Efficacy of an intravenous proton pump inhibitor after endoscopic therapy with epinephrine injection for peptic ulcer bleeding in patients with uraemia: a case-control study.

BACKGROUND: Patients with peptic ulcer bleeding and uraemia are prone to re-bleeding. AIM: To compare the efficacy of an intravenous proton pump inhibitor in treating peptic ulcer bleeding in patients with uraemia and those without uraemia. METHODS: High-risk peptic ulcer bleeding patients received endoscopic therapy with epinephrine (adrenaline) injection plus intravenous omeprazole (40 mg bolus followed by 40 mg infusion every 12 h) for 3 days. Re-bleeding, volume of blood transfusion, hospital stay, need for surgery, and mortality were analysed. RESULTS: The uraemic group had similar 7-day re-bleeding rate (6/42, 14.29% vs. 6/46, 13.04%, P = 0.865) to that of non-uraemic patients, but more re-bleeding episodes beyond 7 days (4/42, 9.52% vs. 0/46, 0%, P = 0.032, OR [95% CI] = 1.105 [1.002-1.219]) and all-cause mortality (4/42 vs. 0/46 P = 0.032, OR [95% CI] = 1.105 [1.002-1.219]). The uraemic group also had more units of blood transfusion after endoscopic therapy (mean +/- s.d. 4.33 +/- 3.35 units vs. 2.15 +/- 1.65 units, P < 0.001), longer hospital stay (mean +/- s.d. 8.55 +/- 8.12 days vs. 4.11 +/- 1.60 days, P < 0.001) and complications during hospitalization (9/42 vs. 0/46, P = 0.001, OR [95% CI] = 1.273 [1.087-1.490]). CONCLUSION: Endoscopic therapy with epinephrine injection plus an intravenous proton pump inhibitor can offer protection against early re-bleeding in uraemic patients with peptic ulcer bleeding, but has a limited role beyond 7 days.

Recurrence of peptic ulcer in uraemic and non-uraemic patients after Helicobacter pylori eradication: a 2-year study.

BACKGROUND: The role of Helicobacter pylori in the pathogenesis of peptic ulcer disease in patients with uraemia remains unclear. AIM: To evaluate the long-term effect of H. pylori eradication in these patients. METHODS: Uraemic and non-uraemic patients with peptic ulcer were enrolled in this study. Patients having history of non-steroidal anti-inflammatory drugs use or cardiovascular disease that need aspirin use were excluded. After confirmation of H. pylori infection, they received a triple therapy and were followed up for 2 years. RESULTS: Between September 1999 and December 2005, 34 patients (41%) of the end-stage renal disease [H. pylori (+) group] and 67 (84%) of the non-uraemic patients with peptic ulcer disease (PU group) received anti-H. pylori therapy. After triple therapy, 32 (94%) from the end-stage renal disease group and 64 (96%) from the peptic ulcer group obtained successful eradication. During the 2-year follow-up, three patients in the end-stage renal disease group were excluded because of the presence of cardiovascular disease and aspirin use in two cases and died of heart failure in one case; two patients in peptic ulcer group refused follow-up. Finally, 29 uraemic and 62 non-uraemic patients had achieved the follow-up. Recurrence of peptic ulcer was more in the end-stage renal disease group than in the peptic ulcer group with intention-to-treat analysis (eight of 32, 25% vs. two of 64, 3%, P = 0.001, OR: 10.0, 95% CI: 1.979-50.540) or per-protocol analysis (eight of 29, 28% vs. two of 62, 3%, P < 0.001, OR: 11.4, 95% CI: 2.245-58.168). CONCLUSIONS: Peptic ulcer recurrence after H. pylori eradication is higher in end-stage renal disease patients with peptic ulcer than in peptic ulcer patients without renal disease. Factors aside from H. pylori play an important role in peptic ulcer recurrence in end-stage renal disease patients.

Breath-hold fast recovery fast spin echo versus conventional non-breath-hold fast spin echo T2-weighted MR imaging of focal liver lesions.

