Intravenous Proton Pump Inhibitor Therapy Research Articles

Peptic Ulcer Disease and Its Implications

Peptic ulcer disease (PUD) is one of the commonest diseases seen throughout the world. Peptic ulcers are open sores that develop on the inside lining of your stomach and the upper portion of your small intestine. The most common symptom of a peptic ulcer is stomach pain. There are various risk factors for the development of peptic ulcer disease, but the most important ones are Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs). Patients generally present with dyspepsia or peptic ulcer bleeding. Acid suppressant therapy, H. pylori eradication, and avoidance of nonsteroidal anti-inflammatory drugs are the cornerstones of treatment of peptic ulcer disease. Peptic ulcer bleeding could be life-threatening. It is managed by appropriate supportive care, intravenous proton pump inhibitor therapy, and endoscopic homeostasis. Trans arterial embolization (TAE), Herbal treated and surgery are rarely required if endoscopic therapy fails.

Randomized controlled trial of early endoscopy for upper gastrointestinal bleeding in acute coronary syndrome patients

Acute upper gastrointestinal bleeding (UGIB) in acute coronary syndrome (ACS) patients are not uncommon, particularly under dual antiplatelet therapy (DAPT). The efficiency and safety of early endoscopy (EE) for UGIB in these patients needs to be elucidated. This multicenter randomized controlled trial randomized recent ACS patients presenting acute UGIB to non-EE and EE groups. All eligible patients received intravenous proton pump inhibitor therapy. Those in EE group underwent therapeutic endoscopy within 24 h after bleeding. The data regarding efficacy and safety of EE were analyzed. It was early terminated because the UGIB rate was lower than expected and interim analysis was done. In total, 43 patients were randomized to non-EE (21 patients) and EE (22 patients) groups. The failure rate of control hemorrhage (intention-to-treat [ITT] 4.55% vs. 23.81%, p < 0.001; per-protocol [PP] 0% vs. 4.55%, p = 0.058) and 3-day rebleeding rate (ITT 4.55% vs. 28.57%, p = 0.033; PP 0% vs. 21.05%, p = 0.027) were lower in EE than non-EE group. The mortality, minor and major complication rates were not different between two groups. Male patients were at higher risk of minor and major complications after EE with OR (95% CI) of 3.50 (1.15–10.63) and 4.25 (1.43–12.63), respectively. In multivariate analysis, EE was associated with lower needs for blood transfusion (HR 0.13, 95% CI 0.02–0.98). Among patients who discontinued DAPT during acute UGIB, a higher risk (OR 5.25, 95% CI 1.21–22.74) of coronary artery stent re-thrombosis within 6 months was noticed. EE for acute UGIB in recent ACS patients has higher rate of bleeding control, lower 3-day rebleeding rate and lower needs for blood transfusion, but more complications in male patients. Further enrollment is mandatory to avoid bias from small sample size (ClinicalTrial.gov Number NCT02618980, registration date 02/12/2015).

Pre-endoscopic intravenous proton pump inhibitors therapy for upper gastrointestinal bleeding: A prospective, multicentre study

Background/AimThe indiscriminate use of high-dose, proton pump inhibitor (PPI) infusion in non-variceal upper gastrointestinal bleeding (UGIB) patients to reduce the rate of peptic ulcers with high-risk stigmata (HRS) has been questioned. We evaluated the prevalence of HRS on peptic ulcer and non-ulcer lesions in patients receiving or not receiving pre-endoscopic PPI therapy. MethodsData of consecutive UGIB patients observed in 50 Italian centres were analysed. The prevalence of both HRS on peptic ulcers and active bleeding on non-ulcer lesions between patients treated or not treated with PPI were compared. Multivariate analysis was performed. ResultsA total of 1,792 (69.8%) out of 2,566 patients received PPI therapy. Prevalence of HRS on ulcers was 51.8% and 53.4% (P = 0.58) in treated and not treated patients, respectively, and the rate of endoscopic therapy did not differ between groups. Prevalence of non-ulcer bleeding lesions was higher in patients treated than in those not treated with PPI (18.7% vs 10.6%; P = 0.023). At multivariate analysis, PPI therapy (OR: 1.16, 95% CI = 0.82–1.64; P = 0.4) was not an independent factor affecting HRS prevalence, which was inversely correlated with timing to endoscopy (OR: 0.85, 95% CI = 0.76–0.95; P = 0.005). ConclusionsOur data failed to detect a significant role of pre-endoscopic PPI therapy in decreasing prevalence of HRS and need for endoscopic treatment in bleeding patients with either peptic ulcer or non-ulcer lesions.

