s-1743 and Stomach-Ulcer

Naproxen/esomeprazole is a fixed-dose combination of the NSAID naproxen and the proton pump inhibitor esomeprazole. In two well designed, 12-week studies, naproxen/esomeprazole fixed-dose combination was noninferior to celecoxib in treating the signs and symptoms of disease in patients with osteoarthritis of the knee, as assessed by the mean change from baseline in Western Ontario and McMaster Universities Osteoarthritis Index pain and function scores and Patient Global Assessment scores (coprimary endpoints). Two other studies showed that the cumulative incidence of gastric ulcers (primary efficacy measure) was significantly lower with naproxen/esomeprazole than with enteric-coated naproxen alone during up to 6 months' therapy in patients with osteoarthritis, rheumatoid arthritis, ankylosing spondylitis or any other condition requiring daily NSAID therapy. The fixed-dose combination was generally well tolerated in these studies, with an upper gastrointestinal tolerability profile generally better than that of naproxen and similar to that of celecoxib.

Topics: Animals; Arthritis; Drug Combinations; Drug Dosage Calculations; Esomeprazole; Humans; Naproxen; Stomach Ulcer

Proton pump inhibitors (PPIs) are the most potent inhibitors of gastric acid secretion available, and they are effective for treating all acid-related disorders. Esomeprazole is one of several most recent PPIs that became available to the market in 2001. Esomeprazole is indicated for the treatment of gastroesophageal reflux disease in adults and children, risk reduction of NSAIDs-associated gastric ulcer, Helicobacter pylori eradication and control of pathological hypersecretory conditions associated with Zollinger-Ellison syndrome. Esomeprazole is available in both oral and intravenous formulations. A number of studies have compared esomeprazole with other PPIs. While differences supporting esomeprazole have been reported, the magnitude of differences has been variable and of uncertain clinical importance. Cost plays a major role in prescribing patterns of PPIs.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Drug Costs; Esomeprazole; Gastroesophageal Reflux; Helicobacter Infections; Humans; Proton Pump Inhibitors; Stomach Ulcer

Esomeprazole (Nexium); S-omeprazole) is a single optical isomer proton-pump inhibitor (PPI) approved for the management of reflux oesophagitis, the symptomatic treatment of gastro-oesophageal reflux disease (GORD), the prevention and healing of NSAID-associated gastric ulcer disease (and the prevention of NSAID-associated duodenal ulcers in the UK), the treatment of Helicobacter pylori infection and associated duodenal ulcer disease (and prevention of relapse of H. pylori-associated peptic ulcers in the UK), and the treatment of Zollinger-Ellison syndrome (and other hypersecretory syndromes in the US).Once-daily oral esomeprazole 40 mg demonstrates greater antisecretory activity than other PPIs. Overall, in well designed clinical studies of 4 weeks' to 6 months' duration in patients with GORD, esomeprazole had similar or better efficacy than other agents. In patients requiring ongoing treatment with NSAIDs, co-therapy with once-daily esomeprazole 20 or 40 mg achieved relief of gastrointestinal symptoms or prevented ulcer occurrence, more effectively than placebo. Esomeprazole was also better than ranitidine 150 mg twice daily in healing NSAID-associated gastric ulcers. In addition, the drug has demonstrated efficacy as part of a triple-therapy regimen for the eradication of H. pylori infection, the healing of H. pylori associated duodenal ulcers and the prevention of relapse of gastric ulcers. Esomeprazole also effectively treated patients with Zollinger-Ellison syndrome. Esomeprazole is generally well tolerated with an adverse-event profile similar to that of other PPIs. Thus, the efficacy and tolerability of esomeprazole for the management of GORD and H. pylori eradication remains undisputed, and the data support its use for the first-line treatment of NSAID-associated gastric ulcer disease and Zollinger-Ellison syndrome.

Topics: Adult; Anti-Ulcer Agents; Duodenal Ulcer; Esomeprazole; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Omeprazole; Proton Pump Inhibitors; Stomach Ulcer; Zollinger-Ellison Syndrome

Non-steroidal anti-inflammatory drugs (NSAIDs) represent one of the most widely used drug classes. However, many patients complain of dyspeptic symptoms impairing their quality of life: ~ 20% of patients taking NSAIDs show endoscopic ulcers with or without symptoms, and up to 2% of chronic NSAID users will develop serious complications each year, such as bleeding or perforation, which are the cause of death in many patients. Coprescription of a proton pump inhibitor is one established option for the healing and prevention of NSAID-associated lesions of the upper gastrointestinal tract in patients at risk. Recent studies evaluated the clinical efficacy of esomeprazole in the management of gastrointestinal problems associated with the intake of selective and non-selective NSAIDs and aspirin.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Dyspepsia; Esomeprazole; Humans; Proton Pump Inhibitors; Stomach Ulcer

Objective Gastric endoscopic submucosal dissection (ESD) is currently a standard procedure, and proton pump inhibitors (PPIs) are most commonly used to treat post-ESD ulcers. Vonoprazan, a potassium-competitive acid blocker (P-CAB), reportedly inhibits gastric acid secretions more effectively than PPIs. Combination therapy of a PPI plus rebamipide is effective for treating larger ulcers. Our goal was to evaluate the effects of vonoprazan plus rebamipide compared to esomeprazole plus rebamipide for the treatment of post-ESD ulcers. Methods First, vonoprazan plus rebamipide (V group) or esomeprazole plus rebamipide (E group) was orally administered to subjects for eight weeks. We then evaluated the ulcer healing process at four and eight weeks after the procedure using a gastric ulcer stage system and by measuring the ulcer size. Patients A total of 84 patients who underwent ESD for gastric neoplasms between September 2015 and December 2017 in Tsuchiura Kyodo General Hospital were included in this randomized controlled trial. Results The ulcer scar rates at week 4 in the V group (n=43) and E groups (n=39) were 20.9% and 15.4%, while those at week 8 were 90.7% and 92.3%, respectively. The ulcer reduction rates at week 4 in the V and E groups were 94.6% and 93.8%, and those at week 8 were 99.7% and 99.3%, respectively. The ulcer scar rates and reduction rates were not significantly different between the two groups. Conclusion Combination therapy consisting of vonoprazan plus rebamipide was not superior to that of esomeprazole plus rebamipide for post-ESD ulcer healing (UMIN000019516).

Topics: Aged; Aged, 80 and over; Alanine; Anti-Ulcer Agents; Drug Therapy, Combination; Endoscopic Mucosal Resection; Esomeprazole; Female; Humans; Male; Middle Aged; Proton Pump Inhibitors; Pyrroles; Quinolones; Severity of Illness Index; Stomach Neoplasms; Stomach Ulcer; Sulfonamides; Wound Healing

Endoscopic submucosal dissection (ESD) is a standard procedure for treating gastric neoplasms. However, ESD causes larger artificial ulcers other than mucosal resection methods. We conducted this prospective randomized controlled study to evaluate the effect of stronger acid suppression on ESD ulcers caused by doubling the proton pump inhibitor (PPI) dose and compare the effects of 20-mg (standard dose) and 40-mg (double dose) esomeprazole (EswonampTM, Daewon Pharmaceutical Co., Ltd., Seoul, Korea) on ulcer healing.. One hundred ninety-seven patients who underwent gastric ESD from July 2017 to December 2017 at Pusan National University Yangsan Hospital were enrolled and randomly assigned to the standard or double-dose group. Change in ulcer size from the day of ESD to 4 weeks after ESD and the scar-change rate were compared between the groups.. There were no significant differences in ulcer contraction (84.5% in 20 mg group vs 86.3% in 40 mg group, P = .91) or scar-change rate (30.9% vs 30.6%, P > .99) between the groups. In a multivariate analysis, initial ulcer size [odds ratio (OR) 0.24; 95% confidence interval (CI) 0.11-0.50] and early gastric cancer (OR 0.22, 95% CI 0.08-0.58) were significantly associated with delayed ulcer healing.. Both 40 and 20-mg esomeprazole have similar effects on ESD-induced ulcer area reduction, suggesting that strong acid suppression does not necessarily result in rapid artificial ulcer healing.. RCT no.: KCT0002885.

