities (80.6% vs 24.6% p<0.001). During the follow up we found a rebleeding rate of 19.4% vs 2.9% (p=0.007) and mortality of 19.4% vs 1.4% (p=0.002) in patients with idiopathic ulcers comparing to peptic ulcers associated with H. Pylori. When we made the analysis of risk factors to mortality and rebleeding, idiopathic ulcers presented a Hazard ratio (HR) of 13.42 (CI 1.71-104.86) p<0.001 and 6.71 (CI 1.47-30.64) p<0.004, respectively. Concerning endoscopic therapy, 10 (27.8%) patients with idiopathic ulcers required it, the same with patients with PU associated with H. Pylori (p=0.11). Besides this, we observed that in the group of idiopathic ulcers, there were 3 patients (22.2%) who required management in the ICU versus 8 patients (4.3%) p=0.007 in the group of H. pylori. On the other hand, we did not find statistical differences in the number of packed red blood cells transfused , neither in the requirement for surgery. Conclusion: Patients who were admitted because of UGIB caused by idiopathic ulcers had higher mortality and more rebleeding, compared to those ulcers associated with H. pylori infection. These patients require a closer monitoring, and likely more time utilizing gastro protective agents. Table 1 Characteristics of the groups with upper gastrointestinal bleeding caused by idiopathic peptic ulcer and H. pylori ulcers
Differential Effects Between Proton Pump Inhibitors on Clopidogrel-Mediated Anti-Platelet Inhibition Paul C. Spizzo Background: It has been suggested that proton pump inhibitors (especially omeprazole and esomeprazole) may reduce the effectiveness of clopidogrel's anti-platelet activity possibly reflecting inhibition of Cytochrome P450 (CYP) 2C19, a hepatic iso-enzyme responsible for conversion of the agent from pro-drug to its active moiety. Whether differences exist between PPIs types on reduction in platelet inhibition during simultaneous PPI and clopidogrel therapy however remains uncertain. The aim of this study was to compare the effects of different PPIs on clopidogrel-mediated platelet inhibition using platelet aggregometry. Methods: 53 patients (29 men, mean age 79±10yrs) concurrently treated with clopidogrel and PPIs were identified. 57% were receiving pantoprazole, 19% omeprazole, 15% esomeprazole, 6% rabeprazole, and 3% lansoprazole. Platelet reactivity was determined on 5ml fresh blood using the Accumetrics VerifyNow® assay system. Results were expressed as P2Y12 platelet reactivity units (PRU) with a value of >235 units indicating suboptimal inhibition of clopidogrel-mediated anti-platelet activity.[i] PRU values were compared for different PPIs using Student's t-test. The prevalence of sub-optimal platelet inhibition was compared with Fisher's exact test. Results: The PRU was >235 in 13 of 53 patients (25%). Of these, 4 were receiving pantoprazole (13% of total patients taking pantoprazole), 4 esomeprazole (4/8, 50%), and the remaining 5 patients omeprazole (5/10, 50%). PRU values in the 5 patients receiving lansoprazole or rabeprazole were <235. The mean PRU was 226±12 units in patients treated with esomeprazole or omeprazole compared to 155±12 units in those receiving pantoprazole, lansoprazole or rabeprazole (p < 0.001). Patients treated with esomeprazole or omeprazole were significantly more likely to have a PRU >235 compared to patients treated with pantoprazole, lansoprazole or rabeprazole (p<0.05). The mean PRU in subjects <80 years was 152.2±16.15 versus 200.0±11.93 in subjects who were aged over 80 (p= 0.0183). Conclusion: Patients receiving a combination of clopidogrel with either esomeprazole or omeprazole have a higher incidence of suboptimal inhibition of clopidogrelmediated platelet activity when compared to other PPIs. Monitoring of platelet function should be considered in patients at high risk of cardiovascular events who receive concurrent clopidogrel and PPI therapy. [i] M.J. Price et al. Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on thrombotic events after drug-eluting stent implantation., European Heat Journal (2008) 29, 992-1000. Mo1156 Predictors for Elevation in Serum Gastrin Following Proton Pump Inhibitor Treatment Holmfridur Helgadottir, Einar Bjornsson BACKGROUND: Gastrin elevation, a known effect of long-term therapy with proton pump inhibitors (PPIs) is highly variable among PPI users. Why only a proportion of patients with prolonged PPI exposure develop hypergastrinemia is unclear. We aimed to determine the predictors for the development of hypergastrinemia in patients on long-term PPIs. METHODS: Gastrin levels in 100 long-term PPI users with previously documented erosive gastroesophageal reflux disease (GERD) were obtained from an unpublished study and from a previous study (Helgadottir et al. Dig Liv Dis 2013) (n=58). Data on age, gender, duration of PPI exposure, the dosage of PPIs and H.pylori (HP) status was obtained. Difference in