A183 UPPER GASTROINTESTINAL CAUSTIC INJURIES: A SINGLE CENTRE CASE SERIES

Abstract Background Caustic esophageal and gastric injury is a rare, but potentially lethal event. The 2017 American Association of Poison Control reported only 193,000 cases of caustic ingestion (1). Caustic agents are acidic or alkaline. The pH of the ingested substance dictates the type of injury and the area of the gastrointestinal track most at risk. The most common culprit agents are alkaline including, for example, bleaches, drain openers and dishwashing detergents. Due to the rarity and natural history of this disease there are very few high-quality studies for clinicians to refer to when managing these patients. Aims We present three cases of caustic ingestion and provide a review of current best practice standards. Methods Between August and September 2019, three patients were admitted to Sunnybrook Health Sciences Centre at the University of Toronto for caustic injury. All three patients were referred to the gastroenterology service and underwent an esophagogastroduodenoscopy (EGD) to assess the degree of esophageal and gastric injury. Patients were followed both in hospital and in the outpatient setting for ongoing surveillance and repeated endoscopic evaluation. Patient demographics, treatment, endoscopic findings and outcomes were collected. Results Three patients intentionally ingested caustic agents, were admitted to hospital and managed by the gastroenterology service. Patients were a mix of ages, genders and ethnicities. All ingestions were strong alkali agents including sodium hydroxide and sodium hypochlorite. All patients underwent an EGD within 24 hours of presentation and caustic injury was graded using the Zargar classification (2). All patients were started on intravenous proton pump inhibitor therapy. All patients were initially made nothing per mouth and ability to resume feeds was assessed based on symptoms. Patient 1, Zargar grade 1, was able to resume oral intake within 48 hours and progressed to a regular diet without complications. Patient 2, Zargar grade 2a, required 5 days of TPN and bowel rest after which a liquid diet was initiated and advanced without complications. The third patient, had a severe injury (Zargar grade 3b), requiring a prolonged hospital stay. He was on TPN for three weeks before transitioned to tube feeds. Conclusions Caustic mucosal injuries are an infrequent, but potentially lethal event requiring urgent assessment and management by a team including gastroenterologists, thoracic and abdominal surgeons, dieticians and intensivists. High-quality evidence to guide management of caustic injuries remains limited. In our case series, there was a wide spectrum of degree of mucosal injury. All 3 patients were managed in a consistent fashion based on current recommendations. Two of three cases had a rapid recovery with the ability to resume oral intake and return home. The third patient remains in hospital, requiring a high level of supportive care. Funding Agencies None

Is a proton-pump inhibitor necessary after endoscopic submucosal dissection for superficial esophageal neoplasms? A propensity score analysis.

Background:Little is known about the efficacy of proton-pump inhibitor (PPI) therapy in the management of esophageal ulcers after endoscopic submucosal dissection (ESD). Therefore, the objective of this study was to investigate the efficacy of PPI in ulcer healing following ESD for superficial esophageal neoplasms, using a propensity score analytic approach.Methods:This retrospective cohort study was conducted at a single referral center. Between April 2005 and August 2015, 199 consecutive patients with superficial esophageal cancer and esophageal dysplasia underwent ESD. For patients with PPI administration, intravenous PPI therapy was commenced immediately after ESD, and oral PPI was administered daily from post-operative day 3, until ulcer healing was identified. We compared the remnant-ulcer rate at 4 weeks after esophageal ESD between the PPI administration and non-PPI groups, using propensity scores and the inverse probability of treatment weighting (IPTW) method.Results:After exclusions, a total of 88 patients were analyzed. The remnant-ulcer rate at 4 weeks after ESD was 25.5% (12/47) and 14.6% (6/41) in the PPI administration and non-PPI groups (p = 0.21). After adjusting for background factors using IPTW, the risk of a remnant ulcer in the PPI administration group was not decreased significantly compared with that in the non-PPI group [odds ratio (OR) = 2.42, 95% confidence interval (CI): 0.73–7.97, p = 0.15]. Furthermore, PPI therapy did not decrease significantly the remnant-ulcer rate on logistic regression analysis after adjusting for the propensity score (OR = 2.40, 95% CI: 0.69–8.32, p = 0.15).Conclusion:PPI administration does not promote ulcer healing after ESD for superficial esophageal squamous cell carcinoma.