Topics: Endoscopic Mucosal Resection; Esomeprazole; Female; Humans; Male; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Republic of Korea; Stomach Neoplasms; Stomach Ulcer; Sulfonamides; Ulcer; Wound Healing

Proton pump inhibitors are effective for the treatment of gastric ulcers after endoscopic submucosal dissection (ESD). However, the most excellent therapy is controversial. Vonoprazan, an active potassium-competitive acid blocker, has a strong gastric acid secretion inhibitory effect, but its efficacy for the treatment of post-ESD gastric ulcers is unclear. Herein, we aimed to determine the healing effect of vonoprazan on post-ESD gastric ulcers.. We carried out a prospective randomized controlled trial examining 92 patients who had undergone ESD for the treatment of gastric neoplasms between April 2015 and June 2016 at Machida Municipal Hospital. Patients were treated with 20 mg/day vonoprazan (V group) or 20 mg/day esomeprazole (E group) for 8 weeks. We evaluated the 8-week cure rate for artificial ulcers and any complications after ESD.. A total of 80 patients (median age, 73.5 years; 71.3% male) were analyzed. Cure rate for the V group was significantly higher than that for the E group (94.9% [37/39] vs 78.0% [32/41], respectively; P = 0.049). In a multivariate analysis, only vonoprazan was correlated with ulcer healing (odds ratio = 6.33; 95% CI = 1.21-33.20; P = 0.029). Delayed bleeding was experienced only in the E group (7.3% [3/41]), but no significant difference compared with the V group was observed (P = 0.241).. Vonoprazan was significantly superior to esomeprazole for the healing of post-ESD gastric ulcers and should be considered as a treatment of first choice.

Topics: Aged; Aged, 80 and over; Endoscopic Mucosal Resection; Esomeprazole; Female; Humans; Male; Postoperative Complications; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Stomach Neoplasms; Stomach Ulcer; Sulfonamides

To evaluate the effects of hydrotalcite combined with esomeprazole on gastric ulcer healing quality.. Forty-eight patients diagnosed with gastric ulcer between June 2014 and February 2016 were randomly allocated to the combination therapy group or monotherapy group. The former received hydrotalcite combined with esomeprazole, and the latter received esomeprazole alone, for 8 wk. Twenty-four healthy volunteers were recruited and acted as the healthy control group. Endoscopic ulcer healing was observed using white light endoscopy and narrow band imaging magnifying endoscopy. The composition of collagen fibers, amount of collagen deposition, expression of factor VIII and TGF-β1, and hydroxyproline content were analyzed by Masson staining, immunohistochemistry, immunofluorescent imaging and ELISA.. Following treatment, changes in the gastric microvascular network were statistically different between the combination therapy group and the monotherapy group (. Hydrotalcite combined with esomeprazole is superior to esomeprazole alone in improving gastric ulcer healing quality in terms of improving microvascular morphology, degree of structure maturity and function of regenerated mucosa.

Topics: Administration, Oral; Adult; Aged; Aluminum Hydroxide; Anti-Ulcer Agents; Collagen; Endoscopy; Esomeprazole; Factor VIII; Female; Gastric Mucosa; Helicobacter Infections; Humans; Hydroxyproline; Immunohistochemistry; Magnesium Hydroxide; Male; Middle Aged; Proton Pump Inhibitors; Stomach Ulcer; Transforming Growth Factor beta1

To compare triple therapy with sequential and concomitant therapies directly in a head-to-head comparison in Helicobacter pylori-infected patients.. Patients were allocated randomly as follows: a triple therapy with esomeprazole (20 mg), amoxicillin (1000 mg) and clarithromycin (500 mg) twice daily for 7 days; a sequential therapy with 5 days of esomeprazole (20 mg) and amoxicillin (1000 mg) twice daily, followed by 5 days of esomeprazole (20 mg), clarithromycin (500 mg) and metronidazole (400 mg) twice daily; or a concomitant therapy consisting of esomeprazole (20 mg), amoxicillin (1000 mg), clarithromycin (500 mg) and metronidazole (400 mg) twice daily for 7 days.. A total of 356 consecutive patients were included. The eradication rates for the triple, sequential and concomitant therapies were 83.6% [95% confidence interval (CI) 76.9-90.4%], 94.2% (95% CI 90.0-98.4%) and 91.7% (95% CI 86.7-96.6%), respectively, in the intention-to-treat population. The differences were significant only between triple and sequential therapies (P=0.01). The primary resistance rates to amoxicillin, clarithromycin and metronidazole were 0.6, 10.5 and 25.9%, respectively. Concomitant therapy was significantly better than triple therapy in cases with clarithromycin resistance (P=0.01).. Ten-day sequential therapy was significantly better than 7-day triple therapy in a clinical setting with low rates of clarithromycin and dual resistance. Concomitant therapy was significantly better than standard triple therapy in the subgroup of patients with clarithromycin-resistant strains.

Topics: Adolescent; Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Clarithromycin; Drug Administration Schedule; Drug Therapy, Combination; Duodenal Ulcer; Dyspepsia; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Peptic Ulcer; Proton Pump Inhibitors; Stomach Ulcer; Treatment Outcome; Young Adult

To compare the therapeutic effects of different doses of intravenous esomeprazole on treating trauma patients with stress ulcer bleeding.. A total of 102 trauma patients with stress ulcer bleeding were randomly divided into 2 groups: 52 patients were assigned to the high-dose group who received 80 mg intravenous esomeprazole, and then 8 mg/h continuous infusion for 3 days; 50 patients were assigned to the conventional dose group who received 40 mg intravenous esomeprazole sodium once every 12 h for 72 h.. Compared with the conventional dose group, the total efficiency of the high-dose group and conventional dose group was 98.08% and 86.00%, respectively (p < 0.05), the hemostatic time was 22.10 h ± 5.18 h and 28.27 h ± 5.96 h, respectively (p < 0.05).. Both doses of intravenous esomeprazole have good hemostatic effects on stress ulcer bleeding in trauma patients. The high-dose esomeprazole is better for hemostasis.