INTRODUCTION: We compare the breath-hold fast recovery fast spin echo (BHFRFSE) T2-weighted and non-breath-hold fast spin echo (NBHFSE) T2-weighted sequences in image quality and lesion characterisation of focal liver lesions. MATERIALS AND METHODS: Fat-suppressed T2-weighted magnetic resonance (MR) images obtained with the 2 sequences (BHFRFSE and NBHFSE) in 79 patients with 113 liver lesions were analysed retrospectively. The image quality and nature of the lesions were evaluated by 2 experienced radiologists. RESULTS: Based on receiver operating characteristic curve analysis, lesion characterisation was comparable for both sequences. The image quality of BHFRFSE was significantly better than that of NBHFSE. The NBHFSE missed 4 malignant lesions while BHFRFSE missed 2 malignant lesions. CONCLUSION: BHFRFSE performs similarly to NBHFSE in image quality and liver lesion characterisation.

Endoscopic haemoclip versus heater probe thermocoagulation plus hypertonic saline-epinephrine injection for peptic ulcer bleeding.

BACKGROUND: Treating patients of bleeding peptic ulcers with heater probe thermocoagulation and haemoclip is considered to be safe and very effective. Yet, there is no report comparing the haemostatic effects of endoscopic haemoclip versus heater probe thermocoagulation plus hypertonic saline-epinephrine injection in these patients. AIM: To compare the clinical outcomes of both therapeutic modalities in patients with peptic ulcer bleeding. METHODS: A total of 93 patients with active bleeding or non-bleeding visible vessels were randomised to receive either endoscopic haemoclip (n = 46) or heater probe thermocoagulation plus hypertonic saline-epinephrine injection (n = 47). Five patients from the haemoclip group were excluded because of the inability to place the haemoclip. RESULTS: Initial haemostasis was achieved in 39 patients (95.1%) of the haemoclip group and 47 patients (100%) of the heater probe group (P > 0.1). Rebleeding occurred in four patients (10.3%) of the haemoclip group and three patients (6.4%) of the heater probe group (P > 0.1). The volume of blood transfused after entry into the study, duration of hospital stay, number of patients requiring urgent surgery and the mortality rates were not statistically different between the two groups. CONCLUSIONS: If the haemoclip can be applied properly, the clinical outcomes of the haemoclip group would be similar to those of the heater probe group in patients with peptic ulcer bleeding. However, if the bleeders are located at the difficult-to-approach sites, heater probe plus hypertonic saline injection is the first choice therapy.

Is submucosal epinephrine injection necessary before polypectomy? A prospective, comparative study.

BACKGROUND/AIMS: Polyps of the gastrointestinal tract are usually removed due to their link to bleeding, obstruction and malignancy. However, complications may occur following polypectomy. The aim of this study was to assess whether submucosal epinephrine injection before polypectomy could reduce the incidence of bleeding and perforation. METHODOLOGY: Between June 1997 and November 1999, patients with sessile polyps of the gastrointestinal tract found in our endoscopic unit were randomized to receive submucosal epinephrine injection (epinephrine group) or no injection (control group) before polypectomy. In the epinephrine group, epinephrine (1:10,000) was injected surrounding the stalk of the polyp until the mucosa was blanched and bulged. The patients were observed for complications in the following month. RESULTS: A total of 120 patients with 151 sessile polyps were enrolled in this study. In the epinephrine group, 75 polyps (n = 68) were randomized to receive epinephrine injection before polypectomy. In the control group, 76 polyps (n = 61) underwent polypectomy without epinephrine injection. In both groups, there was no significant difference in clinical features including the sizes of the polyps and their stalks, the location of polyps and the pathological diagnosis. There were a total of nine episodes of post-polypectomy hemorrhage, two in the epinephrine group and seven in the control group (2/75 vs. 7/76) (P = 0.07). One case in the epinephrine group experienced delayed bleeding (4 days later). Immediate hemorrhage occurred less in the epinephrine group than that in the control group (1/75 vs. 7/76, P = 0.03). There was one case of perforation in each group. CONCLUSIONS: Epinephrine injection prior to polypectomy is effective in preventing immediate bleeding.

A 3-day anti-Helicobacter pylori therapy is a good alternative for bleeding peptic ulcer patients with Helicobacter pylori infection.