2704 Urosepsis Is Difficult to Stomach!

INTRODUCTION: Gastric ischemia is a rare condition associated with poor prognosis typically presenting with abdominal pain, GI bleed and altered mentation and may be caused due to states of shock. We present a rare case of gastric ischemia due to urosepsis. CASE DESCRIPTION/METHODS: A 70 year-old male with past medical history of peripheral vascular disease, chronic Foley catheter and dementia presented with altered mentation, hypotension, tachycardia and decreased urine output. The Foley catheter was replaced revealing purulent urine. Initial labs revealed acute kidney injury, lactic acidosis, and leukocytosis. CT abdomen pelvis without contrast revealed gastric pneumatosis with adjacent left upper quadrant portal venous gas and branching portal venous gas throughout the liver. Esophagogastroduodenoscopy was performed which showed proximal gastric ischemia and necrosis from the midbody to the fundus; biopsies revealed acute hemorrhagic gastritis, and gastroenterology recommended resection. General surgery was consulted who recommended conservative management. Patient improved clinically while receiving antibiotic therapy, intermittent nasogastric tube suction, intravenous proton pump inhibitor therapy and parenteral nutrition. Repeat imaging showed resolution of portal gas and gastric pneumatosis and repeat EGD showed resolution of gastric ischemia. DISCUSSION: Gastric ischemia is a serious condition which is under-recognized clinically. Etiologies include systemic hypotension, vasculitis or disseminated thromboembolism. Gastric pneumatosis or portal venous gas on imaging suggest ischemia; EGD with biopsy is the diagnostic gold standard. Gastric ischemia is either managed surgically or medically with fluid resuscitation, nasogastric tube placement to prevent gastric distension and acid reduction along with antibiotics for patients with gastric pneumatosis.

Diagnosis and management of acute esophageal necrosis.

Acute esophageal necrosis is a rare syndrome classically characterized by a striking endoscopic image of diffuse and circumferential black mucosal discoloration of distal esophagus, with an abrupt transition at the gastroesophageal junction and variable proximal extension. The typical patient is an older male with general debilitation and multiple comorbidities presenting with hematemesis or melena. The pathophysiology usually involves a combination of esophageal ischemia, backflow injury from gastric chemical contents and impaired mucosal reparative mechanisms associated with debilitated physical states. It may arise in the setting of hemodynamic compromise, diabetic ketoacidosis, hypothermia, alcoholic intoxication, trauma, inflammatory diseases, esophageal local infection, solid organ transplantation, postoperative status, drugs or acute gastric outlet obstruction, usually in the background of a chronic debilitating process, where the concurrent presence of multiple risk factors, including diabetes mellitus, hypertension, malnutrition, malignancy or alcohol abuse, places a patient at higher risk. The characteristic endoscopic appearance establishes the diagnosis. Biopsy is supportive but not required. Management is mainly supportive and consists of correcting coexisting conditions, fluid therapy, bowel rest, intravenous proton pump inhibitor therapy and red blood cell transfusion as needed. Although this is a serious life-threatening condition, appropriate treatment may result in a favorable outcome in the majority of patients.