Topics: Adolescent; Adult; Aged; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Esomeprazole; Female; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Stomach Ulcer; Stress, Psychological; Wounds and Injuries

Patients with high Rockall scores have increased risk of ulcer rebleeding after 3-day esomeprazole infusions.. To investigate whether double oral esomeprazole given after a 3-day esomeprazole infusion decreases ulcer rebleeding for patients with high Rockall scores.. We prospectively enrolled 293 patients with peptic ulcer bleeding who had achieved endoscopic haemostasis. After a 3-day esomeprazole infusion, patients with Rockall scores ≥6 were randomised into the oral double-dose group (n=93) or the oral standard-dose group (n=94) to receive 11 days of oral esomeprazole 40 mg twice daily or once daily, respectively. The patients with Rockall scores <6 served as controls (n=89); they received 11 days of oral esomeprazole 40 mg once daily. Thereafter, all patients received oral esomeprazole 40 mg once daily for two more weeks until the end of the 28-day study period. The primary end point was peptic ulcer rebleeding.. Among patients with Rockall scores ≥6, the oral double-dose group had a higher cumulative rebleeding-free proportion than the oral standard-dose group (p=0.02, log-rank test). The proportion of patients free from recurrent bleeding during the 4th-28th day in the oral double-dose group remained lower than that of the group with Rockall scores <6 (p=0.03, log-rank test). Among patients with Rockall scores ≥6, the rebleeding rate was lower in the oral double-dose group than in the oral standard-dose group (4th-28th day: 10.8% vs 28.7%, p=0.002).. Double oral esomeprazole at 40 mg twice daily after esomeprazole infusion reduced recurrent peptic ulcer bleeding in high-risk patients with Rockall scores ≥6.. NCT01591083.

Topics: Administration, Oral; Adult; Aged; Dose-Response Relationship, Drug; Drug Administration Schedule; Duodenal Ulcer; Esomeprazole; Female; Hemostasis, Endoscopic; Humans; Infusions, Intravenous; Male; Middle Aged; Peptic Ulcer Hemorrhage; Proton Pump Inhibitors; Secondary Prevention; Severity of Illness Index; Stomach Ulcer; Treatment Outcome

To evaluate long-term safety of enteric-coated naproxen 500 mg and immediate-release esomeprazole magnesium 20 mg fixed-dose combination (FDC) in patients at risk of NSAID-associated upper gastrointestinal (UGI) ulcers.. In this open-label, multicenter, phase III study, Helicobacter pylori-negative patients aged ≥50 years or 18-49 years with history of uncomplicated ulcer within the past 5 years, who had osteoarthritis, rheumatoid arthritis, or other condition requiring daily NSAIDs for ≥12 months received naproxen/esomeprazole twice daily for 12 months.. NCT00527904.. Adverse events (AEs), vital signs, physical examination, and laboratory tests. Subgroup analyses included age and low-dose aspirin (LDA) use. Predefined NSAID-associated UGI and cardiovascular AEs were analyzed.. Of 239 patients treated (safety population), 135 completed ≥348 treatment days (12-month completers). AE incidence was approximately 70%; dyspepsia, constipation, upper respiratory tract infection, nausea, back pain, and contusion were most frequent (≥5% patients, either population). Treatment-related AEs occurred in 28.0% and 23.7% of patients in the safety and 12-month completer populations, respectively; 18.8% of patients withdrew due to AEs (safety population). Few serious AEs and no deaths occurred. In the safety population, AE incidence was 71.4% and 76.9% in patients aged <65 years (n = 161) and ≥65 years (n = 78), respectively, and 67.6% and 75.8% in LDA users (n = 74) and non-users (n = 165), respectively. Predefined UGI and cardiovascular AEs were observed in 18.8% and 6.3% of patients, respectively, in the safety population, and 16.3% and 5.2%, respectively, in 12-month completers. Dyspepsia and hypertension were most common. Additional assessments showed no unexpected findings.. Based on these outcome measures, long-term treatment with FDC naproxen/esomeprazole is not associated with any new safety issues, including predefined UGI and cardiovascular AEs, in patients requiring NSAID therapy who are at risk of UGI complications.

Topics: Adult; Aged; Aged, 80 and over; Algorithms; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Arthritis, Rheumatoid; Dosage Forms; Drug Combinations; Esomeprazole; Female; Humans; Magnesium Compounds; Male; Middle Aged; Naproxen; Osteoarthritis; Risk Factors; Stomach Ulcer; Time Factors

Gastroprotective co-therapy may reduce the risk of nonsteroidal anti-inflammatory drug (NSAID)-associated gastric ulcers, but adherence is suboptimal.. To compare the incidence of gastric ulcers with PN 400 [enteric-coated (EC) naproxen 500 mg and immediate-release esomeprazole 20 mg], or EC naproxen.. Two randomized, double-blind, multicentre studies (PN400-301, PN400-302). Patients [stratified by low-dose aspirin (< or =325 mg) use] aged > or =50 years or 18-49 years with a history of ulcer, received PN 400 BID (301, n = 218; 302, n = 210) or EC naproxen 500 mg BID (301, n = 216; 302, n = 210) for 6 months. The primary endpoint was the cumulative incidence of endoscopic gastric ulcers.. The cumulative incidence of gastric ulcers was significantly lower with PN 400 vs. EC naproxen (301: 4.1% vs. 23.1%, P < 0.001; 302: 7.1% vs. 24.3%, P < 0.001). PN 400 was associated with a lower combined incidence of gastric ulcers vs. EC naproxen in low-dose aspirin users (n = 201) (3.0% vs. 28.4%, P < 0.001) and non-users (n = 653) (6.4% vs. 22.2%, P < 0.001). The incidence of, and discontinuations due to, upper gastrointestinal (UGI) AEs was significantly lower with PN 400 relative to EC naproxen (P < 0.01, both studies).. PN 400 significantly reduces the incidence of gastric ulcers, regardless of low-dose aspirin use, in at-risk patients, and is associated with improved UGI tolerability relative to EC naproxen (ClinicalTrials.gov, NCT00527782).

Topics: Adolescent; Adult; Anti-Inflammatory Agents, Non-Steroidal; Double-Blind Method; Esomeprazole; Humans; Incidence; Magnesium; Middle Aged; Naproxen; Osteoarthritis; Stomach Ulcer; Tablets, Enteric-Coated; Treatment Outcome; Young Adult

To evaluate endoscopic and histological findings after Helicobacter pylori eradication therapy in gastric ulcer (GU) patients after 12 months' follow-up.. A total of 401 GU patients were randomized to receive either twice-daily (b.i.d.) esomeprazole 20 mg+amoxicillin 1000 mg+clarithromycin 500 mg (EAC) for 1 week followed by placebo for 3 weeks, EAC followed by once-daily (o.d.) esomeprazole 20 mg for 3 weeks or esomeprazole 20 mg b.i.d. plus placebo antibiotics for 1 week followed by esomeprazole 20 mg o.d. for 3 weeks. Endoscopy with biopsy was performed at baseline, after treatment and at 6 and 12 months' follow-up (healed patients).. Endoscopic abnormalities, particularly in the stomach, were common at baseline and remained similar during follow-up, regardless of ulcer status and treatment. Helicobacter gastritis was present (antrum or corpus) in approximately 20% of patients following eradication therapy (versus approximately 80% with esomeprazole alone); these effects were sustained during follow-up. Similar trends were observed for other histological variables (granulocyte and lymphoplasmocytic cell infiltration, replacement of gastric surface cells by regenerative epithelium, and mucous depletion). No changes in atrophy or intestinal metaplasia were observed. Eighteen gastric cancer cases were detected: 11 at baseline endoscopy, and seven during treatment and follow-up.. Endoscopic abnormalities are common in GU patients and persist after proton-pump inhibitor-based triple therapy for H. pylori eradication, which is associated with large, sustained improvements in histological variables. Follow-up endoscopy and histology may be necessary, even in patients with apparently non-malignant GU, to improve the detection rate of gastric malignancy in populations with a high prevalence of gastric cancer.