age, dosage, duration, gender and HP status between those who developed hypergastrinemia and those who did not was estimated with a t-test or Fisher's exact test. Independent predictors for hypergastrinemia were analyzed with multiple linear regression with log transformed gastrin level as the dependent variable and logistic regression. RESULTS: Data from 158 patients on long-term PPI therapy were available for analysis, mean age 60 years (SD 11 years), 10% HP positive, 50% female, mean dosage 28 mg (SD 13 mg, range 1080 mg) and duration 8 years (SD 6 years, range 2-25 years). The mean gastrin levels were 68 pg/ml (SD 54, range 14-465). Female patients had higher fasting gastrin levels than males, 80 pg/ml (SD 66, range 17-465) vs. 57 (SD 35, range 14-204) (p=0.007). Overall 90/158 (57%) had hypergastrinemia (> 49.6 pg/ml). Patients who had hypergastrinemia vs. who did not had higher proportion of females 59% vs. 38% (p=0.0016), higher PPI dose 31 mg (SD 15 mg) vs. 25 mg (SD 9 mg) (p=0.03), and higher HP positivity 14% vs. 4% (p=0.06), but similar age, 61 years (SD 10) vs. 59 years (SD 12) (p=NS) and duration of therapy, 8 years (SD 6) vs. 8 years (SD 6) (p=NS) compared with those who did not have hypergastrinemia, respectively. Female gender was an independent predictor for higher gastrin (β = 0.26, [CI = 0.44 to 0.08], p=0.005) and also positive HP status (β = 0.35, [CI = 0.05 - 0.65], p=0.02). When hypergastrinemia was used as the dependent variable in logistic regression the significant variables for hypergastrinemia were still female gender (OR =2.2, [CI = 1.1-4.3], p=0.023), and positive HP status (OR = 3.8 [CI = 1-18], p= 0.03) as well as the PPI dosage (OR = 1.03 [CI = 1.004-1.07], p=0.03). CONCLUSIONS: Females on long term PPI therapy had significantly higher fasting gastrin levels than males. Female gender was an independent important predictor for the development of hypergastrinemia together with positive HP status and higher dosage in mg. This might suggest increased sensitivity of females to PPIs.
Me: Mean, SD: Standard deviation, CKD: Chronic kidney Disease, CHF: Congestive Heart Failure, COPD: Chronic Obstructive Pulmonary Disease Table 2 Outcomes by group of patients with UGIB caused by idiopathic peptic ulcer and peptic ulcer associated to Helicobacter pylori.
Mo1157 Mortality and Rebleeding in Upper Gastrointestinal Bleeding Caused by Idiopathic Ulcers Eduar A. Bravo Paredes, Patricia Guzman Rojas, Roxana C. Gallegos Lopez, Manuel A. Corzo Maldonado, Alessandra Ciliotta Chehade
ICU: Intensive Care Unit
Introduction: It has been described that idiopathic ulcers (not associated with H. Pylori, NSAIDS or Infections) present an adverse clinical outcome in terms of healing, recurrence, rebleeding and mortality. Aim: Compare patients with upper gastrointestinal bleeding (UGIB) caused by peptic ulcer (PU) associated with Helicobacter Pylori with patients with UGIB caused by idiopathic ulcers in terms of mortality and rebleeding. Methods: Prospective cohort study. Including patients with the diagnosis of UGIB, older than 18 years old, with
S-623
AGA Abstracts
AGA Abstracts
Mo1155
Differential Effects Between Proton Pump Inhibitors on Clopidogrel-Mediated Anti-Platelet Inhibition Paul C. Spizzo Background: It has been suggested that proton pump inhibitors (especially omeprazole and esomeprazole) may reduce the effectiveness of clopidogrel's anti-platelet activity possibly reflecting inhibition of Cytochrome P450 (CYP) 2C19, a hepatic iso-enzyme responsible for conversion of the agent from pro-drug to its active moiety. Whether differences exist between PPIs types on reduction in platelet inhibition during simultaneous PPI and clopidogrel therapy however remains uncertain. The aim of this study was to compare the effects of different PPIs on clopidogrel-mediated platelet inhibition using platelet aggregometry. Methods: 53 patients (29 men, mean age 79±10yrs) concurrently treated with clopidogrel and PPIs were identified. 57% were receiving pantoprazole, 19% omeprazole, 15% esomeprazole, 6% rabeprazole, and 3% lansoprazole. Platelet reactivity was determined on 5ml fresh blood using the Accumetrics VerifyNow® assay system. Results were expressed as P2Y12 platelet reactivity units (PRU) with a value of >235 units indicating suboptimal inhibition of clopidogrel-mediated anti-platelet activity.