A Case of Acute Esophageal Necrosis in a Patient With Multiple Sclerosis

Introduction: Acute esophageal necrosis (AEN) is a rare syndrome with incidence of .01 to .28% on endoscopic series and mortality of 32%. Known as “Black Esophagus,” it's characterized endoscopically by circumferential black mucosa ending abruptly at the gastroesophageal junction. It has been postulated that precipitating events include hypoperfused states and gastric outlet obstruction with concurrent esophageal reflux. Case: A 77-year-old Caucasian female with remote history of peptic ulcer disease and progressive multiple sclerosis (MS) presented with diffuse abdominal pain, nausea, and vomiting. Urinalysis was suggestive of a urinary tract infection (UTI) and she was discharged on five-days of cephalexin. She delayed taking cephalexin and returned four days later with fatigue, worsening dysphagia, and melena. She was hypotensive and labs revealed leukocytosis, acute blood loss anemia, and acute kidney injury. Urine culture grew extended-spectrum beta lactamase producing multi-drug resistant proteus mirabilis. She was admitted for septic and hypovolemic shock secondary to multi-drug resistant UTI and suspected upper gastrointestinal bleeding. Ertapenem was started in light of the resistance and sensitivity pattern of the causative organism. Upper endoscopy revealed diffuse mucosal changes characterized by black discoloration throughout the esophagus and obstructive duodenal ulcer with adherent clot (Figure 1). Endoscopic findings and presentation was consistent with AEN. She improved with vasopressor support, fluid resuscitation, and 14-days of ertapenem. Discussion: AEN is a multifactorial syndrome with notable morbidity. Risk factors include alcohol abuse, hypertension, male gender, diabetes, dyslipidemia, malnourishment, and chronic kidney disease. The most common presentation is upper GI hemorrhage but dysphagia, chest and epigastric pain can also occur. Diagnosis is made endoscopically and histologic confirmation of tissue necrosis is recommended but not required. Treatment involves management of inciting insult(s), acid suppression with intravenous proton pump inhibitor therapy and “nil per os.” A video swallow study revealed mild oral and moderate pharyngeal dysphagia that was attributed to MS. Dysphagia and regurgitation of stomach contents from gastric outlet obstruction predisposed patient to hypovolemia. Septic shock and an obstructive duodenal ulcer with blood loss anemia culminated to promote the development of AEN.1793 Figure 1. Black discoloration of mucosa in the upper third of the esophagus (A), and the middle third of the esophagus (B), normal mucosa at the gastroesophageal junction as seen in retroflexion (C), and duodenal bulb ulcer (D).

Outcomes of peptic ulcer bleeding following treatment with proton pump inhibitors in routine clinical practice: 935 patients with high- or low-risk stigmata

Objective. To assess rates of further bleeding, surgery and mortality in patients hospitalized owing to peptic ulcer bleeding. Materials and methods. Consecutive patients hospitalized for peptic ulcer bleeding and treated with a proton pump inhibitor (PPI) (esomeprazole or pantoprazole) were identified retrospectively in 12 centers in Spain. Patients were included if they had high-risk stigmata (Forrest class Ia–IIb, underwent therapeutic endoscopy and received intravenous PPI ≥120 mg/day for ≥24 h) or low-risk stigmata (Forrest class IIc–III, underwent no therapeutic endoscopy and received intravenous or oral PPI [any dose]). Results. Of 935 identified patients, 58.3% had high-risk stigmata and 41.7% had low-risk stigmata. After endoscopy, 88.3% of high-risk patients and 22.1% of low-risk patients received intravenous PPI therapy at doses of at least 160 mg/day. Further bleeding within 72 h occurred in 9.4% and 2.1% of high- and low-risk patients, respectively (p < 0.001). Surgery to stop bleeding was required within 30 days in 3.5% and 0.8% of high- and low-risk patients, respectively (p = 0.007). Mortality at 30 days was similar in both groups (3.3% in high-risk and 2.3% in low-risk patients). Conclusion. Among patients hospitalized owing to peptic ulcer bleeding and treated with PPIs, patients with high-risk stigmata have a higher risk of further bleeding and surgery, but not of death, than those with low-risk stigmata.

End-stage liver disease complications

Chronic liver disease causes significant morbidity and mortality because of any number of complications including hepatic encephalopathy, ascites, hepatorenal syndrome (HRS), and esophageal variceal hemorrhage (EVH). Predictors of response to lactulose, probiotics, and L-ornithine-L-aspartate therapy in minimal hepatic encephalopathy (MHE) have been reported. Although rifaximin was slightly more effective than lactulose in the maintenance of remission and decreased re-admission in patients with MHE, it was not as cost-effective as lactulose. Beta-blockade has been associated with paracentesis-induced circulatory dysfunction. Those who respond to nonselective beta-blockers have a predictable overall lower probability of developing ascites and HRS. Noradrenaline was as effective as terlipressin for the treatment of type 1 HRS and was less costly. Hemorrhagic ascites, defined as an ascitic fluid red blood cell (RBC) count of at least 10 000/μl, appeared to be a marker for poor outcome in patients with cirrhosis. In patients with acute EVH, band ligation, pharmacologic vasoconstrictors, and antibiotics are effective; notably, intravenous proton pump inhibitor therapy in lieu of vasoconstrictors achieved similar hemostatic effects with fewer side-effects. Refinement in the clinical management strategies for patients with cirrhosis and its complications appear to continue to contribute to improved patient outcomes.