BACKGROUND/AIMS: One-week triple therapy has been recommended as a standard regimen for eradicating Helicobacter pylori infection. The emergence of antibiotic-resistant strains, adverse drug effects, poor compliance and high cost of therapy add problems to the management of these patients. In this study, we assessed whether a 3-day triple therapy could be effective in eradicating Helicobacter pylori infection in bleeding peptic ulcer patients. METHODOLOGY: Peptic ulcer patients with Helicobacter pylori infection were enrolled in this study. Patients enrolled at the outpatient department (group A) received a 7-day oral regimen: bismuth subcitrate colloid 300 mg + amoxicillin 500 mg + metronidazole 250 mg four times per day. Patients who were admitted to the wards due to peptic ulcer bleeding (group B) received a 3-day regimen including omeprazole 40 mg intravenously every 6 hours, amoxicillin 500 mg + metronidazole 250 mg orally four times daily after hemostasis had been achieved. Patients of both groups received omeprazole 20 mg once per day or cimetidine 400 mg twice daily per os for at least-one month after anti-Helicobacter pylori therapy. We followed every patient endoscopically two months after anti-Helicobacter pylori therapy. RESULTS: From June 1997 to April 1999, a total of 57 patients (30 in group A and 27 in group B) with gastric or duodenal ulcer and Helicobacter pylori infection completed anti-Helicobacter pylori therapy. Two months after anti-Helicobacter pylori therapy, peptic ulcer was found to be healed with a scar in 26 (86.7%) of group A and 23 (85.2%) of group B (P > 0.1). The eradication rates of Helicobacter pylori in the two groups were not significantly different in an intention-to-treat analysis [group A: 78.8% (26/33), 95% CI: 64.9-92.7%; group B: 80% (24/30), 95% CI: 65.7-94.3%, P > 0.1] and in a per protocol analysis [group A: 86.7% (26/30), 95% CI: 74.5-98.9%, group B: 88.9% (24/27), 95% CI: 77.1-100.7%, P > 0.1]. Fewer side effects occurred in group B (3/30) than those in group A (7/33) (P > 0.1). CONCLUSIONS: In patients with peptic ulcer bleeding a 3-day anti-Helicobacter pylori therapy is a good alternative for eradicating Helicobacter pylori infection.

Will Helicobacter pylori affect short-term rebleeding rate in peptic ulcer bleeding patients after successful endoscopic therapy?

OBJECTIVE: Helicobacter pylori (H. pylori) can augment the pH-increasing effect of omeprazole in patients with peptic ulcer. A high intragastric pH may be helpful in preventing recurrent hemorrhage by stabilizing the blood clot at the ulcer base of bleeding peptic ulcer patients. Therefore, we hypothesized that omeprazole may reduce short-term rebleeding rate in these patients with H. pylori infection after initial hemostasis had been obtained. METHODS: Between July 1996 and December 1998, 65 bleeding peptic ulcer patients (24 gastric ulcer, 41 duodenal ulcer) who had obtained initial hemostasis with endoscopic therapy were enrolled in this trial. Thirty (46.2%) of them were found to have H. pylori infection by a rapid urease test and pathological examination. For all studied patients, omeprazole was given 40 mg intravenously every 6 h for 3 days. Thereafter, omeprazole was given 20 mg per os (p.o.) once daily for 2 months. A pH meter was inserted in the fundus of each patient under fluoroscopic guidance after intravenous omeprazole had been administered. The occurrence of rebleeding episode was observed for 14 days. RESULTS: In patients with H. pylori infection, intragastric pH (median, 95% confidence interval [CI]: 6.54, 5.90-6.68) was higher than in those without H. pylori infection (6.05, 5.59-6.50, p < 0.001). However, the patients with rebleeding (2 vs 3), volume of blood transfusion (median, range: 1000 ml, 0-2250 vs 750, 0-2000), number of operations (0 vs 1), mortality caused by bleeding (0 vs 0), and hospital stay (median, range: 6 days, 3-14 vs 7, 5-16) were not statistically different from those without H. pylori infection. CONCLUSIONS: Omeprazole does increase intragastric pH in bleeding peptic ulcer patients with H. pylori infection. However, the presence of H. pylori infection does not affect the short-term rebleeding rate in these patients.

The influence of intravenous omeprazole on intragastric pH and outcomes in patients with peptic ulcer bleeding after successful endoscopic therapy--a prospective randomized comparative trial.