Topics: Amoxicillin; Clarithromycin; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Proton Pump Inhibitors; Stomach Ulcer; Treatment Outcome

Patients with comorbidities have an increased risk of ulcer rebleeding, especially within the 28 days after endoscopic therapy. Omeprazole infusion can prevent rebleeding after endoscopic therapy in patients with peptic ulcer bleeding. However, the optimal duration is uncertain, especially for those patients with comorbidities.. To determine whether prolonged low-dose intravenous omeprazole could reduce rebleeding for patients with comorbidities.. A prospective randomized control study.. National Cheng Kung University, Tainan, Taiwan.. A total of 147 patients with comorbidities and peptic ulcer bleeding controlled by endoscopic hemostasis were enrolled.. The enrolled patients were randomized into either the 7-day low-dose group or the 3-day high-dose group, who received 3.3 mg/h or 8 mg/h continuous omeprazole infusion, respectively. After omeprazole infusion, oral esomeprazole 40 mg every day was given.. To compare the rebleeding rates within 28 days after gastroscopy between the 2 study groups.. The 7-day cumulative rebleeding rate was similar between the 2 groups (9.5% vs 9.7%, P > .05), but the 7-day low-dose group had a lower risk of rebleeding between the 8th and 28th day compared with the 3-day high-dose group (0% vs 10.7%, P = .03; relative risk, 0.52 [95% CI, 0.43-0.63]). The Kaplan-Meier curves confirmed that the 7-day low-dose group had a significantly higher cumulative rebleeding-free proportion between the 8th and 28th day than the 3-day high-dose group (P = .02, log-rank test).. In Asian patients, prolonged low-dose omeprazole infusion for 7 days may reduce peptic ulcer rebleeding during the first 28 days in patients with comorbidities.

Topics: Aged; Aged, 80 and over; Comorbidity; Confidence Intervals; Dose-Response Relationship, Drug; Drug Administration Schedule; Duodenal Ulcer; Education, Medical, Continuing; Esomeprazole; Female; Follow-Up Studies; Hemostasis, Endoscopic; Humans; Infusions, Intravenous; Kaplan-Meier Estimate; Male; Middle Aged; Omeprazole; Peptic Ulcer Hemorrhage; Probability; Prospective Studies; Risk Assessment; Secondary Prevention; Severity of Illness Index; Statistics, Nonparametric; Stomach Ulcer; Survival Rate; Time Factors; Treatment Outcome

To compare esomeprazole-based triple therapy with esomeprazole alone for the eradication of Helicobacter pylori (H. pylori), healing of ulcer and prevention of relapse in H. pylori-related gastric ulcer (GU) diseases.. In this double-blind study, 401 H. pylori-positive patients with more than or equal to two GUs were randomized to: esomeprazole (20 mg) twice daily (bid) and amoxicillin (1000 mg) bid and clarithromycin (500 mg) bid (EAC) for 1 week, followed by placebo for 3 weeks (EAC and placebo); EAC for 1 week, followed by esomeprazole (20 mg) once daily (E20) for 3 weeks (EAC and E20); or esomeprazole (20 mg) bid and placebo antimicrobials for 1 week, followed by E20 for 3 weeks (E20 bid and E20). Patients with unhealed GUs at 4 weeks received E20 for an additional 4 weeks. Healed patients were followed up for 12 months.. Eradication rates at 4 weeks or 8 weeks were 82% for EAC and E20, 77% for EAC and placebo and 9.5% for E20 bid and E20 (intention-to-treat analysis). Significantly more patients receiving EAC than those receiving esomeprazole alone remained free of GUs during follow-up [EAC and E20, 90%; EAC and placebo, 87%; P=0.0005 for combined group vs. esomeprazole alone [E20 bid and E20 (74%)]. All treatments were well tolerated.. Esomeprazole-based triple therapy is effective for the eradication of H. pylori, healing of GU and prevention of relapse. Esomeprazole monotherapy for 3 weeks after triple therapy may be beneficial in terms of healing.

Topics: Adult; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Clarithromycin; Double-Blind Method; Drug Therapy, Combination; Esomeprazole; Female; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Secondary Prevention; Severity of Illness Index; Stomach Ulcer; Treatment Outcome; Young Adult

The use of non-steroidal anti-inflammatory drugs (NSAID) is associated with an increased risk of gastric ulcer (GU) development.. This multicentre, randomized, double-blind, parallel-group trial compared endoscopic healing rates at 4 and 8 weeks after treatment with oral esomeprazole 40 or 20 mg once daily, or ranitidine 150 mg twice daily, in patients with 1 baseline GU > or = 5 mm but no GUs or duodenal ulcers >25 mm in diameter who received continued cyclooxygenase-2-selective or non-selective NSAID therapies. The primary outcome was the percentage of patients in each treatment group who had no GUs at week 8.. Four hundred and forty patients were randomized to treatment. At week 8, GU healing rates (95% CI) with esomeprazole 40 mg, esomeprazole 20 mg and ranitidine were 85.7 (79.8-91.7)%, 84.8 (78.8-90.8)% and 76.3 (69.2-83.3)%, respectively; between-group differences were not statistically significant. Week-4 GU healing rates were 70.7 (62.9-78.4)% and 72.5 (65.0-79.9)% with esomeprazole 40 and 20 mg, respectively, and were significantly higher (P < 0.01 for both doses) than those with ranitidine [55.4 (47.1-63.7)%].. In patients who require continued NSAID therapy, GU healing rates at 8 weeks numerically favoured esomeprazole but were not significantly different from ranitidine.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Double-Blind Method; Esomeprazole; Female; Humans; Male; Middle Aged; Ranitidine; Stomach Ulcer; Time Factors; Treatment Outcome

Proton pump inhibitors reduce ulcer recurrence in non-steroidal anti-inflammatory drug (NSAID) users, but their impact in at-risk ulcer-free patients using the current spectrum of prescribed agents has not been clearly defined. We assessed esomeprazole for ulcer prevention in at-risk patients (> or = 60 yr and/or ulcer history) taking NSAIDs, including COX-2 inhibitors. Such studies are particularly relevant, given that concerns regarding adverse cardiovascular outcomes among COX-2 inhibitor users may prompt re-evaluation of their use.. We conducted two similar double-blind, placebo-controlled, randomized, multicenter studies; VENUS (United States) and PLUTO (multinational). A total of 844 and 585 patients requiring daily NSAIDs, including COX-2 inhibitors were randomized to receive esomeprazole (20 or 40 mg) or placebo, daily for 6 months.. In the VENUS study, the life table estimated proportion of patients who developed ulcers over 6 months (primary variable, intent-to-treat population) was 20.4% on placebo, 5.3% on esomeprazole 20 mg (p < 0.001), and 4.7% on esomeprazole 40 mg (p < 0.0001). In the PLUTO study, the values were 12.3% on placebo, 5.2% with esomeprazole 20 mg (p = 0.018), and 4.4% with esomeprazole 40 mg (p = 0.007). Significant reductions were observed for users of both non-selective NSAIDs and COX-2 inhibitors. Pooled ulcer rates for patients using COX-2 inhibitors (n = 400) were 16.5% on placebo, 0.9% on esomeprazole 20 mg (p < 0.001) and 4.1% on esomeprazole 40 mg (p= 0.002). Esomeprazole was well tolerated and associated with better symptom control than placebo.. For at-risk patients, esomeprazole was effective in preventing ulcers in long-term users of NSAIDs, including COX-2 inhibitors.

