The differences between the pharmacokinetics and pharmacodynamics of PPI and Vonoprazan are shown in Table 2 [44,46]

The differences between the pharmacokinetics and pharmacodynamics of PPI and Vonoprazan are shown in Table 2 [44,46]. Table 2 Pharmacological comparisons between PPI and Vonoprazan. = 0.001) [54]. 2.2. a significant global health problem whose prevalence is about 44.3%, from 34.7% in developed countries to 50.8% in developing countries, with a global recurrence rate of 4.3C4.6% [1,2,3]. An epidemiologic meta-analysis study revealed that contamination is most prevalent in Africa (79.1%), followed by Latin America (63.4%) and Asia (54.7%) [4]. In Valproic acid sodium salt Indonesia, contamination prevalence is about 22.1%, suggesting infects approximately one out of five of the population [5]. contamination is usually significantly correlated with incidences of gastritis, gastroesophageal reflux disease, gastroduodenal ulcers, gastric mucosal-associated lymphoid tissue (MALT) lymphoma, and gastric malignancies [6,7,8,9]. The eradication of is vital in reducing peptic ulcer recurrence, in the principal therapy of gastric MALT lymphoma, and in minimizing the risk of gastric malignancy [10,11,12]. removal therapy generally uses proton pump inhibitor (PPI)-based combination Valproic acid sodium salt therapy for 7C14 days by combining a PPI and a minimum of two antibiotics, sometimes with the addition of bismuth. PPI takes a crucial role in eradication by suppressing gastric acid secretion, hence enhancing antibiotics efficacies [13]. However, the success rate of PPI-based eradication therapy declines with antibiotics resistance emergence and inadequate acid suppression [13,14]. Increasing PPI dosage does not increase the eradication rate of PPI-based regimens [15,16,17]. Vonoprazan and tegoprazan are new potential gastric acid suppression brokers, classified as Alcam potassium-competitive acid blockers (P-CAB), that function by H+/K+-ATPase inhibition [18,19] (Physique 1). Japanese guidelines on the management of infections recommend replacing PPI with vonoprazan in first-line and second-line eradication therapies since first launched in 2015, while tegoprazan has been established as treatment for gastroesophageal reflux disease (GERD) in South Korea since 2018 [20,21]. Tegoprazan showed clinical benefits in phase-III studies for erosive esophagitis patients [22] and Valproic acid sodium salt improved both gastric-related diseases and motility defects in a canine study [23]. However, studies of tegoprazan for eradication are still in progress. Several non-randomized control trials (RCT), RCT, and meta-analyses reported encouraging results using vonoprazan-based therapies in eradicating eradication regimens. Open in a separate window Physique 1 The mode of action of proton pump inhibitors (PPIs) and Vonoprazan against contamination. PPI enters parietal cell canaliculus in inactive form and requires acid activation. Protonated pro-drugs will convert to sulphenamide and bond covalently with cysteine groups of H+/K+-ATPase that cause inactivation of H+/K+-ATPase. Unlike PPI, potassium-competitive acid blocker (P-CAB) enters parietal cell canaliculus in active form, has stability in an acidic environment, and does not require acid activation. Protonated P-CAB will make non-covalent bonds with H+/K+-ATPase, thus inactivating the H+/K+-ATPase with a slower dissociation rate and for longer time. * Lacks of PPIs in gastric acid inhibition; ** Benefits of vonoprazan in gastric acid inhibition. We collected all relevant studies after searching comprehensively using predefined keywords through the online databases of PubMed, Web of Science, EMBASE, and The Cochrane Library. We searched all relevant articles for vonoprazan-based eradication regimens (keywords: vonoprazan OR VPZ OR TAK-438 OR Potassium-Competitive Acid Inhibitor AND eradication therapies in human populations using both regimens until April 2020. We extracted data about vonoprazan-based and PPI-based regimens with their dosages and eradication rates. Our exclusion criteria are animal and Non-English studies. Unsatisfactory acid-suppressing therapy outcomes prior to PPI discovery and development expedited research in obtaining new therapeutic agents. Initial studies revealed PPI has a higher efficacy than histamine-2 receptor antagonist-based therapies [24]. Table 1 reviews eradication regimens approved by several gastroenterological societies. Table 1 eradication therapy regimens based on several guidelines. Indonesian Society of Gastroenterology [26]Research [20]with a failure rate of 60C70% [28,29]. Normally, metronidazole-resistant is the main cause of second-line eradication therapy, especially in Southeast Asia [30]. Resistance to levofloxacin has emerged in some countries at a resistance rate of 20C40% [31,32,33]. As established previously, increasing PPI doses does not improve the eradication rate significantly. Consequently, vonoprazan was launched as.

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