In patients with dyspeptic symptoms that persist despite successful eradication, or in naïve patients not infected with EPS, PPI treatment may be tried, achieving a 34% success rate (NNT = 10, 95% confidence interval, 7-33) [216]. PPIs are particularly effective when overlapping reflux symptoms are present, while dyspeptic patients with PDS have no significant benefit [217]. It should be noted that the effect of PPI in FD occurs at standard doses and, since meta-analyses did not reveal a dose-response effect [216, 217], dose escalation in non-responders at standard doses should not be considered. If paroxysmal symptoms occur, antacids or formulations containing alginate may be used .[216] Unlike GERD, long-term PPI treatment is not indicated for FD [217]. After successful treatment, a phase-down strategy is preferable to abrupt discontinuation [217]. Although symptoms may recur in nearly 70% of patients within a 1-year follow-up [82], resuming treatment only in these patients is more beneficial than continuous and expensive treatment, which is prescribed in all cases. a) Comparison of logarithmically processed gastrin levels between women and men on long-term PPI treatment. b) Correlation between exposure to PPIs (mg/kg) and logarithmically processed gastrin levels. c) Correlation between exposure to PPIs (mg/m2) and logarithmically processed gastrin levels. Although endoscopic treatment can lead to hemostasis in most patients, recurrent bleeding is not uncommon [290, 291].
Several meta-analyses [292-294] have shown that adjuvant therapy with a PPI after endoscopic haemostatic treatment reduces the risk of haemorrhagic recurrence and the need for surgery after ulcer bleeding, but has no benefit on all-cause mortality, an effect observed only in Asian studies and in patients with active haemorrhage or a visible non-haemorrhagic vessel. In addition, PPI treatment results in a small but potentially significant reduction in the need for transfusions and length of hospital stay [295, 296]. Although current guidelines [297-299] recommend a regimen of an intravenous bolus (i.v.) followed by continuous infusion of PPIs, a recent meta-analysis [300] found that the effectiveness of continuous and intermittent PPI treatments was comparable. Whether low-dose or oral PPIs can replace high-dose PPIs after endoscopic hemostasis is controversial. In a recent meta-analysis of Taiwan [301], researchers concluded that low- and high-dose therapies were equivalent. However, they included studies with a small number of patients and ulcer patients with low-risk stigmas or even clean ulcers. Similarly, some studies [302, 303] have reported that the effectiveness of oral PPIs is comparable to that of intravenous PPIs, but the results have been combined from open-label studies with a limited sample size. In addition, different oral therapies were combined with each other and compared to different intravenous therapies. It should also be noted that most of the studies included in this setting were conducted in Asian patients [304].
The beneficial effects of antisecretory drugs on the elimination of steatorrhea are mainly caused by the reduction of acidity and volume of secretion. The final results of these actions are the increase of pH in the stomach and duodenum and facilitate the administration and concentration of lipase in the duodenum. However, another important effect is the reduction of duodenal volume flow, which in turn increases the concentration of intraduodenal lipolytic activity [382]. Enteric coated formulations protect pancreatic enzymes from the low pH in the stomach, allowing enzymes to maintain their effectiveness when they reach the duodenum. Enteric-coated enzymes are actually released into the duodenum, where the pH exceeds 5.5 units. Although these formulations are resistant to degradation by stomach acid, some studies have shown improvements in fat absorption when administered with concomitant acid suppression therapy [380]. ZES is a rare disease characterized by the presence of a gastrin-producing tumor (gastrinoma) resulting in persistent hypersecretion of stomach acid and resulting PU disease (often with complications such as perforation, bleeding, etc.), diarrhea or malabsorption. Gastrinomas usually develop in non-islet beta cells of the pancreas or in the duodenal wall (40-90%). Up to two-thirds are clever.
About 20-25% of cases are observed in patients with MEN-1 syndrome [172, 173]. Even more rarely, however, zestic symptoms may come from a cholecystokinin-producing tumor [174], since cholecystokinin (CCK) and gastrin are complete agonists of the gastrin receptor CCK2 in the parietal cell, the stimulation of which results in the secretion of stomach acid. The main drafting group then considered all the proposals made at the Bologna meeting and prepared the final draft. An updated literature search was conducted and the latest findings were recorded. This revised document was then sent to Italian and international experts for consideration (see Acknowledgements section). The amendments resulting from the comments of the external experts were made on the basis of scientific and editorial value in order to prepare the final version of the position paper. Although omeprazole is unable to inhibit the release of amylase from isolated pancreatic acini [366], pantoprazole appears to be able to reduce tissue infiltration of inflammatory cells and necrosis of acin cells in rats with experimentally induced pancreatitis [367], an effect likely caused by reduced expression of inflammatory and adhesion proteins, key mediators in the pathogenesis of PA, is mediated. The only clinical study to date [368] found that treatment with pantoprazole did not affect the clinical course of BP, such as length of hospitalization, time to onset of oral ingestion, or pain relief. In addition, two retrospective studies found that the use of PPIs does not affect the clinical outcomes of patients with severe PA [369] and does not prevent postndoscopic retrograde cholangiopancreatography of pancreatitis [370]. Therefore, most international guidelines for API management don`t even mention PPIs.
The only exception is the Italian Directive [371], which makes it clear that the routine use of PPIs is not recommended in patients with acute PA. This guideline and an earlier Japanese version [372] suggest that these drugs could be considered on a case-by-case basis if specific indications such as the use of NSAIDs, PU disease or bleeding occur. that affect the level of investment in PPPs and PPPs over time. For more information on the FDA`s role in regulating certain PSAs, see: Performance, especially in long-term infrastructure contracts, takes into account factors Proton pump inhibitors are prescribed to treat acid-related gastrointestinal diseases, including gastric and duodenal ulcers, reflux esophagitis and Zollinger-Ellison syndrome. The acid-reducing beneficial properties of PPIs are due to the formation of active metabolites of sulfenamide. PPIs have also been shown to be effective in combination with antibiotics to eradicate Helicobacter pylori. Administered orally as slow-release enteric-coated tablets, PPIs are usually taken before meals, with the dose and duration of treatment depending on the PPI prescribed. Not recommended for children. For more information, see Basic preparations including esomeprazole, magnesium, lansoprazole, omeprazole, pantoprazole (sodium sesquihydrate) and rabeprazole sodium (sodium salt).
PPIs are administered as inactive prodrugs that selectively accumulate in the acidic environment of the secretory canal of the gastric parietal cell. The PPI is quickly protonated and converted into the active form of the drug. Since PPIs covalently bind to active proton pumps, the synthesis of new pumps or the activation of resting pumps is necessary to restore activity.