Gastrointestinal Bleeding and Possible Hypothyroidism

An 88-year-old female, living independently in the community, developed duodenal and gastric ulcers from using overthe-counter naproxen sodium for pain related to a shoulder fracture and arthritis of the knees. She was hospitalized and received packed red blood cells and intravenous proton pump inhibitor therapy. During her hospitalization, she developed atrial fibrillation (AF). Warfarin was not prescribed for stroke prevention because of the gastrointestinal (GI) bleeding. The patient was initially placed on atenolol, and then amiodarone was added. After a two-week hospital stay she was discharged to a nursing facility to gain strength, further correct her anemia, and receive physical therapy for the shoulder and ambulation problems from arthritis of the knees. The amiodarone was continued in the nursing facility. After 15 days of amiodarone therapy (hospital and nursing facility), a laboratory report indicated an elevated thyroid-stimulating hormone level. Levothyroxine was prescribed. The patient was eventually discharged to an assisted living facility once her strength returned and her ambulation improved. GI bleeding with anemia and weakness from nonsteroidal anti-inflammatory drug use and changes in thyroid function with amiodarone therapy for AF will be discussed.

T1955 Retrospective Comparison of Oral vs. Intravenous Proton-Pump Inhibitor Therapy in Patients with Acute Peptic Ulcer Bleeding and High-Risk Endoscopic Stigmata

T1955 Retrospective Comparison of Oral vs. Intravenous Proton-Pump Inhibitor Therapy in Patients with Acute Peptic Ulcer Bleeding and High-Risk Endoscopic Stigmata

Should All Patients With Acute Gastrointestinal Hemorrhage Receive Intravenous Proton Pump Inhibitor Therapy Before Endoscopy?

Should All Patients With Acute Gastrointestinal Hemorrhage Receive Intravenous Proton Pump Inhibitor Therapy Before Endoscopy?

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Pre‐endoscopic PPI therapy reduces recurrent adverse outcomes in acute non‐variceal upper gastrointestinal bleeding: authors' reply

Sirs, Thank you for the insightful comments regarding our manuscript. We would like to address some of the concerns raised by Dr Lin. First, he comments that there is a much higher incidence of high-risk stigmata in the group who received pre-endoscopic proton pump inhibitor (PPI) therapy. We think he may have misinterpreted the table, as the numbers given are not absolute numbers, but instead are proportions (i.e. not 44/132 but 44% out of a total number of 132). Also, as patients may have had multiple lesions and multiple stigmata (i.e. both a non-bleeding visible vessel and oozing from another site) the proportions are not purely additive. In our study, there was a trend towards a decrease in the risk of having high-risk stigmata with pre-endoscopic PPI therapy (47% vs. 57%, P = 0.085), with high-risk stigmata defined as active arterial bleeding, non-bleeding visible vessel, adherent clot or oozing. This finding suggests that pre-endoscopic PPI therapy may assist in stabilizing clots and improving ulcer healing, leading to increased down-grading of high-risk stigmata. Dr Lin also notes that the majority of our patients received oral and not intravenous PPI therapy prior to endoscopy, and expresses concern that oral administration of PPIs may not have sufficiently elevated intragastric pH to a level necessary to promote clot stabilization and prevent rebleeding. We agree that oral PPIs may not always raise the intragastric pH over six, a level thought to be optimal for clot stabilization, but other studies have suggested that there is a little difference between oral and intravenous PPI administration of their immediate effects on intragastric pH. 1, 2 Furthermore, lesser elevations of intragastric pH may also allow some degree of clot stabilization, thus preventing rebleeding. Moreover, oral PPIs have proven efficacy in the prevention of rebleeding in high-risk patients, and meta-analyses have demonstrated that both oral and intravenous PPIs promote an equivalent reduction in rebleeding rates. 3, 4 We also agree with Dr Lin that endoscopic care among our subjects was not standardized, and that endoscopic therapeutic modalities differ in their efficacy. While this is true, the proportion of subjects undergoing any one type of endoscopic haemostasis was not significantly different between treatment groups, and thus is unlikely to have significantly biased our results. Overall, we concur that a randomized controlled trial is necessary to fully evaluate the role of pre-endoscopic PPI therapy in this setting. In the interim, it remains reasonable to offer this low-risk therapy to any patient presenting with signs and symptoms of acute upper gastrointestinal bleeding, especially in situations where endoscopic management is not immediately available.