[i] PRU values were compared for different PPIs using Student's t-test. The prevalence of sub-optimal platelet inhibition was compared with Fisher's exact test. Results: The PRU was >235 in 13 of 53 patients (25%). Of these, 4 were receiving pantoprazole (13% of total patients taking pantoprazole), 4 esomeprazole (4/8, 50%), and the remaining 5 patients omeprazole (5/10, 50%). PRU values in the 5 patients receiving lansoprazole or rabeprazole were <235. The mean PRU was 226±12 units in patients treated with esomeprazole or omeprazole compared to 155±12 units in those receiving pantoprazole, lansoprazole or rabeprazole (p < 0.001). Patients treated with esomeprazole or omeprazole were significantly more likely to have a PRU >235 compared to patients treated with pantoprazole, lansoprazole or rabeprazole (p<0.05). The mean PRU in subjects <80 years was 152.2±16.15 versus 200.0±11.93 in subjects who were aged over 80 (p= 0.0183). Conclusion: Patients receiving a combination of clopidogrel with either esomeprazole or omeprazole have a higher incidence of suboptimal inhibition of clopidogrelmediated platelet activity when compared to other PPIs. Monitoring of platelet function should be considered in patients at high risk of cardiovascular events who receive concurrent clopidogrel and PPI therapy. [i] M.J. Price et al. Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on thrombotic events after drug-eluting stent implantation., European Heat Journal (2008) 29, 992-1000. Mo1156 Predictors for Elevation in Serum Gastrin Following Proton Pump Inhibitor Treatment Holmfridur Helgadottir, Einar Bjornsson BACKGROUND: Gastrin elevation, a known effect of long-term therapy with proton pump inhibitors (PPIs) is highly variable among PPI users. Why only a proportion of patients with prolonged PPI exposure develop hypergastrinemia is unclear. We aimed to determine the predictors for the development of hypergastrinemia in patients on long-term PPIs. METHODS: Gastrin levels in 100 long-term PPI users with previously documented erosive gastroesophageal reflux disease (GERD) were obtained from an unpublished study and from a previous study (Helgadottir et al. Dig Liv Dis 2013) (n=58). Data on age, gender, duration of PPI exposure, the dosage of PPIs and H.pylori (HP) status was obtained. Difference in age, dosage, duration, gender and HP status between those who developed hypergastrinemia and those who did not was estimated with a t-test or Fisher's exact test. Independent predictors for hypergastrinemia were analyzed with multiple linear regression with log transformed gastrin level as the dependent variable and logistic regression. RESULTS: Data from 158 patients on long-term PPI therapy were available for analysis, mean age 60 years (SD 11 years), 10% HP positive, 50% female, mean dosage 28 mg (SD 13 mg, range 1080 mg) and duration 8 years (SD 6 years, range 2-25 years). The mean gastrin levels were 68 pg/ml (SD 54, range 14-465). Female patients had higher fasting gastrin levels than males, 80 pg/ml (SD 66, range 17-465) vs. 57 (SD 35, range 14-204) (p=0.007). Overall 90/158 (57%) had hypergastrinemia (> 49.6 pg/ml). Patients who had hypergastrinemia vs. who did not had higher proportion of females 59% vs. 38% (p=0.0016), higher PPI dose 31 mg (SD 15 mg) vs. 25 mg (SD 9 mg) (p=0.03), and higher HP positivity 14% vs. 4% (p=0.06), but similar age, 61 years (SD 10) vs. 59 years (SD 12) (p=NS) and duration of therapy, 8 years (SD 6) vs. 8 years (SD 6) (p=NS) compared with those who did not have hypergastrinemia, respectively. Female gender was an independent predictor for higher gastrin (β = 0.26, [CI = 0.44 to 0.08], p=0.005) and also positive HP status (β = 0.35, [CI = 0.05 - 0.65], p=0.02). When hypergastrinemia was used as the dependent variable in logistic regression the significant variables for hypergastrinemia were still female gender (OR =2.2, [CI = 1.1-4.3], p=0.023), and positive HP status (OR = 3.8 [CI = 1-18], p= 0.03) as well as the PPI dosage (OR = 1.03 [CI = 1.004-1.07], p=0.03). CONCLUSIONS: Females on long term PPI therapy had significantly higher fasting gastrin levels than males. Female gender was an independent important predictor for the development of hypergastrinemia together with positive HP status and higher dosage in mg. This might suggest increased sensitivity of females to PPIs.
Me: Mean, SD: Standard deviation, CKD: Chronic kidney Disease, CHF: Congestive Heart Failure, COPD: Chronic Obstructive Pulmonary Disease Table 2 Outcomes by group of patients with UGIB caused by idiopathic peptic ulcer and peptic ulcer associated to Helicobacter pylori.
Mo1157 Mortality and Rebleeding in Upper Gastrointestinal Bleeding Caused by Idiopathic Ulcers Eduar A. Bravo Paredes, Patricia Guzman Rojas, Roxana C. Gallegos Lopez, Manuel A. Corzo Maldonado, Alessandra Ciliotta Chehade
ICU: Intensive Care Unit
Introduction: It has been described that idiopathic ulcers (not associated with H. Pylori, NSAIDS or Infections) present an adverse clinical outcome in terms of healing, recurrence, rebleeding and mortality. Aim: Compare patients with upper gastrointestinal bleeding (UGIB) caused by peptic ulcer (PU) associated with Helicobacter Pylori with patients with UGIB caused by idiopathic ulcers in terms of mortality and rebleeding. Methods: Prospective cohort study. Including patients with the diagnosis of UGIB, older than 18 years old, with
S-623
AGA Abstracts
AGA Abstracts
Mo1155