BACKGROUND/AIMS: The role of omeprazole in preventing rebleeding in patients with peptic ulcer bleeding after successful endoscopic therapy has been controversial. In this study, we used 3 different formulas of intravenous omeprazole in the above patients. We wished to compare the intragastric pH and outcomes among them. METHODOLOGY: Between July 1996 and May 1997, after having obtained initial hemostasis with endoscopic therapy, a total of 20 patients with peptic ulcer bleeding (spurting/oozing/non-bleeding visible vessel: 6/4/10) received intravenous bolus of omeprazole 20 mg every 3 hours; 20 patients (3/5/12) received intravenous bolus of omeprazole 40 mg every 6 hours; and, 20 patients (5/4/11) received intravenous bolus of omeprazole 80 mg every 12 hours for 3 days. One intragastric pH meter (Gastrograph Mark III, Medical Instruments Corp. Switzerland) was used to record 24-hour intragastic pH. RESULTS: The intragastric pH in the patients receiving omeprazole 20 mg every 3 hours was 6.1, 6.0-6.2 (mean: 95% CI); in patients receiving omeprazole 40 mg every 6 hours it was 6.4, 6.2-6.5; and, in patients receiving omeprazole 80 mg every 12 hours it was 5.8, 5.7-5.9. The duration of intragastric pH > 6.0 in omeprazole 20 mg every 3 hours was 70.9%, 57.3%-84.4% (mean: 95% CI); in omeprazole 40 mg every 6 hours it was 83.1%, 73.1%-93.1%; and, in omeprazole 80 mg every 12 hours it was 66%, 51.5%-80.4%. Patients with peptic ulcers receiving omeprazole 40 mg intravenous bolus every 6 hours had the highest intragastric pH as compared with the other 2 groups (p < 0.0001). There were no significant differences concerning rebleeding rates, volume of blood transfusion, hospital stay, numbers of operation and mortality among the 3 groups. CONCLUSIONS: After initial hemostasis had been obtained, patients with peptic ulcer bleeding receiving 40 mg intravenous bolus every 6 hours had the highest intragastric pH. However, they had similar outcomes with the other 2 groups.

Influence of Helicobacter pylori on gastric secretion and gastrin release in normal Chinese subjects.

BACKGROUND: Controversy exists concerning the influence of Helicobacter pylori on gastric secretion. Hyper-, normo- and hyposecretion of gastric acid in normal subjects with H pylori infection have been reported, although there is no such report for Chinese subjects. The goal of this study was to identify the effect of H pylori on gastric secretion in normal Chinese subjects. METHODS: Twenty normal subjects with a normal upper gastrointestinal tract by endoscopy were recruited. H pylori status was assayed by a rapid urease test. Gastric secretion and gastrin release were also measured. RESULTS: Among the subjects studied, nine were infected with H pylori. All enrolled subjects were males. Age and body weight were similar between both groups. No significant difference was found in basal acid output, maximal acid output, basal pepsin output or maximal pepsin output between the H pylori-positive group (median, 1.1 mmol/hour, 95% confidence interval 0.2-3.6 mmol/hour; 8.0, 3.0-18.3 mmol/hour; 0, -1.3-11.2 mmol/hour; and 4.1, -4.2-59.3 mmol/hour, respectively) and the H pylori-negative group (2.5, -1.3-11.3 mmol/hour; 12.2, 8.7-26.9 mmol/hour; 4.3, 1.8-13.5 mmol/hour; and 14.8, -5.7-73.0 mmol/hour, respectively). Serum basal gastrin and pepsinogen I concentration were 63.5, 50.0-78.6 pg/ml and 75.1, 50.6-89.8 ng/ml in the H pylori-positive group, and 65.9, 50.2-79.8 pg/ml and 79.1, 59.5-120.1 ng/ml in the H pylori-negative group (p > 0.05). CONCLUSIONS: H pylori plays no role in the gastric secretion and gastrin release in normal Chinese subjects.

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.

Comparison of adrenaline injection and bipolar electrocoagulation for the arrest of peptic ulcer bleeding.