Selection of Proton Pump Inhibitors for Formulary Inclusion

To accurately assess any therapeutic class or specific agent for inclusion in the hospital formulary, a consistent evidence-based review process should be followed. Utilization of any therapeutic class, including the proton pump inhibitors, is more efficient if a single agent is used throughout the healthcare system. The lack of evidence supporting intravenous proton pump inhibitor therapy in stress-related mucosal damage and no comparative data in non-variceal upper gastrointestinal bleeding allows interchange of all agents more readily. Although many factors need consideration, the ideal proton pump inhibitor should be available orally and intravenously, and be prepared easily for administration to patients unable to swallow capsules or tablets. Using these criteria, the hospital system may be able to leverage the best possible cost for selection of a proton pump inhibitor for their formulary.

Review article: the role of antisecretory therapy in the management of non‐variceal upper gastrointestinal bleeding

Non-variceal, upper gastrointestinal bleeding accounts for 300,000 hospitalizations annually in the US and the risk of rebleeding and mortality remain high. The aim of this study was to review the incidence and causes of non-variceal upper gastrointestinal haemorrhage, criteria for early discharge, risk stratification and intravenous vs. oral proton-pump inhibitor use. Peptic ulcer disease accounts for 45% of all admissions for upper gastrointestinal bleeding. Clinical and endoscopic predictors of adverse outcome have been identified. The Rockall scoring system identifies patients who can be considered for early discharge after endoscopy. Evidence supports the use of intravenous proton-pump inhibitor therapy for patients with bleeding ulcers associated with high-risk stigmata. Patients who are clinically stable and in whom upper endoscopy has shown an ulcer with a clean base or a flat pigmented spot have a low risk for rebleeding and may be discharged early on oral proton-pump inhibitor therapy. Proton-pump inhibitor treatment reduces ulcer rebleeding but does not affect overall mortality. In the US, most patients with ulcer bleeding have low-risk stigmata, and thus, can be treated with oral proton-pump inhibitors and discharged early.

Intragastric Acid Control with Oral Esomeprazole or Pantoprazole after Intravenous Pantoprazole Administration in Healthy Adults

Purpose: After a prescribed course of intravenous proton pump inhibitor therapy, patients may require continued oral antisecretory therapy. The objective of this study was to compare intragastric acid control with oral esomeprazole 40 mg once daily with that of oral pantoprazole 40 mg once daily after 5 days of intravenous pantoprazole 40 mg once daily. Methods: In this randomized, open-label, comparative, 2-way crossover study (D9612L00066), healthy adults were randomized to 1 of 2 dosing sequences. Each 10-day dosing period included 5 days of daily injections over 2 minutes of intravenous pantoprazole followed by 5 days of once-daily oral doses of esomeprazole 40 mg or pantoprazole 40 mg. There was a 10–21-day washout period between dosing periods. All doses were administered, under observation at the investigator's site, 30 minutes before breakfast. Non–high-fat, non–high-calorie meals were provided to study subjects. On days 1 and 5 of oral dosing (before receiving the daily dose), a calibrated electrode was positioned 10 cm below the lower esophageal sphincter for 24-hour pH monitoring. The pH technicians and readers were blinded to subject treatment sequence. Only data from patients who had evaluable tracings from both day-5 tests were included. Results: All 38 subjects with evaluable data were H. pylori-negative and white, 63% were men, and the mean age was 25 years (range, 19 to 57 years). The mean number of evaluable hours of pH data for both treatment groups on both days was 24. Oral esomeprazole was significantly more effective for gastric acid suppression than oral pantoprazole on days 1 and 5 (steady state) of oral dosing (see table) immediately after a course of intravenous pantoprazole. The 16% difference between treatment means on day 5 is equivalent to 3.9 hours of pH > 4 during a 24-hour period.Table: Least-Squares Mean (SEM)% Time of 24 Hours Intragastric pH was >4 on Days 1 and 5 of Oral DosingConclusions: Switching from intravenous pantoprazole to oral esomeprazole 40 mg once daily more effectively suppressed intragastric acid than switching from intravenous pantoprazole to oral pantoprazole 40 mg once daily. Supported by AstraZeneca LP.

Proton pump inhibitors in acute peptic ulcer bleeding

Proton pump inhibitors in acute peptic ulcer bleeding

Proton pump inhibitors in acute peptic ulcer bleeding

Proton pump inhibitors in acute peptic ulcer bleeding