Topics: Aged; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Arthritis, Rheumatoid; Cyclooxygenase 2 Inhibitors; Double-Blind Method; Duodenal Ulcer; Esomeprazole; Female; Humans; Male; Middle Aged; Osteoarthritis; Proton Pump Inhibitors; Risk Factors; Stomach Ulcer

The role of clopidogrel in patients at risk for gastrointestinal complications is uncertain, although it has been recommended for patients who have gastrointestinal intolerance to aspirin. We tested the hypothesis that clopidogrel is as effective as esomeprazole and aspirin in preventing recurrences of ulcer complications.. This was a prospective, double-blind, randomized, controlled study of 170 patients who developed ulcer bleeding after the use of low-dose aspirin between November 2002 and January 2005. After healing of ulcers and eradication of Helicobacter pylori, if present, patients were assigned randomly to treatment with esomeprazole 20 mg/day and aspirin 100 mg/day (n = 86) or clopidogrel 75 mg/day (n = 84) for 52 weeks. The primary end point was recurrent ulcer complications.. During a median follow-up period of 52 weeks, no patient in the esomeprazole group, as compared with 9 patients in the clopidogrel group, developed recurrent ulcer complications. The cumulative incidences of recurrent ulcer complications were 0% in patients receiving esomeprazole and aspirin and 13.6% in patients receiving clopidogrel (absolute difference, 13.6%; 95% confidence interval for the difference, 6.3-20.9; log-rank test, P = .0019).. The combination of esomeprazole and aspirin is superior to clopidogrel in preventing ulcer complications in patients who have a past history of aspirin-related peptic ulcer bleeding.

Topics: Aged; Aged, 80 and over; Anti-Ulcer Agents; Aspirin; Clopidogrel; Cohort Studies; Double-Blind Method; Esomeprazole; Female; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Platelet Aggregation Inhibitors; Secondary Prevention; Stomach Ulcer; Ticlopidine; Treatment Outcome

To compare orally administered esomeprazole 40 mg once daily and 20 mg once daily with ranitidine 150 mg twice daily for the healing of gastric ulcers (GUs) during 8 wks in patients who continued to receive daily nonsteroidal anti-inflammatory drug (NSAID) therapy.. This multicenter, randomized, double-blind, parallel-group trial included patients who were receiving nonselective or cyclo-oxygenase-2 (COX-2)-selective NSAIDs and had at least one GU >or=5 mm but no gastric or duodenal ulcer >25 mm in diameter at the baseline esophagogastroduodenoscopy (EGD). After 4 and 8 wks of treatment, ulcer-healing status was confirmed by EGD. The primary outcome was the percentage of patients in each treatment group who had no GUs (GU healing rate) at week 8.. A total of 406 patients were randomized to treatment. At week 8, GU healing rates with esomeprazole 40 and 20 mg were 91.5% (118/129; 95% CI, 86.7-96.3%) and 88.4% (122/138; 95% CI, 83.1-93.7%), respectively, and were significantly higher than the 74.2% rate (98/132; 95% CI, 66.8-81.7%) with ranitidine (p<0.01 for both comparisons). GU healing rates at 4 wks (78.3%[101/129] and 79.0%[109/138] in the esomeprazole 40- and 20-mg groups, respectively) were also significantly higher (p<0.05) than in the ranitidine group (66.7%[88/132]). All treatments were well tolerated.. Esomeprazole 40 and 20 mg once daily are effective and well-tolerated therapies compared with ranitidine 150 mg twice daily for healing GUs in patients who need to continue NSAID therapy.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Confidence Intervals; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration Schedule; Drug Therapy, Combination; Esomeprazole; Female; Follow-Up Studies; Gastric Mucosa; Humans; Male; Middle Aged; Probability; Ranitidine; Reference Values; Risk Assessment; Severity of Illness Index; Stomach Ulcer; Treatment Outcome

The present study investigated the gastroprotective activity of benzyl isothiocyanates (BITC) on indomethacin (IND)-induced gastric injury in a rat model and explicated the possible involved biochemical, cellular, and molecular mechanisms. The rat model with gastric ulcers was established by a single oral dose of IND (30 mg per kg b.wt). BITC (0.75 and 1.5 mg kg

Topics: Animals; Anti-Ulcer Agents; Apoptosis; Caspase 3; Esomeprazole; Female; Heme Oxygenase-1; Humans; Indomethacin; Inflammation; Intestinal Mucosa; Isothiocyanates; Male; NAD(P)H Dehydrogenase (Quinone); NF-E2-Related Factor 2; NF-kappa B; Oxidative Stress; Rats; Rats, Wistar; Signal Transduction; Stomach Ulcer

Endoscopic submucosal dissection (ESD) is widely used as a treatment modality for gastric mucosal neoplasia. While proton pump inhibitors (PPIs) have been used for the control of artificial ulcers created by ESD (ESD-ulcers), complete healing of the ulcers is not always achieved in all the cases. The purpose of this study was to identify the clinical factors that are predictive of refractory ESD-ulcers.. We recruited 90 patients with 102 artificial ulcers that formed after the patients underwent ESD for gastric tumours. All the patients received a 20-mg capsule of esomeprazole daily until the 56th day after ESD, and underwent endoscopy at 1, 4, 6 and 8 weeks after the ESD. We analyzed the clinical factors that were associated with the complete healing at 8 weeks after the ESD (CH-8w). The ulcers in the scar stage were defined as the complete healing in this study.. Of the 102 ESD-ulcers, 16.7% failed to show complete healing after the 8 weeks of PPI therapy. Univariate analysis identified the percent reduction of the ulcer size at 4 weeks after ESD (PR-4w) as being significantly associated with CH-8w. Multivariate analysis identified ulcer location in the lower-third of the stomach and PR-4w > 95% as being independently correlated with the CH-8w (odds ratio = 4.86 and 7.89, respectively). Analysis of the area under the receiver operating characteristic (AUROC) curve demonstrated that the AUROC curve of PR-4w for predicting the CH-8w was 0.78.. Based on the results of our study, endoscopic observation at 4 weeks after ESD would help in the early identification of refractory ESD-ulcers.

Topics: Endoscopic Mucosal Resection; Esomeprazole; Gastric Mucosa; Gastroscopy; Humans; Proton Pump Inhibitors; Stomach Neoplasms; Stomach Ulcer; Ulcer

The purpose of this study was to evaluate the co-prescription efficacy of esomeprazole and flupenthixol/melitracen relative to that of solitary esomeprazole on erosive gastritis complicated with negative feelings. 140 erosive gastritis patients complicated with negative feelings enrolled in the present study. Seventy cases in the control group took esomeprazole, and 70 cases in the observation group received esomeprazole plus flupenthixol/Melitracen, both for 4 weeks. We gastroscopically checked the clinical symptoms, mucosal erosion, PGE2 and MDA levels in gastric mucosa, anxiety, depression, and recurrence before and after treatment in the groups. After treatment, the observation group had lower scores of clinical symptoms, mucosal erosions, Hamilton Depression Rating Scale (HAMD), and Hamilton Depression Rating Scale (HAMA) than the control group (p<0.05); as well, the observation group showed higher PGE2 and lower MDA levels than the control group (p<0.05); during six months of follow-up (100% follow-up rate), 16 and 34 recurrent cases occurred, respectively, in the observation and control groups (p<0.05).  Co-prescription of esomeprazole and flupenthixol/melitracen improved the clinical symptoms and mucosal erosions, relieved negative feelings and reduced the recurrence rate. The efficacy of the co-prescription is higher than that of the solitary prescription.

