Editorial: deja vu all over again – let the P‐CAB wars begin. Authors' reply
Abstract
We appreciate Dr. Metz's insightful comments on the development and clinical use of various potassiumcompetitive acid blockers (PCABs). While PCABs are considered as potential substitutes for proton pump inhibitors (PPIs), there are concerns regarding the risk of hypergastrinaemia in patients on longterm PCABs. Vonoprazan, the first PCAB to be approved in Japan, causes marked increase in serum gastrin compared with PPIs including esomeprazole and lansoprazole. Vonoprazan 20 mg oncedaily increased gastrin level to over 500 pg/mL after 1 week and to about 300 pg/mL after 8 weeks, which were over 2fold and about 1.5fold greater than with esomeprazole and lansoprazole, respectively (Table 1).1,2 One possible explanation for this phenomenon could be binding selectivity to gastric H+/K+ ATPase. The discharge of vonoprazan into the lumen is inhibited by both its deep binding site on the proton pump and an electrostatic barrier that is formed at the pump's inlet.3 This may result in slow dissociation and prolonged inhibition of gastric acid secretion, which contribute to the elevated gastrin level.4 In contrast, other PCABs such as tegoprazan and fexuprazan have shown comparable increases in serum gastrin levels to esomeprazole, despite their more potent inhibition of gastric acid secretion.5– 8
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