Therapies gastric-acid suppression

Evenepoel P, Claus D, Geypens B, Maes B, Hiele M, Rutgeerts P, et al Evidence for impaired assimilation and increased colonic fermentation of protein, related to gastric acid suppression therapy. Aliment Pharmacol Ther 1998 12 1011-1019. 

B. Termanini, F. Gibril, V. Sutliff, et al. Effect of long-term gastric acid suppressive therapy on serum vitamin B12 levels in patients with Zollinger-Ellison syndrome. American Journal of Medicine 104,422 (1998). 

Gastric outlet obstruction occurs in approximately 2% of patients with PUD and is usually caused by ulcer-related inflammation or scar formation near the peripyloric region. Signs and symptoms of outlet obstruction include early satiety after meals, nausea, vomiting, abdominal pain, and weight loss. Ulcer healing with conventional acid-suppressive therapy is the primary treatment, but if this is unsuccessful then an endoscopic procedure (e.g., balloon dilation) is required. 

Promotility agents may be useful as adjuncts to acid suppression therapy in patients with a known motility defect (e.g., LES incompetence, decreased esophageal clearance, delayed gastric emptying). However, these agents are generally not as effective as acid suppression therapy and have undesirable side effects. 

The risk of infection rises with conditions that increase gastric pH and subsequent bacterial overgrowth, such as obstruction, hemorrhage, malignancy, or acid-suppression therapy (clean-contaminated). 

Peptic ulcer Adjunctive therapy for peptic ulcer. These agents suppress gastric acid secretion. 

Pancrelipase is available in both non-enteric-coated and enteric-coated preparations. Pancrelipase enzymes are rapidly and permanently inactivated by gastric acids. Therefore, non-enteric-coated preparations (eg, Viokase tablets or powder) should be given concomitantly with acid suppression therapy (proton pump inhibitor or H2 antagonist) to reduce acid-mediated destruction within the stomach. Encapsulated formulations contain acid-resistant microspheres (Creon) or microtablets (Pancrease, Ultrase). Enteric-coated formulations are more commonly used because they do not require concomitant acid suppression therapy. 

The PPIs (omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole) dose-dependently inhibit basal and stimulated gastric acid secretion. When PPI therapy is initiated, the degree of acid suppression increases over the first 3 to 4 days of therapy, as more and more proton pumps are inhibited. Upon discontinuation of therapy, full restoration of acid secretion takes 3 to 5 days. Because PPIs inhibit only those proton pumps that are actively secreting acid, they are most effective when taken 15 to 30 minutes before meals. ... 

Intravenous pantoprazole or lansoprazole clearly is the preferred therapy in patients with acute bleeding ulcers. The theoretical benefit of maximal acid suppression in this setting is to accelerate healing of the underlying ulcer. In addition, a higher gastric pH enhances clot formation and retards clot dissolution. 

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