Topics: Aged; Anthracenes; Anxiety; Combined Modality Therapy; Depression; Emotions; Esomeprazole; Female; Flupenthixol; Gastric Mucosa; Gastritis; Humans; Male; Middle Aged; Recurrence; Stomach Ulcer; Treatment Outcome

Stress ulcer is a severe complication in critically ill patients and causes a high mortality. The proton pump inhibitor esomeprazole is widely applied in the treatment of stress ulcers because of its powerful acid suppression ability. However, the mechanism of stress ulcer and the precise gastroprotective effect of esomeprazole in stress ulcer remain unclear.. In the present study, the rats with water-immersed and restraint (WIR)-induced stress ulcer were used to further elucidate the anti-ulcerogenic capacity of esomeprazole in stress ulcer in addition to its anti-acid secreting ability.. The rats were randomly divided into 5 groups: control group (NS), water-immersed and restraint group (WIR), high-dose application of esomeprazole plus stress ulcer-induced group (HE+WIR), low-dose application of esomeprazole plus stress ulcer-induced group (LE+WIR), and high-dose application of esomeprazole without stress ulcer-induced group (HE). Our study showed that the pretreatment of esomeprazole alleviated gastric tissue damage in both macroscopic and histopathological manifestations. Pretreatment of esomeprazole elevated the decline in PEG2 level affected by WIR; and it inhibited the secretion of gastric acid, gastrin and pepsin. Moreover, esomeprazole exerted its antioxidant effects by reducing malondialdehyde levels, enhancing the expressions of antioxidant factors like glutathione and superoxide dismutase (SOD) and reducing the compensatory transcriptional elevation of SOD1 gene. Esomeprazole also reduced the levels of MPO (myeloperoxidase), tumor necrosis factor (TNF)-α and interleukin (IL)-1β according to its anti-inflammatory effects. We further explored the possible mechanism of esomeprazole pretreatment on stress ulcer and demonstrated that esomeprazole attenuated the high phosphorylation levels of nuclear factor kappa B (NF-κB) p65 and p38 MAPK, and decreased the NF-κB p65 nuclear translocation induced by WIR related stress ulcer.. Our study provides some evidence that the esomeprazole pretreatment exerts gastroprotective effects in WIR-induced stress ulcer through not only its antisecretory effect but also its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways.

Topics: Administration, Oral; Animals; Anti-Ulcer Agents; Antioxidants; Dose-Response Relationship, Drug; Esomeprazole; Gastric Mucosa; Injections, Intraperitoneal; Male; MAP Kinase Signaling System; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Stress, Psychological

The role of Helicobacter pylori eradication is still not clear in endoscopic submucosal dissection (ESD)-induced artificial ulcer. This study investigates the therapeutic effects of H. pylori eradication on ESD-induced artificial ulcers.. Eighty-four patients with ESD-induced artificial ulcers were enrolled. H. pylori eradication success subgroup (Group A1) and H. pylori eradication failure subgroups (Group A2) received standard triple therapy orally for 7 days, followed by esomeprazole 20 mg bis in die (bid) orally for the remainder of the treatment period (4 weeks in total). The H. pylori positive (Group B1) and H. pylori negative subgroups (Group B2) received esomeprazole 20 mg bid orally for 4 weeks. Ulcer healing was evaluated by gastroscopy, and H. pylori was identified by a C13 breath test or an Hp-RUT 2 and 6 months after treatment.. Successful eradication of H. pylori can promote healing of ESD-induced artificial ulcers. The ESD-induced artificial ulcer healing rate in Group A1 was statistically higher than that in Groups A2, B1, and B2.. Our results indicated that early H. pylori eradication therapy can promote ESD-induced artificial ulcer healing in H. pylori positive patients with ESD-induced artificial ulcers.

Topics: Adult; Aged; Anti-Bacterial Agents; Anti-Ulcer Agents; Drug Therapy, Combination; Endoscopic Mucosal Resection; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Retrospective Studies; Stomach Ulcer

Gastric ulcer is a common problem affecting the gastrointestinal tract. Spirulina and wheatgrass are natural substances that have anti-inflammatory and antioxidant effects. The aim of the Work was to elucidate the possible protective role of spirulina and wheatgrass versus standard treatment esomeprazole on indomethacin-induced gastric ulcer in adult male albino rats. Eighty adult male albino rats were divided into eight groups: group I (the control group), group II that received indomethacin (100 mg/kg orally), group III that received esomeprazole (20 mg/kg orally), group IV that received spirulina (1000 mg/kg orally), group V that received wheatgrass (1000 mg/kg orally), group VI that received indomethacin (100 mg/kg) + esomeprazole (20 mg/kg), group VII that received indomethacin (100 mg/kg) + spirulina (1000 mg/kg) and group VIII that received indomethacin (100 mg/kg) + wheatgrass (1000 mg/kg). Six hours after indomethacin treatment, all rats were anesthetized and their stomachs obtained for measures of gastric acidity, pepsin activity, mucin content, gastrin, ulcer index, total antioxidant capacity (TAC), tumor necrosis factor -α (TNF-α), interleukin-8 (IL8), proapoptotic protein (Bax). Histological (using H&E stain, PAS reaction) and immunohistochemical (using anti Ki67 immunostain) techniques were performed. Western immunoblot analysis for heat shock protein 70 (HSP70) was also done. Moreover, a morphometric study was done for area% of positive immunoreactive cells for Ki67 and optical density and area% of PAS reaction. All performed measurements were followed by statistical analysis. Indomethacin induced loss of normal architecture of gastric mucosa with sloughing of surface epithelium and inflammatory cellular infiltration. It also led to a significant increase in gastric acidity, inflammatory mediators (TNF-α, IL-8), pro-apoptotic protein Bax and a significant decrease in TAC levels and HSP-70 expression. There was also a significant decrease in area% of Ki67 immunoreactivity and area% and optical density of PAS reaction as compared with the control group and other pre-treated rats. These disturbed parameters were associated with increased ulcer index. In pre-treatment groups, the structure of the mucosa was similar to control with marked improvement in the biochemical assay. In conclusion, Spirulina and wheatgrass can partly protect the gastric mucosa against indomethacin-induced damage to a degree similar to that of the classical treatment eso

Topics: Animals; Antioxidants; Biomarkers; Biopsy; Cytokines; Disease Models, Animal; Esomeprazole; Immunohistochemistry; Indomethacin; Inflammation Mediators; Male; Phenotype; Plant Extracts; Poaceae; Protective Agents; Rats; Spirulina; Stomach Ulcer

Topics: Aged; Anti-Ulcer Agents; Body Mass Index; Duodenal Ulcer; Duodenitis; Esomeprazole; Humans; Hypertension, Portal; Ischemia; Liver Cirrhosis, Alcoholic; Male; Risk Factors; Stomach Ulcer; Treatment Outcome

Proton pump inhibitors (PPI) are effective at healing artificial ulcers after endoscopic submucosal dissection (ESD) for gastric neoplasms; however, the efficacy of vonoprazan is not completely understood. The aim of the present study was to determine the healing effect of vonoprazan on artificial ulcers post-gastric ESD relative to PPI.. Thirty-five patients who underwent gastric ESD between April and November 2015 were treated with vonoprazan 20 mg/day for 4 weeks and subsequently underwent endoscopy for evaluation of ulcer size (V group). Ulcer contraction rate was determined by the following formula: ([ESD specimen size] - [ulcer size at 4 weeks after ESD])/(ESD specimen size) × 100%. We compared the results with those of a historical control group treated with esomeprazole 20 mg/day for 4 weeks after gastric ESD and subsequently measured their ulcer size (33 patients, E group) by propensity score-matching methods.. Sixty-two subjects were enrolled after propensity score-matching. Ulcer contraction rate at 4 weeks after ESD in the V group was significantly higher than that of the E group (97.7 ± 3.2% vs 94.5 ± 6.7%, respectively, P = 0.025). Number of subjects with a scar-stage ulcer (100% contraction rate) tended to be higher in the V group relative to the E group (32% [10 of 31] vs 13% [4 of 31], respectively, P = 0.070, McNemar's chi-squared test).. Vonoprazan has a faster post-gastric ESD artificial ulcer contraction rate than esomeprazole. Vonoprazan may supersede PPI in treating post-ESD artificial ulcers of the stomach.