BACKGROUND: Peptic ulcers with active bleeding or a non-bleeding visible vessel require aggressive endoscopic treatment. AIMS: To determine whether endoscopic adrenaline injection alone or contact probe therapy following injection is a suitable treatment for peptic ulcer bleeding. METHODS: A total of 96 patients with active bleeding or non-bleeding visible vessels received adrenaline alone, bipolar electrocoagulation alone, or combined treatment (n=32 in each group). RESULTS: Initial haemostasis was not achieved in one patient in the adrenaline group, two in the gold probe group, and two in the injection gold probe group (p>0.1). Rebleeding episodes were fewer in the injection gold probe group (2/30, 6.7%) than in the gold probe group (9/30, 30%, p=0.04) and in the adrenaline group (11/31, 35.5%, p=0.01). Treatment failure (other therapy required) was rarer in the injection gold probe group (4/32, 12.5%) than in the adrenaline group (12/32, 37.5%, p=0.04). The volume of blood transfused after entry of the study was less in the injection gold probe group (mean 491 ml) than in the adrenaline group (1548 ml, p<0. 0001) and the gold probe group (1105 ml, p<0.01). Duration of hospital stay, numbers of patients requiring urgent surgery, and death rate were not statistically different among the three groups. CONCLUSIONS: For patients with peptic ulcer bleeding, combined adrenaline injection and gold probe treatment offers an advantage in preventing rebleeding and decreasing the need for blood transfusion.

Predictive factors for rebleeding in patients with peptic ulcer bleeding after multipolar electrocoagulation: a retrospective analysis.

The role of endoscopic therapy for peptic ulcer bleeding is well-documented. Nevertheless, rebleeding occurs in 10% to 30% of patients, and such patients are at high risk for death without early retreatment or definitive surgery. The aim of our study was to predict which patients would rebleed within 1 month after successful multipolar electrocoagulation of 100 patients with active peptic ulcer bleeding (spurting, oozing, or nonbleeding visible vessel). We had achieved initial hemostasis in 97 patients and carried out univariate and multivariate analyses to predict which patients would rebleed. Rebleeding occurred within 1 month in 17 (17.5%) patients. we correlated 20 clinical and endoscopic factors with rebleeding episodes. With univariate analysis, blood transfusion of 500 ml or more at entry (p < 0.0001) and use of cimetidine (p = 0.01) were statistically significant for rebleeding. With multivariate analysis, use of omeprazole was an independent factor for preventing rebleeding (odds ratio, 7.68; 95% confidence interval, 1.642-35.929). We suggest that omeprazole may help to prevent rebleeding in patients who have had hemostasis with multipolar electrocoagulation.

A prospective randomized comparative trial showing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful endoscopic therapy.

BACKGROUND: A blood clot in a peptic ulcer is unstable in a low pH environment. The use of omeprazole may prevent rebleeding by elevating intragastric pH in patients with bleeding peptic ulcer after hemostasis has been achieved. OBJECTIVES: To assess the influence of using omeprazole and cimetidine on 24-hour intragastric pH and to determine their ability to prevent rebleeding after having achieved initial hemostasis in patients with active bleeding or nonbleeding visible vessels. METHODS: One hundred patients with bleeding peptic ulcers who had obtained initial hemostasis were enrolled in this randomized comparative trial. In the cimetidine group (n = 50), a 300-mg intravenous bolus of cimetidine was given, followed by a 1200-mg continuous infusion daily for 3 days. Thereafter, 400 mg of cimetidine was given orally twice daily for 2 months. In the omeprazole group (n = 50), a 40-mg intravenous bolus of omeprazole was given, followed by 160 mg of continuous infusion daily for 3 days. Thereafter, 20 mg of omeprazole was given orally once daily for 2 months. A pH meter was inserted in each patient's fundus under fluoroscopic guidance after the intravenous bolus of cimetidine or omeprazole had been administered. RESULTS: The stigmata of recent hemorrhage before endoscopic therapy in the omeprazole and cimetidine groups were, respectively, spurting (9 vs 12), oozing (4 vs 9), and nonbleeding visible vessel (37 vs 29) (P > .05). The duration of intragastric pH higher than 6.0 was longer in the omeprazole group (mean [+/- SD], 84.4% +/- 22.9%) than that of the cimetidine group (mean [+/- SD], 53.5% +/- 32.3%) (P < .001). Rebleeding occurred in 2 patients (4%) in the omeprazole group and in 12 patients (24%) in the cimetidine group by day 14 after enrollment (P = .004). There was a tendency for patients in the omeprazole group to require less blood transfusion (median, 0 mL; range, 0-2500 mL) than those in the cimetidine group (median, 0 mL; range, 0-5000 mL) (P = .08). The hospital stay and number of operations and mortality rate were similar between both groups. CONCLUSIONS: The use of omeprazole is more effective than cimetidine in increasing intragastric pH and reducing rebleeding episodes in patients with bleeding peptic ulcers after successful endoscopic therapy. This suggests that omeprazole should be used routinely after successful endoscopic therapy.