Topics: Aged; Endoscopic Mucosal Resection; Esomeprazole; Female; Follow-Up Studies; Gastroscopy; Humans; Male; Postoperative Complications; Propensity Score; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Stomach Neoplasms; Stomach Ulcer; Sulfonamides; Treatment Outcome

Esomeprazole warrants further investigation as a treatment for equine gastric ulcer syndrome.. To investigate the duration of intraday acid suppression achieved with two doses of esomeprazole under two dietary conditions.. A four way crossover design.. Six adult Thoroughbreds instrumented with percutaneous gastrotomy tubes were used. Intragastric pH was measured for continuous 23 h periods (08.00-07.00 h) for 6 consecutive days (Days 0-5). Baseline data was recorded on Day 0 and esomeprazole was administered on Days 1-5. Two doses (0.5 and 2.0 mg/kg bwt/day per os once daily) and two diets (a high grain/low fibre (HG/LF) and ad libitum hay (HAY) diet) were studied. Data for the percentage of time pH was above 4 (%tpH>4) and median intraday pH was reported for two measurement points and analysed using generalised estimating equations.. An inconsistent effect of both diet and dose was evident with mean %tpH>4 and mean of the median intraday pHs typically higher at the 2.0 mg/kg bwt dose and in HG/LF diet. A cumulative effect of dosing was present with the magnitude of acid suppression observed on Day 5 consistently higher than that observed on Day 1. The magnitude of acid suppression, at measurement point 1, compared favourably with previous reports on omeprazole and exceeded human therapeutic breakpoints for the 0.5 mg/kg bwt dose in the HG/LF diet and 2.0 mg/kg bwt dose in the HAY diet.. Instrumentation may have modified gastric function and horses were not fasted or exercised.. The findings of the present study suggested that both dose and diet affect the response to esomeprazole in the horse and that a cumulative effect is present over the first 5 days of treatment. Further investigation into the clinical efficacy of esomeprazole and trials directly comparing esomeprazole and omeprazole appear to be warranted.

Topics: Animals; Anti-Ulcer Agents; Cross-Over Studies; Diet; Dose-Response Relationship, Drug; Esomeprazole; Horse Diseases; Horses; Humans; Hydrogen-Ion Concentration; Stomach Ulcer

Spondias mombin Linn (Anacardiaceae) and Ficus exasperata Valh (Moraceae) are botanicals with known phytotherapeutic potentials in the traditional system of medicine in the world.. The objective of this study is to investigate the quantitative polyphenolic constituents and gastroprotective effects of aqueous leaf extracts of Spondias mombin and Ficus exasperata against indomethacin-induced gastric ulcer in rats.. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg body weight (b.w.)). Ulcerated rats were orally administered with esomeprazole (a reference drug) at a dose of 20 mg/kg body weight, and Spondias mombin and Ficus exasperata at a dose of 100 and 200 mg/kg b.w. once daily for 21 d after ulcer induction. Gastric secretions and antioxidant parameters were thereafter evaluated.. The significantly increased (p < 0.05) ulcer index, gastric volume, malondialdehyde level, and pepsin activity by indomethacin were effectively reduced by 65.40, 36.47, 45.71, and 53.79%, respectively, following treatment with F. exasperata at 200 mg/kg b.w. S. mombin at this regimen also attenuated these parameters by 71.70, 46.62, 50.16, and 55.73%. Moreover, the extracts significantly increase the reduced activity of superoxide dismutase as well as pH and mucin content in the ulcerated rats.. These findings are indicative of gastroprotective and antioxidative potentials of the extracts which is also evident in the degree of % inhibition against ulceration. The available data in this study suggest that the extracts proved to be capable of ameliorating indomethacin-induced gastric ulceration and the probable mechanisms are via antioxidative and proton pump inhibition.

Topics: Anacardiaceae; Animals; Anti-Ulcer Agents; Cytoprotection; Disease Models, Animal; Dose-Response Relationship, Drug; Esomeprazole; Ficus; Gastric Mucosa; Hydrogen-Ion Concentration; Indomethacin; Malondialdehyde; Mucins; Pepsin A; Phytotherapy; Plant Extracts; Plant Leaves; Plants, Medicinal; Proton Pump Inhibitors; Rats, Wistar; Stomach Ulcer; Superoxide Dismutase; Time Factors

Topics: Administration, Oral; Adult; Drug Eruptions; Esomeprazole; Female; Gastroesophageal Reflux; Hand Dermatoses; Humans; Lansoprazole; Male; Proton Pump Inhibitors; Stomach Ulcer

Quadruple concomitant non-bismuth therapy has recently become the most widely prescribed first-line treatment for Helicobacter pylori infection in Spain. Whether optimized conventional triple therapy can achieve comparable efficacy rates remains to be seen.. Retrospective study comparing the efficacy of triple and quadruple concomitant therapy, and sub-analysis following administration of both for 10 days with esomeprazole 40mg/12h.. A first-line therapy was administered to 657 patients from 1st January 2012 to 31st December 2014. Quadruple therapy (n=371) showed higher efficacy than triple therapy (n=248) for both intention-to-treat (85.9% vs. 65.7%; P<.001) and per protocol analysis (92.5% vs. 68.4%; P<.001). When both therapies included esomeprazole 40mg/12h administered for 10 days, quadruple concomitant therapy (n=108) also had higher efficacy than triple therapy (n=76) for intention-to-treat (90.7% vs. 73.6%; P=.003) and per protocol analysis (92.5% vs.74.6%; P=.002).. Quadruple concomitant therapy with high dose proton pump inhibitor (PPI) for 10 days achieves a significantly higher eradication outcome than optimized triple therapy, with rates of over 90% when the PPI prescribed is esomeprazole 40mg/12h.

Topics: Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Clarithromycin; Drug Administration Schedule; Drug Therapy, Combination; Dyspepsia; Esomeprazole; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Proton Pump Inhibitors; Retrospective Studies; Spain; Stomach Ulcer

YF476 differs from the proton pump inhibitor (PPI) esomeprazole in mode of action by antagonizing the type 2 receptor of cholecystokinin/gastrin (CCK-2R). YF476 protection against diclofenac-induced gastric ulcers was compared to esomeprazole and correlated with plasma levels of hormones related to gastric pH (gastrin, ghrelin, and somatostatin), gastric gene expression of these hormones, their receptors, and inducible nitric oxide synthase (iNOS). YF476 or esomeprazole pretreatments were followed by diclofenac. Four hours later, gastric tissue was excised and analyzed for ulcer index. An intragastrically implanted Bravo capsule measured pH for 5 days during YF476 plus pentagastrin treatment. Changes in gene expression were assayed for gastrin, ghrelin, and somatostatin; their receptors; and iNOS. YF476 acutely (within 4 h) protected against diclofenac-induced gastric ulcers equivalent to esomeprazole. Gastric pH recorded during 5 days in the presence of pentagastrin was 1.83 (±0.06). YF476 raised pH to 3.67 (±0.09) and plasma ghrelin, gastrin, and somatostatin increased. YF476 increased gene expression of somatostatin receptor and gastrin, while ghrelin receptor decreased; transcripts coding ghrelin, somatostatin, and CCK-2R remained unchanged. In the presence of diclofenac, esomeprazole increased expression of all these transcripts and that of iNOS, while YF476 yielded only decreased CCK-2R and increased iNOS transcripts. YF476 is a potential new preventative treatment for patients at risk of nonsteroidal antiinflammatory drug (NSAID)-induced ulceration. Gastric gene expressions of ghrelin, gastrin, and somatostatin and their receptors differ between esomeprazole and YF476. Despite these differences and different modes of action to raise gastric pH, both drugs acutely increase iNOS, suggesting iNOS expression parallels pH.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Benzodiazepinones; Diclofenac; Esomeprazole; Gastric Mucosa; Gene Expression Regulation; Hydrogen-Ion Concentration; Male; Nitric Oxide Synthase Type II; Phenylurea Compounds; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin B; Stomach Ulcer

Proton pump inhibitors promote ulcer repair in nonsteroidal anti-inflammatory drug (NSAID)-treated patients with ongoing NSAID-induced gastric toxicity, although the underlying mechanisms remain unclear. We examined the healing mechanisms of esomeprazole on NSAID-induced gastric ulcerations in the presence of a continued NSAID treatment. Ulcerations were induced in rats by oral indomethacin (6μmol/kg/day) for 14 days. Indomethacin administration was continued, alone or combined with equivalent acid inhibitory doses of esomeprazole (5μmol/kg/day), lansoprazole (15μmol/kg/day) or famotidine (20μmol/kg/day), for additional 7 days. Stomachs were then processed for: histomorphometric analysis of mucosal injury; mucosal levels of prostaglandin E(2) (PGE(2)) and malondialdehyde (MDA); expression of vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), caspase-3, and cyclooxygenase-2 (COX-2) (Western blot); expression of Ki-67 (immunohistochemistry). Indomethacin for 14 days elicited mucosal damage, reduced PGE(2) levels and increased MDA. After additional 7 days, indomethacin induced the following effects: further enhancement of mucosal damage and MDA content; decrease in PGE(2) levels; increase in COX-2 and activated caspase-3 expression; decrease in VEGF, PCNA and Ki-67 expression. In the presence of indomethacin, esomeprazole and lansoprazole were more effective than famotidine in promoting resolution of mucosal damage. Concomitantly, esomeprazole and lansoprazole, but not famotidine, restored PCNA and Ki-67 expression, and normalized MDA levels. Moreover, esomeprazole, lansoprazole and famotidine partly counteracted caspase-3 activation, without affecting VEGF expression. The healing activity of esomeprazole on indomethacin-induced gastric ulcerations can be ascribed to two mechanisms: (1) acid-dependent reduction of pro-apoptotic signalling; (2) acid-independent restoration of proliferating/repairing pathways.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Apoptosis; Blotting, Western; Caspase 3; Cell Proliferation; Cyclooxygenase 2; Dinoprostone; Disease Models, Animal; Esomeprazole; Famotidine; Gastric Acid; Gastric Mucosa; Histamine H2 Antagonists; Immunohistochemistry; Indomethacin; Ki-67 Antigen; Lansoprazole; Male; Malondialdehyde; Proliferating Cell Nuclear Antigen; Proton Pump Inhibitors; Rats; Rats, Wistar; Stomach Ulcer; Time Factors; Vascular Endothelial Growth Factor A; Wound Healing

The efficacy of proton pump inhibitors in patients at high risk of gastrointestinal injury receiving non-steroidal anti-inflammatory drugs is currently debated.. To evaluate the effects of esomeprazole on the impairment of gastric ulcer healing associated with non-steroidal anti-inflammatory drug treatment.. Gastric ulcers were induced in rats by acetic acid. Four days later, animals were treated daily with equivalent acid-inhibiting doses of esomeprazole or famotidine, alone or in combination with indomethacin. At day 3 or 7 of treatment, ulcerated tissues were processed to assess: ulcer area; malondialdehyde; prostaglandin E(2); nuclear factor-kB; proliferating cell nuclear antigen and caspase-3 (Western blot).. In indomethacin-treated animals, esomeprazole was more effective than famotidine or the antioxidant melatonin in promoting ulcer healing. Malondialdehyde levels were increased by indomethacin, and this effect was counteracted by esomeprazole, but not famotidine. Esomeprazole and famotidine, given alone or in combination with indomethacin, increased proliferating cell nuclear antigen expression. Increased levels of prostaglandin E(2) were detected in ulcerated tissues. Ulcer prostaglandin E(2) production was reduced by indomethacin, alone or in combination with esomeprazole or famotidine, while it was enhanced when esomeprazole or famotidine were tested alone. The activation of caspase-3 was induced by indomethacin, and this effect was prevented by esomeprazole, but not famotidine. In the presence of indomethacin, esomeprazole, but not famotidine, enhanced nuclear factor-kB activation in gastric ulcers.. Esomeprazole counteracts the detrimental action of indomethacin on ulcer repair through both acid-dependent and acid-independent effects. The acid-independent actions are related to decrease in tissue oxidation and apoptosis and to enhancement of nuclear factor-kB activation.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Antioxidants; Caspase 3; Dinoprostone; Disease Models, Animal; Esomeprazole; Famotidine; Indomethacin; Male; Malondialdehyde; Melatonin; NF-kappa B; Proliferating Cell Nuclear Antigen; Rats; Rats, Wistar; Stomach Ulcer; Treatment Outcome; Wound Healing

Topics: Aged, 80 and over; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Esomeprazole; Female; Humans; Infusions, Subcutaneous; Palliative Care; Peptic Ulcer Hemorrhage; Stomach Ulcer

The two prevailing approaches to decrease risks of nonsteroidal anti-inflammatory drug (NSAID)-associated gastrointestinal (GI) events are the use of a COX-2 inhibitor or co-therapy with a proton-pump inhibitor (PPI). A major limitation of each approach is that, in patients at the highest risk for NSAID-induced ulcers, neither treatment is effective when used as a stand-alone strategy. An important question is whether combination therapy with a COX-2 inhibitor plus a PPI has improved GI safety compared to a traditional NSAID plus a PPI. This study evaluated high GI risk patients who were taking, along with their NSAID or COX-2 inhibitor, either the PPI, esomeprazole, or the placebo. It confirms that our current approach of adding PPIs to reduce NSAIDs' ulcer risks is an effective strategy. However, this study did not show a safety advantage for using a COX-2 inhibitor instead of a traditional NSAID in high GI risk patients who take PPIs. Thus, there continues to be no prospective data to support a GI benefit of COX-2 inhibitor plus a PPI over traditional NSAID plus a PPI in high-risk patients.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Cyclooxygenase 2 Inhibitors; Duodenal Ulcer; Esomeprazole; Humans; Proton Pump Inhibitors; Risk Factors; Stomach Ulcer